Hazardous Chemicals: Agents of Risk and Change, 1800-2000 9781789203202

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HAZARDOUS CHEMICALS

The Environment in History: International Perspectives Series Editors: Dolly Jørgensen, University of Stavanger; Christof Mauch, LMU Munich; Kieko Matteson, University of Hawai’i at Mānoa; Helmuth Trischler, Deutsches Museum, Munich

Recent volumes: Volume 17 Hazardous Chemicals: Agents of Risk and Change, 1800–2000 Edited by Ernst Homburg and Elisabeth Vaupel Volume 16 Planning for the Planet: Environmental Expertise and the International Union for Conservation of Nature and Natural Resources, 1960–1980 Simone Schleper

Volume 12 Managing Northern Europe’s Forests: Histories from the Age of Improvement to the Age of Ecology Edited by K. Jan Oosthoek and Richard Hölzl Volume 11 International Organizations and Environmental Protection: Conservation and Globalization in the Twentieth Century Edited by Wolfram Kaiser and Jan-Henrik Meyer

Volume 15 Changes in the Air: Hurricanes in New Orleans from 1718 to the Present Eleonora Rohland

Volume 10 In the Name of the Great Work: Stalin’s Plan for the Transformation of Nature and its Impact in Eastern Europe Edited by Doubravka Olšáková

Volume 14 Ice and Snow in the Cold War: Histories of Extreme Climatic Environments Edited by Julia Herzberg, Christian Kehrt, and Franziska Torma

Volume 9 The Nature of German Imperialism: Conservation and the Politics of Wildlife in Colonial East Africa Bernhard Gissibl

Volume 13 A Living Past: Environmental Histories of Modern Latin America Edited by John Soluri, Claudia Leal, and José Augusto Pádua

Volume 8 Disrupted Landscapes: State, Peasants and the Politics of Land in Postsocialist Romania Stefan Dorondel

For a full volume listing, please see the series page on our website: http://berghahnbooks.com/series/environment-in-history.

Hazardous Chemicals Agents of Risk and Change, 1800–2000

/ Edited by

Ernst Homburg and Elisabeth Vaupel

berghahn NEW YORK • OXFORD www.berghahnbooks.com

First published in 2019 by Berghahn Books www.berghahnbooks.com © 2019, 2022 Ernst Homburg and Elisabeth Vaupel First paperback edition published in 2022 All rights reserved. Except for the quotation of short passages for the purposes of criticism and review, no part of this book may be reproduced in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system now known or to be invented, without written permission of the publisher. Library of Congress Cataloging-in-Publication Data Names: Homburg, Ernst, 1952- editor. | Vaupel, Elisabeth, 1956- editor. Title: Hazardous chemicals : agents of risk and change, 1800-2000 / edited by Ernst Homburg and Elisabeth Vaupel. Description: New York : Berghahn Books, 2019. | Series: Environment in history: international perspectives ; volume 17 | Includes bibliographical references and index. Identifiers: LCCN 2019013898 (print) | LCCN 2019017289 (ebook) | ISBN 9781789203202 (ebook) | ISBN 9781789203196 (hardback : alk. paper) Subjects: LCSH: Hazardous substances--History. | Hazardous substances--Environmental aspects--History. | Poisons--History. Classification: LCC T55.3.H3 (ebook) | LCC T55.3.H3 H3764 2019 (print) | DDC 363.1709--dc23 LC record available at hfps://lccn.loc.gov/2019013898 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library ISBN 978-1-78920-319-6 hardback ISBN 978-1-80073-434-0 paperback ISBN 978-1-78920-320-2 ebook

Dedicated to the memory of Joost Mertens (1943–2015) and Masanori Kaji (1956–2016)

/ Contents List of Figures and Tables

ix

Acknowledgments xi List of Abbreviations

xii

Introduction. A Conceptual and Regulatory Overview, 1800–2000 1 Ernst Homburg and Elisabeth Vaupel Part I. From Acute to Chronic Poisoning: Regulating Old Poisons in the Industrial Age   1.  Schweinfurt Green and the Sanitary Police: The Fight against Copper Arsenite Pigments Joost Mertens†

63

  2. The Banning of White Lead: French and International Regulations 87 Laurence Lestel   3. Old Situations, New Complications: Lead and Lead Poisoning in a Changing World Christian Warren

107

Part II. Discovering New Health Impacts: Carcinogenesis, Mutagenesis, and More in Times of Uncertainty and Non-knowledge   4. Discovering Chemical Carcinogenesis: The Case of Aromatic Amines Heiko Stoff and Anthony S. Travis

137

  5. Cyclamates: A Tale of Uncertain Knowledge (1930s–1980s) 179 Alexander von Schwerin

viii Contents

  6. Cadmium Poisoning in Japan: Itai-itai Disease and Beyond 211 Masanori Kaji†   7. Dioxins: The “Total Poison” Stefan Böschen

235

Part III. New Products, New Effects: The Discovery of the Environment and the Long Shadow of the 1960s  8. Organophosphates Frederick Rowe Davis   9. A Tale of Two Nations: DDT in the United States and the United Kingdom Peter J. T. Morris

267

294

10. War and Peace: The Phenoxy Herbicides Amy M. Hay

328

11. Raising a Stink: The Short, Happy Life of MTBE John K. Smith

354

Conclusion Ernst Homburg and Elisabeth Vaupel

376

Index 393

/ Figures and Tables

Figures Fig. 0.1 Illustration of the five symbols for dangerous substances adopted by the Council of Europe in 1962. 33 Fig. 1.1 Dr. Gustav Kletschke’s scheme of the color trade (1854). 71 Fig. 1.2 “Information policy” as exemplified by the labeling of a can with Paris green of Sherwin-Williams, Canada. 79 Fig. 2.1 Cases of lead poisoning in the Seine department. 92 Fig. 2.2 Lead poisoning of white lead workers in two factories in the Seine department. 93 Fig. 2.3 Picture illustrating the poem L’empoisonné (The poisoned), written about white lead by Clovis Hugues, a socialist, who often defended workers. 96 Fig. 2.4 Consumption of white pigments based on lead and zinc in France. 98 Fig. 3.1 “Uncle Sam’s Experience with Paints.” 108 Fig. 3.2 “Lead Helps to Guard Your Health.” 110 Fig. 3.3 BP Ethyl advertisement. 118 Fig. 3.4 Parallel decreases in blood-lead levels and lead used in gasoline. 125 Fig. 4.1 Meister Lucius & Brüning (later Hoechst) advertisement (dated 1892). 140 Fig. 6.1 Map of the polluted area in the Jinzū River basin of the Toyama Plain. 212 Fig. 6.2 The Jinzū River basin and the location of the Kamioka mine. 213 Fig. 7.1 Diagram of stages in the evolution of the “network of experimentation.” 250 Fig. 9.1 Image of DDT-impregnated cardboard parrot to kill houseflies. 309

x  Figures and Tables

Table Table 2.1 Key points concerning white lead in France (from various sources).

89

/ Acknowledgments

A

s the editors of this book, we are grateful for the help we received from many people, without whom this publication would not have been possible. Above all, we would like to thank Helmuth Trischler for his continued support for us to work on this project. We also thank the numerous colleagues from Canada, France, Germany, Britain, India, Israel, Japan, the Netherlands, and the United States—active in fields as diverse as toxicology, environmental history, chemistry, sociology, history of science, and philosophy—with whom we could collaborate while working on this book. It was also a great pleasure to discuss elements of the introduction with colleagues at the Science History Institute in Philadelphia, as well as during presentations at the Deutsches Museum in Munich, and at a Science, Technology and Society research meeting at Maastricht University. In particular, we would like to mention the comments by Karin Zachmann, Jens Lachmund, and Peter Morris. Last but not least, we thank the two referees of this book for their stimulating, informative, and thought-provoking comments. We very much thank the authors of the eleven studies published in this book for their valuable insights, for all the hard work that went into their chapters, and for their patience. Together with our introduction, the book covers a large domain, and occasionally we thought our project was perhaps a bit too ambitious. We have no doubt, though, that our book can and will stimulate further research on the history and current practices of (environmental) regulation, on the production of knowledge about chemicals and risks, and on the roles of politics, industry, and social movements in issues of human health and ecology. It is with deep regret that we must announce the loss of two dear colleagues who passed away during the process of completing the book: Joost Mertens in June 2015, and Masanori Kaji in July 2016. We dedicate this book to their memory and to their loved ones. Maastricht and Munich, November 2018

/ Abbreviations 2,4-D 2,4,5-T AAAS ABCM ACPOTC

2,4-dichlorophenoxyacetic acid 2,4,5-trichlorophenoxyacetic acid American Association for the Advancement of Science Association of British Chemical Manufacturers Advisory Committee on Pesticides and Other Toxic Chemicals (UK) ADI acceptable daily intake Agfa Actiengesellschaft für Anilin Fabrication (Joint Stock Company for Aniline Manufacture) API American Petroleum Institute BASF Badische Anilin und Soda Fabrik (Baden Aniline and Soda Factory) BMG Bundesministerium für Gesundheit (German Federal Ministry of Health) BMWi Bundesministerium für Wirtschaft (German Federal Ministry of Economics) CATS Citizens Against Toxic Sprays CCNR Central Commission for Navigation of the Rhine CDC Centers for Disease Control and Prevention (US) CIBA Chemical Industry Basel CLP Classification, Labeling, and Packaging CMR Carcinogenic, Mutagenic, or Toxic to Reproduction CNRA Citizens Natural Resources Association of Wisconsin COPR Control of Pesticides Regulations (UK) CPC Council on Pharmacy and Chemistry (US) CRA Cumulative Risk Assessment DDD dichlorodiphenyldichloroethane DDT dichlorodiphenyltrichloroethane DFG Deutsche Forschungsgemeinschaft (German Research Foundation) DGCH Deutsche Gesellschaft für Chirurgie (German Society of Surgery)

Abbreviations  xiii

DSD EDF EEC EIS EMS EPA EPN ETBE EWC FAO FDA FDRL FFDCA FIFRA FQPA GHS GRAS HAC HETP HEW I-TEQ IARC ICI ICMESA ICR IDRA ILC ILO JECFA JMPPC LD50 MAC MCPA MHW MMT MP MTBE

Dangerous Substances Directive Environmental Defense Fund (US) European Economic Community Environmental Impact Statement Environmental Mutagen Society Environmental Protection Agency (US) ethyl-4-nitrophenyl phenylphosphonothionate ethyl tert-butyl ether East-West Center Food and Agriculture Organization (UN) Food and Drug Administration (US) Food and Drug Research Laboratory Federal Food, Drug, and Cosmetic Act (US) Federal Insecticide, Fungicide, and Rodenticide Act (US) Food Quality Protection Act (US) Globally Harmonized System of Classification and Labeling of Chemicals generally recognized as safe Herbicide Assessment Committee hexaethyl tetraphosphate Department of Health, Education, and Welfare (US) international toxic equivalent International Agency for Research on Cancer Imperial Chemical Industries (UK) Industrie Chimiche Meda Società Azionaria (Meda Chemical Industries Company) Institute of Cancer Research (UK) Itai-itai Disease Residents’ Association (Japan) International Labour Conference International Labour Organization (UN) Joint FAO/WHO Expert Committee on Food Additives Jinzū Mining Pollution Prevention Council (Japan) lethal dose 50 (median lethal dose) maximum allowable concentration 2-methyl-4-chlorophenoxyacetic acid Ministry of Health and Welfare (Japan) methylcyclopentadienyl manganese tricarbonyl member of Parliament methyl tert-butyl ether

xiv Abbreviations

NAS NCI NGO NIH NIOSH

National Academy of Sciences (US) National Cancer Institute (US) nongovernmental organization National Institutes of Health (US) National Institute for Occupational Safety and Health (US) NRC National Research Council (US) NTP National Toxicology Program (US) OMPA octamethyl pyrophosphoramide PCA Pollution Control Agreement PCB polychlorinated diphenyl PCN polychlorinated naphthalene PCP pentachlorophenol POW prisoner of war PR public relations PVC polyvinyl chloride REACH Registration, Evaluation and Authorisation of Chemicals (EU) RFG reformulated gasoline RMEA Rubber Manufacturing Employers’ Association SA Sturmabteilung (“Storm Detachment”) SS Schutzstaffel (“Protection Squadron”) TCDD tetrachlorodibenzodioxin (“Seveso dioxin”) TEL tetraethyl lead TEPP tetraethyl pyrophosphate TLV threshold limit value Tox Lab Toxicity Laboratory (University of Chicago) UNEP UN Environment Programme USAF US Air Force USAID US Agency for International Development USDA US Department of Agriculture USFS US Forest Service VA Veterans Administration (US) VCM vinyl chloride monomer WHO World Health Organization (UN)

/ Introduction A Conceptual and Regulatory Overview, 1800–2000 Ernst Homburg and Elisabeth Vaupel

On 20 April 1895, the Frankfurt physician and surgeon Ludwig Rehn

(1849–1930) reported at the annual Congress of the German Society of Surgery (Deutsche Gesellschaft für Chirurgie) in Berlin that he had diagnosed three cases of bladder tumors among a group of forty-five workers from the magenta department of one of the largest German aniline dyeworks, at Hoechst on the Main. In the following years, similar cases were found in other German aniline dyeworks, and, as a result, this form of bladder cancer was soon called “aniline cancer.” It was one of the earliest industrial carcinomas diagnosed with certainty. In the century after this discovery, many other industrial chemicals would be shown to be carcinogenic.1 Magenta had then been produced from aniline on an industrial scale for almost four decades. It was made in dozens of aniline dyeworks all over Europe and the United States. By 1895, some twenty thousand workers were employed in the German dyestuffs industry alone, along with several thousands in other countries.2 Why was this particular occupational disease discovered so late?​ Apart from the obvious possibility that entrepreneurs and physicians connected to these factories might not always have been very keen to publish about the health problems among their workers, there are at least four major reasons. First, we now know cancers such as anilineinduced bladder cancer have a latency period of ten to more than twenty years, so the material properties of substances and organisms matter: the workers diagnosed ill in 1895 had been working with aniline already around 1880. Second, the industry was relatively small in its first ten to fifteen years and only started to employ large numbers of workers after the mid-1870s, so for a long time, the number of affected workers

2  Ernst Homburg and Elisabeth Vaupel

was simply too small to discover cause-effect relationships. Third, getting occupational cancers is to some degree a matter of chance: some workers are more sensitive to chemicals than others. Finally, only in the course of the twentieth century were statistical-epidemiological data on mortality and morbidity collected systematically on a large scale.3 Because of these four factors, it would have been difficult to discover aniline cancer before the mid-1890s. In a nutshell, this example illustrates one of the topics discussed at a workshop that stood at the basis of the present book. Learning processes such as the discovery of new diseases depend not only on the occupational and disciplinary backgrounds of the actors involved but also on processes going on in the material world. In the example given, these material processes include the growing production of aniline dyes and the marked increase in the number of workers involved, but the biomolecular mechanisms that make the metabolites of aniline can also induce cancer in the human bladder.4 Aniline is just one example among many. Since the Industrial Revolution, numerous new chemicals have been produced industrially in exponentially growing quantities. Today, more than seventy thousand different chemicals are manufactured, thirty to fifty thousand on a significant scale.5 In most of these cases, the toxic and environmental properties of these substances were unknown when they were introduced to the market and in many cases still are. Often, toxic and other hazardous properties were discovered only after years of production and use. The amount of synthetic chemicals produced today is staggering. Annual production figures in millions of metric tons for some key basic chemicals illustrate this very well: sulfuric acid 230, ammonia 145, ethylene 135, chlorine 65, sodium carbonate 50, and benzene 45, to which almost one hundred million of metric tons of nonferrous metals could be added.6 All these tons find their way somewhere in society and the environment every year. For more than two hundred years, industrial societies have struggled to cope with many unknown hazards. In modern knowledge society, there is a permanent tension between innovation and risk. Several chapters of this book illustrate this phenomenon well. Socioeconomic forces and knowledge production give rise to a permanent stream of new products and to growing production units that, in their turn, have unforeseen and initially poorly understood impacts on social life, human health, and the environment. Societies, as well as individuals and groups, have responded to these risks by developing new knowledge on such diverse fields as toxicology, environmental sciences, and

Introduction  3

technology assessment; introducing a wide variety of regulatory actions, procedures, and systems; and changing cultural and political attitudes and practices in coping with risk and uncertainty.7 In recent decades, authors from a broad range of disciplines have written an increasing number of historical studies on toxic and other hazards of industrial societies.8 In this volume, we analyze that double-faced interaction between innovation and risk by following a limited number of substances over long periods of time and in different national settings. Over the past twenty years, several such “histories (or biographies) of substances” have been published, thereby illustrating the genre’s epistemological potential.9 In the following chapters, the historical analysis of several poisonous, or hazardous, chemicals has been combined to provide insights into the interplay between industry, substances, citizens, governments, the environment, and science over the past two centuries. The substances portrayed in depth are the arsenic-containing pigment Schweinfurt green in France and Germany from the late eighteenth century to 1890; lead compounds in France and the United States (1800–1980); aromatic amines in Germany, the United States, and the United Kingdom (1880–1980); dioxins in Germany, the United States, Vietnam, and Italy (1900–1990s); cadmium in Japan (1910–2010); cyclamates in the United States and Germany (1930s–1980s); organophosphates in the United States (1930s–2000); phenoxy herbicides in the United States and Vietnam (1940s–2000); DDT in the United States and the United Kingdom (1945–2000); and MTBE in the United States (1980s–2000s). Although there is a predominance of histories on the health and environmental debates in the United States, interesting comparisons with developments in Germany, France, the United Kingdom, and Japan will help construct the larger picture, which is also the aim of this introduction.10 The “biographical approach” of chemical substances looks at the entire “life cycle” of a compound: at its production and uses; at the problems it caused in different realms; at issues of risk assessment, legal control, management strategies, disposal; and, finally, at the development of alternatives. It follows the substance through domains that are usually studied in isolation in the scholarly literature, such as occupational health and safety, food safety, environmental pollution, transport and storage of hazardous substances, agricultural production, and military technologies. This volume aims to shed more light on the interaction between those—legally and institutionally—separated

4  Ernst Homburg and Elisabeth Vaupel

domains and to trace how borders and interactions between them shifted over time and across national borders. Among those domains, the ones concerned with health issues often figure most prominently in public debates and were among the first to be regulated. We will therefore start with a section on the history of the poison concept. Next, we will discuss how poisons were regulated in the course of history in different social domains. Then, we will address the regulation of hazardous substances and articles in general, excluding the poisons proper, before ending with a brief overview of the book. We will argue that the regulatory fields of both poisonous and nonpoisonous hazardous chemicals had gradually developed by the early twenty-first century toward the regulation of chemicals in general and in Europe especially. On the one hand, this result of a more preventive and precautious philosophy takes serious account of the consequences of uncertainty and risk. On the other hand, it also fits, paradoxically, well into neoliberal policies of deregulation in which economic interests have a greater “say” and are consulted extensively in the implementation of the new legal frameworks. The chemical industry has objected for decades—with a reference to Paracelsus (1493–1541)—to a strict separation between poisonous and nonpoisonous industrial products. That policy seems to have worked out well for the industry.

Poisons: A Conceptual History Although poisons and hazards are as old as humanity, “hazardous substances” is relatively new and became popular only after the mid-1970s, when it started to partly replace the older “dangerous substances.”11 Although some languages translate both concepts as the same term(s) (in German, e.g., gefährliche Stoffe or Gefahrstoffe), the distinction between the two terms in English is significant. “Hazard” takes into account both danger and risk, thereby including potential dangers of which the actual occurrence is uncertain. The shift from “danger” to “hazard” coincides perfectly with the growing popularity of risk studies and arguments in the 1970s. The category of “dangerous” substances and goods thereafter obtained a narrower meaning in the field of transport.12 The shift in terminology illustrates a new phase in the conceptual history of chemicals considered dangerous. For many people, the concepts of poison, dangerous substances, and hazardous substances will probably be identical, and, indeed, all the chemicals discussed in

Introduction  5

this book were primarily, though not exclusively, a matter of social and political concern because of the suspicion that they were poisonous. However, it is important to realize there is no perfect identity between these concepts. Dangerous and hazardous chemicals are a broad category that, next to poisons, also includes chemicals that are dangerous because they are, for instance, explosive, corrosive, or inflammable. The broader category gradually took shape in the first half of the twentieth century. The concept of poison, by contrast, dates back to antiquity and biblical times, so we will start our overview with a history of the poison concept. Poisons in Antiquity and the Middle Ages Most conceptual histories of poison go back to antiquity, where the Greek pharmakon (poison) and toxon (arrow) and the Latin venenum, virus, and potio are the most relevant terms in this context. Potio, for instance, returns in the English and French “poison,” and venenum in the French venin. Greek and Roman authors mostly classified poisons according to the three realms of nature: animal poisons (from, e.g., vipers and scorpions) received the most attention, followed by plant poisons. Mineral poisons, then, were the least important category.13 An important dimension of the ancient concept of poison is that it referred both to medicines (“good poisons”) and to magic potions and substances that could kill people or seriously damage someone’s health (“bad poisons”). Some authors relate the difference between the good and bad properties of a substance to differences in quality, whereas others refer to the importance of the quantity involved. Galen and Celsus in some of their writings made a more rigorous distinction between medicamentum and venenum, the latter being a harmful substance often deliberately applied to murder someone that should be feared. Despite that, the close relation between medicines and poisonous substances was preserved in the Middle Ages, when Arab scholars such as Geber and Avicenna wrote treatises that included both pharmaceuticals and poisons.14 Poisons, Contagions, and Miasmas From the early sixteenth century onward, the concept of poison received a new meaning, mainly because of the impact of the plague and other pestilences on European medicine. Medical authors started

6  Ernst Homburg and Elisabeth Vaupel

to believe the devastating infectious diseases affecting Europe, such as typhus, syphilis, and the plague, were caused by a poisonous fever, seed, or agent, which the Italian doctor Girolamo Fracastoro (1478–1553) called “contagion.” In the next century, authors such as Guillaume de Baillou (1538–1616) and Thomas Sydenham (1624–1689) reintroduced Hippocrates’s atmospheric miasma theory to account for the occurrence of infectious and other acute diseases, in which noxious vapors emerging from putrescent organic matter, or stagnant water, acted as a kind of atmospheric poison to make people ill. Until far into the nineteenth century, authors of textbooks on poisons and toxicology included contagions and miasmas in their classification of poisons. Alongside the usual categories of animal, plant, and mineral poison, some authors now added aerial poisons, but others preferred to include the miasmas under animal poisons.15 In addition, the terms poison (e.g., venenum and virus in Latin, “poison” in French and English, and Gift in German) acquired a stronger negative connotation, which lacked the ambiguity of the Greek pharmakon. Although many authors were aware of relations between medicines and poisons, the latter term stood for dangerous substances of death, secrecy, witchcraft, and fear. The often cited, and mostly misunderstood, quote from Paracelsus’s Sieben Defensiones (manuscript from 1537/1538, published 1564 as part of the Drei Bücher)—“What is there that is not poison, all things are poison and nothing (is) without poison. Solely the dose determines that a thing is not a poison”—seems to have had no impact whatsoever on the medical and pharmaceutical discourses in the early modern period. More importantly, “dose” in Paracelsus’s writings meant something completely different than today. It was a purely qualitative concept, in which terms such as larger or smaller played no role. The “right dose,” for instance, referred to a harmonious equilibrium of forces in nature.16 The now famous Paracelsus quote was rarely cited before 1900, and it would be another fifty years until it started to be used frequently, by medical men and producers of pesticides or foodstuffs, often for apologetic reasons. The most common idea on the action of poisons in the eighteenth century seems to have been that—similar to the ideas of Cartesians such Sylvius and Lemery on medicines—the qualities such as shape of the subtle particles of a poison meant that even small quantities could already kill someone via an unknown mechanical force.17

Introduction  7

The Influence of Experimental Physiology and Chemistry Around 1800, the concept of poison again changed greatly. The concepts of health and illness in medicine got a new meaning when the dominant humoral pathology gave way to more mechanistic views on the human body. Intertwined with this, developments in physiology and chemistry, as well as the growing importance of toxicological expertise and chemical analysis in forensic medicine, played a role. The use of animal experiments, for instance, by Felice Fontana (1730–1803) and Anton Störck (1731–1803) in the 1760s, followed by the gradual rise of experimental physiology as a branch of medicine after 1800, made it possible to classify poisons not only according to their origin from a realm of nature but also based on a more precise description of their action on organisms, such as corrosive, astringent, paralyzing, or narcotic effects. Also, “dose” had obtained by this time a quantitative meaning. Animal experiments had led to the discovery of a clear relationship between that new concept of the dose of a poison and its physiological effect. By the 1780s, this was only a surmise, but it was for many poisons a widely held scientific view by the 1840s. As a result, the relationship between poisons and medicines became an attractive topic to investigate. The rise of modern chemical theories in the late eighteenth century, through the influence of Lavoisier and his fellow chemists, did perhaps have an even greater impact on the new way to look at poisons. Instead of being entities of natural history, they were increasingly seen as chemical substances, and the effects of poisons were now understood in chemical, and not mechanical, terms. Part of the new chemistry was the emergence of organic chemistry and the attempts to extract plants’ essential, active, poisonous principles. As a result of experiments by Johann Christian Dölz (1792) and Friedrich Sertürner (1805), poisons were increasingly viewed as physiologically potent chemical substances. All these developments in physiology, animal experiments, chemical theory, and chemical plant analysis found their way in an influential textbook of the young Spanish-French professor of medicine Mateo Orfila (1787–1853), Traité des poisons tirés des règnes minéral, végétal et animal, ou Toxicologie Générale: Considerée sous les rapports de la Physiologie, de la Pathologie et de la Médicine légale, published in four parts from 1814 to 1815. This hybrid book marks perfectly the transition from poisons as an object of natural history and forensic medicine to poisons as a chemical and physiological object. Orfila stood, so to speak, with one leg in each approach.18

8  Ernst Homburg and Elisabeth Vaupel

These conceptual changes should therefore not be understood as radical breaks. Knowledge of poisons is not confined to the esoteric circle of one particular scientific discipline, within which paradigm changes can take place, but rather is part of the cultural and social history of humanity, and part of a complex matrix of interacting scientific disciplines. As a result, it is better to visualize these conceptual changes as a kind of sedimentation process in which new layers of meaning are deposited on top of the older ones, whereby the latter are still present. Even after 1800, poisons were still an object of secrecy, danger, fear, and perhaps even mystery for many people. Within the world of eighteenthcentury science, poisons and toxicology had primarily been the domain of medical police and forensic medicine, focusing on murder, and that would not really change in the first third of the nineteenth century. So, in disciplinary terms, there was also a strong continuity across the fundamentally new approaches that had been launched around 1800.19 During the first period discussed in this book, especially in the chapters on Paris green (Mertens) and white lead (Lestel), the concept of poison and the study of toxicology were still very much in flux. It would take the first three-quarters of the nineteenth century before toxicology would change fundamentally into a more experimental and chemical direction, and only by 1900 had the new disciplinary profile of toxicology as an independent scientific field stabilized.20 Occupational Diseases At the end of the eighteenth century, the field of toxicology was the domain of physicians. But when that field moved into a more chemical direction, and especially when new, more complex chemical tests to detect poisons were developed in the mid-nineteenth century, new groups such as pharmacists and the emerging profession of the chemist stepped in. Also, content-wise, the scope of toxicology widened. Traditionally, the study of poisons focused strongly on detection and treatment of criminal acts of poisoning, or accidental acute poisoning. But when the Industrial Revolution gained momentum, increased attention was also given to occupational diseases, often caused by chronic exposure to toxic substances, thereby building on Paracelsus’s book De morbis fossorum metallicorum about diseases among miners and on Bernardino Ramazzini’s (1633–1714) book on occupational diseases among artisans and skilled workers (published in the early eighteenth century and still translated in the mid-nineteenth century). The latter,

Introduction  9

with its emphasis on slowly acting chronic poisons, was not part of the traditional literary corpus of toxicology. In the nineteenth century, that separation between occupational medicine and toxicology gradually disappeared, as the role of poisonous workplace substances became a concern. Chronic poisoning, which was hardly an issue for toxicologists in the early decades of the century, now also received attention. Only in the course of the nineteenth century did a clear conceptual distinction between acute and chronic poisoning emerge. John A. Paris and John S. M. Fonblanque (1823) devoted a few pages to “the chronic operation of poisons,” and Robert Christison (1832) mentions chronic poisoning in passing, but only with Alfred S. Taylor (1848) and, especially, Ludwig Hirt (1875) were both forms of poisoning clearly opposed to each other. By 1900, Hirt’s field of industrial toxicology had become a subfield of the study of poisons.21 Poisonous Gases The broadening scope of toxicology, in terms of the different social groups and professions involved, was further widened in the 1850s. The metallurgical and chemical industries had grown to such a scale that the noxious vapors pouring into the atmosphere and the massive pollution of canals and rivers did not escape the population’s attention. The significant, sometimes even massive, public protests in several countries against these evils, and the subsequent advice given by different professional groups in response, offer a unique insight into the views about poisons at the time. The protests were partially directed against the devastating effects of poisonous and noxious industrial waste gases on vegetation. It would be wrong to see this as an early sign of environmental consciousness, although that might have played a role in some cases. Within the legal frameworks of the time, financial interests of farmers and landowners fueled the debates on the impact of the industry on vegetation. Property rights, and loss of property, played a major role. Next to that were serious worries about human health. In 1855, the Belgian pharmacist Léon Peeters published a small brochure entitled Salubrité publique: Guérison radicale de la maladie des pommes de terre et d’autres végétaux, in which he argued that the devastating epidemic disease of potato plants that had caused serious famine in Europe in the late 1840s resulted from dangerous vapors of the chemical industry and that small children were suffering from aerial poisons. In the protests and expert testimony that followed these accusations,

10  Ernst Homburg and Elisabeth Vaupel

an interesting mix can be encountered between purely chemical and toxicological views on gaseous substances such as hydrogen chloride, sulfur dioxide, and nitrogen oxides, and older but still popular views on the roles played by miasmas and contagions in public hygiene. In 1865, the German state physician responsible for the Rhineland, Hermann Eulenberg (1814–1902), summarized these impacts on human health and vegetation in a five-hundred-page textbook on noxious and poisonous gases. Within a mainly physiological structure—in which suffocating gases and three types of toxic gases (narcotic, irritating, biolytic) were distinguished—his approach was primarily chemical, discussing the gases as chemical entities with distinct formulae. Nevertheless, gaseous miasmas and their epidemic consequences were also discussed. The book therefore illustrates quite perfectly the view on (gaseous) poisons during the third quarter of the nineteenth century. At the same time, it also was a milestone at the interface of public health and toxicology, and a specimen of “external” industrial hygiene, which much later would be named environmental toxicology.22 Then, as a result of the well-known research from 1870 to 1900 by Louis Pasteur (1822–1895), Robert Koch (1843–1910), and several others including Ferdinand Cohn (1828–1898), John Tyndall (1820–1893), Wilhelm Roux (1850–1924), Martinus Willem Beijerinck (1851–1931), and Dimitri Ivanovski (1864–1920), the ideas on infectious diseases changed completely. Bacteria were discovered, and later viruses. The final publications on miasmas appeared in the 1880s. Toxicology on the one hand, and bacteriology, microbiology, and virology on the other, now followed different paths. The concept of poison changed again. Scientific circles no longer saw it as a cause of infectious diseases, but ideas on miasmas and contagions lingered in other circles. In Crop Production, Poisoned Food, and Public Health (1925), the farmer John Hepburn, for instance, argued fertilizer and pesticide use in agriculture was a major cause of cancer, which he considered a contagious disease.23 By the time Hepburn wrote his book, though, the massive public protests against the chemical industry were something of the past. Why?​As we will discuss, most countries introduced some form of factory regulations or made existing regulations more stringent. In most European countries, officers of health and factory inspectors were appointed to control industry; give advice to municipal, provincial, and national authorities; and handle citizens’ complaints. For more than a century, they functioned as a technocratic elite that mediated between government, industry, and the population. Often coming from the same

Introduction  11

engineering and scientific schools as the leaders of industry, and from the same social strata, they frequently handled upcoming issues in an industry-friendly manner. Pollution of air, water, and soil continued, although in a somewhat limited way, until the 1960s, when broad public concerns and protests surfaced again.24 The Threshold Paradigm of Industrial Toxicology In the early twentieth century, the study of poisons had, in principle at least, widened itself to the investigation of the toxic properties of almost any chemical substance that was suspected to be dangerous to some degree. In addition to its forensic origins, toxicology had assimilated elements of analytical chemistry (chemical toxicology, toxicological chemistry), pharmacology (animal experiments, the study of drugs’ “side effects”), “internal” industrial hygiene (occupational poisoning, industrial toxicology), and “external” industrial hygiene (release of poisonous substances into the atmosphere, surface waters, and the soil). At the same time, it had dissociated itself from the study of infectious diseases.25 Whereas the development of analytical chemistry and experimental physiology had revolutionized the field of toxicology in the nineteenth century, industry would now take on that role until the 1960s.26 The number of industry-produced chemicals grew enormously, and their often-unknown toxicological properties posed a risk to workers’ health. Industrial toxicology moved center stage, and its paradigm started to dominate the field as whole and how poisons were understood.27 A key ingredient of that paradigm was the concept of threshold, or limit, value. “Minimal lethal dose” had entered toxicology around 1880 as a quantitative measure to compare the toxicity of different acute poisons. Given the large variation in the response of different test animals of one species, the British pharmacologist John William Trevan (1887–1956), at the Wellcome Physiological Research Laboratories, in 1927 invented the more robust measure LD50, the lethal dose at which half the population of test animals in a certain experiment would die. It would play an important role in toxicological research and the regulation of poisonous chemicals until at least the 1980s.28 Toxicologists were therefore used to threshold values when industrial toxicologists started to search for the opposite of the minimal lethal dose, namely a maximum allowable concentration. Whereas nineteenth-century labor unions, some medical doctors, and other experts made efforts to ban certain chemicals such as white phosphorus

12  Ernst Homburg and Elisabeth Vaupel

and white lead from the industry (Lestel; Warren), early twentiethcentury industrialists promoted the idea that industrial work would not be dangerous as long as the exposure to chemicals stayed under certain limits. They tried to keep the dangers manageable and avoid a total ban of their products and processes. The idea of safe limits rested on the assumption that organisms, and ecosystems such as rivers, could transform or excrete poisonous substances via their metabolism, as long as the concentration of these substances was not too high. In German debates about river pollution around 1900, Carl Duisberg (1861–1935), a leader of the chemical industry, defended the notion that companies could discharge all their harmful and poisonous wastewaters into rivers, because the rivers’ dilution, as well as their “self-cleaning capacity,” would make the waste harmless. In World War I, two German pharmacologists—Ferdinand Flury (1877–1947) and Wolfgang Heubner (1877–1957)—further developed the key notion of the existence of a safe threshold value working under Fritz Haber (1868–1934) on poison gases, a program in which his “intimate enemy” (befreundeter Feind) Duisberg also played a role. Flury and Heubner published their results on hydrocyanic acid in 1919, and other colleagues, including Russian and American industrial toxicologists, took up the notion of threshold values from there. Alice Hamilton (1869–1970), the leading US expert in occupational medicine and industrial toxicology, published Industrial Poisons in the United States (1925), the first textbook in the field. After retiring from Harvard Medical School in 1935, she became a medical consultant to the US Division of Labor Standards and as such played a major role in preparing a system of occupational exposure limits, or maximum allowable concentration values, published for the first time in 1947. Animal experiments played a large role in establishing these threshold limit values. Whereas nineteenth-century industrial hygienists had visited the workshops and workers themselves (Mertens), the industrial toxicologists were now largely in the laboratories.29 Environmental Poisons and Low-Dose Uncertainty As is widely known, the 1960s saw an upsurge of environmental concern, the start of a rapidly growing environmental movement throughout the industrialized world, and increased government activity on monitoring and regulating pollution. These concerns did not come out of the blue. In the 1950s, national and international experts had discussed extensively the growing problems of air pollution, the presence of pesticide

Introduction  13

residues and toxic dyes in foodstuffs, and worries about pesticides in general (Morris; Stoff and Travis). In the 1960s, all these issues reached the public at large. Rachel Carson’s Silent Spring (1962) played a major role. A similar spark was ignited by thousands of children born in Germany and elsewhere with severe malformations of their limbs as a result of the pharmaceutical drug thalidomide, which their mothers had taken during pregnancy. Large-scale health disasters in Japan with mercury and cadmium compounds (Kaji), as well as massive air pollution by the then exponentially growing chemical, oil, and steel industries in almost all industrial countries, made the picture complete. Next to Carson’s book, Murray Bookchin’s Our Synthetic Environment (1962), Barry Commoner’s Science and Survival (1963), and Jerome Rodale’s Our Poisoned Earth and Sky (1964) reached audiences worldwide. In the same decade, the instrumental revolution in analytical chemistry meant ever smaller amounts of chemical substances could be measured in foodstuffs, human and animal bodies, and the environment. Toxic substances such as PCB, DDT, and dioxins suddenly seemed to be literally everywhere on the globe.30 The concerns addressed in the 1960s are still with us. Scanning scientific, activist, and political texts from 1965 to the early 1980s, one can conclude that the concept of poison again changed significantly in at least two ways. “Environmental poison” emerged, with layers of meaning that the older poison concept lacked, and, moreover, growing evidence—though debated—that an exposure to even low doses of certain chemicals could cause serious health problems undermined the dominant threshold paradigm of industrial toxicologists from the 1910s to the 1960s. Terms such as environmental toxicology, ecotoxicology, and environmental poisons, and their equivalents in other languages, entered the literature in the mid-1960s. “Environmental poison” appears to be used with two rather different meanings. On the one hand, the term refers to poisonous substances such as pesticides or other pollutants that are dispersed throughout the environment and pose a danger to human health. To some extent, there is a continuity here with the “external” industrial hygiene of the third quarter of the nineteenth century, although Gerd Spelsberg has argued that smoke and noxious gases were seen in the past mainly as a nuisance that destroyed or devaluated property but in the 1950s were reconceptualized as causing health problems.31 On the other hand, “environmental poison” could also refer to substances that poison the (nonhuman) environment. This particular

14  Ernst Homburg and Elisabeth Vaupel

meaning certainly was a major break with earlier poison concepts that always had been strongly anthropocentric since their ancient origins, even though they had been applied to (other) warm-blooded animals since the eighteenth century. John Prestwich, in Dissertation on Mineral, Animal and Vegetable Poisons (1775), defines poisons, for instance, as “those things, which are experienced to be in their whole nature, or in their most remarkable properties, so contrary to the animal life, as in a small quantity to prove destructive to it.” In Johann Friedrich Gmelin’s Allgemeine Geschichte der Gifte (1776) and writings of other authors around 1800, we encounter similar definitions. It was Rachel Carson’s concept of the food chain that opened the eyes of the public at large for the poisoning of other forms of life than man and (higher) animals. The German Chemicals Act (Chemikaliengesetz) of 1982 aimed to protect both humans and the environment, and required, for instance, toxicological tests on fish, earthworms, water fleas, and algae.32 Research in the 1950s and 1960s on the recently discovered mutagenic and teratogenic properties of certain chemicals further widened the concept of poisons, introducing effects not yet discussed in textbooks on forensic and industrial toxicology. New groups of geneticists and toxicologists entered the field, and in the US founded the Environmental Mutagen Society, which successfully acted as an activist pressure group to link mutagens and teratogens to the well-recognized and well-funded problems of cancer research (Schwerin). Mutagens and teratogens also became subject to regulatory measures in the 1970s and 1980s. The Ames test, introduced by the biochemist Bruce Ames (*1928) in 1973, provided a quick method for testing the carcinogenic and mutagenic properties of chemicals. As a result, research in this area grew exponentially in the following two decades.33 This research in genetics also helped undermine the idea defended by chemical companies and industrial toxicologists that toxic chemicals could be handled safely as long as the exposure to humans remained below a threshold limit value. In the 1970s, that idea came under pressure when two research traditions met. On the one hand, as Soraya Boudia has shown, research on the effects of low doses of radiation concluded that the effects were not negligible under any threshold value. Instead, the cumulative effect of low doses of radiation over longer periods could have a serious impact on human health. On the other hand, as argued Alexander von Schwerin, Beat Bächi, and Heiko Stoff and Anthony Travis (this volume), research into the carcinogenic properties of chemicals led to a similar conclusion: in many cases, there was no

Introduction  15

minimum safe dose. The defenders of the “old school” heavily contested these results, but when it became clear that they could not be denied, the battle lines shifted to the question of whether the new toxicological insights could be generalized to types of poisons whose mode of action was not based on genetic defects. By 1975, the discussion on poisons was increasingly characterized by terms such as uncertainty and risk.34 The broad concept of environmental poisons and the insight that almost all chemicals could have an effect on some organisms, together with the insight that in many cases there might be no safe dose at all, has the potential to completely undermine the traditional notion of a poison. Even though the term poison remained very popular in the press and many public debates,35 the 1980s can be seen as the end of “era of the poison,” in the sense of the existence of specific dangerous substances with unique toxic properties. Any chemical substance could form a risk. Because of this blurring of boundaries between chemicals and poisons, we will discuss the regulation in the “risk society” of two more general categories, namely those of hazardous substances and of chemicals in general. However, we will first give a brief historical overview of the regulation of poisonous substances more narrowly conceived, making this broad conceptual overview more concrete by showing in somewhat more detail how poisons were handled in different subsystems of society.36

Regulation of Poisons Regarding the regulation and governance of risks and dangers, most people will perhaps primarily think of juridical and administrative laws, rules, and regulations. Over the past twenty to thirty years, though, several scholars have argued that a far broader view on issues of regulation is needed to understand how hazards and risks are handled in practice. In the footsteps of Jean-Paul Gaudillière’s studies on the regulation of pharmaceuticals, one can distinguish, for instance, between “industrial,” “professional,” and “public” ways of regulating the uses of poisons, alongside the more well-known “juridical” and “administrative” procedures. Industrial ways of regulating chemicals would include the roles played by business associations on quality control or storage safety, supplying instruction leaflets for (dangerous) products, or surveillance of industrial practices by insurance companies and accountancy firms. Examples of professional regulation are activities of corporations and

16  Ernst Homburg and Elisabeth Vaupel

scientific associations in collecting and distributing information on health and safety issues, for instance, the making of codices. Public forms of regulation would include activities of consumer groups, the impact of media exposure, or litigation initiated by citizens, to mention a few examples.37 Given the present state of the historiography of the regulation of poisons, it would be hardly possible to sketch the entire spectrum of regulatory measures over the long period of time discussed in this book. We can only scratch the surface and will mainly focus on regulations of a juridical and administrative nature. But it is good to make the desideratum explicit that further research into other ways of regulating poisons and other hazardous substances should be initiated. On top of that, we will give examples of those other ways of regulation when possible.38 Pharmaceuticals In antiquity (e.g., in Galen’s writings), poisons, medicines, and foodstuffs were often mentioned in one breath. They were distinct, but related, because they could all be administered orally. Food could be poisoned, medicines were sometimes too potent and dangerous, and so on. It is therefore perhaps no great surprise that the first explicit regulatory measures on poisons had to do with pharmaceuticals and foodstuffs.39 The oldest regulations on poisons concerned the apothecary, or pharmacy. This was the place where poisonous chemicals were for sale, and from the fourteenth century onward, many town governments issued prohibitions, sanctions, or ordinances on the selling and storing of poisons. From the eighteenth century onward, common practice ordered poisons be stored in a separate, locked cabinet and all sales of poisons be noted in a special housekeeping book, to be controlled regularly by the town physician.40 Since the Renaissance, the composition of official drugs made in pharmacies was also regulated by local and, later, national pharmacopoeias. In the mid-nineteenth century, these regulations were amended by acts that tried to prevent the adulteration of drugs, as a result of the advent of industrial medicines and the growing commercialization of the drugs market (e.g., British Pharmacy Act 1868 and the US Pure Food and Drug Act of 1906). Control of narcotic drugs, according to most toxicological handbooks classified as poisons, was stricter and became increasingly regulated internationally from 1906 onward. In that respect, the control for pharmaceuticals and narcotics was a forerunner of the regulation of chemicals in general.41

Introduction  17

Apart from the standardization of the composition of drugs, many other aspects of pharmaceuticals were not regulated at all for a long time. In the early decades of the twentieth century, there were generally no strict procedures for the admission of drugs, no legal criteria for their efficacy, and no mandatory tests for harmful side effects or for safety. The US Federal Food, Drug, and Cosmetic Act (1938) took a first great step into the opposite direction. The burden of proof for the safety of drugs was put on the shoulders of the manufacturers, and, just as in the case of toxic substances, a precautionary principle (avant la lettre) was implemented for pharmaceuticals, although it was abandoned in practice only a few years later.42 Since the 1930s, the number of new medicines on the market has grown tremendously, leading to an increasing number of cases of poisoning by these new drugs, whose (side) effects were often not well known. Despite these serious signals, the regulation of drugs was not put on a totally new basis until the early 1960s, due to the shock produced by the aforementioned “thalidomide affair.” From 1962, therefore, most countries, with the US Food and Drug Administration in a leading role, considerably tightened up the required testing procedures for drug safety. In the German Federal Republic, the Law on Pharmaceuticals (Arzneimittelgesetz) of 1961 was revised again in 1964 as a result of disastrous side effects of thalidomide use. From now on, preclinical and clinical studies became mandatory before new drugs were admitted to the market. In 1976, the West German parliament passed an improved Law on Pharmaceuticals, which came into force on 1 January 1978. Similar laws were established in other countries.43 The disastrous effects of thalidomide put, for the first time, the then quite unexpected teratogenic side effects of drugs clearly on the map. After new laws on the admission of novel drugs had been passed in the United States, Germany, and most other developed countries, tests on the teratogenic properties became mandatory, as did tests for the possible toxic, carcinogenic, and (recently discovered) mutagenic effects of drugs. The impact of these ever more stringent regulations on the pharmaceutical industry and on the innovation of new drugs cannot be overestimated. Bringing new drugs to the market became a timeconsuming and costly process. Within that force field between risk and innovation, only the largest and most wealthy pharmaceutical companies could keep a stream of innovations flowing, in only by taking over new start-ups.44

18  Ernst Homburg and Elisabeth Vaupel

Foodstuffs Local regulations on forbidding the use of poisonous substances in foodstuffs also date back to the Middle Ages, but France, as far as we know, was the first country to regulate these issues on the national level. After Louis XIV had issued a general ordinance on the possession of and the trade in poisons in 1682, a 1742 police ordinance on making desserts forbade confectioners from using dangerous colors such as copper and lead compounds in preparing their sweet dishes. Later nineteenth-century regulations on foodstuffs invariably referred back to that eighteenth-century decree on the duties of the police. The law of October 1800 on the police control of the hygiene of cities, including foodstuffs, remained in force during a large part of the nineteenth century, not only in France but also in several countries that had been part of the French empire during the Napoleonic wars.45 The chapter on Schweinfurt green gives a good insight in the responses of different legal and political regimes on the introduction of that new pigment to the market (Mertens). Within three years after its large-scale introduction in France, the authorities in 1830 issued ordinances that forbade the use of the green coloring matter not only in certain foodstuffs but also in the wrappers around confectionaries. Prussia followed in 1838, but the prevailing statute law afforded less legal possibilities to act in Britain. For a long time, such legal measures were rather ad hoc, limited to individual products and specific applications. But by the end of the nineteenth century, countries started regulating the quality of foodstuffs more generally on a national basis, not only in view of adulteration practices but also often to protect human health. Whereas the British Sale of Food and Drugs Act 1875 focused mainly on adulteration, the German Food Law (Nahrungsmittelgesetz) of 1879 gave more room to health concerns. Apart from foodstuffs, it included other consumer products that could cause dangers, such as toys painted with poisonous pigments. More specific bans of poisonous pigments in foodstuffs and other goods of consumption followed in 1882 and 1887. Similar steps were made in other countries after 1900, for example, the US Pure Food and Drug Act of 1906, which was partly an achievement of the “pure food movement” that had emerged in the United States in the late nineteenth century and later spread to Britain, Germany, and other countries.46 From the movement’s viewpoint, food additives and pesticide residues in foodstuffs were highly suspicious. When these substances were found, the pure food movement soon labeled these

Introduction  19

foodstuffs “poisoned food.” The dangerous aniline dye butter yellow was banned from use in foodstuffs in the United States in 1918. Stoff and Travis show in their chapter how the debate on “poisoned food,” and butter yellow in particular, evolved in Germany. In 1939, the first German legal measures on food additives were taken. In the 1950s, both in Germany and on the European level, the debate on food additives gained another dimension when it appeared that several of those additives were probably carcinogenic. Butter yellow was forbidden in Germany in 1951. A few years later, the Joint FAO/WHO Expert Committee on Food Additives was created and would play a major role in expert advice on regulations. From 1957 to 1963, “acceptable daily intake” was developed within that body. This concept implied a fundamental break with the earlier practice of using negative and positive lists. It introduced the “threshold paradigm” into the domain of foodstuffs and did not do justice to the suspicion that carcinogenic chemicals could also be dangerous as a result of exposures to low doses. The legal implementation of these ideas differed between countries, though. In 1958, in both Germany and the United States, new food laws, or amendments to existing laws, were enacted that included rules on additives. Because of a specific amendment moved by Senator James Delaney (the “Delaney clause”), “any chemical additive found to induce cancer in man, or, after tests, found to induce cancer in animals” should not be approved for use in food. The clause, therefore, went much further than the JECFA’s proposals, but included an escape for questionable substances that had been used for some time and thus were “generally recognized as safe” (Schwerin). The Delaney clause would be heavily contested for years to come, concerning both the GRAS status of cyclamates and the applicability of the clause to pesticide residues in food (Morris; Schwerin). It played a key role in 1969/1970 in the decision to ban cyclamate use in the United States. In Germany, by contrast, these sweeteners then stayed on the market.47 Residues of pesticides in food provoked similar debates. Concern about these residues emerged already well before World War II. However, powerful industrial and agricultural lobbies prevented the creation of strict and binding regulatory measures. In 1963, the Joint FAO/WHO Meeting on Pesticide Residues was established, but regulation continued to diverge greatly between countries. The US Food Quality Protection Act, signed by President Bill Clinton in 1996, finally required a systematic reassessment of all food threshold levels, with respect to residues of organophosphate pesticides in the first place

20  Ernst Homburg and Elisabeth Vaupel

(Davis).48 Parallel to these discussions about where to draw the line between “acceptable food” and “poisoned food,” the past few decades have witnessed frequent struggles on the borderline between “health foods” and pharmaceuticals. In Germany, for instance, different rules applied to legal complications of sweeteners used in foodstuffs and in pharmaceuticals (Schwerin). Producers of foodstuffs often advertised products with certain pharmaceutical claims to promote sales and higher margins while simultaneously trying to avoid their products being subject to the strict and extensive procedures of the legislation on pharmaceuticals. Unilever, for instance, first promoted from 1959 to 1961 its cholesterol lowering margarine Becel (Flora in the United Kingdom) only via apothecary shops before launching it as a healthy product in supermarkets. In the past twenty years, the market of “health foods” has grown exponentially, so the EU, followed by other countries, in 2002 tried to draw a clear legal borderline between pharmaceuticals and foodstuffs, thereby solving Galen’s problem in a Solomon-like manner.49 Transport and Storage The trade, transport, and storage of poisonous substances was initially regulated via decrees on the pharmacies and even, in France, via the more general ordinance of 1682. Also, in Germany, proponents of an improved “medical police” such as Johann Peter Frank made a strong case at the end of the eighteenth century for regulating the trade of poisons. Their pleas were successful, because Gustav Kletschke, in 1854, said packing, shipping, and storing of poisonous materials had been sufficiently regulated, at least in the wholesale trade (Mertens).50 Regulation of issues such as these also extended to the international sphere. At the Congress of Vienna of 1815, the Central Commission for Navigation of the Rhine (CCNR) was created, of which all countries on the then navigable portions of the Rhine became members: Baden, France, Bavaria, Hesse-Darmstadt, Nassau, Prussia, and the Netherlands. After years of rivalry, mainly between Prussia and the Netherlands, an international convention on the navigation on the Rhine was signed in Mainz on 31 March 1831. Under Prussian leadership, in practice at least, the CCNR coordinated and regulated the shipping on the Rhine in the remainder of the nineteenth century. The commission still exists. In July 1838, an agreement was reached on the packing and shipping of arsenic and other inorganic poisons such as quicksilver preparations, sugar of lead,

Introduction  21

and Spanish green, and the control thereof. As far as we know, this constitutes the earliest example of an international regulation on poisons, and even on chemicals in general. It stayed in force for many decades.51 In the 1870s, tensions between Prussia and the Netherlands grew again. In 1865, the Prussian Minister of Trade had passed an edict that prohibited aniline dye manufacturers from dumping their arsenic waste, resulting from the manufacture of magenta, in rivers. After the opening in 1872 of an improved connection to the sea at Rotterdam, ships with arsenic waste started to sail down the Rhine to dump it into the North Sea. Protests by fishermen led to prolonged negations between the Dutch and Prussian governments and finally to the adoption of a Law on the Import, Transit, and Export of Poisonous Substances by the Dutch parliament in June 1876.52 Concerning storage and transport in non-river environments, for instance, by rail or aircraft, there were many national laws and international conventions, but we will discuss those in the larger framework of the handling of hazardous chemicals in general. Poisons in the Workplace Regulations on the dangers and nuisances of industry materials were first mainly limited to the effects they had on factory neighbors, such as stench, smoke, irritation by noxious gases, pollution of wells and rivers, and so on. Although occupational diseases had been known since the times of Paracelsus and Ramazzini, little was done for the workers in terms of legal protection. It was left to the factory owners to decide what measures should be taken to avoid workers becoming ill. There were striking cultural differences between countries regarding labor relations. In the white lead industry, for instance, workers were suffering a great deal from poisonous dust of white lead (Lestel), but while British and later French manufacturers improved the process by breaking the white lead coils under water with special machines, Dutch factory owners only advised workers to protect their noses and mouths with a wet handkerchief and to perform some other tasks every few hours, as a kind of “job rotation.”53 In the 1860s, the French mining engineer Charles de Freycinet (1818–1923) concluded after a broad survey that the international differences on the regulation of health issues in the workplace were marked. In England, which he visited in early 1863, there was no legal protection worthy of the name. Working conditions differed from factory to factory, depending on the manufacturers’

22  Ernst Homburg and Elisabeth Vaupel

attitudes. In Belgium and Prussia, state-appointed factory inspectors played an important, positive role, and a lot had still to be done in France, but the manufacturers themselves were improving their processes. The British Alkali Act 1863 was passed to reduce the emission of noxious gases by the heavy chemical industry, and the alkali inspectors appointed as a result changed the situation for the better. The act was modernized several times, and other laws were passed. Nevertheless, as David Walker demonstrated, the situation of workers in dangerous productions was often deplorable until far after World War II.54 In their chapters on the Schweinfurt green and white lead industries in France, Joost Mertens and Laurence Lestel both demonstrate how long it took before alarming observations on the health of the workers resulted in legal measures of a binding nature. However, other kinds of regulation played their part, in the form of the distribution of information on dangerous manufactures, technical advice by sanitary committees, procurement policies by the state, and activities by people such as Jean-Pierre Darcet, who tried to reduce workplace dangers by technical means. Due to the prevailing liberal political views, a strong conviction held that manufacturers’ self-regulation would be the best way to proceed. Similar regulatory mechanisms were quite successful in the case of producing phosphorous matches. There, the dangerous white phosphorous was replaced gradually from around 1850 onward by the less harmful red phosphorous, on the advice of the Austrian chemist Anton Schrötter (1802–1875). Nevertheless, legal measures to truly prohibit the use of white phosphorous were not taken until the twentieth century. It was banned from the production of matches in the Netherlands in 1901, followed by Germany in 1903. International agreements followed two decades later.55 Tackling the causes instead of the symptoms often depended on the availability of good and affordable alternatives. After decades of debates in France on the dangers of pigments such as white lead and Schweinfurt green, the use of white lead was finally banned in 1909—though not for self-employed ­painters— when zinc white and lithopone had become available as alternatives (Lestel).56 Schweinfurt green, by contrast, despite legal measures taken in 1893 and 1895, remained in use in the shipbuilding industry, where its poisonous properties were in demand for protecting ships’ bottoms against algae (Mertens). From 1886 to 1918, measures for the protection of factory workers and painters were also taken in Germany, Britain, Austria, and the Netherlands. In the international arena, the International Labour Organization, established in June 1919, that

Introduction  23

actively strove to ban the use of white lead, white phosphorous, and other poisonous substances in industry (Lestel). But ratification of the conventions was often slow. Britain and the United States, for instance, did not sign the White Lead Convention of 1921 to ban the use of white lead from most interiors (Warren).57 In 1877 and 1878, Switzerland and Germany were the first countries to pass laws that included provisions for workers’ health. Germany was, in 1884, also first to introduce financial compensation for injured workers. Britain followed in 1906. The United States and France introduced similar schemes in the next decade (Lestel; Warren). Initially only intended to compensate income losses as a result of (acute) injuries, it would take many years before chronic occupational diseases were also brought under these laws. That happened in Germany, for instance, in 1925. These laws only applied to workers who became sick from officially recognized occupational diseases. The official listing of an occupational disease could often take several decades after the first alarming symptoms had been discovered (Stoff and Travis). Even then, as Walker shows for Britain, poisoned workers were often just sent home with financial compensation, while the labor conditions were not improved.58 As discussed earlier as part of the conceptual history of poison, initiatives to ban certain poisonous products were gradually giving way to regulatory policies in terms of threshold values in the interwar years, leading to the MAC values published shortly after World War II. During the same years, an increasing number of workplace chemicals were recognized as causing chronic occupational diseases, such as cancer. All these developments took place mainly within the legal frameworks of factory acts dating from the late nineteenth to early twentieth century. In the 1960s and 1970s, that situation would change, starting with the British Factories Act 1961, the Carcinogenic Substances Regulations 1967, and the Health and Safety at Work Act 1974. The US Occupational Safety and Health Act was passed in 1970, followed in 1976 by the Toxic Substances Control Act (Stoff and Travis). Laws such as these reinforced processes going on within industries to improve working conditions. Nevertheless, the “industrial hazard regimes” differed from country to country and between different industries. Products and processes forbidden in the United States, Europe, or Japan were often still used and practiced elsewhere.59 The 1970s were characterized by an increasing turmoil about toxic chemicals, concerning not only the environment and consumers but also the workplace. The number of laws, ordnances, and other

24  Ernst Homburg and Elisabeth Vaupel

r­egulations grew steeply. Other regulatory interventions multiplied: increased involvement of labor unions, NGOs, and political parties in health and safety issues; more publicity and public debate; the creation of safety committees inside the factories in which workers now got a voice; and, finally, a growing number of experts from an increasing number of fields who had, or wanted to have, a “say” in issues on toxic chemicals in industry and trade. In clear contrast to the interwar period and the 1950s, experts now often disagreed, for example, on the dangers of prolonged exposures to low doses of carcinogenic chemicals (Schwerin). The robustness of TLVs such as MAC values came into question. In the 1960s, the possible carcinogenic effects of chemicals had already received much attention, but when it became known in January 1974 that vinyl chloride monomer—the starting material for the much-used plastic PVC—had most probably caused liver cancer (angiosarcoma), a “publicity bomb” exploded. After the MAC value of VCM had already been lowered from 500 ppm to 200 ppm around 1970, it now was almost immediately lowered to 50 ppm and, in October 1974 in the United States, even to 1 ppm. Great improvements in the analytical-chemical instrumentation were required to measure levels such as these at all, especially in the less than ideal work atmospheres in the production halls. By 1990, it proved possible to lower VCM concentrations in factories to 0.1 ppm, a fact that puts previous working conditions, when exposures of 3,000 ppm or higher had not been rare, into a poignant perspective. Also, when TLVs in the United States and later Europe had been lowered to 1 ppm, discussions on the dangers of low doses continued, because of not only different theories about the mechanisms of cancer but also different views on precautionary policies in industry (Hay). In the late 1970s and early 1980s, a vast number of books, brochures, and articles on industrial poisons was published, on carcinogenic chemicals in particular.60 As we will argue, in the 1980s and the decades thereafter, the regulation of toxic workplace chemicals became part of the larger network of legal, political, and public documents and practices on the regulation of chemicals in general. Toxic Pesticides (and Chemical Weapons) Many of the substances discussed in this volume are pesticides. As recognized poisons, they were employed intentionally because of their deadly effects on organisms regarded as pests in agriculture and for humans. Since the 1870s, pesticides have been released in huge

Introduction  25

amounts into the environment. They massively contributed to a growing awareness of hitherto unknown problems connected with the use of poisonous substances. With few exceptions, the first generations of pesticides used in the nineteenth and the first third of the twentieth century were inorganic compounds, containing heavy metals such as mercury, lead, arsenic, or copper. Their harmfulness to organisms had often been known empirically for centuries; others were byproducts of certain industries such as coal tar dye production. In either case, they were not optimized for application on the farm. Schweinfurt green (Mertens) began to be used as a pesticide as soon as it became clear it was too toxic to be used as pigment. Its first large-scale use was in the United States, where vast monocultures favored the occurrence of pests on mass-produced crops. The regulation of pesticides took the form of advice: users were recommended to apply protective measures known from industrial hygiene—tidiness and cleanliness above all.61 Initially, Europe watched these developments in the United States rather skeptically. Germany, however, gave up its reservation against the use of arsenicals as pesticides in World War I due to the lack of other plant protection agents and to the food shortages caused by the war. The fact that the Germans used arsenicals as chemical weapons in the war, as well as the necessity to find new civil utilizations for the production capacities they had built up during the war, played an additional role for the acceptance of arsenicals in agriculture. The history of the first synthetic pesticides is closely connected to the use of poisons for military purposes.62 The first attempt to regulate the handling of hazardous chemicals on an international level was—significantly enough—directly related to chemical weapons, the use of which had, at least theoretically, already been regulated by the Hague Convention of 1899. After World War I, the international community of states tried to agree on how to handle chemical weapons in the future, leading to the Geneva Protocol of 1925, which did not, however, prevent the development of even more poisonous substances.63 Furthermore, the history of these new weapons was closely connected to the history of pesticides. A chemist employed by IG Farben, Gerhard Schrader (1903–1990), had been asked to develop new insecticides based on organic fluorinephosphorous compounds (Davis). By unintentionally poisoning himself in 1937, he became aware of the extreme toxicity of the compound later known as Tabun, produced from 1942 onward. In the meantime, Schrader continued his work on organophosphate insecticides. In 1944,

26  Ernst Homburg and Elisabeth Vaupel

he finally discovered several substances that could be used as pesticides, among them one that would become known as malathion in the United States. After World War II, arsenicals were replaced relatively quickly by a second generation of pesticides, the contact insecticides based on organic chlorine compounds. The most prominent example was DDT, the insecticidal properties of which were discovered in 1939. The WHO used DDT as key chemical in its worldwide malaria-eradication programs: it was cheap to manufacture, was easy to use, and had longlasting effects (Morris).64 However, already in 1946, it was discovered that mosquitos had become resistant against DDT. Because DDT was highly fat-soluble, it accumulated in organisms, especially those at the end of the “food chain,” a concept that emerged in the DDT discussion. The concerns about the problematic environmental effects of DDT and other chlorinated hydrocarbons found a voice in Carson’s aforementioned Silent Spring.65 The book was a major catalyst for public debates about the dangers of chemicals for people and the environment, as well as for new legislation on the environment in general and pesticides in particular. A few years after the publication of Silent Spring, the US government established the National Institute of Environmental Health Sciences (1966) and the Environmental Protection Agency (1970). Other countries founded similar institutions: in West Germany, for instance, the Umweltbundesamt, the equivalent to the EPA, was founded in 1974. Also, legislation on pesticides was adapted to the toxicological and ecological lessons learned in the 1950s and 1960s. In 1962, the Council of Europe created a Working Party on Pesticides, which developed procedures for the registration of these dangerous substances, and since 1963, the FAO and the WHO has held annual joint meetings on pesticide residues. The German Pflanzenschutzgesetz of 1968 had similar aims and was followed by ordinances that specified the testing methods and the criteria for accepting new pesticides for entering the market. In 1971, Japan revised its existing Agricultural Chemicals Control Law in the same direction. Four years later, the WHO adopted a classification of pesticides based on their formulation (solids, liquids, aerosols) and their acute and dermal toxicity to rats.66 New pesticides were tested not only for their toxic properties but also for their ecotoxicological behavior, which partly depended on their formulation. The new academic discipline of ecotoxicology looked at the mode of action of chemicals and asked about the interaction of pesticides with organisms and ecosystems; the distribution and transport

Introduction  27

of these substances over the environmental compartments soil, water, and air; and the impacts on flora and fauna. It was of high symbolic significance that the Nixon administration, when it created EPA in 1970, moved the responsibility for pesticides from the US Department of Agriculture to the new agency. In the same year, Sweden banned DDT use, followed two years later by a ban in the United States (Morris). These bans were partly based on the suspicion that DDT could be carcinogenic. Although that suspicion could not be confirmed (Böschen), governments of many industrialized countries found it necessary to apply what is today known as the precautionary principle, which became an important concept in the legislation on chemicals discussed later.67 After its ban, DDT was largely replaced by organophosphates, a third generation of pesticides (Davis). Their success was because their properties differed significantly from DDT: they did not accumulate in food chains and were not persistent in the environment. Also, in 1954, a group of carbamate pesticides came on the market. The progression from organochlorine to organophosphate to carbamate pesticides involved an increase in degradability in the environment but at the cost of increased mammalian toxicity. Therefore, scientists concentrated on reducing the mammalian toxicity of the next pesticide generation, which led to the development of neonicotinoids. They came on the market in 1985 but were later discovered to be harmful for bees even at low concentrations.68 Closely connected to the history of pesticides and chemical weapons is the history of herbicides (Hay; Böschen). Herbicides based on 2,4-D and 2,4,5-T were developed in the United Kingdom and soon extensively used in US agriculture, but also in the Vietnam War from 1961 to 1970, because of their potential to defoliate trees. They are dangerous, because dioxins are present as containments in these products. Agent Orange—a mixture of these two herbicides—contaminated with dioxins was used in Vietnam, leading to severe health effects among Vietnamese and US soldiers. Only after the 1976 dioxin accident in a Seveso chemical plant in Northern Italy did the damage caused by the herbicides to war veterans begin to be discussed in the United States on a larger scale. Because of the Seveso disaster, scientists began investigating the mutagenicity and teratogenicity of dioxins—categories of risks not really regarded as relevant before. In addition, as mentioned earlier, the phenomenon of ecotoxicity was discovered, followed by the discovery of unexpected effects of nonlethal doses on the immune and endocrine systems.69 Pesticide use played an important role in the

28  Ernst Homburg and Elisabeth Vaupel

widening of these toxicological debates. Next, we will investigate how the regulation of toxic substances started to be linked to the regulation of hazardous substances more generally and even to the control of chemicals in general.

Regulating of Hazardous Chemicals Having analyzed the history of the poison concept, we discussed the regulation of health hazards posed by toxic substances in different domains, such as pharmaceuticals, foodstuffs, transport, workshops, and industries, and, lastly, pesticides. The aim of this section is to place these issues within the larger framework of the regulation of hazardous substances causing non-health hazards—at least, not only health hazards—such as explosions and fires. We will show how, after around 1980, regulations of those types of hazards partly merged in Europe and other developed countries with regulations on poisons, leading to legal frameworks on chemicals in general. “Hazardous substances” or “hazardous chemicals” refer to a broader set of potentially dangerous chemicals than poisons alone. It includes, for instance, flammable materials, corrosive substances, irritating gases, radioactive chemicals, or substances with an unpleasant or disgusting smell. The most influential early law that regulated hazards was the French Empire’s Factory Decree of 15 October 1810 (Décret impérial relatif aux manufactures et ateliers qui répandent une odeur insalubre ou incommode) that formed the basis for most nineteenth-century European factory laws. Although smell was the major hazard addressed by the title of the act, a much larger set of potential dangers and nuisances was considered in practice. We will not follow the development of industry legislation in detail here, because we partially addressed it already, but want to highlight the classification of hazards implied by this law that forms an interesting precedent to the classifications we will discuss later. Napoleon’s Factory Decree was characterized by a combined political-administrative and spatial-geographical type of regulation. Workshops and industry were divided into three categories. The first, most dangerous, class included black powder mills, storage facilities for explosives, gun foundries, ironworks, and, later, town gas factories. As a rule, they had to be situated outside the towns and villages, and only the emperor could give authorization. The second category included most of the chemical industry, and other industries with fire hazards,

Introduction  29

such as potteries and distilleries. They were authorized by the prefect of the department or province and could only be situated inside town or villages when the hazards involved were considered small. The factories and workshops in the third, least dangerous, category could be situated anywhere. They had to be authorized by local government. This legal framework dominated the authorization of new factories in Continental Europe for decades. In practice, not only nuisances (smoke, stench, noise) but also health issues (dangerous vapors, effluents, waste) and other dangers (fire, explosions) were taken into account.70 The regulation of hazardous substances we will discuss can be divided into three categories or legal traditions: regulations on the safety of transport and storage facilities; regulations on the classification and communication of hazardous workplace substances; and regulations on the authorization of hazardous chemicals. Although the first two categories were often related, they had been cast into distinct supranational legal frameworks since the 1950s: the Orange Book on the transport of dangerous goods on the one hand, and the Yellow and Purple Books on the classification, labeling, and packaging of dangerous chemical substances (in the workplace) on the other. Transport and Storage The earliest international regulation in this category was the aforementioned agreement on the packing and shipping of arsenic and other inorganic poisons on the Rhine of July 1838. It included not only strict descriptions of how the barrels or boxes with arsenic should be constructed but also rules on labeling. On each barrel or box, “Arsenic (poison)” should be painted with black oil paint. Working with symbols was considered as well. Mertens says in his chapter that Gustav Kletschke proposed in 1854 to paint a black cross on barrels or boxes containing poisons.71 New laws and regulations were often a response to serious accidents and disasters. In the 1860s, two new substances entered the market that proved to be extremely dangerous: petroleum and nitroglycerine. In view of possible accidents, local authorities acted swiftly under pressure of insurance companies, and a huge petroleum fire in the Port of Antwerp in 1866 stimulated measures on the national and international levels. Within a few years, several local, national, and transnational ordinances and agreements were issued on the handling and storage of these products, for instance, in the Netherlands, as well as within the CCNR. Nitroglycerine, in its turn, was banned from rail

30  Ernst Homburg and Elisabeth Vaupel

transport, and shipping explosives and inflammable liquids such as petroleum, in the same cargo was prohibited.72 Kerosene, then used in lamps, soon became an article of great international trade and commerce, so national and international regulations on safety measures soon came into being. In the 1860s, instruments had already been developed to determine the flash point of petroleum and were soon improved by chemists from France, England, Russia, and the United States. As a result, kerosene and other petroleum fractions became the first products, as far as we know, for which TLVs were defined. When the testing methods prescribed in the British Petroleum Act 1871 were found to be unsound, the chemist Frederick Abel (1827–1902) developed a new instrument to measure the flash point that received mandatory status in the Petroleum Act 1879. For use in lamps, trade/commerce, transport, and storage, the minimum flash point was defined at 23 degrees Celsius, slightly above room temperature. Fractions with a higher flash point were considered safe, and those with a lower flash point hazardous. Other countries adopted similar types of legislation, often with different national instruments and, as a result, different flash points. Also, (inter)nationally operating railway and shipping companies introduced binding rules based on the flash points of the cargo. Later, more refined schemes based on two parameters (the flash point and the boiling point) came into use.73 The precautions concerning nitroglycerine were part of more wideranging legal frameworks on rail transport. In Britain, for instance, the Railway Clauses Consolidation Act 1845 had removed dangerous goods from the obligation that railway companies should transport all kinds of goods. Due to pressures from the industry, though, railway companies started to transport some dangerous goods from 1855 onward. The issues were finally regulated by the Explosives Act 1875, which adopted a classification of explosives into seven categories and specified the transport regulations of these materials for each class. In 1890, the transport of dangerous goods by rail was for the first time regulated by an international agreement, the Berne Convention. In Britain, from 1892 to 1922, chemists working for the railway companies were heavily involved in developing methods, criteria, and standardized labels for safe transport. One outcome of their work was H. Joshua Phillips’s The Handling of Dangerous Goods: A Handbook for the Use of Government and Railway Officials, Carriers, Shipowners, Insurance Companies, Manufacturers and Users of Such Goods (1898), showing the entire spec-

Introduction  31

trum of actors involved. An updated version of the Berne Convention was issued in 1961, and the US Federal Railroad Safety Act was adopted in 1974. Regulations such as these, however, could not prevent the fact that increased rail transport of chemicals could lead to accidents such as the 1979 Mississauga train derailment, not far from Toronto, from which two hundred thousand people had to be evacuated.74 From 1910 onward, the Antwerp branch of the Lloyd’s insurance market published guidelines for the maritime shipping of dangerous goods in French, English, and German that went through several editions until the 1960s. On the political level, the first international convention on sea transport—the very general International Convention on the Safety of Life at Sea—was reached in 1929, which included a chapter on all types of cargo (except liquids and gases in bulk) that, “owing to their particular hazards to ships or persons on board, may require special precautions.” Precise agreements on sea transport of hazardous substances, comparable to the agreements for rail transport, were still lacking. There were only many local and national regulations on the loading and shipping of dangerous goods and explosives on ships. On the international level, the Intergovernmental Maritime Consultative Organization and the International Maritime Organization took the lead, developing the International Maritime Dangerous Goods Code (1965) and the Code for the Construction and Equipment of Ships Carrying Dangerous Chemicals in Bulk (1972) that went through many updated editions.75 Regarding air transport of dangerous goods, the International Air Transport Association in 1950 took the initiative to issue the first list of recommendations. An improved edition came out in 1956. Around the same time, US and European measures were taken to regulate road transport of dangerous goods, and the handling, transport, and storage of such goods more generally. Various US laws were adopted to regulate such issues, including the Dangerous Cargo Act (1952) and the Hazardous Materials Transportation Control Act (1970). The European Agreement Concerning the International Carriage of Dangerous Goods by Road, the first international agreement that regulated road transport, was adopted in 1957 and regularly upgraded in the next few decades. Moreover, individual European countries also issued national laws and regulations such as the Law on the Transport of Dangerous Goods (Gesetz über die Beförderung gefährlicher Güter) of 1975 and the Dangerous Goods Ordinance Road (Gefahrgutverordnung Strasse) of 1985 in Germany.76

32  Ernst Homburg and Elisabeth Vaupel

Regulations on the safety of transporting dangerous goods were of course closely linked to issues on the classification and labeling of hazardous cargo. Railway chemists in Britain undertook one of the first attempts to arrive at a more comprehensive classification of dangerous substances in 1892, agreeing on a classification of four types of dangerous goods: explosives, inflammable liquids, dangerous and corrosive chemicals, and miscellaneous. Each category was subdivided according to the magnitude of the hazards involved—the explosives into the seven categories introduced in 1875, and the inflammable liquids, for instance, into categories based on the flash point. On top of that, the committee specified the “conditions of carriage,” forming guidelines on how each material should be stored, packed, and labeled and which precautions should be taken during loading and unloading. By 1914, the British railway companies had adopted a uniform system of labels—consisting of the name of the hazard class and a symbol—that indicated whether a wagon was carrying explosives (circle), inflammable liquids (cross), or dangerous goods (rectangular box).77 That British system formed the basis for later international classification and labeling systems intended to improve the safety of transport. An important milestone was reached when the UN published in 1957 the “Orange Book” (Transport of Dangerous Goods: Recommendations Concerning the Classification, Listing and Labelling of Dangerous Goods and Shipping Papers for Such Goods), which classified hazardous materials into nine groups: explosives, compressed gases, inflammable liquids, inflammable solids, oxidizing substances, poisonous and infectious substances, radioactive materials, corrosives, and miscellaneous. The Orange Book listed some 2,500 items of commonly carried dangerous goods. This first important international set of recommendations created a framework for more specific regulations for the transport by rail, ship, air, and road and found its way into many countries’ national legislation. In an updated fashion, it remains in force today.78 Classification and Labeling of Workplace Chemicals In the 1950s, attempts were also made to extend these transport rules and regulations to the classification and labeling of hazardous substances in the workplace (factories, laboratories, etc.). The ILO played a crucial role in developing those “communication systems,” especially after World War II. From 1950 onward, the ILO Chemical Industries Committee was busy with classifying and labeling dangerous, obnox-

Introduction  33

Figure 0.1  Illustration of the five symbols for dangerous substances adopted by the Council of Europe in 1962. The symbols for corrosive, explosive, inflammable, oxidizing, and poisonous substances are shown from left to right. The ILO had already proposed four of these symbols in 1952. Source: Rodgers et al., International Labour Organization, 123, fig. 3. Published with permission.

ious, and toxic chemicals and, in 1952, proposed five basic symbols for hazardous materials: liquids spilling (corrosion), bomb (explosion), flame (fire), skull and crossbones (poison), and trefoil (radioactivity). However, the UN Economic and Social Council did not adopt this ILO system until 1958. In the following decade, these symbols found their way into the “Yellow Book” for workplace chemicals, which the Council of Europe adopted in 1962. In that document (Dangerous Chemical Substances and Proposals Concerning Their Labelling), the symbol for radioactive substances, regulated by a separate convention, was replaced by a symbol for oxidizing agents (see fig. 0.1). It specified the required labeling of five hundred chemical substances frequently used in factories and other workplaces. A few years later, new symbols were added for noxious chemicals and irritating chemicals—for instance, in the EEC Dangerous Substances Directive of 1967. The hazards considered in the Yellow Book and the DSD were related to explosions, fire (oxidizing substances, inflammable substances, highly inflammable substances), health (noxious or unhealthy substances, toxic substances, highly toxic substances), and skin damage (corrosive substances, irritating substances). In the next decade, new pictograms were added for highly inflammable chemicals, highly toxic chemicals, and, finally, environmental hazards. These were incorporated in the recommendations of the International Organization for Standardization.79 For the subclassification of certain hazards, TLVs were increasingly used in the twentieth century. The distinction between corrosive and irritating substances in the DSD was still qualitative: corrosive substances destroyed the human tissue, whereas irritating substances “only” caused inflammation. In the case of fire hazards, the flash point criterion had already been used since the late nineteenth century and

34  Ernst Homburg and Elisabeth Vaupel

divided at first all substances into two classes: flammable and nonflammable. By the 1960s, this had developed into a system with three classes: highly flammable (flash point less than 21 degrees Celsius), flammable (flash point between 21 and 55 degrees Celsius), and nonflammable. In the case of toxic substances such as pesticides, the LD50 was the usual criterion. In the case of acute oral poisons, the WHO had distinguished four categories since 1975: extremely toxic substances with an LD50 less than 5 ppm; highly toxic substances with am LD50 between 5 and 25 ppm; moderately toxic substances with an LD50 between 25 and 200 ppm; and noxious, or unhealthy, substances with an LD50 between 200 and 2,000 ppm.80 In the 1970s, the evaluation, handling, regulation, and management of hazardous materials, substances, and chemicals became a booming field, with its specific conferences, handbooks (e.g., those by James H. Meidl in 1970 and 1972), and scientific journals (e.g., Journal of Hazardous Materials, launched in 1975). The paradigm of industrial toxicology—with its rather technical use of exposure models, risk calculations, and TLVs—was the dominant approach, despite growing debates on the effects of low doses and an increased awareness of the role of uncertainties. Regulation of hazardous substances in the last two decades of the twentieth century was characterized by the introduction of an increasing number of hazard categories and of ever more danger classes within each category.81 This approach culminated in the Globally Harmonized System of Classification and Labeling of Chemicals developed under the auspices of the UN after the 1992 Rio de Janeiro Earth Summit. The GHS was codified in the “Purple Book” adopted at the 2002 World Summit on Sustainable Development at Johannesburg, together with the Strategic Approach on International Chemicals Management, of which the GHS became a component. The introduction of the GHS did not occur rapidly. Japan and New Zealand adopted the system in 2008, and the EU ratified a new classification, labeling, and packaging legislation based on the GHS in 2009, which replaced the DSD of 1967. The GHS was gradually introduced in practice at the end of 2010 for chemical substances and before June 2015 for mixtures. Instead of five classes for physical hazards, nine for health hazards, and one for environmental hazards, the new UN system distinguished no less than sixteen types of physical hazards, eleven of health hazards, but still only one of environmental hazards. Also, the number of hazard pictograms changed from seven to nine. The six old pictograms stayed more or less the same, but three new symbols were introduced: a gas cylinder, for gases under pressure; an

Introduction  35

exclamation mark for harmful substances, dangerous to health, without being a poison; and a torso for health hazards as a result of carcinogenic, mutagenic, or teratogenic chemicals. By putting the last types of hazards in a separate class, apart from the classes of poisons in which they had been included before, the UN finally did some justice to the debates on these types of risks that had taken place since the 1950s.82 In the past ten to fifteen years, these regulations on the classification and labeling of chemicals have increasingly been related to, and integrated into, the legislation on poisonous substances and to rules on admitting chemicals to the market. We will discuss those recent developments in this volume’s conclusion.

The Structure and Content of This Book: From Schweinfurt Green to MTBE We have divided the chapters of this book into three parts. This division into three clusters is partly chronological and partly thematic. The scientific paradigms and regulatory mechanisms dominant in one period do not suddenly cease to exist during the next one. Hence, the three phases, or parts, are “cumulative.” Issues characteristic for an earlier period still can play a role in the next one, but new insights and procedures begin to be important as well. Part I In part I, we have grouped three chapters on pigments and other substances containing lead and arsenic, that were already known to be acute poisons for a long time. There was no doubt those substances were dangerous. So, the toxicological aspects themselves are not the main issue in this cluster, although those aspects certainly played a role in the debates on the hazards of tetraethyl lead in Christian Warren’s chapter, in which he extensively discusses Robert Kehoe’s theory of “a threshold for lead absorption below which no illness [would] occur.” As a result, the chapters’ focus is on the regulation of these poisonous substances in different domains such as food and nutrition, the workplace, homes, and, finally, the environment. Together, these chapters show the importance of the establishment and existence of regulatory and advisory bodies in the nineteenth and early twentieth centuries, with France and Germany being ahead of the United States. These chapters also

36  Ernst Homburg and Elisabeth Vaupel

demonstrate differences in legal and political cultures, with, according to Joost Mertens, a quite strict separation between French politicians and scientific advisers, as contrasted to a stronger integration of experts within the German state bureaucracies. Although toxicological issues are generally not prominent on most of pages of part I, and differences between acute and chronic poisoning are not addressed explicitly, they do play a role “between the lines.” Arsenic and lead, and their chemical compounds, were known to be very dangerous acute poisons, but some health effects of a more chronic character were already known by around 1800. But the conceptual distinction between acute and chronic poisoning was only made systematically in the mid-nineteenth century, Alfred S. Taylor’s textbook On Poisons in Relation to Medical Jurisprudence and Medicine (1848) being one of the earliest examples. To some degree, the great differences in morbidity between workers in white lead factories and (house)painters, shown in Lestel’s chapter, can also be interpreted as resulting from acute versus chronic poisoning. In the early nineteenth century, white lead workers were sent to hospitals by the dozen each year, and many of them died. By the end of the century, after technological improvements in the factories had reduced the exposure, the public debates shifted to the more gradual and cumulative health problems encountered by painters using white lead. Warren’s chapter mentions other serious consequences of chronic lead poisoning such as illness, or even death, of children under five in the United States, living in houses painted with white lead inside. Since the mid-1960s, the dangers of chronic poisoning by low doses of lead compounds dissipated through the ­environment—as a result of using TEL in gasoline—were heavily debated again, after Kehoe’s theory had come under attack. Part II By contrast to part I, the four chapters of part II address to a much larger degree the discovery of new diseases, health effects, and, as a result, insights in toxicology. Stoff and Travis analyze in their chapter how the carcinogenic properties of chemical substances were discovered and addressed in the first six decades of the twentieth century. Although examples of carcinogenic effects of substances, such as chimney soot,83 can be identified with hindsight, these effects were absolutely no issue in nineteenth-century toxicology. Only since the late nineteenth century were specific chemicals gradually identified as a possible cause of cancer,

Introduction  37

next to radiation and genetic factors. Aromatic amines had the doubtful privilege to be among the earliest suspects, because of bladder cancer found among workers in the synthetic dyestuffs industry, as discussed earlier. It took industrial toxicologists and factory physicians—as early “merchants of doubt”—several decades of debate to agree on which aromatic amines were the most dangerous.84 As a result, the regulation of these substances mostly occurred after World War II. The related synthetic food colorant “butter yellow” played a key role in that respect. The chapter shows that the substance was important not only in accelerating debates on the regulation of (carcinogenic) food additives but also in the emerging insight that there was probably no threshold level below which carcinogenic chemicals were safe. In Schwerin’s chapter, food additives also play a central role, now in form of cyclamates sweeteners. The interesting aspect here is that in the 1960s and 1970s, next to carcinogenic effects, mutagenic effects also increasingly received attention, thereby widening the entire spectrum of toxicological effects from acute and chronic effects to totally different types of acute and chronic physiological, histological, cellular, and genetic changes. Schwerin shows the complexity of the issues involved—for instance, of the (assumed) relationships between mutagenic and carcinogenic effects—the role uncertainty played in the debates on these issues, and the influence of the different political cultures in the United States and Germany, leading to contrary outcomes in the regulation of cyclamates. The novelty of the chemical substances involved is not a major issue in part II. Aromatic amines were already produced for decades before the debates of their carcinogenic properties started. Cyclamates, by contrast, were fairly new, but the chapter focuses more on the health effects themselves and regulatory issues. An even stronger example of an old substance creating new problems is the discovery of the cause of the so-called itai-itai disease in Japan in the early 1960s, as described by Masanori Kaji. The element cadmium had been known for more than 150 years, but by 1960, there were still no systematic insights about its health effects but only scattered reports. The painful itai-itai disease was first described in the 1930s in the basin of the Jinzū River, where a Mitsui Group zinc factory discharged its effluents upstream. But it took another three decades before it could be proved that the cadmium content of the effluents was the major cause of the disease. One of the most fascinating aspects of Kaji’s chapter is how it illustrates the great changes in political culture that took

38  Ernst Homburg and Elisabeth Vaupel

place in Japan in the 1960s—just as in other highly developed market economies. Although the Mitsui Group experts continued to deny, as they had done in earlier decades, any relation between their effluents and the disease, a special grassroots coalition of victims, lawyers, and physicians, together with some allies belonging to the establishment, won several lawsuits, culminating in 1972 in a total defeat of the Mitsui Group’s case. The itai-itai case illustrates well not only the fundamental political changes of the 1960s but also how different professional groups seized the opportunity to team up with the victims and being to act as their spokespersons. Schwerin underlines the same point in the cyclamate debates when he signals the sometimes-opposing views of “agencies, media, politicians, and scientists, all of them claiming to speak for the interests of the consumer.” Both the role of the 1960s and issues of spokesman ship return in Stefan Böschen’s chapter on the changing perceptions of the dangers of dioxins. After decades of obscurity, since around 1900, as an acute and a chronic industrial poison in the electrochemical industry, dioxins in the 1960s and 1970s completely broke out of the confines of industrial toxicology due to their presence as a highly toxic contaminant of phenoxy herbicides (Agent Orange) used in Vietnam, as well as to the Seveso disaster on 10 July 1976. As a result, in the 1980s, dioxins developed into a “total poison,” debated in several arenas, to the degree that only mentioning “dioxins” was enough to end every discussion of the actual risks involved. Böschen also highlights the roles played by uncertainties, analyzed by Schwerin as well, and “nonknowledge,” sometimes used by “merchants of doubt” to avoid regulatory decisions. The extremely high acute toxicity of several dioxins, as well as the great diversity within this family of chemicals, for a long time masked the more complex chronic effects of low doses of these substances, be they carcinogenic, mutagenic, or teratogenic. Because of all these diverse aspects, almost all the issues discussed in part II, and even part I, culminate in Böschen’s chapter. Dioxins are the “collective symbols” in which the old and newly discovered health effects come together, because they combine a high acute toxicity with carcinogenicity. Moreover, they shed light on many other hazardous malpractices and “surprises”: think of the role of accidents (Seveso), of side effects of intended uses (Vietnam), and of the global effects of industrial behavior (burning waste, exporting hazards to under­ developed countries).85

Introduction  39

Part III Part III focuses on the environmental effects of hazardous chemicals. Although Rachel Carson’s iconic Silent Spring is also discussed in several of the aforementioned chapters, it plays a key role in this part. Three of the four chapters here specifically discuss the social, political, and natural history of pesticides, which play a great role in Carson’s book, and all four are very much focused on the environmental effects of chemicals, a topic put strongly on the map generally in the 1960s, and by Silent Spring in particular. Although the environmental and ecotoxicological effects of chemicals to some degree are already foreshadowed in the chapters by Warren, Kaji, and Böschen, they form the overarching topic of part III. The four chapters bring the reader to the start of twenty-first century and all address issues such as environmentalism and political culture that fully unfolded only in the 1960s. In that sense, the long shadow of the 1960s unites them all. In the first part of Frederick Davis’s chapter, the reader is struck by the important role played by sophisticated chemical and toxicological detail and research in the development of the organophosphates. Through taking a step backward, it is important to note this phenomenon unites almost all the chapters of parts II and III. Although scientific expertise played a role in the nineteenth century as well, the huge development in the twentieth century of industrial toxicology, medical science in general, ecology, and, last but not least, chemical analysis with highly sophisticated instruments—as well as the increased specialization and institutionalization of these fields—have fundamentally transformed debates on risk and safety. The second part of Davis’s chapter focuses on organophosphates as problematic successors to DDT, the other “collective symbol” in the domain of hazardous chemicals, next to dioxins (Böschen). DDT, which played a major role in Silent Spring, is the subject of a very interesting chapter by Peter Morris in which the “substance histories” of DDT in the United States and the United Kingdom are compared. The differences appear to be huge: in terms of not only the quantities used in agriculture in the first place (the United Kingdom being dwarfed by the United States) but also political culture and regulatory policies. In the United States, the precautionary principle implied by the Delaney clause regarding cancer risks (see Böschen; Morris; Schwerin) played a role, but even more so did the numerous law suits initiated by citizen groups, biologists, environmentalists, and lawyers. In that respect, there

40  Ernst Homburg and Elisabeth Vaupel

are quite some parallels with the Japanese story told by Kaji, and with Amy Hay’s chapter on Agent Orange and other herbicides in which law suits fought by Vietnam veterans are shown to have played an important role. In the United Kingdom by contrast, as Morris argues, backroom negotiations between government officials and various interest groups dominated the scene. Schwerin notes a similar distinction between the United States and, in that case, Germany. Although the book lacks a specific chapter on the great global atmospheric and stratospheric chemical hazards heavily debated in the past few decades—climate change and the depletion of the ozone layer—the issue lurks around in John Smith’s chapter on the fate of MTBE as a gasoline additive in the United States. Introduced in the 1970s as a replacement for TEL as a high-octane component that would not affect the exhaust pipe catalyst, it later grew in importance when the oxygen content of gasoline had to be raised for environmental reasons. In that role, it entered into competition with bioethanol, which finally won the battle for political reasons, Smith argues, because assumptions about the greenhouse effect sparked the desire for an allegedly renewable fuel. Smith also nicely shows how the economic interests of corn and sugar producers played a role in the MTBE debates, a topic foreshadowed in Schwerin’s chapter when he addresses the role of sugar producers in discussing cyclamate sweeteners in the United States. That does not mean, of course, the importance of industrial lobbies is limited to the United States. One could argue the role of litigation in the US system, as well as the local interests defended by senators and other politicians, make that role in the United States just more visible. For a long time in Europe, these influences were more hidden because of informal, confidential consultation and backroom negotiations. As the example of the REACH legislation shows, discussed in our conclusion, industrial interests and lobbies are now very present in Europe. This brief discussion of some important aspects of the chapters of this book, without discussing all their rich details, suffices to demonstrate that the book as a whole gives a broad and interesting picture of the changing ways in which societies coped with chemical hazards. In our conclusion, we will return to some of these issues and analyze the outcomes of the chapters chronologically in relation to important recent studies. We will then also discuss more explicitly the differences and similarities between the three parts.

Introduction  41

Ernst Homburg is Professor Emeritus of History of Science and Technology at Maastricht University. He studied chemistry in Amsterdam and was connected to the universities of Groningen, Nijmegen, Eindhoven, and Maastricht. From 1989 to 2003, he coedited two book series on the history of technology in the Netherlands in the nineteenth and twentieth centuries. He has published widely on the history of the chemical profession, technical education, the chemical industry, textile printing, and the environment. He was president of the Dutch Society for the History of Medicine, Mathematics, Science, and Technology (1995–1998) and of the European Working Party on the History of Chemistry (2003–2009). In 2014, he received the American Chemical Society HIST Award. His most recent books are, with Nicolas Coupain and Kenneth Bertrams, Solvay: History of a Multinational Family Firm (2012), and, with Ineke Pey, Een kabinet vol kleur: De collectie schildersmaterialen van de Amsterdamse verfhandelaar Michiel Hafkenscheid (1772–1846) (2018). Elisabeth Vaupel is a historian of chemistry at the Forschungsinstitut of the Deutsches Museum. She focuses on the history of chemistry in the nineteenth and twentieth centuries. Recent publications include “Ersatzgewürze (1916–1948): Der Chemie-Nobelpreisträger Hermann Staudinger und der Kunstpfeffer” (Technikgeschichte, 2011), “Edelsteine aus der Fabrik: Produktion und Nutzung synthetischer Rubine und Saphire im Deutschen Reich (1906–1925)” (Technikgeschichte, 2015), and “Kinder, sammelt Knochen! Lehr- und Propagandamittel zur Behandlung des Themas Knochenverwertung an deutschen Schulen im ‘Dritten Reich’” (NTM, 2018). She coedited, with Stefan L. Wolff, Das Deutsche Museum in der Zeit des Nationalsozialismus: Eine Bestandsaufnahme (2010). Notes   1. Rehn, “Blasengeschwülste”; Berenblum, “Aniline Cancer”; Schmähl, “Krebser­ zeugende Stoffe”; Blackadar, “Historical Review.” See also Stoff and Travis, this volume.  2. Haber, Chemical Industry.   3. Struyker Boudier et al., Risiko’s meten, 37–55.  4. For a theoretical reflection on, as well as the empirical study of, relations between material processes and knowledge production, see Latour, Pasteurization; Vries, Bruno Latour, 53–81.

42  Ernst Homburg and Elisabeth Vaupel

  5. Gelbke and Fleig, “Entwicklung,” 303–4; Lönngren, International Approaches, 19–20; Führ, “REACH,” 110; Langston, “New Chemical Bodies,” 260; Golding, History, 96.   6. See the page “Basic Chemicals” of “The Essential Chemical Industry—Online”, last consulted 31 March 2019, which lists the most important chemicals and their production figures. http://www.essentialchemicalindustry.org/chemicals. html. For historical figures, see Goertz, World Chemical Industry; Reuben and Burstall, Chemical Economy.  7. Bora, Henkel, and Reinhardt, “Einleitung”; Versluis et al., “EU Seveso”; Böschen, “Risikogenese”; Scheringer et al., “Will We Know,” 700.  8. For references to literature from the 1970s to the 1990s, see Homburg, “Industrie”; Homburg, “Schrikbeelden”; Homburg, “Pollution.” For reviews of recent literature on toxicants and regulation, see Jas, “Chemicals”; GuillemLlobat, “Science”; Bertomeu-Sánchez and Guillem-Llobat, “Following Poisons”; Demortain, “Expertise”; Kirchhelle, “Toxic Tales.”  9. Simon, DDT; Ball, H2O; Whorton, Arsenic Century; Böschen et al., “Stoffgeschich­ten”; Chang and Jackson, Element; Hahn and Soentgen, “Acknowledg­ ing Substances,” 19–33. 10. An even broader view can be obtained by considering the “substances histories” that were presented at the same conference on which this book is based but have been published elsewhere. Erker, “Hazardous Substances” (on quicksilver, benzene, asbestos, organobromine compounds, carbon dioxide, picloram, and Agent Orange); Tyabji, “Hazard Concerns.” For a recent history of toxic substances and pollution in a non-Western country (India), see Arnold, Toxic Histories. 11. Based on searches in large (national) library catalogs on these terms. 12. Boudia, “Managing Scientific.” Today, “dangerous goods” is limited to transport regulations, although “hazardous materials” is more common in that field in the United States. “Dangerous goods” is in some respects narrower than “hazardous chemicals” (namely, now, only relating to transport and, mainly, acute dangers), and in other respects broader (namely, articles such as air bags and lithium batteries, as well as radioactive substances, that are mostly regulated separately). See CSP, “Differences.” 13. Stevenson, Meaning, 1–22; Wahrig, “Gift,” in Literatur; Dilg, “Griechischen.” 14. Mead, Mechanical Account, 131–32; Steinschneider, Toxikologischen Schriften; Kuhlen, “Gift”; Kreek, “Alexander Willem Michiel,” 6. 15. Kegler, Nützlichs und tröstlichs; Wood, From Miasmas, 1–23; Bynum et al., Dictionary, 75–76, 409, 428; Fischer-Homberger, Medizin, 361–64; Montfort, “Venenum,” 309–23; Wahrig, “Organisms”; Crowther, “Toxicology”; Mead, Mechanical Account, 149–83; Hunter, “Of Poisons.” 16. Montfort, “Venenum”; Gmelin, Allgemeine Geschichte, 18–21; Deichmann et al., “What Is There”; Ickert, “Von der rechten Dosis”; Papadopoulos, “Gift.” 17. Mead, Mechanical Account; Halle, Gifthistorie, 2; Wahrig, “Gift,” in Enzyklo­ pädie; Sudhoff, Versuch, 100–101; Paracelsus, Sieben Defensiones, 8, 25;

Introduction  43

Stadlinger, “Paracelsus,” 349; McLean, “Pesticides,” 614. The only historian, as far as we know, who related late eighteenth-century discourses on doses directly to the ideas of Paracelsus is Esther Fischer-Homberger, but she does not give any direct evidence for that link or seem to have realized that Paracelsus’s concept of dose was totally different from the eighteenth-century notions. See Fischer-Homberger, Medizin, 377–78, 393–95, 401, 406. 18. Plenk, Toxikologie, 11; Paris and Fonblanque, Medical Jurisprudence, 131; Fischer-Homberger, Medizin, 395–99, 402–6; Earles, “Experiments”; Kreek, “Alexander Willem Michiel,” 7–13; Wahrig, “Zeit”; Wahrig, “Organisms”; Crowther, “Toxicology”; Wahrig, “Geheimnis”; Bertomeu-Sánchez et al., Chemistry. See also Watson, Forensic Medicine. 19. Schneider, Ueber die Gifte; Marx, Lehre; Christison, Treatise; Wahrig, “Erzählte Vergiftungen”; Wahrig, “Geheimnis.” 20. We refer to this book’s chapters by mentioning the name(s) of the author(s) in in-text parentheticals. 21. Ramazzini, Abhandlung; Paris and Fonblanque, Medical Jurisprudence, 143– 49; Christison, Treatise, 162, 207, 364–65; Taylor, On Poisons, 98–99; Hasselt, Handbuch; Hirt, Gewerblichen Vergiftungen, esp. 3–4, on the distinction between acute and chronic poisoning; Weichardt, “Gewerbetoxikologie,” 198– 206; Wahrig, “Organisms”; Crowther, “Toxicology”; Wahrig, “Geheimnis”; Reinhardt, “Expertise”; Friedrich, “Apotheker”; Whorton, Arsenic Century, 174, 188–92. Joseph Adams (Observations), building on earlier ideas by Thomas Sydenham and John Hunt, distinguishes between chronic and acute but refers to diseases, not to the contagious poisons themselves. 22. Boens, Étude hygiénique; Eulenberg, Lehre; Spelsberg, Rauchplage; Homburg, “Schrikbeelden”; Wilmot, “Pollution,” 121–47. Although the mid-nineteenth century views were ambiguous, some actors, such as Eulenberg, also saw the nuisances and toxic effects caused by some gases as a chemical affair. We therefore disagree with Rachel Rothschild (“Turn towards Toxins”), who argues the “toxic fog” of December 1930 in the Meuse Valley was the historical turning point for understanding chemicals as toxic. 23. Hepburn, Crop Production; Wood, From Miasmas, 29–32, 37–40, 95; Bynum et al., Dictionary, 22–23, 39, 75–77, 200; Fischer-Homberger, Medizin, 378; Langston, “New Chemical Bodies,” 261. 24. Spelsberg, Rauchplage, 205–14; Homburg, “Schrikbeelden”; Homburg, “Pollution”; Walker, “Occupational Health,” 33–36, 155–56, 238–40, 265–66; Zimmer, “Brouillard”; Zimmer, “Dodelijke nevels”; Rothschild, “Turn towards Toxins,” 128; Newman, Love Canal. 25. Lewin, Lehrbuch, iii–v; Mohr, Chemische Toxicologie; Kobert, Lehrbuch; Baumert, Lehrbuch; Lewin, Gifte; Kreek, “Alexander Willem Michiel,” 14;  Wahrig and Neubaur-Stolte, “1929”; Bertomeu-Sánchez, “From Forensic,” 92. 26. Mohr, Chemische Toxicologie; Bertomeu-Sánchez et al., Chemistry; Reinhardt, “Expertise.”

44  Ernst Homburg and Elisabeth Vaupel

27. Moeschlin, Klinik, preface; Walker, “Occupational Health,” 152, 155; Wahrig and Neubaur-Stolte, “1929,” 83; Scheringer et al., “Will We Know,” 700; Boudia, “From Threshold.” See also Langston, “New Chemical Bodies,” 260. 28. The date 1880 is based on a search for “minimal lethal dose” in Google Books. See Trevan and Dale, “Error”; Gaddum, “John William Trevan”; Leake, “Scientific Status,” 2073. 29. Hamilton, Industrial Poisons; Hamilton and Johnstone, Industrial Toxicology; Cage, “Development,” 227; Moeschlin, Klinik, 37–45; Lönngren, International Approaches, 23, 43; Weichardt, “Gewerbetoxikologie,” 206–8, 217–18; Gelbke and Fleig, “Entwicklung,” 327–28; Andersen, “Pollution”; Reinhardt, “Limit Values”; Sellers, “Cold War,” 25–45; Langston, “New Chemical Bodies,” 260–61; Plumpe, Carl Duisberg, 466–80, 661–70. See also “Haber’s Rule,” Wikipedia, last edited 4 October 2018, 16:51, https://en.wikipedia.org/wiki/ Haber%27s_​rule. 30. Carson, Silent Spring; Briejèr, Zilveren sluiers; Spelsberg, Rauchplage, 205–14; Lönngren, International Approaches, 28, 45–48, 60–62, 66–67; Tesh, Uncertain Hazards, 43–49; DeSombre, Domestic Sources, 81–88; Böschen, Risikogenese, 266–76; Morris, “Parts per Trillion”; Forths et al., “Arzneimittel,” 65–68; Kirk, Contergan-Fall; Botting, “History”; Jas, “Adapting.” See also Stoff and Travis, Schwerin, Morris, Kaji, and several other authors, this volume. 31. An illuminating study of the rise of ecotoxicology that addresses the change in focus from humans to nonhuman biota, is Halffman, Boundaries, esp. 116– 17, 157–58, 167, 322–23, 413–18. See also JMPR, Evaluation; Spelsberg, Rauchplage, 209–10; DeSombre, Domestic Sources, 81–88; Langston, “New Chemical Bodies,” 262–63. 32. Prestwich, On Mineral, 1; Gmelin, Allgemeine Geschichte, 22; Schlemper, Over den invloed; Matsumura et al., Environmental Toxicology; Engelhardt and Lange, Chemikaliengesetz, 22–24; Andersen, “Pollution,” 196–97; Böschen, Risikogenese, 276–301; Wahrig, “Organisms,” 162–63, 179. 33. Creager, “Political Life,” 46–64. 34. “ACS Updates Environmental Report,” Chemical & Engineering News, 56, no. 49 (1978): 34–36; Reinders, Risico’s; Tesh, Uncertain Hazards; Schwerin, “Low Dose Intoxication,” 401–18; Bächi, “Zur Krise”; Reinhardt, “Limit Values,” 596; Scheringer et al., “Will We Know,” 700; Jas, “Adapting,” 64–65; Boudia, “From Threshold”; Boudia, “Managing Scientific.” An early example of risk concept is Weisburger and Weisburger, “Chemicals,” 124–42. 35. Cf. Margerison et al., Superpoison; Hemminger, Vorsicht Gift; Henseling, Planet. 36. Beck, Risk Society; Lönngren, International Approaches, 21; Bora, Henkel, and Reinhardt, “Einleitung.” 37. Schot, Geven; Gaudillière and Hess, Ways of Regulating; Gaudillière, “DES,” 91; Bora, Henkel, and Reinhardt, “Einleitung”; Demortain, “Expertise.” 38. For an overview, see Boudia and Jas, “Introduction,” 3–14; Boudia and Jas, “Gouverner.”

Introduction  45

39. Kuhlen, “Gift,” 1446; Steinschneider, Toxikologischen Schriften, 16–18. 40. Lenihan and Fletcher, Chemical Environment, 99; Wahrig, “Stoff der Macht,” 311–12; Wahrig, “Erzählte Vergiftungen,” 100–101; Fischer-Homberger, Medizin, 79, 96, 98; Gelbke and Fleig, “Entwicklung,” 341–42. 41. Rücker, “Langer Weg”; French and Phillips, Cheated, 34; Weber, Food; Lönngren, International Approaches, 22–23, 30, 47–49. 42. Gelbke and Fleig, “Entwicklung,” 297–98; Brosnan, “Law,” 538; Langston, “Precaution,” 30–31; Gaudillière, “DES,” 68. 43. Moeschlin, Klinik, preface; Homburg, “Era,” 437; Le Fanu, Rise and Fall, 211–20; Forth et al., “Arzneimittel”; Gelbke and Fleig, “Entwicklung,” 341–44; Rücker, “Langer Weg”; Kirk, Contergan-Fall; Jungmayr, “ConterganTragödie”; Blasius, “25 Jahre”; Schmidt, “50 Jahre”; Johnson et al., Thalidomide Catastrophe. 44. Chandler, Shaping, 239–56; Homburg, “Era,” 544–51. On the actual European practice of regulation, see Hauray, “From Regulatory Knowledge.” 45. Gelbke and Fleig, “Entwicklung,” 313–14; Fischer-Homberger, Medizin, 96; Hartman, Bestuur, 299–302. 46. French and Phillips, Cheated, 1, 5, 34–37, 112; Baumert, Lehrbuch, 27, 30; Dennstedt, Chemie, 400–403; Hahn and Winters, “Neuordnung,” 399; Vaupel, “Arsenhaltige Verbindungen,” 40; Weber, Food, 1, 14; Gelbke and Fleig, “Entwicklung,” 314, 341–43. 47. Hepburn, Crop Production; Bogaers, Blaastumoren, 60; French and Phillips, Cheated; Gelbke and Fleig, “Entwicklung,” 314–15, 327; Lönngren, International Approaches, 68–70; Jas, “Adapting,” 49–65. 48. Langston, “New Chemical Bodies,” 262–71; Jas, “Adapting,” 49. 49. Helvoort et al., Gesmeerde kennis, 39–42; Hahn and Winters, “Neuordnung,” 398–99. 50. Fischer-Homberger, Medizin, 96, 98. 51. Klemann, “Central Commission,” 35, 37, 39, 46–47; “Reglement betrekkelijk den vervoer van Arsenicum en andere metaal-vergiften: Aanhangsel van het protocol no. XVII van 24 julij 1838,” Staatsblad van het Koninkrijk der Nederlanden 1 (1844): 16–18; Hartman, Bestuur, 53. 52. Andersen, “Pollution,” 186–89; Graaff, “Milieuvervuiling.” 53. Müller, Paracelsus; Homburg and Vlieger, “Victory,” 38; Weichardt, “Gewer­ betoxikologie,” 220–24. 54. Freychinet’s reports were published in several issues of the Annales des Mines vols. 5–10 (1864–1866). For the final report, see Freycinet, Traité. Walker, “Occupational Health.” 55. Graham, “Class II,” 92; De La Rue and Hofmann, “Class XXIX,” 1410–12; Schrötter and Anthon, “Classe II,” 84–89; Hahn and Winters, “Neuordnung,” 399; Lönngren, International Approaches, 23, 43. For conflicting views on the role of Darcet, see Le Roux (Laboratoire, 305–448; “Governing,” 76–78), who points to Darcet as a key chemist and industrialist who “liberalized” (i.e., weakened) the traditional industrial regulations in the interests of industry,

46  Ernst Homburg and Elisabeth Vaupel

and Jorland (“Review”), who emphasizes his role as technical innovator, also with positive effects for workers and neighbors. 56. See also Rainhorn, “Santé.” 57. Fuchsloch, “Blau—Weiss,” 213–14; Lenihan and Fletcher, Chemical Environment, 68–70, 76–77; Walker, “Occupational Health,” 33; Lönngren, International Approaches, 23, 38, 41–43; Golding, History, 145–46. 58. Cinquième congres international d’hygiène et de démographie à La Haye (du 21 au 27 août 1884): Comptes rendus et mémoires, publiés par le secrétaire général avec le concours de MM. les Secrétaires de Séances et MM. les Secrétaires des Sections, vol. 2 (The Hague, 1884–1885), 209–14; Weber, Arbeitssicherheit, 17, 19, 103–4; Walker, “Occupational Health”; “Bekanntmachung über die Gewährung von Sterbegeld und Hinterbliebenenrenten bei Gesundheitsschädigung durch aromatische Nitroverbindungen,” Reichsgesetzblatt, 12 October 1917, 900; Weichardt, “Gewerbetoxikologie,” 208–14; Gelbke and Fleig, “Entwicklung,” 341–43; Bächi, “Zur Krise,” 419. 59. Lenihan and Fletcher, Chemical Environment, 58; Walker, “Occupational Health,” 34, 117–18, 121, 150, 155–57, 241–42; Bogaers, Blaastumoren, 45–46, 79–80; Weichardt, “Gewerbetoxikologie,” 212–17; Sellers and Melling, Dangerous Trade. 60. Gelbke and Fleig, “Entwicklung,” 300, 341–44; Walker, “Occupational Health,” 157; Levinson, PVC; Homburg, “Era,” 369–73; Markowitz and Rosner, Deceit and Denial, 178–233; Krimsky, “Low-Dose Toxicology”; Golding, History, 152–59. 61. Vaupel, “Arsenhaltige Verbindungen,” 44–58; Weber, Food, 32; Gelbke and Fleig, “Entwicklung,” 342. 62. See Russell, War and Nature. 63. Lowe, International Protection; Rodgers et al., International Labour Organization. 64. Lönngren, International Approaches, 27, 47–48, 55–57; Kinkela, DDT, 7, 15–21, 28–29; Vaupel, “Arsenhaltige Verbindungen,” 60. 65. Lear, Rachel Carson. 66. Lönngren, International Approaches, 28, 48, 51, 55–66, 72–74; Vaupel, “Arsen­ haltige Verbindungen,” 44, 50, 52, 57, 62; Gelbke and Fleig, “Entwicklung,” 312–13, 341, 343; Weber, Food, 1. 67. Roberts, “Unruly Technologies,” 256–57; Rosner and Markowitz, “Industry Challenges.” For a history of ecotoxicology, see Halffman, Boundaries. 68. Goulson, “Review.” 69. Schug, “Minireview.” 70. Koelma, Handboek, 4–6; Hartman, Bestuur, 179–81; Coronel, Gezondheidsleer, 16–20; Homburg, “Schrikbeelden,” 440–51; Le Roux, Laboratoire; Klein, “Risques industriels,” 260–65; Jarrige and Le Roux, Contamination, 92–102. 71. “Reglement betrekkelijk den vervoer van Arsenicum.” 72. Koelmans, “Van pomp,” 10–21, 24–26, 50; Hartman, Bestuur, 62, 128–29, 182, 223.

Introduction  47

73. Forbes and O’Beirne, Technical Development, 57; Peckham, Report, 220, 223–37; Wischin, Vademecum, 88–95; RDSG, Petroleum Handbook, 176–77; Koelmans, “Van pomp,” 50. 74. Lönngren, International Approaches, 78–80, 85; Russell and Hudson, Early Railway Chemistry, 151–63; Gelbke and Fleig, “Entwicklung,” 343; “1979 Mississauga Train Derailment,” Wikipedia, last edited 17 January 2019, 17:24, https://en.wikipedia.org/wiki/1979_​Mississauga_​train_​derailment. 75. Aeby, Dangerous Goods; Lönngren, International Approaches, 40, 80–81, 86. 76. Lönngren, International Approaches, 78, 80; Gelbke and Fleig, “Entwicklung,” 342–43. 77. Russell and Hudson, Early Railway Chemistry, 152–61. 78. EC, Chemicals, 7–8. 79. Lönngren, International Approaches, 27, 78–86; Rodgers et al., International Labour Organization, 122–23; “Richtlinie des Rates vom 27. Juni 1967 zur Angleichung der Rechts- und Verwaltungsvorschriften für die Einstufung, Verpackung und Kennzeichnung gefährlicher Stoffe,” Amtsblatt der Euro­ päischen Gemeinschaften 10, no. 196 (1967): 1–98; Seidl, “GHS.” 80. Lönngren, International Approaches, 63–64, 78–79; Seidl, “GHS.” 81. Reinhardt, “Regulierungswissen,” 351. 82. Fischer, “International einheitlich”; Darschnik, “Stolperstellen”; Jeschke, “Sicherheit koordinieren”; Karavezyris and Koch-Jugl, “Globale Chemikalien­ sicherheit”; EC, Chemicals; Seidl, “GHS.” 83. Brown and Thornton, “Percivall Pott.” 84. Oreskes and Conway, Merchants of Doubt. 85. Cf. Sellers and Melling, Dangerous Trade, 202–5; Kirchhelle, “Toxic Tales,” 219–20; Jas, “Chemicals,” 195–96; Jas, “Gouverner,” 53–60.

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Reinders, Lucas. Risico’s van wetenschap en techniek: Conflicten tussen gezondheid en vooruitgang. Amsterdam, 1980. Reinhardt, Carsten. “Expertise in Methods, Methods in Expertise.” In Science in the Context of Application, edited by Martin Carrier and Alfred Nordmann, 143–59. Dordrecht, 2011. _____. “Limit Values and Boundaries of Science and Technology.” Comptes Rendus Chimie 15, no. 7 (2012): 595–602. _____. “Regulierungswissen und Regulierungskonzepte.” Berichte zur Wissen­ schafts­geschichte 33, no. 4 (2010): 351–64. Reuben, B. G., and M. L. Burstall. The Chemical Economy: A Guide to the Technology and Economics of the Chemical Industry. London, 1973. Roberts, Jody A. “Unruly Technologies and Fractured Oversight: Towards a Model for Chemical Control for the Twenty-First Century.” In Boudia and Jas, Powerless Science?​254–68. Rodgers, Gerry, Eddy Lee, Lee Swepston, and Jasmien van Daele. The International Labour Organization and the Quest for Social Justice, 1919–2009. Geneva, 2009. Rosner, David, and Gerald Markowitz. “Industry Challenges to the Principle of Prevention in Public Health: The Precautionary Principle in Historical Perspective.” Public Health Reports 117, no. 6 (2002): 501–12. Rothschild, Rachel Emma. “The Turn towards Toxins: An Essay Review.” Endeavour 40, no. 2 (2016): 128–30. RDSG (Royal Dutch/Shell Group). A Petroleum Handbook. London, 1933. Rücker, Daniel. “Ein langer Weg zum Arzneimittelgesetz.” Pharmazeutische Zeitung 151, no. 3 (19 January 2006): 12. Russell, Colin A., and John A. Hudson. Early Railway Chemistry and Its Legacy. Cambridge, 2012. Russell, Edmund. War and Nature: Fighting Humans and Insects with Chemicals from World War I to Silent Spring. Cambridge, 2001. Scheringer, Martin, Stefan Böschen, and Konrad Hungerbühler. “Will We Know More or Less about Chemical Risks under REACH?​” Chimia 60, no. 10 (2006): 699–706. Schlemper, Pieter. Over den invloed van chemische stoffen op lagere organismen. Utrecht, 1942. Schmähl, Dietrich. “Krebserzeugende Stoffe.” In Amberger-Lahrmann and Schmähl, Gifte, 167–96. Schmidt, Michael. “50 Jahre Arzneimittelgesetz.” PTA heute, 23 December 2011, 44–46. Schneider, Peter Joseph. Ueber die Gifte in medicinisch-gerichtlicher und medicinisch-polizeylicher Rücksicht: Ein Handbuch für öffentliche und gerichtliche Aerzte, Apotheker und Rechtspfleger. 2nd ed. Tübingen, 1821. Schot, Johan W., Bas de Laat, and Ronald van der Meijden. Geven om de omge­ ving: Milieugedrag van ondernemingen in de chemische industrie. The Hague, 1990.

Introduction  57

Schrötter, Anton, and Friedrichs Anthon. “Classe II: Chemische Substanzen und Producte, pharmaceutische Processe.” In Österreichische Bericht über die Internationale Ausstellung in London 1862 im Auftrage des k.k. Ministeriums für Handel und Volkswirthschaft, edited by Joseph Arenstein, 63–95. Vienna, 1863. Schug, Thaddeus T., Anne F. Johnson. Linda S. Birnbaum, et al. “Minireview: Endocrine Disruptors: Past Lessons and Future Directions.” Molecular Endocrinology 30, no. 8 (2016): 833–47. Schwerin, Alexander von. “Low Dose Intoxication and a Crisis of Regulatory Models: Chemical Mutagens in the Deutsche Forschungsgemeinschaft (DFG), 1963–1973.” Berichte zur Wissenschaftsgeschichte 33, no. 4 (2010): 401–18. Seidl, Manfred. “GHS: Global Harmonisiertes System.” Chem-Page.de, last updated 3 October 2018. https://www.chem-page.de/sicherheit/ghs-globalharmonisiertes-system.html. Sellers, Christopher. “The Cold War over the Worker’s Body: Cross-National Clashes over Maximum Allowable Concentrations in the Post–World War II Era.” In Boudia and Jas, Toxicants, Health and Regulation, 25–45. Sellers, Christopher, and Joseph Melling, eds. Dangerous Trade: Histories of Industrial Hazard across a Globalizing World. Philadelphia, 2012. Simon, Christian. DDT: Kulturgeschichte einer chemischen Verbindung. Basel, 1999. Spelsberg, Gerd. Rauchplage: Zur Geschichte der Luftverschmutzung. Köln, 1988. Stadlinger, Hermann. “Paracelsus. 10 November 1493, † 24. September 1541.” Chemiker-Zeitung 65 (1941): 349–50. Steinschneider, Moritz. Die toxikologischen Schriften der Araber bis Ende des XII. Jahrhunderts: Ein bibliographischer Versuch, grossenteils aus handschriftlichen Quellen. Hildesheim, 1971. Stevenson, Lloyd G. The Meaning of Poison. Lawrence, KS, 1959. Struyker Boudier, Harry, Klaus Heilmann, and John Urquhart. Risiko’s meten: Een antwoord op de angst voor een technologische kultuur. Baarn, 1985. Sudhoff, Karl. Versuch einer Kritik der Echtheit der Paracelsischen Schriften, Theil 1: Die unter Hohenheim’s Namen erschienenen Druckschriften. Berlin, 1894. Taylor, Alfred S. On Poisons in Relation to Medical Jurisprudence and Medicine. Philadelphia, 1848. Tesh, Sylvia Noble. Uncertain Hazards: Environment Activists and Scientific Proof. Ithaca, NY, 2000. Trevan, John William, and Henry Hallett Dale. “The Error of Determination of Toxicity.” Proceedings of the Royal Society of London B 101, no. 712 (1927): 483–514. Tyabji, Nasir. “Hazard Concerns: MIC at Bhopal and Virginia and the Indian Nuclear Liability Act.” Economic and Political Weekly 47, no. 41 (2012): 41–50. Vaupel, Elisabeth. “Arsenhaltige Verbindungen vom 18. bis zum 20. Jahrhundert: Nutzung, Risikowahrnehmung und gesetzliche Regulierung.” Blätter für Technikgeschichte 74 (2012): 31–63.

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Versluis, Esther, Marjolein van Asselt, Tessa Fox, and Anique Hommels. “The EU Seveso Regime in Practice: From Uncertainty Blindness to Uncertainty Tolerance.” Journal of Hazardous Materials 184, nos. 1–3 (2010): 627–631. Vries, Gerard de. Bruno Latour. Cambridge, 2016. Wahrig, Bettina. “Erzählte Vergiftungen: Kriminalitätsdiskurs und Staatsarz­ neikunde 1750–1850.” In Fallstudien: Theorie—Geschichte—Methode, edited by Johannes Süßmann, Susanne Scholz, and Gisela Engel, 97–111. Berlin, 2007. _____. “Geheimnis und Publizität des pharmakon: Verhandlungen über den Umgang mit Giften im 18. Jahrhundert.” In Kulturen des Wissens im 18. Jahrhundert, edited by Ulrich Johannes Schneider, 45–59. Berlin, 2008. _____. “Gift.” In Enzyklopädie der Neuzeit, vol. 4, edited by Friedrich Jaeger, 896–900. Stuttgart, 2006. _____. “Gift.” In Literatur und Medizin: Ein Lexikon, edited by Bettina von Jagow and Florian Steger, 304–8. Göttingen, 2005. _____. “Organisms That Matter: German Toxicology (1785–1822) and the Role of Orfila’s Textbook.” In Bertomeu-Sánchez and Nieto-Galan, Chemistry, Medicine, and Crime, 153–82. _____. “Der Stoff der Macht: Gift und Elixier in E. T. A. Hoffmanns Erzählung ‘Ignaz Denner’.” In Rosarium Litterarum: Beiträge zur Pharmazie- und Wissen­schaftsgeschichte: Festschrift für Peter Dilg zum 65. Geburtstag, edited by Christoph Friedrich and Sabine Bernschneider-Reif, 311–20. Eschborn, 2003. _____. “Zeit des Gifts: Formen der Temporalität in Claude Bernards Arbeiten über Curare.” In Lebendige Zeit: Wissenskulturen im Werden, edited by Henning Schmidgen, 79–96, 393–99. Berlin, 2005. Wahrig, Bettina, and Angelika Neubaur-Stolte. “1929: Louis Lewin und das Ende der Toxikologie.” In Arzneimittel des 20. Jahrhunderts: Historische Skizzen von Lebertran bis Contergan, edited by Nicholas Eschenbruch, Viola Balz, Ulrike Klöppel, and Marion Hulverscheid, 77–102. Bielefeld, 2009. Walker, David. “Occupational Health and Safety in the British Chemical Industry, 1914–1974.” PhD diss., University of Strathclyde, 2007. Watson, Katherine D. Forensic Medicine in Western Society: A History. London, 2011. Weber, Gustavus A. The Food, Drug, and Insecticide Administration: Its History, Activities and Organization. Baltimore, 1928. Weber, Wolfhard. Arbeitssicherheit: Historische Beispiele—Aktuelle Analysen. Reinbek, 1988. Weichardt, Heinz. “Gewerbetoxikologie und Toxikologie der Arbeitsstoffe.” In Amberger-Lahrmann and Schmähl, Gifte, 197–252. Weisburger, John H., and Elizabeth K. Weisburger. “Chemicals as Causes of Cancer.” Chemical & Engineering News 44, no. 6 (1966): 124–43. Wilmot, Sarah. “Pollution and Public Concern: Response of the Chemical Industry in Britain to Emerging Environmental Issues, 1860–1901.” In Homburg et al., Chemical Industry, 121–47.

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Wischin, Rudolf. Vademecum des Mineralöl-Chemikers: Ein Nachschlagebuch für den täglichen Gebrauch in Betriebe und Laboratorium der Mineralöl-Fabriken. 2nd ed. Braunschweig, 1900. Wood, W. Barry. From Miasmas to Molecules. New York, 1961. Whorton, James C. The Arsenic Century: How Victorian Britain Was Poisoned at Home, Work, and Play. Oxford, 2010. Zimmer, Alexis. “‘Le brouillard mortel de la vallée de la Meuse’: Décembre 1930— Naturalisation de la catastrophe.” In Débordements industriels: Environne­ ment, territoire et conflit, edited by Thomas Le Roux and Michel Letté, 115–34. Rennes, 2013. _____. “Dodelijke nevels in het Maasdal bij Luik tussen 1897 en 1938: Ontdekking en ontkenning van den industriële luchtvervuiling.” Studies over de sociaaleconomische geschiedenis van Limburg 59 (2014): 26–50.

/ PART I From Acute to Chronic Poisoning Regulating Old Poisons in the Industrial Age

/

CHAPTER 1

Schweinfurt Green and the Sanitary Police The Fight against Copper Arsenite Pigments Joost Mertens†

In 1775, Carl Wilhelm Scheele published a detailed study of the chemi-

cal properties of white arsenic (arsenic trioxide), which he had found to be an acid. He investigated the reactions of this acid with various substances, including a series of metals such as gold, silver, mercury, cobalt, and copper. The combination of copper and white arsenic resulted in a green-colored compound.1 He then started to experiment with this copper arsenite green as a painter’s pigment and found it worked quite well. Moreover, the color did not show any signs of fading or discoloration, even after three years. So, the Royal Swedish Academy of Sciences invited Scheele to publish the mode of preparation of this green color. He did so in 1778. His method consisted essentially in adding a solution of blue vitriol (copper sulfate) to a solution of potassium arsenite. A German translation of this synthesis appeared in 1783, followed by a French translation in 1785 and English in 1786.2 Despite Scheele’s and the academy’s optimism, and despite the many arsenite green hues in J. M. William Turner’s Guildford from the Banks of the Wey (1805), the new pigment was never very popular. The reviewer of Thomas Beddoes’s translation of Scheele’s recipe remarked that, in Great Britain at least, Scheele’s green was sold at a high price. In Thomas Bardwell’s Treatise on Painting (1795), Scheele’s green appears in the list of green colors, as does a short description of its preparation, but was absent from the usual palette of British painters.3 There were some technical problems as well. When Scheele’s laboratory synthesis was scaled up to commercial quantities, the resulting green was not always of the same shade due to impurities in commercial potash, white arsenic, and blue vitriol. Moreover, the precipitate was sometimes very

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hard to grind.4 All these problems—chemical, mechanical, commercial, esthetic—were solved by the invention of an industrial method to produce a modified copper arsenite green, by Ignaz von Mitis in Vienna (1805) and Wilhelm Sattler in Schweinfurt (1814). This new green, superior to Scheele’s green, was a double salt, copper acetoarsenite. Mitis, who produced it between 1805 and 1818, sold it under the name Mitis Grün, and Sattler, who produced and exported large quantities of it, called it Schweinfurter Grün. Over the years, many new names such as Vienna green, Brunswick green, Paris green, and parrot green were adopted. In England, it came to be known as emerald green. Up to 1822, both the composition and the method of preparation of Schweinfurt green were kept secret, which gave Sattler a virtual monopoly all over Europe. In 1822, however, both secrets were published: in Germany by Justus Liebig and in France by Henri Braconnot. In 1822, a Mr. Noël, who owned a paper hangings manufactory in Nancy and used a “secret” green pigment imported from Schweinfurt, asked Braconnot to carry out a chemical analysis of this mysterious substance. Braconnot quickly discovered the green pigment consisted of three components: white arsenic, copper oxide, and acetic acid. It resembled Scheele’s green but was much more beautiful. Braconnot also tried hard to find a method of synthesis and, after many experiments, succeeded in finding a method that combined copper sulfate, white arsenic, and acetic acid. Scaling up this laboratory synthesis to manufacturing conditions led to some modifications, but in the end, Noël produced his own beautiful arsenical green. Braconnot published his results “in order to do a service to the arts.”5 Braconnot’s article provoked a reaction from Liebig. In a letter to the editors of the Annales de chimie et de physique, Liebig said he had found a better method than Braconnot’s, which he had published in the Repertorium für die Pharmacie and was both less cumbersome and less costly. His method consisted in combining verdigris (a mixture of copper acetate and copper carbonates), acetic acid, and arsenic, verdigris being cheaper than copper sulfate.6 In his original article, Liebig said he had already begun to investigate the “secret” substances called Mitis green and Schweinfurt green in 1820 to find a mode of preparation of these green colors and thus subvert “commercial speculations” in the interests of science and the diffusion of inventions.7 Both Braconnot’s and Liebig’s methods were widely publicized. At the end of the 1820s, the French were no longer dependent on imports from abroad. From about 1827, they began to manufacture their own Schweinfurt green,

Schweinfurt Green and the Sanitary Police  65

one of the first producers being Henri Ringaud (1805–1876), of Paris. More importantly, the arsenical color was used not so much as a ­painter’s pigment but rather as a coloring material in the manufacture of confectionary and wallpaper. And this was the source of worries and concerns among hygiénistes on public health, and of the emerging field of forensic medicine (médecine légale).8

Green Confectionary In 1830, Gabriel Andral—a professor of hygiene (public health) at the University of Paris Faculty of Medicine and a member of the Royal Academy of Medicine—wrote a report to the Paris Police Prefecture on the dangers of colored confectionary.9 Andral proposed that the new prefect, Achille Libéral Treilhard, issue an ordinance that would list all coloring substances to be prohibited, including many mineral pigments, among which Schweinfurt green received special attention. To understand Andral’s report and its position in the French fight against copper arsenite green, we must go into the history of the Council of Sanitation (Conseil de Salubrité), the role played by the police prefect, the meaning of the ordinances issued by this prefect, and some events preceding Andral’s report. Every ordinance against Schweinfurt green, from 1830 onward, refers explicitly to a series of previous ordinances, laws, and regulations pertaining to hazardous chemicals in consumer products. The first in this series dates from 1742 and was addressed to the kingdom’s confectioners, pastry chefs, and traiteurs, who were told not to use dangerous colors such as copper and lead compounds for preparing their sweetmeats, sugarplums, jams, and marzipan figurines.10 Infractions of these rules would lead to confiscation of merchandise, severe fines, and even imprisonment. This ordinance also presented a series of allowable colors, all of them innocuous dyestuffs such as cochineal, saffron, turmeric, litmus, indigo, and so on. The structure of this Ancien Régime regulation—what colors were prohibited in what kind of goods, what punishments were incurred, what colors were allowed— survived into the nineteenth century. On 22 July 1791, the National Assembly issued a decree on the organization of the municipal police. The police received the explicit authority to visit public places such as markets, cafés, and shops (butchers, bakers, grocers, apothecaries) to check the wholesomeness of foodstuffs and medicines. At the same time, offering bad or harmful

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foodstuffs was defined as an offence to be punished with confiscation and a heavy fine.11 On 1 July 1800, this authority was attributed to the newly created magistrate, the police prefect, who was responsible for public health in the city of Paris.12 This legal structure survived Waterloo, and in the Bourbon Restoration and the July Monarchy, the fight against copper arsenite green was undertaken against this legal background. The police prefect presided over the Council of Sanitation, which had been instituted in 1802 on the instigation of Charles Louis Cadet de Gassicourt, a professional pharmacist, who served as this council’s secretary until his death in 1821. Just before he died, he prepared an agreement between the prefect and the editors of the Annales de l’Industrie on publishing the council’s reports. It was a further step in the evolution of the scientific disciplines of public hygiene and legal medicine. After the discontinuation of the Annales de l’Industrie in 1827 and to “fill a serious gap in our medical literature,”13 the new discipline founded its own journal in 1829, the Annales d’Hygiène Publique et de Médecine Légale.14 Gabriel Andral was both a member of the Council of Sanitation and a cofounder of the Annales, in the fourth volume of which his report to the police prefect on dangerous confectionary was published. Andral was not the first to worry about green confectionary. In January 1827, Claude François Barruel, a préparateur for chemistry lessons at the University of Paris Faculty of Science, became curious about the beautiful green color of the New Year sugarplums. He subjected these sweets to a chemical analysis and soon found they contained substantial amounts of copper acetoarsenite (Schweinfurt green). Arsenic and its compounds were known for centuries to be toxic, so the police authorities ordered an investigation to be carried out among several Parisian confectioners. Their arsenic-containing sweets were confiscated and destroyed, and no such sweets were allowed to be sold.15 These measures were probably based on the decrees issued in 1800. Furthermore, in 1827, Jean Baptiste Alphonse Chevallier wrote an article about two cases of green confectionary, which chemical analysis proved to contain copper arsenite. To prevent serious mishaps, Chevallier proposed an educational strategy: those engaged in preparing foodstuffs, and confectionary in particular, should acquire some elementary chemical knowledge and acquaint themselves with recent developments in public health.16 For the dangers of Schweinfurt green, Chevallier referred to Wilhelm Remer’s Traité de police judiciaire, the French translation of the second

Schweinfurt Green and the Sanitary Police  67

edition of Remer’s Lehrbuch der polizeilich-gerichtlichen Chemie.17 Remer wondered whether the use of Scheele’s green by confectioners, bakers, and pastry chefs ought not to be prohibited altogether, a measure much more drastic than Chevallier’s “information strategy.”18 In 1829, Barruel was inclined to think no confectioner would use poisonous colors for their sweets in the future. He was proved wrong by the police prefect who had ordered Henri-François Gaultier-Claubry to analyze various green confectionary articles imported from Germany, which turned out to contain significant amounts of copper arsenite. Alarmed, the police prefect sent out a circular authorizing the Paris police to confiscate confectionary containing poisonous mineral colors such as Schweinfurt green. Chevallier showed this circular to some of his pharmacy colleagues of the Royal Academy of Medicine. They decided to investigate the problem of colored confectionary and encourage the Council of Sanitation to publish a list of innocuous colors. Nothing came of this initiative, because of the Revolution in Paris of 1830.19 Prefect of Police Treilhard took up the problem and ordered the Council of Sanitation to report on the dangers resulting from colored confectionary and on how to remove those sweets from the market. Gabriel Andral wrote the report. Andral’s report is important in two respects. First, the dangers arising from the presence of Schweinfurt green pertained not only to the sweets themselves but also to the wrappers around them. Wrappers and wrapping paper were the next issues in the fight against copper arsenite. Second, the report led to an ordinance issued by Treilhard dated 10 December 1830.20 It refers to the ordinances of 1742 and 1791, mentioned earlier, but also to articles 319 and 320 of the Penal Code, which specify the punishments for manslaughter or injury by negligence. These articles were applicable to the problems of green confectionary and green liqueurs, because the confectioners producing and selling these goods were held personally responsible for accidents resulting from their consumption. One of Andral’s proposals further stipulated that a special committee would visit Paris confectioners to ensure the observance of the new ordinance. Finally, the ordinance specified the colors that were prohibited and those that were not. Schweinfurt green was strictly prohibited and should be replaced by a mixture of Prussian blue and Persian berry, which was as brilliant as Schweinfurt green, according to the Council of Sanitation experts. William Brooke O’Shaughnessy was very jealous of France, where such strict measures could be taken: “The statute law of England affords

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the public little protection against any system of this kind, no matter how deadly in its nature . . . In these particulars it is that our continental brethren, whether medical or judicial, have most outstripped us in their race with the progress of knowledge.”21 But O’Shaughnessy was far too optimistic about his “continental brethren,” for even after fifty years, in 1881, an ordinance against using mineral colors such as Schweinfurt green in sweets, liqueurs, and wrapping paper was issued, repeating the regulations of 1830, 1838, 1853, and 1862.

Green Wallpaper The coloring of confectionary was not the only use of copper arsenite green. Another early use of Schweinfurt green was the coloring of wallpaper, especially the tufted or flock variety, called papier velouté in France and Flocktapete in Germany.22 Before 1845, its hazards received only scant attention. In 1817, Sigismund Hermbstädt proposed a green pigment invented by Christian Barth, of Osnabrück, as a harmless alternative to arsenical green. If swallowed, the dust particles coming off arsenite green wallpaper would lead to dangerous fits of illness.23 In 1836, to prove the innocuousness of “new silver” (a nickel-copper-zinc alloy), Liebig compared it to the Schweinfurt green on the walls of many living rooms and bedrooms, applied not to repel flies but to please the eye. It would be better to prohibit this green color altogether.24 Then, in 1839, several warnings appeared in the German press. On 11 April 1839, the Intelligenzblatt for Unterfranken and Aschaffenburg gave an official warning against the use of wallpapers containing copper arsenite green, which had been proved harmful.25 The warning was extended to wall paints prepared from copper arsenite pigments. Ten days later, a similar warning appeared in the Intelligenzblatt for Schweinfurt, the lion’s den so to speak. In November and December 1839, Leopold Gmelin, a University of Heidelberg chemistry professor, published a more elaborate warning in the Carlsruher Zeitung and the Schwäbischer Merkur. According to Gmelin, the danger of green wallpaper was greatest in badly ventilated, damp rooms. There, a “foul smell” developed, no doubt caused by some arsenic compound. Maybe this arsenical pigment should be banned altogether. These warnings were the occasion for the Grand Duchy of Baden government to invite Gmelin to formulate some sanitary police regulations on the use of copper arsenite green. Gmelin did so in June 1844.

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The Grand Duchy of Baden constitution provided for an active policy of public health. To that end, the administration appointed medical officers, a health commission, and sanitary police. It also encouraged the development of a scientific Staatsarzneikunde, which was left to the Baden association of medical officers, which began to publish its own journal in 1835. Gmelin’s study of the dangers of Schweinfurt green, published in this journal, is important for at least three reasons.26 First, it was quoted repeatedly in subsequent reports on the problem of green wallpaper, not only in Germany but also in France and England.27 Second, it triggered an international toxicological debate on whether the dangers of green wallpaper arose from the “foul smell” or the dust particles coming off the wall. The “foul smell” school was internally divided as to the nature of the gaseous emanations. Was it arsine, an organometallic compound such as cacodyl, or metallic arsenic?​Third, it already showed many of the later problems of a rational sanitary policy: decisionism, information, and innovation. Gmelin presented several cases of persons who slept in a room with green wallpaper waking up with a headache, nausea, a dry mouth, and a persistent cough. These symptoms proved this kind of wallpaper produced a poisonous air. Next, Gmelin considered whether this arsenical wallpaper should be banned. It would be very difficult to ban the pigment itself from the market, since it was sold under many different names, and inventing a new name was easy. So, what should be forbidden was the use of copper arsenite green in wallpaper production. But then a whole army of administrative chemists would be needed to control these artisans’ workshops. Moreover, whether such a prohibition should be imposed was a political question that should be decided by the government, not by a scientific expert. Should the government decide to ban arsenical green wallpaper, Gmelin would be more than willing to write instructions for analyzing wallpapers. Should the government decide against such a ban, Gmelin would be more than willing to provide the factual material needed for official warnings. But the real solution of the problem must come from technological innovation. Gmelin considered the possibility of a prize for the invention of a substitute for Schweinfurt green: “It is only by the invention of such a color that one can succeed in completely suppressing arsenical green.”28 In the same year, 1845, a Dr. Blandet published a memoir on the dangers of Schweinfurt green, not so much during the “consumption” of wallpaper as during its manufacture. The workers involved in the various stages of green wallpaper production not only suffered

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from headaches and sore throats but also presented edema, pimples, pustules, vesicles, swollen lips, and ulcerated genitals.29 Wallpaper production took place in a series of stages, some of which were very dangerous if Schweinfurt green was the color employed. Blandet mentioned (1) the operation of sifting powdered Schweinfurt green in a bolting machine to sift the right particle size for preparing the green paint needed for (2) the operation called “grounding” by which the worker spread a uniform layer of green paint on one of the wallpaper’s surfaces, and (3) the operation called “satinizing” by which the worker gave a brilliant polish to the painted surface by means of a hard brush. To reduce the dangers of sifting, Blandet proposed the concentration of Schweinfurt green production in a limited number of special chemical factories that would provide the market with ready-to-use arsenical green powder. As to grounding, the operation could easily be prohibited, as the fashion of green backgrounds had passed. For the serious dangers presented by satinizing the paper, Blandet proposed the innovative solution made possible by the polishing machine newly invented by Jules-Otto Ebert, a Parisian wallpaper manufacturer. According to Blandet, these measures could prevent a total ban on Schweinfurt green, which was desirable, for how else could the tender green of all kinds of vegetation—leaves, trees, fields, meadows—be imitated on a piece of wallpaper?​ This memoir provoked Chevallier into a response. After reading Blandet’s memoir, he wondered if the arsenic-related edemas and pustules reported by Blandet were widespread and if they were serious enough to be brought to the attention of the authorities. He also wondered if the manufacture of arsenical green wallpaper ought not be prohibited altogether, adding that there was no unanimity among jurists as to whether the authorities had the right to ban an industry if it proved detrimental to public health. Chevallier sent a letter to several wallpaper manufacturers, asking if they had encountered any occupational health problems while producing Schweinfurt green or green wallpaper. From their responses, Chevallier concluded the arsenical paper industry was not very dangerous, provided some preventive measures were taken (regular baths, gloves, wet masks, ventilation) and the Ebert machine was universally adopted for satinizing.30 Thus, around 1850, the fight against copper arsenite green had led to a proposal of measures that consisted of a mixture of information, preventive manufacturing arrangements, and the encouragement of substitute colors and innovative production methods. But banning arsenical green from the market

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Figure 1.1  Dr. Gustav Kletschke’s scheme of the color trade (1854). Figure created by the author.

was out of the question. It was generally thought the hazards of this green color could be contained by a set of more or less strict regulations of the industries using the color for various consumer products on the one hand and protective measures in the chemical manufacturing of the color on the other. In 1854, Gustav Kletschke made a detailed analysis of the various stages of both the production and the application of hazardous chemicals including Schweinfurt green, with a view to detailing the responsibilities of the Prussian sanitary police. Kletschke’s essay opened on a radical note: most cases of poisoning by mineral colors were to be attributed to profit seeking and ignorance. Neither source could be completely eradicated, but they could be regulated, which was precisely the task of the sanitary police. Kletschke indicated four areas of regulation: the color trade, specific prohibitions, information, and sanctions. For the discussion of the first area, he presented a tripartite chain of color trading (fig. 1.1). According to Kletschke, the wholesale trade was sufficiently regulated. For this, he referred to a series of ministerial circulars issued between 1817 and 1840 on packing, shipping, and storing poisonous materials including white arsenic and other arsenic compounds. Moreover, the dangers could not be located here, since “this trade . . . is conducted by experts, owners of chemical factories and wholesale druggists.”31 The dangers arose from the ignorance of the retailer. The druggist, often a chemist himself, would not be fooled by a new name. But the retailer, the Materialist, was wholly at the mercy of the druggist’s conscientiousness. To counteract this dependence, Kletschke proposed to compel the druggist to place a label on his wares carrying both the commercial name such as Schweinfurter Grün and the official chemical designation such as copper arsenite. As to the retail trade, Kletschke reminded readers that, since 1845, grocers needed some police permit to sell poisonous materials.32 And to clear the retailer from responsibility, Kletschke proposed putting a black cross on bags containing poisonous materials so that, in case of mishaps, the retailer could blame either the druggist or the artisan who bought the material.

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The artisans and manufacturers at the end of the chain needed more than a black cross. They needed additional information on the products that were not allowed to contain hazardous chemicals. Kletschke mentioned several prohibitions issued in the Kingdom of Prussia between 1839 and 1851 applicable to toys, confectionary, gingerbread, wrapping paper, wall paint, and wallpaper. And he was happy to extend the list to include liqueurs, wafers for sealing letters, paint boxes, cosmetics, and leather. Information and education were needed to fight one of the main causes of all these problems: ignorance. To persons involved in the retail trade, Kletschke recommended Julius Stoeckhardt’s color manual, which moreover offered a vocabulary that might facilitate communication between color traders and the public health authorities.33 When the color retailer receives his sales permit, he should be given a pamphlet with information on the various trade names of, for instance, copper arsenite green, an indication as to the chemical identification of this substance, and a summary of the existing sanitary laws and regulations. Finally, by way of a finishing touch to this package of regulations, Kletschke proposed severe punitive measures. Labels, permits, black crosses, lists of unauthorized colors, educational pamphlets—all these sanitary measures were meant to regulate the production, trade, and application of harmful colors such as Schweinfurt green. If an accident nevertheless occurred under these conditions, it could be attributed unequivocally to negligence or malicious intent. Then, severe punishment was necessary. Most of the studies, reports, and ordinances pertaining to arsenite green focused on the right side of Kletschke’s chain of color trading, that is, on the making of consumer products containing Schweinfurt green and the trade providing them with this poisonous color. An exception was Blandet’s aforementioned 1845 memoir. Another study of the symptoms produced by handling copper arsenite green appeared in 1857 by Eugène Follin, a professor at the University of Paris Faculty of Medicine, who referred to Blandet’s “curious” paper and Chevallier’s “interesting” paper.34 He then went on to remark that these peculiar affections had not attracted the attention of the medical profession for nearly a decade. He presented detailed clinical observations of the ulcerations on the nose, scrotum, hands, and feet of François Pamard, who worked in a Schweinfurt green factory, where he prepared this compound by mixing hot solutions of arsenious acid and copper acetate. Similar eruptions could be observed in wallpaper manufacture workers, especially those engaged in chemical operations, sifting,

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grounding, and satinizing. Should this be a reason to ban Schweinfurt green or its application to wallpaper production?​No. Arsenical disease could easily be treated. What should be recommended was a couple preventive measures, especially for workers exposed to Schweinfurt green dust flying about in the workshop. Prosper de Pietra-Santa lectured on the Schweinfurt green disease before the Academy of Sciences on 23 August 1858. He had observed a dozen workers, prisoners of the Madelonnettes, who handled copper arsenite in the manufacture of green paper. He concluded that they suffered from a specific occupational disease, which, however, could be prevented by simple hygienic measures. Thus, “one could, without inconvenience, maintain this industry.” A detailed report on his observations in the Madelonnettes Prison was published in the Annales d’Hygiène.35 In the special circumstances of a prison, Pietra-Santa could regularly observe the appearance of various symptoms and the effect of therapeutic means and prophylactic measures. In this way, he studied sixty-some prisoners engaged in the manufacture of lampshades made of Schweinfurt green paper that was produced on the spot, involving the preparation of green paint and the operations of grounding and satinizing. He found that the Madelonnettes lampshade workers developed vesicles, pustules, mucous membranes, and ulcerations on their fingers, toes, and genitals, the scrotum in particular. But none of these symptoms were of a serious nature, and all could be prevented by proper hygiene measures (baths, gloves) and cured by a specific treatment (salt water and calomel). In 1864, Pietra-Santa presented the results of another six years of observations in the Madelonnettes Prison. He found complete corroboration of his earlier results. So, it would be easy to “respect the wise principles of industrial liberty.”36 In 1859, Chevallier published a sixty-page review of the dangers of Schweinfurt green, a material that in view of its widespread applications and toxic properties deserved the attention of the authorities. It showed that, forty-five years after Sattler began to produce it on an industrial scale, this green color had found many applications: paper, artificial flowers, confectionary, wrappers, pastry, wallpaper, paint boxes, ball dresses, sealing wafers, toys, bird cages. It also showed that the ordinances against the use of copper arsenite in these consumer products had not been very effective. For example, arsenical green wrapping paper could still be found in many Parisian shops: “If one takes a glance at the shop windows of grocers, greengrocers, butchers, sellers of chocolate or pastry, one sees almost everywhere that all these foodstuffs

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are in contact with or wrapped in toxic papers.”37 And this deplorable state of affairs was prolonged despite the studies and recommendations made over the years by scientists, doctors, chemists, and pharmacists such as Blandet, Pietra-Santa, Barruel, O’Shaughnessy, Andral, Gmelin, and Chevallier himself. The case of arsenical wallpaper is interesting because it shows how the German handling of the Schweinfurt green problem provoked the jealousy of French hygienists. In 1838, the Prussian government issued a decree prohibiting the use of poisonous materials including Schweinfurt green in colored paper. A year later, the decree was repealed because importation of arsenical green paper considerably exceeded domestic consumption. But then, in 1846, a detailed report by the Royal Scientific Deputation for the Medicinal System (Königliche wissenschaftliche Deputation für das Medicinalwesen) proposed to prohibit all applications of Schweinfurt green to paper and textiles. In 1848, the Prussian government followed its deputation’s proposal with an ordinance against copper arsenite in paper and wallpaper. In 1852, this decree was reissued, while the report was translated into French and presented to the Paris police prefect in the hope that he would follow his Prussian counterpart. In 1856, the deputation produced a new report on arsenical colors. The 1848 prohibition was fairly effective, at least in Prussia. The commission proposed to ban not only the application but also the production of Schweinfurt green, not only in the Kingdom of Prussia but also in the Zollverein states. It was further proposed that the police would force homeowners who still had their walls covered with arsenical green paper to remove it. To set the example, all green wallpaper should be removed from royal and public buildings.38 In France, the official hygienists shied away from this kind of ruling. In 1854, Chevallier and Édouard-Adolphe Duchesne, both members of the Council of Public Health and Sanitation (Conseil d’Hygiène Publique et de Salubrité), the successor to the Council of Sanitation, asked themselves whether the manufacture of toxic papers should be prohibited. The answer was “no.” Confectioners should not be allowed to use green wrappers, but the production of green paper was not to be prevented, a conclusion probably made in deference to the wise principles of industrial liberty.39 In England, the Prussian laws made a deep impression and reminded the English of the precarious tension between economic freedom and public health. In 1857, William Hinds discovered the arsenical wallpaper problem and the solutions the Prussians had found. He first quoted a Dr. Seoffern:

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As you intend to reside some considerable time in the Prussian dominions, you will, perhaps, set about papering your rooms. Take care in doing this you do not give the police cause to pounce down upon you . . . An Englishman whom I knew took it into his head to hang his sitting-room with paper of a certain green tint . . . The Englishman absented himself . . . He then came back, and was surprised to find the chamber, not merely hung, but unhung. The police had sent people there to strip the paper off.

Hinds then turned into a political philosopher: It is unquestionable, that while in England we enjoy so much liberty of action and such an extent of self-government, we, on the other hand, lose much in some respects in a sanitary or hygienic sense by that same freedom from interference . . . No rational man can . . . doubt . . . that [the] Government are most anxious . . . to suppress any proceedings really injurious to the public health and safety . . . Let us hope that the facility with which Her Majesty’s lieges can procure arsenic . . . for the destruction of themselves and others will be removed . . . while any of us may be unconsciously poisoned in our very food and delicacies, and even by our own firesides.40

Deadly Green Then, in 1865, two Schweinfurt green workers died in France. This event and the subsequent trial not only formed an important episode in the fight against copper arsenite green but were also very instructive on the nineteenth-century chemical technology of Schweinfurt green production, which was far removed from the neat laboratory syntheses devised by Braconnot or Liebig. In the summer of 1865, two chemical workers died, Pierre Beidel on 6 June and Sylvain Chimbeau on 3 July. Both were employed by the chemical manufacturer Florentin-Joseph Ansart to sift large quantities of Schweinfurt green in a bolting machine. Ansart was arrested on suspicion of manslaughter by negligence (homicide par imprudence). Charles de Gonet, the examining magistrate, charged two expert witnesses to examine the bodies, by autopsy (Paul Lorain) and by chemical analysis (Zacharie Roussin). Roussin found both arsenic and copper in the victims’ organs and skin by using the method of detecting small quantities of arsenic invented by James Marsh in 1836.

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A short history of this Marsh test illustrates the importance of analytical chemistry in the fight against copper arsenite. Marsh, a chemist at the Royal Arsenal, Woolwich, had devised his very sensitive test out of frustration. In 1833, John Bodle had been acquitted for poisoning his grandfather, notwithstanding the analysis Marsh had carried out using the common sulfide method developed by Samuel Hahnemann in 1785. The new method Marsh published in 1836 could be applied to not only white arsenic but also arsenical pigments such as orpiment, realgar, and Scheele’s green.41 The Marsh test became standard procedure after 1840, when Marie Lafarge was convicted for poisoning her husband. During the trial, Mathieu Orfila not only detected arsenic in the body of the victim but also assured the legitimacy of both forensic toxicology and legal chemistry, as well as the institutionalization of the Marsh test.42 Roussin’s results were a sufficient reason for Gonet to send him to Ansart’s factory to report on the various chemical operations carried out in Schweinfurt green production and to evaluate the factory’s hygienic conditions. The trial took place on 20 October. After hearing Ansart, Lorain, Roussin, and Maître Grandmanche, the defense lawyer, the court found Ansart guilty of manslaughter by negligence, as stipulated in the Penal Code, and sentenced him to eight days’ imprisonment and a fine of 300 francs. The court was much impressed by Roussin’s report, which clearly showed the dangers of Ansart’s bolting machines, which produced clouds of green dust that crept into the workers’ mouths, noses, lungs, and skin.43 Ansart appealed to the imperial court. This appeal took place on 18 November. Grandmanche tried to shed some doubt on the experts’ reports but also defended the chemical industry in general, including its hazardous processes: “If men like Ansart did not manufacture copper sulfate, what would become of the electric telegraph; if no Schweinfurt green was produced, what would become of our navy which consumes millions of kilograms of this substance, and what would become of our painting enterprises?​. . . And who but the state is the big fulminate entrepreneur?​” However, the judge was not impressed by this rhetoric and confirmed the verdict of the magistrate’s court.44 Roussin incorporated his report on Ansart’s factory into an essay on copper arsenite poisoning in 1867.45 Referring to research by Chevallier and Pietra-Santa, he said it was fairly well known how Schweinfurt green entered the body by inhaling or swallowing, but how it entered the body by skin absorption was largely unknown. This question is the subject of the second part of Roussin’s essay. The first

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part presents the results of his investigation of Ansart’s factory carried out by Gonet’s order. Ansart’s factory was nothing more than a shed with a roof with some holes in it and therefore insufficiently ventilated. Schweinfurt green production took place in various stages: preparation of copper sulfate, the addition of this salt to a solution of arsenious acid, drying the resulting precipitate, powdering it, sifting it, filling barrels with the finished product. The preparation of copper sulfate consisted of dissolving metallic copper in nitric acid, adding sulfuric acid, and cooling the resulting solution. Ansart used not pure copper but rather a wide variety of waste copper and scrap copper: gilder’s copper scouring, waste copper solutions from André Gaupillat’s percussion cap factory in Meudon, copper cinders, copper filings, discarded telegraph batteries. In the first stage, the various reactions produced many noxious vapors. They were, however, a minor problem compared to the dangers arising from the handling of dry copper arsenite. The real problems began after the green precipitate had been dried. First, the cakes of Schweinfurt green were crushed into smaller fragments by means of wooden hammers. This action led to clouds of green powder throughout the workshop. Then, this powder was transferred to a mechanical sieve (bolting machine) to subject it to particle-size fractionation. This operation again produced a cloud of Schweinfurt green that settled on the workers’ clothes and skin. Then, the finely divided material was transferred from the bolting machine to packing cases, to be shoveled, finally, into sacks or barrels ready to be sold to customers. All this transferring was done by means of wooden bowls, leading to green clouds being flown around. When Gonet instructed Roussin to visit Ansart’s factory, he in fact ordered him to carry out a comparative investigation. So, Roussin visited another Schweinfurt green manufacturer who used similar technologies and coped with similar hygienic problems, the Ringaud firm, which had since 1828 produced Schweinfurt green that found its way to housepainters, wallpaper manufacturers, and the French Navy. Ringaud’s factory stood in glaring contrast to Ansart’s production shed. Here, neat and regular ways of handling the various materials according to a methodical chain of operations were used—no waste or secondhand materials, and no disagreeable smells. Most important, the dangerous operations of pulverizing and sieving Schweinfurt green were done in separate workrooms by means of wellclosed bolting machines. Roussin’s report had two consequences. First, it contributed heavily to Ansart’s imprisonment because the deaths

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of Beidel and Chimbeau were attributed to personal negligence that could have been easily avoided, as was shown by Ringaud. Second, Roussin’s description of Ringaud’s operations saved the Schweinfurt green industry, because it showed unequivocally that the manufacture of arsenite green was possible without any objection, provided a series of strict hygienic measures were taken. Ringaud was the living proof of that. His factory had become a model of harmless Schweinfurt green production. Within four months of Ansart’s conviction, the Paris Police Prefecture published an official instruction drawn up by the Council of Sanitation that faithfully mirrored Ringaud’s arrangements and Roussin’s recommendations. Workers should wear masks. They should put talcum powder on their hands. Bolting machines should be well closed and placed in a separate, well-aired room. A tank with diluted acid should be kept in readiness. Workers should not be allowed to eat in the workshop. They should wear special overalls and impermeable shoes. In the case of a rash or other symptoms, they should be sent to the doctor immediately. And the manager should pin up these instructions.46

The Wise Principles of Industrial Liberty In France, the fight against Schweinfurt green was fought by means of ordinances issued by police prefects. They were aimed at artisans, manufacturers, and merchants who made and sold consumer products such as confectionary, wallpaper, ball dresses, artificial flowers, and so on that contained this green poison. The measures taken were of a wide variety: prohibition of certain goods, supported by confiscations, fines, and regular inspection rounds; information including instructions written by the Council of Sanitation; promotion of substitute colors such as Barth’s green, green earth, green ultramarine, or a mixture of Prussian blue and some harmless yellow color. When the manufacturing of arsenical green was the subject of regulation, it was never prohibited but rather subjected to preventive measures (fig. 1.2), and managers were encouraged to adopt innovative procedures or machines. This approach was not very effective. For one, the public health problem had to be tackled on the département level. Only when someone died of Schweinfurt green poisoning was the problem raised to the state level. Chevallier and Duchesne, speaking on the problem of toxic wrapping paper and the easy way of dodging the regulations valid in Paris,

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Figure 1.2  “Information policy” as exemplified by the labeling of a can with Paris green of Sherwin-Williams, Canada, twentieth century. Wikimedia Commons, public domain.

urged the adoption of general measures: “This question touches public health on all sides; we may even declare it is a question of universal salubrity, since there is no family, rich or poor, that does not daily consume the goods of a confectioner, chocolate maker, grocer, butcher, pastry

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cook, etc.”47 Five years later, speaking on the same problem, Chevallier proposed to generalize the Parisian ordinance of 1853 to every French department: Such a decree would absolutely prohibit in the whole of France the manufacture and sale of toxic papers for confectioners. Until the government takes this wise measure, demanded for so long by the Council of Public Health and Sanitation of the Seine department, we think the prefects should make haste to adopt the 1853 ordinance for their respective departments and command its rigorous execution.48

The ineffectiveness of Schweinfurt green regulation was because of not only administrative fragmentation but also deeply ingrained tenets of political philosophy, such as the principles of individual liberty in general and industrial liberty in particular. The first regulation against green confectionary dated from 1830. After fifty years, in 1881, the Paris Police Prefecture issued an ordinance against, yet again, the use of Schweinfurt green in confectionary and wrapping paper. In 1893, a new law on industrial hygiene was adopted.49 In 1895, this law was applied specifically to the Schweinfurt green industry. More than half the annual production went to the shipbuilding industry for protecting ships’ bottoms against algae, but part of the rest was used to produce green lampshades, as if the problem of arsenical paper had never existed. Why did the fight against copper arsenite green take so long?​An answer can be found in Gérard Jorland’s study of nineteenth-century French public health. The general decisionistic structure of public medicine, its “metaparadigm,” in Jorland’s words, was a kind of trias hygienica: “The hygienist recommends the measures to be taken in the field of public health, the legislator converts these recommendations into laws and regulations, and the administrator, the executive, enforces the law.”50 Jorland wondered why the institution of public health in nineteenth-century France never broke out of its advisory role, always remaining a scientific discipline, while Germany created executive bodies like the Sanitätspolizei (Medical Police) that could pounce on you when you were decorating your bedroom with arsenical wallpaper. According to Jorland, the heart of the matter was the shrill contrast between the ruling ideology of liberalism and individual liberties, and an alternative ideology of collective liberties and collective safety that he called “solidarism” and better fit the basic assumptions of public health. Maxime Vernois perfectly

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formulated the essential tension between hygienic measures and industrial liberty: The industrial use of arsenic compounds can always develop into a hazard. From a hygienic point of view, an absolute prohibition would certainly be a beneficial and wise measure. Yet, no harm should be done to the free development of industry. The best course to follow is to warn the public against the dangers attached to their use and search for inoffensive substitutes.51

The ideology of laissez faire led to two results. The hygienists “wrote novels” that implied analyses, studies, memoirs, treatises, and the like without subsequent legislative action. The state recoiled from intervening in industry. According to Jorland, this political restraint had to be attributed to a lack of legitimacy to intervene in the population’s individual rights. And this lack of legitimacy was due to the instability of the short-lived regimes that spanned the nineteenth century: First Republic, First Empire, Bourbon Restoration, July Monarchy, Second Republic, Second Empire, Third Republic. There was no time for the state to “become rooted” in civil society.52 “A public health policy is an excellent test of the confidence granted to the state by civil society.”53 In other words, the Schweinfurt green problem could be solved only in a stable, trustworthy political environment. Joost Mertens† was an independent researcher in the history of applied sciences, chemical technology in particular, with an intellectual background in physical chemistry, philosophy of science, and history of technology. His publications included articles on the long-term history of the electric battery, the French version of Beckmannian technology, and topics from the history of chemistry (Anselme Payen, artificial ultramarine). Before he passed away on 29 June 2015, at the age of seventyone, he was working on a French translation of Johann Beckmann’s Entwurf der allgemeinen Technologie, the technocratic utopia of Étienne Cabet, the dangers of green ball dresses dyed with Schweinfurt green, and the history of science writing (Charles Barreswil).

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Notes   1. Scheele, “Vom Arsenik,” 287–88.   2. Scheele, “Zubereitungsart”; Scheele, “Manière”; Scheele, “Method.”  3. Bardwell, Practical Treatise. For the reluctant acceptance of Scheele’s green, see Ball, Bright Earth, 154–55.  4. Mérimée, De la peinture, 194–97.   5. Braconnot, “Sur une très-belle couleur.” All translations in this chapter are mine.   6. Liebig, “Sur une couleur verte.”   7. Liebig, “Darstellung.”   8. For the notions of forensic medicine, medical police, Staatsarzneykunde, and legal medicine, see Burg, “Forensic Medicine.”   9. Andral, “Rapport.” An English translation can be found in O’Shaughnessy, “Poisoned Confectionary.” [See also Whorton, Arsenic Century, 153–68.] 10. “Ordonnance de Police concernant les compositions qui entrent dans les desserts, du 10 octobre 1742,” in Collection des lois, ordonnances et réglements de police, depuis le 13e siècle jusqu’à l’année 1818, Vol. 5: 1739–1749 (Paris, 1818), 170–72. 11. “Décret relatif à l’organisation d’une police municipale et correctionelle,” in Collection complète des lois, décrets, ordonnances, réglemens, 2nd ed., vol. 3 (Paris, 1834), 114–18. 12. “Arrêté qui détermine les fonctions u préfet de police de Paris (messidor an 8, 1er juillet 1800),” in Collection complète des lois, décrets, ordonnances, réglemens, vol. 12 (Paris, 1826), 251–53. 13. “Prospectus,” Annales d’hygiène publique et de medicine légale 1 (1829): v–viii. 14. Jorland, Société, 29–39, 76–83; Mertens, “Annales,” 150; “Extrait du compte rendu sur les dépenses de la Préfecture de police pour l’exercice 1819,” Annales de l’industrie nationale et étrangère 3 (1821): 216. 15. Barruel, “Dangers,” 420. 16. Chevallier, “Note sur la coloration.” 17. Remer, Police. 18. Remer, Lehrbuch, 288–89. 19. Chevallier, “Section de Pharmacie”; Chevallier, “Note sur la vente.” 20. “Préfecture de police: Ordonnance concernant les pastillages, les liqueurs et sucreries coloriées—Paris, le 10 décembre 1830,” in Chevallier, “Note sur la vente,” 41–46. 21. O’Shaughnessy, “Poisoned Confectionary,” 198. 22. For the German situation, see Andreas, “Schweinfurter Grün.” 23. Hermbstädt, “Anweisung,” 136–38. See also “Préparation d’une peinture verte économique,” Annales des arts et manufactures 4 (1817): 84–85. 24. Liebig et al., “Vermeintliche Schädlichkeit.” 25. In the rest of this chapter, the general “arsenite green” is used, as was quite common during the nineteenth century, when “acetoarsenite green” also could have been meant in practice.

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26. Gmelin, “Nachtheile.” 27. For the debates on green (arsenical) wallpaper in England, see Whorton, Arsenic Century, 203–28; Hawksley, Bitten. 28. Gmelin, “Nachtheile,” 414. 29. Blandet, “Mémoire.” 30. Chevallier, “Essais.” 31. Kletschke, “Aufgaben,” 143. 32. “Polizeiliche Genehmigung zum Handel mit Giften und Droguen,” in Die allgemeine Gewerbe-Ordnung vom 17. Januar 1845 (Magdeburg, 1847), 37. 33. Stoeckhardt, Ueber die Zusammensetzung. 34. Follin, “Note”; Blandet, “Mémoire”; Chevallier, “Essais.” 35. Pietra-Santa, “Existe-t-il une affection.” 36. Pietra-Santa, “Sur la fabrication,” 656. 37. Chevallier, Recherches, 16–17. 38. “Ueber Arsenikfarben und deren Anwendung, in sanitätspolizeilicher Beziehung: Gutachten der Königlichen wissenschaftlichen Deputation für das Medicinalwesen (2. Juli 1856),” Vierteljahrsschrift für gerichtliche und öffent­ liche Medicin 16 (1859): 8–25. 39. Chevallier and Duchesne, “Dangers,” 75. 40. Hinds, “Another Case.” 41. Marsh, “Account.” A French translation appeared in Journal de Pharmacie 23 (1837): 553–61 and a German translation in Annalen der Chemie und Pharmacie 23–24 (1837): 207–16. See also Campbell, “Landmarks.” 42. Bertomeu-Sanchez and Nieto-Galan, Chemistry. 43. “Tribunal correctionne de Paris, Homicide par imprudence—Fabrication du vert de schweinfurt—Mort de deux ouvriers par intoxication l,” Gazette des tribunaux, Journal de jurisprudence et des débats judiciaires, 21 October 1865, 1010. 44. “Cour impériale de Paris, Homicides par imprudence—Fabrication de produits chimiques—Mort de deux ouvriers par intoxication d’arsenic de cuivre—Responsabilité du patron,” Gazette des tribunaux, Journal de jurisprudence et des débats judiciaires, 26 November 1865, 1129. 45. Roussin, “Double empoisonnement.” 46. “Instruction concernant les précautions à prendre par les fabricants et par les ouvriers qui s’occupent de la preparation du vert de Schweinfurt, approuvée par le préfet de police le 16 mai 1866,” Moniteur d’hygiène et de salubrité publique 1 (1866): 417–18. 47. Chevallier and Duchesne, “Dangers,” 81. 48. Chevallier, Recherches, 17. 49. Jorland, Société, 307; Guérard, “L’inspection.” 50. Jorland, Société, 82. 51. Vernois, Traité pratique, 259. 52. Jorland, Société, 322. 53. Jorland, “Comment,” 11.

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Bibliography Andral, Gabriel. “Rapport fait à M. le Conseiller d’état, Préfet de Police, sur le danger qui peut résulter de l’emploi des bonbons colorés.” Annales d’hygiène publique et de médecine légale 4 (1830): 48–51. Andreas, Holger. “Schweinfurter Grün: Das brillante Gift—Der lange Weg zum Verbot einer gesundheitsgefährdenden Substanz.” Chemie in unserer Zeit 30, no. 1 (1996): 23–31. Ball, Philip. Bright Earth. Chicago, 2003. Bardwell, Thomas. Practical Treatise on Painting in Oil-Colours. London, 1795. Barruel, Claude-François. “Des dangers que l’on court en mangeant certains bonbons colorés.” Annales d’hygiène publique et de médecine légale 1 (1829): 420–24. Bertomeu-Sanchez, José Ramón, and Agustí Nieto-Galan, eds. Chemistry, Medi­cine, and Crime: Mateu J. B. Orfila (1787–1853) and His Times. Sagamore Beach, 2006. Blandet, Dr. “Mémoire sur l’empoisonnement externe, produit par le vert de Schweinfurt (vert arsenical), ou de l’œdème, et de l’éruption professionnels des ouvriers en papiers peints.” Journal de médecine 3 (1845): 112–16. Braconnot, Henri. “Sur une très-belle couleur verte.” Annales de chimie et de physique 21 (1822): 53–56. Burg, Thomas N. “Forensic Medicine in the Nineteenth-Century Habsburg Monarchy.” Center for Austrian Studies Working Paper 96-2. University of Minnesota, 1996. Campbell, W. A. “Some Landmarks in the History of Arsenic Testing.” Chemistry in Britain 1 (1965): 198–202. Chevallier, J. B. Alphonse. “Essais sur les maladies qui atteignent les ouvriers qui préparent le vert arsenical et les ouvriers en papiers peints qui emploient dans la préparation de ces papiers le vert de schweinfurt; moyens de les prévenir.” Annales d’hygiène publique et de médecine légale 38 (1847): 56–78. _____. “Note sur la coloration de quelques sucreries par un composé vénéneux, le vert de schweinfurt, l’arsénite de cuivre.” Journal de chimie médicale, de pharmacie et de toxicologie 3 (1827): 1–4. _____. “Note sur la vente des sucreries coloriées, bonbons, pastilles, etc.” Journal de chimie médicale 7 (1831): 37–50. _____. Recherches sur les dangers que présentent le vert de Schweinfurt, le vert arsenical, l’arsénite de cuivre. Paris, 1859. _____. “Section de Pharmacie: Séance du 16 mai.” Revue médicale française et étrangère 2 (1829): 555–56. Chevallier, J. B. Alphonse, and Édouard-Adolphe Duchesne. “Des dangers que présente l’emploi des papiers colorés avec des substances toxiques.” Annales d’hygiène publique et de médecine légale 2 (1854): 66–82. Follin, Eugène. “Note sur l’éruption papulo-ulcéreuse qu’on observe chez les ouvriers maniant le vert de Schweinfurt.” Archives générales de médecine 10 (1857): 683–89.

Schweinfurt Green and the Sanitary Police  85

Gmelin, Leopold. “Die Nachtheile der grünen Tapeten für die Gesundheit betreffend.” Annalen der Staats-Arzneikunde 10 (1845): 407–16. Guérard, Bruno. “L’inspection du travail et les débuts de la prévention des risques spécifiques.” Les cahiers du comité d’histoire 2–3 (2000): 57–90. Hawksley, Lucinda. Bitten by Witch Fever: Wallpaper and Arsenic in the Victorian Home. London, 2016 . Hermbstädt, Sigismund Friedrich. “Anweisung zur Verfertigung einer der Gesundheit völlig unschädlichen grünen Malerfarbe (Barthsches Grün).” Gemeinnützlicher Rathgeber für den Bürger und Landmann 2 (1817): 136–38. Hinds, William. “Another Case of Arsenical Poisoning by a Decorative WallPaper.” Medical Times and Gazette 35 (1857): 520–22. Jorland, Gérard. “Comment on a obligé les Français à se faire vacciner.” L’Histoire 361 (2011): 8–15. _____. Une société à soigner: Hygiène et salubrité publiques en France au XIXe siècle. Paris, 2010. Kletschke, Gustav. “Die Aufgabe der Medicinal-Polizei zur Verhütung von Vergiftungen durch schädliche Farben.” Vierteljahrsschrift für gerichtliche und öffentliche Medicin 6 (1854): 139–61. Liebig, Justus. “Darstellung der unter dem Namen Wienergrün im Handel vor­ kommenden Malerfarbe.” Repertorium für die Pharmacie 13 (1822): 446–57. _____. “Sur une couleur verte.” Annales de chimie et de physique 23 (1823): 412–13. Liebig, Justus, Johann Bartholomäus Trommsdorff, and Emanuel Merck. “Ueber die vermeintliche Schädlichkeit des Neusilbers in dem Haus- und Küchengebrauche.” Annalen der Pharmacie 17 (1836): 125–37. Marsh, James. “Account of a Method of Separating Small Quantities of Arsenic from Substances with Which It May Be Mixed.” Edinburgh New Philosophical Journal 21 (1836): 229–36. Mérimée, Léonor. De la peinture à l’huile. Paris, 1830. Mertens, Joost. “The Annales de l’Industrie: A Technological Laboratory for the Industrial Modernization of France.” History and Technology 20, no. 2 (2004): 135–63. O’Shaughnessy, William Brooke. “Poisoned Confectionary: Detection of Gamboge, Lead, Copper, Mercury, and Chromate of Lead in Various Articles of Sugar Confectionary.” The Lancet 16, no. 402 (1831): 193–98. Pietra-Santa, Prosper de. “Existe-t-il une affection propre aux ouvriers en papiers peints qui manient le vert de schweinfurt?​” Annales d’hygiène publique et de médecine légale 10 (1858): 339–56. _____. “Sur la fabrication des abat-jour peints en vert par les préparations arsenicales de Scheele et de Schweinfurt.” Comptes rendus hebdomadaires des séances de l’Académie des sciences 59 (1864): 653–56. Remer, Wilhelm Hermann Georg. Lehrbuch der polizeilich-gerichtlichen Chemie. 3rd ed. Helmstädt, 1827.

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_____. Police judiciaire pharmaco-chimique, ou Traité des alimens salubres. Translated by Edme-Jean-Baptiste Bouillon-Lagrange and Heinrich August Vogel. Paris, 1816. Originally published as Lehrbuch der polizeilich-gerichtlichen Chemie, 2nd ed. Helmstädt, 1812. Roussin, Zacharie. “Double empoisonnement par le vert de schweinfurt, nouvelles expériences relatives à l’absorption cutanée.” Annales d’hygiène publique et de médecine légale 28 (1867): 179–205. Scheele, Carl Wilhelm. “Manière de préparer une nouvelle couleur verte.” In Mémoires de Chymie de M. C. W. Schéele, translated by Claudine Picardet, 261–64. Dijon, 1785. _____. “Method of Preparing a New Green Colour.” In The Chemical Essays of Charles William Scheele, translated by Thomas Beddoes, 253–54. London, 1786. _____. “Method of Preparing.” Monthly Review 75 (1786): 351. _____. “Vom Arsenik und dessen Säure.” Translated by Abraham Gotthelf Kästner. Der Königl: Schwedischen Akademie der Wissenschaften Abhandlungen . . . auf das Jahr 1775 37 (1781): 265–94. _____. “Zubereitungsart einer neuen grünen Farbe.” Translated by Abraham Gotthelf Kästner Der Königl: Schwedischen Akademie der Wissenschaften Abhandlungen . . . auf das Jahr 1778 40 (1783): 316–17. Stoeckhardt, Julius Adolf. Ueber die Zusammensetzung, Erkennung und Benutzung der Farben im Allgemeinen und der Giftfarben insbesondere, wie über die Vorsichtsmaßregeln beim Gebrauche der letzteren. Leipzig, 1844. Vernois, Maxime. Traité pratique d’hygiène industrielle et administrative des ­établissements insalubres, dangereux et incommodes. Vol. 1. Paris, 1860. Whorton, James C. The Arsenic Century: How Victorian Britain Was Poisoned at Home, Work, and Play. Oxford, 2010.

/

CHAPTER 2

The Banning of White Lead French and International Regulations Laurence Lestel

The massive recall of lead-contaminated toys in 2007 reminded us

that white lead is still not banned everywhere in the world.1 A comparison of the evolution of white lead legislation in each country would be tedious and would not give a clear idea of the reasons for a white lead ban. For example, France, the first country to ban white lead in painting in 1909, was one of the last European and developed countries to ban lead in gasoline (in 2000). If one looks closely at the arguments, which motorists and the powerful automobile industry lobby put forward in France, the toxicity of lead is clearly not the only factor that determines legislation. Lead consumption is still increasing in the world, even in European and developed countries.2 To fully describe how the use or production of white lead has been regulated or banned, many aspects must be considered: What was the knowledge about white lead toxicity?​Was it local or international knowledge?​What was regulated or banned—production or use?​Why have some uses been regulated while others have not?​Who took action for banning or regulating white lead?​Who were the opponents?​What kinds of arguments were developed?​What kinds of regulations were adopted?​How were these regulations adapted over time?​How did these regulations or bans enter into force?​Were there some controls, and were they efficient?​Can we correlate the regulation or ban of white lead with the appearance of alternative products?​ To give elements of answers to all these questions, I shall focus on two bodies of data: the nineteenth-century situation in France, from the introduction of white lead production in 1809 to its ban for painting in 1909;3 and the 1920s debate at the International Labour Organization,

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which helps see the limits of the different national approaches to the white lead problem.4 White lead has many uses. One of the oldest, dating back to ancient Egypt, is its use in cosmetics, as was widely practiced in Japan.5 In France, recipe books and inventories from perfume shops likewise testify its eighteenth-century use in cosmetics.6 But the properties of white lead also made it useful in sealants and as a drying agent for colorless varnish for business cards or shoes since the nineteenth century. Lace makers used its bleaching power to clean their work.

White Lead Production and Producers in France in the Nineteenth Century The increase of white lead use in France, as in most countries, that started in the eighteenth century was because of its use as white pigment in paints. Most discussions about the toxicity of white lead were related to that application (see table 2.1). In the early nineteenth century, the toxicity of white lead affected mostly workers in factories that produced white lead; by the end of the century, it had become a problem that concerned mostly painters. France did not know how to produce white lead and instead imported it from England and Holland, but the increasing demand for it as white pigment in paints led to a technical challenge that structured what can be called the time of inventors. In Paris, this era of chemists, with the help of Antoine Lavoisier’s modern chemistry, discovered a way to manufacture white lead in two days instead of the two months the traditional “Dutch process” required.7 In 1809, Jean-Louis Roard (1775–1853) developed the new process in a firm in Clichy, near Paris.8 The Clichy process is rather different from the classical Dutch process, which is slow and involves leaving sheets of lead in contact with vinegar and carbonic acid generated by horse dung for about two months.9 White lead is obtained in the form of flakes, which are then crushed and sold as bars. The Clichy method is a rapid process in aqueous media, where the litharge (lead oxide) reacts with vinegar and then carbon dioxide, which is bubbled through hundreds of tubes into the solution. Using this process, very high-quality white lead in the form of a fine powder is obtained in less than forty-eight hours. But this very fine powder is dangerous, as workers easily inhale it. Like many occupations related to lead, white lead production was required to receive a formal permission from the French government

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Table 2.1 Key points concerning white lead in France (from various sources). Usage

Century

Key Actors

Cosmetic Eighteenth Chemists

Painting

Early Chemists, nineteenth industrials

Late Doctors, nineteenth chemists

Late twentieth

Municipalities, health department

Advantage

Risk Perception

Some disadvantages (premature skin aging) White “pure” Risk for workers in interior; white lead cities less dark at night production (Toulouse) Risk for Good painters covering properties, hard to match with substitutes

Risk for inhabitants

Action

Technical responses (process modifications) Prohibited use

Renovation of degraded residences

as a result of the 1810 decree concerning dangerous or unhealthy manufactures.10 White lead production entered the second of three danger classes because of its harmful emissions. In 1810, Clichy was the only major firm, which opened in 1809 and was scheduled to produce enough white lead, in the order of six hundred tons, to cover a third of French needs. Many small establishments were also attempting to develop the Dutch process in Paris, Orleans, Givet, Rouen, and Pezenas. But one region later took the lead, both in the number of factories created and the quality of white lead produced: the Lille region (North of France) and some neighboring municipalities (Wazemmes, Esquermes, Fives). While the number of white lead factories remained constant or declined in the rest of France, Lille saw significant growth from 1820 to 1840 and from 1865 to 1885.11 Discussions on the toxicity of white lead thus focused on two areas: the Seine department, because of the Clichy factory, which operated from 1809 to 1882, and the Nord department, with ten companies. What is of interest is the importance of the debate on white lead, even though relatively few workers were concerned: estimates arrive at 450 workers throughout France in 1836; Théodore

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Lefebvre & Co. employed 100 workers in the middle of the century, as did the firm of Veuve Jules Perus et Cie. in 1885, these being the most important firms for white lead production near Lille.12 From all these companies, only the pioneer (Roard in Clichy) used a special process. The rest used the traditional Dutch method.13 White Lead Production and Lead Poisoning Most producers of white lead recognized its toxicity very early: the life of white lead factory workers was remarkably shortened, and white lead was already known as a cause of occupational disease. Various records suggest manufacturers had recognized this problem and attempted to ameliorate it since the beginning of the nineteenth century. As early as 1827, white lead producers who presented products at industrial fairs received awards for making their industry safer for their workers.14 This was an exceptional situation: other chemicals displayed at the fairs received awards based on their qualities, their manufacturing processes, or the proper use of manufacturing residues, but white lead received awards for how its toxicity was managed. White lead producers introduced many technical innovations to reduce the impact of white lead on workers. They followed several strategies, including the introduction of protective equipment and practices for workers such as gloves and masks formed by a sponge between two wire meshes, sinks to wash their hands in, and a rotation of the most exposed workers. Other strategies included mechanization and workspace modification to provide better ventilation and better chimney draughts. In 1837, Théodore Lefebvre developed a machine to detach white lead flakes from lead sheets in Lille with the help of Aimé Laurenge, a carpenter and mechanical engineer.15 Interestingly, instead of keeping his invention secret, Lefebvre immediately communicated to other manufacturers the drawings of this machine, which was intended to eliminate manual operations at one of the most dangerous steps of the process. But this machine would soon be abandoned: the workers called it “the devil,” because a machine with violent movements was inevitably a dust generator. The most significant advance was using water to moisten white lead powder before any handling. A small producer from Orléans in central France had adopted grinding with water in 1823, but this practice became widespread in France only in the 1870s, a few decades after this had happened in England.16 Replacing vertical grinding stones with horizontal ones allowed the use of copper trims, which made it

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possible to grind with water without splashing the workers. The positive effects were immediate: “For eighteen months, we have passed on the white lead to wet grinding, and we clean the pots only after they have stayed under water for several days: there are not half as many workers with saturnine diseases as in the past.”17 The last great improvement by manufacturers was promoting the sale of white lead as paste in oil, taking advantage of white lead’s higher affinity for oil than for water, a characteristic reported by the chemist Nicolas Clément-Desormes (1778–1841) in 1834.18 The firm of Louis Pierre Bezançon (1810–1878), the other producer of white lead in Paris, first introduced this innovation in Paris and seemed to have completely stopped the manufacture of white lead as powder in favor of white lead in oil in 1852.19 Lefebvre in Lille introduced white lead in oil in 1850. In 1870, he sold half his white lead as powder, the other half as paste, in either water or oil. He maintained the production of white lead as powder at the request of a few customers. In 1917, we know the company’s stocks were eighty-eight tons of white lead ground in water, eighty-one tons of white lead ground in oil, and four tons of white lead as powder. Consequently, these two industry leaders, who applied the most advanced techniques in their factories, had a particularly low rate of lead poisoning in their companies.20 All these efforts were officially recognized. French Public Health Advisory Committee (Comité Consultatif d’Hygiène Publique de France) reported in March 1901 that the Expert-Bezançon process of grinding and mixing white lead in water, with the addition of oil as it passed through the rollers, had made the white lead industry less harmful. The report also underlined the effect of careful medical examinations and of job rotations at places with a high exposure.21 Management of White Lead Poisoning in Factories by the State We also have evidence that the state concerned itself with the hazards of white lead. The first whistleblowers were hospitals, which started lead poisoning statistics in 1818 (see fig. 2.1).22 French doctors at the Charity and Beaujon hospitals knew about lead poisoning, leading to the publication of a two-volume treatise by the physician Louis Tanquerel des Planches (1810–1862) in 1839 (drawing on more than 1,200 patients).23 This was the era of the hygienists, who severely denounced the dangers of white lead, although without much success. One leading figure in the public campaign against white lead, the pharmacist Jean Baptiste

92  Laurence Lestel

Figure 2.1  Cases of lead poisoning in the Seine department. Figure created by the author. Source: See Lestel, “Production,” notes 24 to 26.

Alphonse Chevallier (1793–1879), aimed to produce statistics about lead poisoning to monitor the positive impact of technical changes in factories. His regular factory visits led him to suggest useful changes to “encourage manufacturers on the road of progress.”24 In the Seine department (Paris and its surroundings), the number of white lead workers going to the hospital grew to more than 350 in 1846 and then stabilized 100 to 200 per year. The proportion of patients from white lead factories was about 65 percent from 1838 to 1851, the other patients being professional painters working with white lead. This decreases to 35 percent on average from 1867 to 1880 for workers employed in white or red lead factories. These figures must be compared to the number of workers employed in each sector. Throughout this period, only two white lead factories of importance existed in Paris: Bezançon, created in 1839, which employed thirty to fifty workers, and Roard in Clichy, which employed forty-five to sixty-five workers. These figures led the chemist E. J. Armand Gautier (1837–1920), assisted by the Prefecture of Police in charge of public health, to conduct a survey in which he classified occupations according to their healthiness (or lack thereof) by counting the number of cases of lead poisoning occurring for each hundred workers.25 Factories of white lead and red lead (a lead oxide, sometimes produced in the same firms) were by far the worst, with a percentage of workers suffering from lead poisoning at well above one hundred. An annual percentage over one hundred means that the factories sent more patients to the hospital than the number of their workers: either a worker went to the hospital several times, or the

The Banning of White Lead  93

Figure 2.2  Lead poisoning of white lead workers in two factories in the Seine department. Figure created by the author. Source: See Lestel, “Production,” notes 24 to 26.

turnover of workers was very high. This drops to 1.8 percent for painters (250 patients out of 14,000 workers).26 Not all factories of white and red lead were equally dangerous. Gautier, as all observers of the time, sets apart the Clichy factory, which indeed provides a quite exceptional amount of patients (400 percent or more): for example, 209 patients for 45 workers in 1880.27 In comparison, Bezançon, which employed the same number of ­workers, sent fifteen workers to hospital in the same year. Figure 2.2 shows clearly the qualitative difference between the two factories. Moreover, the number of patients in the Bezançon factory clearly decreased significantly in the 1850s, which can be attributed to technical advances in the manufacturing process of white lead, as described earlier. Data on factories in Lille are more fragmented. From 1878 to 1880, the number of annual admissions to hospital did not exceed 155 of more than 300 workers. The Lefebvre factory was by far the healthiest, with only 4 to 6 percent of its workers becoming sick each year.28 Again, this can be attributed to the quality of the operations in the Lefebvre manufacture. What is important to note is that the Clichy factory, determined to keep its hold on the market niche for lead powder, refused to finish its white lead in a wet state, which explains the high number of patients. Chevallier wrote many reports about the special case presented by this

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factory, but his recommendations were never put into practice. This shows the limits of the surveillance system of factories in France in the nineteenth century.29 The number of patients coming from this factory dropped only when the factory closed in 1882, after the death of its owner.30 At the end of the nineteenth century, white lead production was no longer considered a problem in France. Even after the ban of white lead in painting in 1909, new factories received authorization to produce white lead: the Villemot Company at Aubervilliers in 1926 and Expert-Bezançon at Saint-André-lez-Lille in 1930.

Painters and the Regulation of White Lead Use White lead became a very attractive product in the nineteenth century. All interior walls (and some exterior walls, as in Toulouse)31 of even the smallest towns and villages were painted with white lead, which led to an increase in production and consumption throughout the nineteenth century. But the toxicity of white lead, along with the fact that the lead carbonate it contained blackened in the presence of the sulfurous gas coming from new lighting sources such as gas lamps, led the French government to regulate the use of white lead in paints and propose alternative products such as zinc white (a zinc oxide). Again, as for the factories, nineteenth-century regulations were not very efficient. Only in the early twentieth century did real changes occur. French Regulations against White Lead in Paint In 1849, the Minister of Public Works ordered all the government buildings in France be painted with zinc oxide instead of lead carbonate (white lead). This was followed in 1852 by a similar request addressed to the departments by the Minister of the Interior. However, these recommendations seemed to be abandoned very rapidly: the use of zinc white at first increased (reaching six thousand tons in 1854) but soon decreased again.32 The only place where the request was implemented was in the French Navy. In a corrosive marine environment, protecting exposed surfaces was essential. An 1837 article of a regulation required sailors to paint with tallow and white lead all parts of dismantled ships. Navy ships were regularly whitened with white lead paint. White lead was also used in sealants. However, in the 1840s and 1850s, many cases of dry colic were observed, and their origin was discussed. Among

The Banning of White Lead  95

­ fficers, those who were “melancholic” and spent more time in their o cabins than others were more often ill. After several years of epidemiological studies with the help of a dense network of correspondents on many ships, Doctor-in-Chief of the Navy Amédée Lefèvre (1798–1869) finally proved the negative effect of lead in 1858.33 His work was followed by a series of regulations to limit lead use in Navy ships. When the question of the use of white lead for painting arose again in 1901, the Ministry of Trade asked for an opinion from the Navy, which by then had fifty years of experience using zinc white instead of white lead.34 However, painters did not easily adopt zinc white because it was considered to have a less satisfactory covering effect than white lead, as well as little durability, and more expensive. In 1901, the physician and politician Georges Clemenceau (1841– 1929) and the newspaper L’Aurore were the main actors in a movement against the use of white lead in paints.35 This led to the first national decree against the use of white lead as powder in 1902.36 At that time, Germany and England had already adopted regulations on white lead, but the situation moved more rapidly in France, spurred on by vigorous parliamentary debates initiated by Jules-Louis Breton (1872–1940), who wrote a report on white lead in 1903, and Clovis Hugues (1851–1907), who wrote a poem on the painters (fig. 2.3). Charles Frédéric Expert-Bezançon (1845–1916), a senator and white lead producer, actively opposed these texts, but Clemenceau and L’Aurore launched a new campaign in 1904.37 Painters, who began to organize their opposition to white lead in 1904,38 also began to strike, first in Lille in 1905 and then in Lille and Paris during three weeks in 1906. For the first time, many workers suffering from visible diseases were gathered together, which certainly had an effect on public opinion. It is noteworthy that this painters’ movement was not supported by classical labor unions, none of which took action against occupational diseases.39 One leader of the painters’ movement was Abel Craissac, who tried to promote collaboration with experts and physicians and greatly influenced the first ILO director (1919–1932), the French politician Albert Thomas (1878–1932). Many involved in these debates blamed the workers, arguing they became sick because they did not wash their hands, drank alcohol, and so forth. Others underlined the difficulties in ensuring that the working conditions of painters were hygienic. However, some began to say the workers’ degraded health was not their fault and that more radical

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Figure 2.3  Picture illustrating the poem L’empoisonné (The poisoned), written about white lead by Clovis Hugues, a socialist, who often defended workers (© Bibliothèque nationale de France).

solutions were necessary. This led to a new law that went further than in any other country: white lead was strictly prohibited in any interior and exterior works done by employed painters (ouvriers peintres). The law passed in 1909 and was to enter into force in 1915 but was applied only

The Banning of White Lead  97

after World War I. This six-year delay between the law’s passing and entry into force was to avoid paying any compensation to manufacturers and leave them time to change their activities. The Slow Replacement of White Lead by Zinc White and Lithopone The pioneer in the use of zinc white was Edme-Jean Leclaire (1801– 1872). His painting company, founded in 1828, employed sixty workers, of which nineteen suffered from lead poisoning. After testing different white pigments, he patented a new process in 1845 for the preparation of zinc white, which was soon put into practice in both Paris and Belgium.40 Well-known for a mutual aid society he created in 1838, Leclaire was supported by Chevallier, who published a report on zinc white in 1849. France and Belgium kept their position as leaders in zinc oxide production until the beginning of the twentieth century. However, despite the recommendations of the state, zinc white did not succeed in supplanting white lead. Painters argued it did not cover surfaces very effectively, but these claims were contradicted by reports and even in a film presented by Breton at the beginning of the twentieth century in the battle against white lead and the promotion of zinc white.41 It seems the major obstacle was its price.42 Instead, painters adopted another zinc-based pigment: lithopone. The industrial process for its production was developed in England in 1874. Lithopone is a mixture of zinc sulfate and barium sulfide. Gradually, manufacturers mastered this mix to make the lithopone impermeable and less mealy so that it was considered satisfactory for indoor use in 1914.43 Statistics show that French manufacturers did not produce much lithopone until white lead was banned. While France had deposits of barium, it imported the barium sulfide necessary for manufacturing this paint.44 There was almost no lithopone production in France before the 1920s. Lithopone was mainly imported from Germany.45 White lead was replaced by zinc white and lithopone shortly after World War I (fig. 2.4). It is interesting to see that hygienists initiated the replacement of white lead, but the dominant arguments in practice were all about technical aspects, such as the physical and chemical nature of the different paints, their comparative coverage properties, and their lightfastness. This technical approach is also that of the thirty-minute film produced by the French physician, biologist, and filmmaker Jean Comandon (1877–1970) on white lead, presented at the Sorbonne in 1923 and in Geneva in 1927.46 In these expert reports, zinc

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Figure 2.4  Consumption of white pigments based on lead and zinc in France. Figure created by the author. Sources on white lead, see Lestel, “Comment”; on zinc white, see annual customs statistics and the journal Le Mois Chimique et Électrochimique, 1905ff.

white is promoted more often than lithopone, showing the preferences of experts and painters had shifted.

Comparison with Other Countries Because of its international character, the Third Session of the International Labour Conference (ILC) in Geneva in 1921, with “the use of white lead in painting” as its main topic, gives valuable information on the different national practices regarding white lead. Before the conference, the ILO had sent a questionnaire to not only governments but also manufacturers and labor organizations. The first question was very controversial, and some saw it as evidence of the ILO’s bias: “In view of the fact that it is now possible to replace white lead by efficient substitutes, are you of the opinion that a Draft Convention, prohibiting the use of white lead in painting, should be admitted to the Conference?​”47 The ILO also decided to publish all documents it received.48 First, there was no doubt about the toxicity of white lead. Many countries had already gathered statistics on lead poisoning, although it is not easy to compare them because of the different criteria used (Were painters set apart?​ What was considered: death or illness?​Was there a legal obligation to report lead poisoning or not?​). Knowledge about lead poisoning was

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currently shared between countries: in the first official reports on the toxicity of white lead in France at the beginning of the nineteenth century, there were letters from England and Holland, giving details about how lead poisoning was avoided in those two countries.49 Tanquerel des Planches’s book on white lead diseases in 1839 was even published in the United States, a country that is not known to have considered lead poisoning in the nineteenth century.50 What was regulated or banned was the use of white lead in painting, never its production. There was fierce debate at the 1921 ILC on whether to completely ban the use of white lead or just regulate it. Proponents of a total prohibition (like France, which practiced total prohibition since 1909, as far as employed painters were concerned) said the number of patients had declined only after the ban was in effect, while other countries such as Germany and England thought regulation was sufficient. The major reasons given to continue using white lead were technical ones, particularly the absence of convenient substitutes, especially for exterior applications, as already seen in France.51 The only unanimous decision taken was about the prohibition of employment of women in seven categories of work where lead and its compounds were used, but that resolution had already been adopted at the first ILC in Washington in 1919. An interesting point was the introduction of financial compensation for sick workers. Germany introduced compensation in 1884, England in 1906, and several US states from 1911 to 1920.52 But that issue was not debated in France, because compensation for occupational disease was not introduced until October 1919 and thus after the use of white lead had already been banned. At the 1921 ILC, four main points were discussed: medical knowledge about lead poisoning, statistics on lead poisoning, the technical properties of the substitutes for white lead, and the legal solutions to enable substitution. The proposal by the French politician Justin Godart (1871–1956) to ban white lead for all interior and exterior works was considered too controversial and replaced by a proposal concerning only interiors, which was adopted unanimously.53 Countries that ratified this text were supposed to ban white lead and lead sulfate from interior works, with the exception of railway stations and some special cases. Five years later, thirteen countries had ratified the text (Austria, Belgium, Bulgaria, Chile, Czechoslovakia, Estonia, France, Greece, Latvia, Poland, Romania, Sweden), three other countries had decided to ratify it (Hungary, Italy, the Netherlands) and five recommended ratification (Argentina, Cuba, Denmark, Germany, Uruguay). After the

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ratification of the text, France extended the prohibition of the use of white lead in painting for all workers (i.e., for independent painters as well) by law in 1926. Britain was strongly criticized for obstructing the ratification of the text and for even campaigning in other countries against ratification.54 English producers still opposed zinc white, using technical arguments, and complained about the lack of a convenient substituent for white lead. Although the ratification of the proposed text appeared to take a long time and was never completed, the ILO helped standardize practices regarding this occupational disease.

Conclusion The toxicity of white lead was well known by many actors, but that was not sufficient to produce relevant regulations to prevent its further diffusion, use, or effects.55 The use of white lead in painting, not its production, was regulated or banned, even if many of the debates were about processes for producing white lead. The numbers of workers concerned can explain this: a few hundred in the case of white lead production, many tens of thousands in the case of painting. However, painters were often isolated workers, and they only organized quite late. Their opponents were manufacturers very close to political power. In France, labor unions took no action against occupational diseases. The crucial factor was the intervention of newspapers and politicians, more than physicians and hygienists, whose knowledge was necessary but not sufficient. In the twentieth century, new international organizations such as the ILO started their work with the white lead as a case, leading to the first standards for international regulation, in which each country must ratify a common text, here on white lead use restriction. As seen in the 1921 ILC, the predominant arguments were technical and economic. Workers were considered more through statistics than through their suffering. The story of white lead is not over. In the 1980s, France rediscovered white lead by means of several cases of childhood lead poisoning. The victims were poor inhabitants in contact with degraded painted walls. White lead became a symbol of the slums. The situation led to a 2003 law that required all property owners who rent or sell houses or apartments to have a “lead diagnosis.”56 Previously a symbol of luxury, white lead has become a toxic product that must be covered or removed by law.

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Laurence Lestel is Research Director at the Centre National de la Recherche Scientifique (CNRS) and a member of the UMR 7619 METIS at Sorbonne University. After working in the CNRS Department of Chemical Science (1988–1999), she switched to environmental history, looking for the environmental impact of increasing industrialization and urbanization nineteenth- and twentieth-century France. Her work aims to analyze how environmental problems were detected and managed by several actors such as the state, experts, and the public. She wrote “Non-ferrous Metals (Pb, Cu, Zn) Needs and City Development: The Paris Example (1815–2009)” (Regional Environmental Change, 2012) and coedited a book, with Catherine Carré, on the complex relationships between European cities and their waters, Les rivières urbaines et leur pollution (2017). Notes   1.   2.   3.   4.   5.

Story, “Lead Paint”; Gilbert and Wisner, “Mattel.” Sellers, “Cross-Nationalizing”; Lestel, “Non-ferrous Metals.” Lestel, “Production”; Lestel, “Comment.” Heitmann, “ILO”; Lespinet-Moret and Viet, L’organisation. On Egypt, Walter et al., “Making Make-Up”; for white lead (oshiroi) production in Japan, see Takamatsu, “On Japanese Pigments.” I thank Yoshitomo Kikuchi for sending me the relevant pages.   6. Lanoë, “Céruse.”   7. Louis-Jacques Thenard (1777–1857), a chemistry professor at the Collège de France in Paris, developed this chemical process. See Emptoz, “Procédé.”   8. Roard was a French chemist and manufacturer and a friend of the chemists who developed the chemical process. Before developing the production of white lead in Clichy, he was the director of dyes at the Manufacture des Gobelins. After Roard, it was directed by his son-in-law Théophile Joseph Orsat (from 1850 until his death in 1862) and then by the latter’s son Louis Hengist Orsat (from 1862 until his death in 1882). For details, see Lefort, “Fabriquer.”  9. For the development of the Dutch process, see Homburg and Vlieger, “Victory.” Details of the Dutch process and the same process used in England were known in France with the publication of Chaptal, Chimie appliquée, 302–8. 10. This 1810 decree followed a question at the Institut de France about the dangers of odors emitted by the new types of chemical factories emerging at that time. Many books have been written on it in the past few years. Guillerme et al., Dangereux; Le Roux, Risques industriels. 11. At the beginning, this was probably because of the proximity with Holland, which first developed its own process. Later, it was because of the strength

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of the firms in the Lille region, all connected by family links (families Faure, Brabant, Bériot, Perus, Lefebvre), which facilitated the transfers of knowledge and of technologies between them. These family connections were quoted by one of their descendants, Georges Dulouard, and can be seen through genealogic research at Archives Départementales du Nord, accessed 13 February 2019, https://archivesdepartementales.lenord.fr. 12. The Veuve Perus Company is described in Turgan, “Usine Perus.” Documents on Théodore Lefebvre & Co. can be found in Lefebvre, Fabrique, but the story of the company (which still exists and produces paint mixtures) has not yet been written. Perus was Lefebvre’s sister-in-law. 13. Lestel, “Production,” 39. 14. Ibid., 41. 15. Lefebvre, Fabrique, 59. 16. Arnould “Oral Contribution.” 17. Lefebvre, Fabrique, 48. 18. Clément-Desormes, from 1819 to 1836, was the first professor of industrial chemistry at the Conservatoire des Arts et Métiers. 19. Bezançon began his activity as a white lead producer in Paris in 1839 with his brother Eugène. The firm, which used the Dutch process, expanded with the help of his son-in-law Charles Expert-Bezançon, a senator and a member of the commission of inquiry of the senate about white lead in 1905. Two new firms began white lead production under the name Expert-Bezançon, near Lille in 1900 and near Paris in 1919. See Bezançon Frères, Note présentée, 5. 20. Lestel, “Comment,” 45. 21. Oliver, Dangerous Trades, 294. Some white lead manufacturers had employed physicians since the mid-nineteenth century, while the organization of medical examination in companies was legislated only in 1909. 22. Administration Générale des Hospices et Hôpitaux civils de Paris, “Etat des Peintres et des ouvriers employés à la fabrication de la Céruse atteints de la colique de plomb, admis pendant les années 1818, 1819, 1820, 1821 et 1822 dans les Hôpitaux dépendant de la 1ère et de la 2ème division (3 tableaux),” AN, F12 2428. 23. Tanquerel des Planches, Traité. 24. Chevallier had been a member of the Conseil de Salubrité (Council of Sanitation) since 1837 and wrote about two thousand reports, many on white lead factories. 25. Gautier was a chemistry professor at the University of Paris Faculty of Medicine and a member of the Academy of Medicine and of the Academy of Science. He published several reports on hygiene at the request of state services. 26. Gautier, Cuivre, 237–52. 27. Gautier’s interpretation was that “every worker in this factory is sent on average four times per year to hospital!” Ibid., 247. 28. Ibid., 251; Desplats, “Histoire sanitaire.”

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29. Jorland, “L’hygiène professionnelle.” 30. For details, see Lestel, “Comment.” 31. Nègre, “Céruse.” 32. Thibaut, Céruse, 39. 33. Lefèvre was named Commander of the Legion d’Honneur for his work on the effect of lead in the Navy ships. See, e.g., Sardet, Médecins, 130–41. 34. SHD, Archives de la Marine, 6 DD1 402. 35. Georges Clemenceau is most known for his role in politics as a supporter of Dreyfus and in World War I. He was the French prime minister from 1906 to 1909 and from 1917 to 1920. 36. Décret du 18 juillet 1902, réglementant l’emploi du blanc de céruse dans l’industrie de la peinture en bâtiment. 37. Mainly for the workers’ self-protection and to improve the hygiene inside the white lead factories. 38. At the First International Congress of Painters Labour Organization in Grenoble, 4–11 September 1904. 39. Rainhorn, “Mouvement.” 40. See Peters and Laloux, “Adolphe Stoclet.” 41. Breton was also director of the National Office for Scientific and Industrial Research and Inventions in Meudon-Bellevue and the first Minister of Hygiene, Assistance, and Social Welfare. 42. On the role of regulation in the competition between white lead and zinc white, see Rainhorn, “Santé.” 43. Vila, “Peintures industrielles.” 44. CSEP, “Lithopone.” 45. For more on the production of lithopone in Germany, see “75 Jahre deutsche Lithophone,” Die Zeit, 10 January 1952. 46. I thank Thierry Lefebvre, the CNRS, and the Archives Françaises du Film– CNC for restoring the film and presenting it at the “semaine de la science” in October 2011. 47. English translation in Heitmann, “ILO.” 48. BIT, Céruse. 49. The letter from England was from Gilbert Blanc, the king’s physician-in-chief. 50. As clearly written in Alice Hamilton’s books. See Warren, Brush with Death. 51. In his article, Heitmann says British nonunion observers often viewed French authorities as being motivated by economic self-interest, since the zinc oxide industry was centered in France and Belgium. French observers could have answered that Britain was the second producer of white lead in the world with about 50,000 tons per year, about 20,000 of which were exported (after the United States with 120,000 tons per year), whereas France was only selfsufficient, producing about 25,000 tons in 1910. So, Britain had an economic interest in the use of white lead in paints. France and Belgium were producers of zinc white, but Germany was the first producer of lithopone, with 100,000

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tons in 1923 (50,000 tons in the United States and only a few in France, which was obliged to import it). 52. Rainhorn, “Banning.” 53. Godart represented France at the ILO and was very close to Thomas. For details, see Viet, “Médiation.” 54. Conférence Internationale sur la Céruse du 2 juin 1927 à Genève, where Comandon’s film was presented. 55. Rainhorn, “Interroger.” 56. This required developing methods for detecting lead in painted walls. Mostly based on X-ray fluorescence, the analytical methods still must be improved, because the presence of other types of white pigments such as zinc oxide can lead to false results. AFSSE, Détection.

Bibliography Archives AN (Archives Nationales), Pierrefitte-sur-Seine. SHD (Service Historique de la Défense), Vincennes.

Publications AFSSE (Agence Française de Sécurité Sanitaire Environmentale). “Détection du plomb dans les peintures anciennes.” Report of the working group, June 2005. Arnould, J. “Oral Contribution.” [In French.] In Congrès international d’hygiène: Tenu à Paris du 1er au 10 août 1878, vol. 1, 638–642. Paris, 1880. Bezançon Frères. Note présentée par MM. Bezançon frères, fabricants de céruse à Paris, Classe 44–n°91 à la commission impériale de l’Exposition de 1867. Paris, 1867. BIT (Bureau International du Travail). La céruse: Documentation réunie par le Bureau international du travail sur l’emploi de la céruse dans l’industrie de la peinture. Genève, 1927. Chaptal, Jean-Antoine. Chimie appliquée aux arts. Vol. 4. Paris, 1807. CSEP (Chambre Syndicale des Entrepreneurs de Peintures de la Ville de Paris). “Lithopone.” Bulletin de la Chambre de commerce et d’industrie (Paris) 40–42 (1909): 1247–48. Desplats, Henri. “Histoire sanitaire des fabriques de céruse à Lille, depuis 1866 jusqu’à 1878.” Annales d’hygiène publique et de médecine légale 47 (1878): 385–406. Emptoz, Gérard. “Un procédé de fabrication de la céruse issu de la ‘chimie moderne’ au début du XIXe siècle.” In Lestel and Lefort, La céruse, 49–60. Gautier, E. J. Armand. Le cuivre et le plomb dans l’alimentation et l’industrie au point de vue de l’hygiène. Paris, 1883.

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Gilbert, Joseph, and Joel Wisner. “Mattel, Lead Paint and Magnets: Ethics and Supply Chain Management.” Ethics and Behavior 20, no. 1 (2010): 33–46. Guillerme, André, Anne-Cécile Lefort, and Gérard Jigaudon. Dangereux, insalubres et incommodes: Paysages industriels en banlieue parisienne, XIXe–XXe siècles. Seyssel, 2004. Heitmann, John. “The ILO and the Regulation of White Lead in Britain during the Interwar Years: An Examination of the International and National Campaigns in Occupational Health.” Labour History Review 69, no. 3 (2004): 267–84. Homburg, Ernst, and Johan H. de Vlieger. “A Victory of Practice over Science: The Unsuccessful Modernisation of the Dutch White Lead Industry (1780–1865).” History and Technology 13 (1996): 33–52. Jorland, Gérard. “L’hygiène professionnelle en France au XIXe siècle.” Le mouvement social 4, no. 213 (2005): 71–90. Lanoë, Catherine. “La céruse dans la fabrication des cosmétiques sous l’Ancien Régime (XVIe–XVIIIe siècles).” Techniques et culture 38 (2002): 17–33. Lefebvre, Théodore. Fabrique de céruse de Théodore Lefebvre et Cie à Lille, section des Moulins (Nord): Rapports, notices, documents, extraits divers, etc. 1825–1865. Lille, 1865. Lefort, Anne-Cécile. “Fabriquer de la céruse aux portes de Paris: L’usine de Clichy, 1809–1883.” In Lestel and Lefort, La céruse, 101–10. Le Roux, Thomas, ed. Risques industriels: Savoirs, regulations, politques d’assistance, fin XVIIe–début XXe siècle. Rennes, 2016. Lespinet-Moret, Isabelle, and Vincent Viet, eds. L’organisation internationale du travail. Rennes, 2011. Lestel, Laurence. “Comment concilier développement industriel et protection de l’ouvrier: Le cas de la céruse en France au XIXe siècle.” Archiv für Sozialgeschichte 43 (2003): 79–99. _____. “Non-ferrous Metals (Pb, Cu, Zn) Needs and City Development: The Paris Example (1815–2009).” Regional Environmental Change 12, no. 2 (2012): 311–323. _____. “La production de céruse en France: Évolution d’une industrie dangereuse.” Techniques et culture 38 (2002): 35–66. Lestel, Laurence, and Anne-Cécile Lefort. La céruse: usages et effets, Xe–XXe siècles. Paris, 2003. Nègre, Valérie. “La céruse et le blanchiment des villes de brique au milieu du XVIIIe siècle.” Techniques et culture 38 (2002): 5–16. Peters, Arnaud, and Pierre-Olivier Laloux. “Adolphe Stoclet et les débuts de la production de blanc de zinc en Belgique (1845–1855).” In Les innovations et transferts de technologie en Europe du Nord-Ouest aux XIXe et XXe siècles, edited by Jean-François Eck, and Pierre Tilly, 179–94. Bruxelles, 2011. Oliver, Thomas. Dangerous Trades. London, 1902. Rainhorn, Judith. “The Banning of White Lead: French and American Experiences in a Comparative Perspective (Early Twentieth Century).” European Review of History / Revue européenne d’histoire 20, no. 2 (2013): 197–216.

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_____. “Interroger l’opacité d’une maladie: Le saturnisme professionnel comme enjeu sanitaire, scientifique et politique dans la France du XIXe siècle.” Histoire, Économie et Société 36, no. 1 (2017): 8–17. _____. “Le mouvement ouvrier contre la peinture au plomb: Stratégie syndicale, expérience locale et transgression du discours dominant au début du XXe siècle.” Politix 23, no. 3 (2010): 9–26. _____. “La santé au risqué du marché. Savoir medical, concurrence économique et regulation des risques entre blanc de zinc et blanc de plomb (France, XIXe siècle),” in Le Roux, Risques industriels, 21–44. Sardet, Michel. Médecins et pharmaciens de la marine à Rochefort au XIXe siècle. Paris, 2005. Sellers, Christopher C. “Cross-Nationalizing the History of Industrial Hazard.” Medical History 54, no. 3 (2010): 315–340. Story, Louise. “Lead Paint Prompts Mattel to Recall 967,000 Toys.” New York Times, 2 August 2007. Takamatsu, Toyokichi. “On Japanese Pigments.” PhD diss., University of Tokyo, 1878. Tanquerel des Planches, Louis. Traité des maladies de plomb ou saturnines. 2 vols. Paris, 1839. Thibaut, Anthelme. La céruse. Lyon, 1907. Turgan, Julien. “Usine Perus et Cie à Lille (Nord).” In Les grandes usines, vol. 16, no. 321, 1–16, Paris, 1885. Viet, Vincent. “La médiation de Justin Godart entre la France et l’Organisation international du Travail dans l’entre-deux-guerres.” In Lespinet-Moret and Viet, L’organisation internationale du travail, 89–106. Vila, A. “Les peintures industrielles succédanés de la céruse et peinture anti rouille.” Chimie et industrie 24 (1930): 1052–67. Walter, Philippe, Pauline Martinetto, Georges Tsoucaris, et al. “Making Make-Up in Ancient Egypt.” Nature 397, no. 6719 (1999): 483–84. Warren, Christian. Brush with Death: A Social History of Lead Poisoning. Baltimore, 2000.

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CHAPTER 3

Old Situations, New Complications Lead and Lead Poisoning in a Changing World Christian Warren

In 1900, the National Lead Company distributed a pamphlet entitled

“Uncle Sam’s Experience with Paints,” narrated by Uncle Sam himself. The recent “scrap” with Spain, he observed, had created the need for some major repainting: “I have been furbishing up the new places that have come under my flag and feel that I have repaid the people for any inconvenience I may have put them to while bringing them into line and giving them their freedom.” Havana and Santiago were now free, from not only tyrants but also “the smudge of yellow fever,” because, Sam crowed, “wherever I go I introduce cleanliness. And for cleanliness there is nothing like paint—the best paint—Pure White Lead and Pure Linseed Oil” (fig. 3.1).1 A century ago, US lead industries were well on their way to becoming the world’s largest suppliers of lead products, ready to “cover the earth”—if not with lead paint, then with the post-combustion byproducts of tetraethyl lead. But the United States was still a largely disinterested consumer of foreign ideas about recognizing, preventing, and, especially, regulating lead poisoning. By World War II, however, the United States also achieved preeminence in studying lead poisoning: in the workplace, the general environment, and the home, with an increasing emphasis on childhood plumbism. The growing attention by US researchers made pediatric lead poisoning appear to the world as a uniquely American problem. The international medical world saw this “silent epidemic” as a peculiar product of the US urban population, shaped by the nation’s racial and class divides and aggravated by its comparatively backward system of health care for the poor. By the end of the twentieth century, the United States

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Figure 3.1  “Uncle Sam’s Experience with Paints” (© National Lead Company, 1900).

had dramatically reduced its own population’s exposure to lead but continued to market the poison to the rest of the world. Currently, the United States is the second largest producer of lead (China has become the first), remains a leading exporter of lead products, and, somewhat ironically, because of its mixed history of responding to the poisoning of its people and lands, is an international leader in anti-lead-poisoning activism.2

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Similarly, the historiography of lead and lead poisoning has until recently been decidedly lopsided in its coverage of North American stories, but that is changing, with important nation-specific studies by Laurence Lestel, Judith Rainhorn, Didier Fassin, Frank Uekötter, and others, and cross-national studies by Rainhorn and Christopher Sellers.3 This chapter is a brief and largely synthetic look at a few themes in the history of lead, focusing mostly on the United States and Western Europe in the twentieth century. Those themes frame three intertwined histories: the changing nature of exposure to bioavailable lead compounds, the creation of knowledge about the health effects of lead, and the regulatory efforts to minimize those health consequences. My working thesis has a good-humoredly jingoistic “America First” thrust, namely that as this new crop of local and transnational studies collectively widens the lens to something resembling a global perspective, we will see that today’s global pattern of distribution of lead’s risks, which imposes the greatest harms on the poorest and most vulnerable populations, is far from new—that variations on this pattern in fact have always defined the distribution of lead’s risks in each lead-using nation and region and that nowhere was this tragic and counterproductive dynamic clearer than in the twentieth-century United States.

Climax of the Old Lead World (1890–1920) Through the first half of the twentieth century, the US lead industry promoted its product as the “useful metal” and ran advertisements in popular magazines showing the many products in homes, cars, and industry that relied on lead (fig. 3.2).4 In claiming lead’s indispensability, the industry had history on its side: from the days of the ancient Greeks, who quickly found applications for the tons of lead that piled up as a byproduct of silver smelting, metallic lead and its oxides formed the basis of a truly mind-numbing array of products, from paints to medicines to weights to water pipes. Lead’s ubiquity rose with industrialization, so by the twentieth century, inhabitants of much of the Northern Hemisphere lived, in the words of a pediatrician’s grim assessment, in “a lead world.”5 Every step in the long history of lead’s rise to “indispensability” was matched with incremental knowledge of its toxicity. In the fourth century BCE, Hippocrates described a possible case of saturnine colic in a metalworker; two centuries later, the Greek physician and poet

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Figure 3.2  “Lead Helps to Guard Your Health” (© National Geographic Magazine, 1923).

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Nicander of Colophon described in detail the symptoms of poisoning from compounds of lead (and prescribed several purgative treatments). Observers from Pliny in ancient Rome to Bernardino Ramazzini in eighteenth-century Italy noted lead’s deadliness and indispensability, even to physicians: “How strange it is,” Ramazzini wryly noted, “that lead—which . . . is commonly called the surgeon’s mainstay . . . should . . . throw up merely by exhalation seeds so deadly that potters who need its aid are thus stricken.”6 The applications for leaden compounds extended far beyond the pharmacopeia; their chemical attributes made them indispensable in hundreds of applications. Among the deadliest was vintners’ addition of lead salts to their wines, both to inhibit fermentation and to sweeten inferior wines. The resulting health effects probably went largely undetected or misunderstood, but in a few notable instances, physicians identified lead at the heart of dramatic epidemics of abdominal and neurological illness. In 1639, for example, François Citois, a French physician in the town of Poitiers, recorded an epidemic of severe colic that left its victims “like ghosts or statues. Walking artificially, pallid, squalid, lean . . . their gait laughable if it were not so pitiable.”7 Later in the seventeenth century, Eberhard Gockel, the city physician of Ulm, surveyed the practices of winemakers in his region; he found widespread lead adulteration and lead colic. Gockel’s interest had been piqued by personal experience: he had contracted a severe case of lead colic after a stay at a local monastery whose vintner relied on lead compounds.8 Not all lead adulteration of spirits was intentional. Apple cider was a big business in Devonshire, England; for years, cider season produced hundreds of people suffering the excruciating stomachaches that came to be known as the Devonshire Colic. The physician George Baker conducted a methodical survey of hospitals, farms, and cider presses, searching for the cause. In 1767, Baker published his findings. “An Essay Concerning the Endemial Colic of Devonshire” found that metallic lead was used in the presses, mills, and storage barrels. Making matters worse, some cider producers added metallic lead into casks of cider for the same reason vintners did—to sweeten inferior cider and control fermentation.9 Early in his inquiry, Baker sought the advice of Benjamin Franklin, who informed him of the widespread history of lead-tainted rum in the American Colonies and confirmed the similarity of symptoms.10 In a letter to another of Franklin’s medical correspondents, in which he rehearsed his long experience with lead and lead poisoning, Franklin cautioned: “You will observe with Concern

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how long a useful Truth may be known, and exist, before it is generally receiv’d and practis’d on.” Before the mid-twentieth century, most of those “useful truths” came from the study of the lead trades, with much less attention paid to adulterated foods and beverages, or leaden water pipes, and almost none devoted to the dangers particular to children. Franklin was intimately aware of occupational lead poisoning: from his youthful days in the printing trade, when he contracted the early symptoms of clinical plumbism, to his 1767 trip to Paris, where he learned of the Charité Hospital’s progress in treating lead poisoned workers.11 Of course, it was at Charité that Louis Tanquerel des Planches conducted his groundbreaking studies published in 1839.12 The generally wretched conditions in most lead factories, with their heavy toll in morbidity and mortality, made them obvious targets for state-sponsored inspectors and reformers. Well into the 1920s, most products that relied on lead used it in its ancient forms, and while the considerable risks posed by these products increased arithmetically with production and consumption, the dangers they posed to human health were, likewise, the old accustomed ones often bearing old, evocative names: gastrointestinal illnesses such as “painter’s colic,” localized paralyses such as “ankle drop” or “wrist drop,” and the panoply of neurologic conditions from headache to tremors to convulsions. The persistence of ancient products poisoning in old accustomed ways is nowhere clearer than in the case of white lead (ceruse, lead carbonate), a product of perennial importance from the days of the ancient Greeks, and one whose ancient pedigree paint companies in the early twentieth century frequently pointed to, boasting that their pure white lead was made by the “Old Dutch Process.” White lead has proved an excellent case history to track the uneven efforts by various Western nations to make its production and use less deadly. A substantial body of historical studies shows that the timing, pace, and consequences of lead pigment regulation in France, Britain, and Germany from the midnineteenth century to about 1920 reflect the particular alchemy of state power, industry influence, and labor activism at work in each nation.13 Still, the major players were moving in the same direction: monitoring worker health; modifying production methods, and implementing workplace regulations to protect workers; and building a professional cadre of occupational scientists with ties to the academy and the state. Meanwhile, US lead industries were quickly surpassing the Old World in the mining, smelting, and consumption of lead, and because

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of a very different set of dynamics between labor, management, and the state, lead manufacturers leapt to the ignominious top spot for the production of lead-poisoned workers. Conditions in US lead factories were every bit as bad as those in the French lead works whose poisoned workers Tanquerel des Planches studied at Charité in the 1830s, every bit as deadly as the potteries Thomas Oliver wrote of in the early twentieth century. But unlike Europe, where the light inspectors shone on lead factories turned relatively quickly into national factory inspection acts, national workers’ compensation laws, and a growing army of occupational hygienists, the United States fell far behind Europe in keeping its workers safe. As late as 1910, a Belgian labor department official haughtily sniffed to Alice Hamilton that, when it came to industrial hygiene in the States, “Ça n’existe pas.”14 It was undoubtedly true the United States lagged far behind the nations of Europe in lowering rates of occupational lead poisoning (there, medical and occupational hygiene reports were so numerous to support at least one journal entirely devoted to the subject: Austria’s Bleivergiftungen, published from 1905 to 1915).15 Still, it is not accurate to assert there was no industrial hygiene in the United States. As studies by me, Christopher Sellers, Mark Aldrich, and others make clear, from before the 1890s, dozens of disparate and disconnected points of surveillance emerged in cities across the industrial Northeast, as medical professionals, labor groups, and city and state labor bureau statisticians started tallying the health costs of lead poisoning in factories and workplaces under their purview.16 But with the still-weak federal government, hobbled by obeisance to local and state law and authority, these well-intentioned studies could do little against the nation’s headlong rush for production that paid little heed to the health of its workers. It would take a generation more of activism, the accumulation of convincing statistical data linking factory conditions to social measures of health, promulgated by government reports and muckraking journalists, and the decline in the supply of new immigrant laborers, but by the 1920s, a uniquely American system of state workers’ compensation laws emerged, with its marriage of insurer, devotion to industrial efficiency, and empowered medical experts. By most measures, US lead factories became far less fatal after World War I.17 These improvements were unevenly distributed, of course. Workers in large factories, especially those in industrial states, faced regular health inspections, and occupational health specialists monitored factory conditions. Conditions in smaller plants, or in factories in regions

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with the weakest workers’ compensation laws, remained as deadly as ever. Worst off were American painters; these end users of the deadliest consumer product of old, white lead paint, benefited from neither effective workers’ compensation schemes nor the sort of restrictions on the use of lead paint enacted by most signatories to the White Lead (Painting) Convention of 1921.18 ILO Convention 13 is significant for many reasons. It essentially banned the use of lead paint (defined then as any paint containing more than 2 percent lead by weight) for most interiors and restricted how lead paint was distributed (only in paste form, not as lead carbonate powder) and used. And so, although imperfectly implemented, and only gradually adopted (eventually by dozens of nations, from Czechoslovakia to Cuba—but not the United States), the White Lead (Painting) Convention of 1921 had a significant impact on the health of workers, its chief intended beneficiaries. Its unintended health benefits—to those who lived in buildings that would hence be painted with nontoxic paints—are impossible to measure. Comparing rates of childhood lead paint poisoning in Europe in the subsequent years with those in the United States—a nation of “white leaders”—would seem to demonstrate the convention’s positive impact. Reports of American children poisoned by paint increased dramatically in the 1920s and 1930s. In the 1920s, children under five counted for less than 5 percent of all lead poisoning deaths in the United States. Twenty years later, infants composed more than 25 percent.19 In Europe, pediatric lead paint poisoning remained remarkably rare, seemingly proof that the ILO convention succeeded beyond its framers’ intentions. Yet, this dramatic rarity gives pause. Without convincing data on the incidence of elevated blood-lead levels in Europe over the twentieth century, historians face making an argument from silence. And the silence in the published record is deafening—almost. The few reports from European medical journals in the Index Medicus are instructive, and tantalizing. One from 1910 reported the death of a child who gnawed the paint off furniture. It turned out the father was a bookkeeper in a lead paint plant and had repainted the child’s crib with his employer’s product. In this case, as in so many from the United States in the same years, lead became suspected only because there was an occupational connection to the child. This death was because of a deadly but uncommon combination—a child who gnawed on everything, and a handyman father who worked in a lead plant. “Curious cases” such as this maintained the comforting illusion that childhood

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lead poisoning was rare, and steered attention from the everyday exposures in every child’s home.20 Another report, from 1922, started with an announcement that seemed to belie the historian’s assumption that pediatric lead poisoning was unknown in Germany. Chronic lead poisoning in children had become “a rarity” in the last decade. Did this suggest there had been a “silent epidemic” in Germany predating that of the United States?​No— the improvement under discussion came from recent German child labor laws restricting the employment of children in lead industries.21 Decades later, two German specialists performed a meta-analysis of postwar pediatric literature, finding once more that childhood lead poisoning was a rarity in Germany because of protective legislation. In the United States, on the other hand, lead poisoning was an “extraordinarily frequent disease,” with Baltimore alone accounting for a remarkable fraction of all known lead poisoning cases among children.22 It was no coincidence that the Germans’ analysis pointed to Baltimore as a lead poisoning hot spot, but that choice raises troubling questions. Did Germany’s apparent refractoriness to childhood lead poisoning reflect epidemiological reality, or was it merely an artifact of very different epidemiological priorities and presumptions?​The lack of concerted case-finding efforts in Germany and elsewhere in Europe in the postwar years does not mean there was no harm to find. The American experience in case finding demonstrated again and again that lead poisoning “occurred” most where health professionals were actively looking for it. For instance, Baltimore’s efforts to study and reduce lead poisoning from the early 1930s led to its erroneous distinction as America’s (and consequently the world’s) childhood lead poisoning capital, reporting nearly a quarter of all childhood lead-poisoning fatalities in the United States.23 The correct inference to take from Baltimore to the wider world—that greater vigilance on the part of other cities on both sides of the Atlantic would have found the true incidence and led to preventive measures—seems to have been ignored by health practitioners and historians in both the United States and Europe.24 This myopia is due in part to the legacy of the ILO convention of 1921, whose purpose and hygienic impact have been misunderstood and exaggerated. One significant lapse has been the ongoing assumption that the ILO outlawed white lead paint to protect children. Advocates for US lead poisoning prevention often voice this myth to criticize America’s blindness to the dangers of lead, which European authorities saw so much more clearly. And the myth supports monocausal

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a­ rguments about the US lead industry’s hegemonic tentacles controlling the polity there; by ignoring the machinations (both overt and otherwise) of European lead industries in the lead-up to the convention, America’s failure to join the ban can be safely laid at the lead industry’s door, letting broader US forces (such as deep postwar animosity toward internationalism and rabid isolationism) off the hook for the “silent epidemic” of childhood lead poisoning that developed after 1921. A final problem with the myth is that it downplays the significance of the benefits that accrue crosscutting regulations. Properly understood, the ILO’s labor-oriented restriction was not a case of the ILO doing the right thing for the wrong reason; instead, the convention did one right thing for one right reason. History would prove that restricting white lead in home interiors to protect painters was also right for other reasons that played little or no role in its establishment. Lead’s opponents need to find allies in places they think have little overlap—and that goes for disciplinary boundaries as much as geographic ones.

TEL Changes the Game If the world of the early 1920s was “a lead world,” it was one where lead’s dangers came chiefly from old accustomed sources whose unquestionable dangers appeared to be falling before rational programs of occupational hygiene. Into this complacent world, Du Pont, General Motors, and Standard Oil introduced TEL. A “gift of God,” in the words of Ethyl Corporation Vice President Frank Howard, TEL’s inherent toxicity was incontrovertible—at least after its dangers were made visible in a series of scandalous industrial accidents that left dozens of workers dead and hundreds mentally impaired for life.25 Far greater was ethyl’s impact in the realm of public health, but this was so insidious and subtle as to take decades to fully comprehend. The introduction of TEL as a gasoline additive in the mid-1920s changed the game in a few fundamental ways. First, its toxicity is quite distinct from its leaden predecessors. Unlike metallic lead and almost all lead compounds in use since ancient times, TEL is an organic compound, easily absorbed by the skin and wickedly fluent in passing the blood-brain barrier, two traits that produced the lightning-fast and shocking symptoms displayed in the poisoned workers from the “loony gas” factories where TEL was first manufactured.26 But TEL entered the market as a crucial new product of strategic importance to the

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automotive, petroleum, and lead industries. This meant its production must continue despite the scandalous industrial accidents that marred its introduction. This imperative gave rise to the Kettering Laboratory of Applied Physiology at the University of Cincinnati, headed by Robert Kehoe. Kehoe’s research came to dominate the field in both the United States and around the world, defining risks, setting regulatory agendas, and defending a coherent (if misguided) set of principles that would last for generations, convincing the world that lead—even TEL—could be used with acceptable risks to workers, and with essentially no danger to the public.27 Tetraethyl lead was taken off the US market for a little over a year in 1925, while a hastily concocted study into the fatal manufacturing accidents of the early 1920s reached the foregone conclusion that TEL posed little risk to workers and, hence, presumably, even less to the public. In the process of gaming the inquiry, the Ethyl Corporation achieved remarkable cultural power. With Kehoe serving simultaneously as Ethyl’s medical director and as director of the Kettering Laboratory, the lead industry controlled a mighty link to the academic research community.28 In the absence of government-directed research, the US lead industry set the agenda. For the next forty years, industry-owned or industry-financed clinics conducted the most influential research, usually with pro-lead results.29 Kehoe’s research convinced the government and the public that Ethyl had controlled the occupational hazards related to manufacturing and distributing TEL. Furthermore, Kettering research produced “scientific” proof that nature had equipped the human body with mechanisms to cope with the levels of environmental lead that the use of leaded gasoline might produce. A crucial leadusing industry, with powerful ties to the nation’s largest automotive and chemical industries, acquired the power to define lead poisoning. By late 1926, Americans could once again buy leaded gasoline; ten years later, almost all US gasoline was ethylized, and Europe’s slow march toward reliance on lead for octane enhancement had begun, albeit at a slow and uneven pace. Britain jumped right in: Standard Oil introduced Ethyl into the British fuel market in 1928 through the Anglo-American Oil Company; by 1931, BP had adopted Ethyl as its octane booster for its premium “BP Plus” petrol, renamed “BP Ethyl” after a couple years (fig. 3.3).30 German hygienists viewed the US studies skeptically, but as TEL was not marketed in Germany in the 1920s, authorities adopted a wait-and-see attitude; Frank Uekötter quotes a 1929 German Ministry of Transport report, which proposed “to keep

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Figure 3.3  BP Ethyl advertisement (© Grace’s Guide to British Industrial History, 1933).

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track of the large-scale experiment currently underway in the United States.” Germany did not permit domestic ethyl sales until 1939, the same year as France.31 Switzerland held out for almost a decade longer: remarkably prescient warnings of the public health dangers came from such critics as the forensics professor Heinrich Zangger, who called Ethyl a “dangerous improvement,” and while it improved fuel efficiency and reduced destructive engine knock, such improvements should not be made at the risk to the public’s health. He correctly foresaw the threat looming in the “dust or vapor blown out and sprayed in the streets of the cities,” and concluded this was a case where “medicine and the state have important roles.” Gasoline sold in Switzerland remained lead free until 1947.32 Although adopting TEL was never inevitable, its eventual universality makes it seem so; it is important to assess the factors that explain European nations’ change of heart. Chief among these are developments in auto manufacturing and fuel production that brought US and European markets into more direct competition in the postwar years, which meant America’s increasing reliance on high compression engines would filter into the European auto market. And with those engines came US dependence on TEL as a cheap means to bolster octane ratings.33 As for the health objections, they fell away with assurances based in reality and perception. By the late 1930s, the Ethyl Corporation, under the strict guidance of Robert Kehoe, had established an impressive safety record for the manufacture and distribution of liquid TEL, with no replaying of anything like the debacle of the Bayway and Deepwater disasters.34 Kehoe was proud to discuss in print and at professional conferences the stringent protocols he was able to put in place and enforce in every factory operated under Ethyl’s license. He seemed eager to help other lead-using industries improve their health records. He seldom if ever spoke publicly about lead manufacturers who failed to meet his exacting standards, or of accidents involving TEL. In internal correspondence, he was considerably more forthcoming.35 Kehoe reported in conference reports some of the bad things that could happen when he and his well-disciplined engineers lost control of the process of manufacturing and distributing TEL, an extremely rare occurrence, except in the aftermath of World War II. He told of the Soviets dismantling and moving to Russia two of Germany’s TEL plants (together with some of the plants’ Ethyl-trained engineers), and the disasters resulting when the deadly chemical was mishandled. Large quantities

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of pure TEL made its way out of the carefully circumscribed settings Kehoe had demanded and into the hands of the public. People used it to fuel lamps or wash their floors; train cars that carried poorly sealed containers of TEL one day carried hundreds of passengers the next; Kehoe cited Soviet studies reporting hundreds of deaths, including a Polish village where, he reported, “everyone . . . either died or became seriously ill.” Similar disasters took place in Japan in the months after the war ended.36 As bad as these disasters were, Kehoe would have had no difficulty defending TEL use going forward. First, he would note that all these reports concerned pure liquid TEL, which no one since 1926 had claimed was anything but deadly. Second, these horror stories highlighted Ethyl’s track record for minimizing the human costs of working with TEL, demonstrating why Ethyl should continue to control all facets of its manufacture and distribution. Finally, he would jump on the opportunity to remind critics that almost twenty years of experience had shown, just as the Surgeon General’s report of 1926 predicted, the use of leaded gasoline was not producing the deaths in the streets naysayers warned of. These points relied on the KehoeKettering paradigm about lead toxicity that had dominated the field of occupational health since the mid-1930s. The so-called Kehoe rule arose from dozens of experiments in animal and human physiology, as well as practical experience in lead factories. The rule had four parts: some lead absorption is normal, as lead occurs naturally in the environment; thus, the human body has mechanisms to absorb and excrete lead; there is a threshold for lead absorption below which no illness will occur; finally, since the public’s exposure was far below that which would produce absorption above that threshold for harm, TEL posed no public health risk.37 Thus assured, more nations followed the anthropomorphized Ethyl’s advice in magazine ads to “take me with you and get a kick out of driving instead of a knock.” The alchemy of the internal combustion engine transformed the deadly occupational TEL fluid into an aerosolized miasma of various inorganic lead compounds. The peat bogs, lake sediments, and arctic snows of the Northern Hemisphere tell the story of what resulted. Recent assays of these and other silent and passive biometric markers show that from the 1930s, as TEL use in gasoline rose, so did the amount of bioavailable lead in the environment—a risk to the public’s health raised and dismissed in the 1920s, ignored until the late 1950s, and only proved when, for reasons largely unrelated to

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public health, the compound was removed from petrol burned in US automobiles. It was this universality of risk that marked the second distinction between the dangers TEL posed and those from an earlier day’s metallic and inorganic compounds of lead. The geochemist Clair Patterson set a fire in the house of Kehoe in 1965, when he published some of the first noteworthy observations to this effect. His article “Contaminated and Natural Lead Environments of Man” first appeared not in the hard science journals he was accustomed to but the leading applied toxicology journal, the Archives of Environmental Health. What was more audacious was his thesis, reached by way of a thought experiment that tied his evidence of rising environmental lead contamination to a presumed but unmeasured rise in health outcomes from typical exposures of more than two hundred times what Patterson calculated was in the preindustrial environment. He asserted, “The average resident of the United States is being subjected to severe chronic lead insult.” Howls of derision echoed through the pages of US occupational hygiene publications, but Patterson’s thesis introduced an element of doubt that began eroding the lead industry’s forty-year-old certitude. A second rhetorical catalyst appeared the same year: the sociologist Colum Gilfillan’s thesis tying lead poisoning to the fall of ancient Rome. Lead, contaminating their water and food, weighed heavily on the mental and reproductive health of Rome’s elites, amounting to “the major influence in the ruin of the Roman culture, progressiveness, and genius.”38 The geophysicist’s and the sociologist’s assertions injected deep cynicism about the Kehoe paradigm, doubt that would be crucial for lead’s critics, who initially had more logic than evidence on their side. The evidence was not long in coming, however, primarily from new approaches to studying the effects of lead absorption in children, effects far below the “threshold for harm” that lay at the heart of the old paradigm.

The United States Leads in Exposure of Childhood Lead Poisoning Childhood lead poisoning was recognized later than occupational plumbism, though earlier than the pandemic of low-level effects of lead compounds broadcast throughout the general environment. Of the three modes of exposure that dominated the twentieth century, pediatric lead poisoning remains the most divisive. The dramatic increase in

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reported childhood lead poisoning deaths after the 1930s in the United States cannot be attributed to suddenly deteriorating housing, changing behavior, or the increased use of leaded gasoline. What did change was the number of health professionals on the lookout for lead poisoning, due to the mature subdiscipline of pediatrics, greater sensitivity by medicine and public health to non-biotic, environmental disease causation, and greater awareness of lead’s ubiquity.39 These changes can be seen in the transformations in public and professional perceptions of the typical lead-poisoned child. Those rare reports of lead-poisoned children before the 1930s often emphasized the bizarre or exotic, the most famous today being the innocent Australian children poisoned by an ill-fated combination of climate and housing style in semitropical Brisbane.40 By the mid-1940s, lead-poisoned children clearly were not victims of rare or bizarre circumstance but rather had been poisoned by the paint in their homes. Childhood lead poisoning came to be understood as the tragic medical outcome of social problems: bad housing, “backward” children, and “ignorant” parents. It was just another of the insoluble “ghetto problems,” one bound inextricably with the racial and economic changes associated with the Great Migration of African Americans from the South. Many concerned health workers found themselves reluctantly agreeing with the lead poisoning researcher who concluded in 1940, “like the poor, lead poisoning is always with us.”41 But deep cultural changes occurred in the postwar years, marked by a shift from the neglect and social Darwinism of earlier years to the birth of the modern civil rights movement and the Great Society. Throughout this sea change, the same children were presumed to be at greatest risk from lead: poor children, usually of color. But now, the lead poisoned child became proof that slums kill, a rallying point for advocacy. The dramatic expansion of lead poisoning prevention programs in the 1970s was crucial. But these efforts would pale in comparison to those prompted by the reassessment of risks from low-level lead exposures, which once again transformed the image of the lead poisoned child.42 Julian Chisolm, a pediatrician at Johns Hopkins University, conducted some of the most important childhood lead poisoning investigations in the early 1970s, examining the effects of lead below levels associated with clinical symptoms. His research prompted the US Public Health Service to redefine “undue lead absorption,” from 60 µg/dL to 40 in 1971 and to 30 in 1975.43 In contrast, the psychiatrist Herbert Needleman studied the mental and psychological costs of even lower

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levels of exposure. In 1979, he published a study implicating subclinical lead exposure in diminished IQs and school performance among Boston-area children.44 Needleman and Chisholm’s redefinition of “low-level” cast lead’s menacing shadow over middle-class children, rousing their parents’ ire and political clout. By the mid-1990s, assertive measures to limit lead in the human environment lowered average American blood-lead burdens to levels unheard of in the 1940s.45 This remarkable achievement in true primary prevention through dramatic reductions in universal exposures was, however, incomplete: while much of the miasma of universal lead exposure cleared away, most of the old lead paint remained on walls, in the dust inside homes, and in the soils around old buildings and throughout cities. The perception, and largely reality, casts the poor child of the inner city as most at risk.46 It would be useful to determine if America’s experience with childhood lead poisoning was unique and that other industrialized nations somehow avoided this particular toxic plague, or if the United States is in effect the world’s “Baltimore”—infamous for its high rates of childhood lead poisoning but mostly because it was the focus of early and intensive investigations and preventive programs. Those decades of investigation certainly produced an abundance of data, at least compared to other regions. Innovative methods for getting around this dearth of historical data may eventually produce more than comparative conjecture or dismissal of the issue as unknowable. Two recent trends, in lead epidemiology and European social history, may encourage more ambitious research in comparative histories, not incidentally because they align in so many ways the now (in)famous history of childhood lead poisoning in the United States. In the past fifty years, as European nations began grappling with their own Great Migration of non-Europeans from the old colonial periphery to their cities, where those populations’ cultural practices and limited housing options made them—as it had African Americans in Northern cities in the 1940s—a coherent “other.” Doctors in a Parisian hospital in 1986 reported a case that could have come straight from New York City in the 1950s: a two-year-old is admitted in a coma and soon becomes convulsive. Doctors suspect viral encephalitis; lumbar punctures do not turn up an infectious etiology. Not until two weeks have passed is a blood sample taken monitored for lead: “The child’s blood lead level was found to be 2630 μg/L . . . The father, a Malian immigrant, explained that his daughter regularly ingested paint at home.” The misdiagnosis

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(with presumption of a biotic cause, not an environmental toxicant), public health officials’ subsequent attempts to make this about culture and personal behavior and not deadly slum conditions, the resulting call for government action (in 1990)—all these elements suggest a much older American story retold in Paris.47 Ten years later, France had taken great strides in screening its children for lead exposure, although with yet another familiar result, with Paris standing in for Baltimore. A report on screening efforts found that “66% of the new cases lived in Paris or the suburbs even though the population of children was less than 20% of the total of French children.”48 The fact that “new cases” were defined as children whose blood lead levels exceeded the EU’s definition of 100 g/L (equivalent to 10 µg/dL, the ratio used by the CDC) raises the second factor that has brought childhood lead poisoning to greater prominence as a public health problem in Europe and elsewhere—the dramatic reduction in how high a blood-lead level passed the “threshold” for case definition. Even if clinical lead poisoning was rare in European children of earlier generations, many thousands now have lead burdens above today’s more stringent standards. Those standards derive from large-scale studies that implicate “low-level” blood-lead levels in a range of mental and emotional problems, as well as possible chronic health effects. The modern concern with levels that once could be ignored has prompted greater vigilance and greater curiosity about the shifting suite of environmental lead exposures and their impact over decades. The authors of a 2011 meta-analysis of EU blood-lead studies concluded that researchers need “harmonized and accessible data collection in environmental and other exposure media (food, drinking water), designed to enable exposure assessments and integration with exposure and health data.” Again, this call echoes similar plaints from American epidemiologists in the 1960s dealing with inconsistent standards from city to city, state to state.49 While the search for children at potential risk of lead widens across Europe and industrialized nations around the world, one heartening fact stands out: there has been a general decline in average blood leads. The causes of this drop in any one area will depend on many factors, from the age and condition of housing, the area’s history of industrial sources of lead pollution, and other low-level but endemic sources such as public water systems. What will be almost universal, however, will be the salubrious impact of phasing out the use of leaded gasoline.

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Figure 3.4  Parallel decreases in blood-lead levels and lead used in gasoline (United States, 1976–1980). Source: Rutter and Jones, Lead versus Health (New York, 1983).

Deleading the World’s Gasoline The government interventions that did the most to lower lead exposures, both in the United States from the late 1970s and in the world since, had almost nothing to do with paint. Of these projects in primary prevention, the most effective has been the phaseout of leaded gasoline. The American side of the story is well known, with its dramatic impact on average blood-lead levels, a correlation clearly depicted in a powerful and widely viewed and graph charting the parallel decline in TEL consumption and human lead absorption (fig. 3.4).50 Ironically, most of the early progress in the United States, and much of the anti-Ethyl advocacy in Europe, were undertaken to reduce automotive air pollution in general, with little attention given to the risks of environmental lead. The biggest exception to this rule seems to have been the Soviet Union, which restricted sales of TEL in major cities in the mid-1950s for, it would seem, the protection of the public’s health. Elsewhere, smog was a far more visible and troubling issue for environmental regulators well into the late 1960s and early 1970s. Even in the years after Patterson had shown the reality of lead contamination, and the new epidemiological truths about low-level lead absorption were

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gaining ground, an earlier era’s portfolio of nuisance pollutants from sulfur dioxide to carbon monoxide carried more weight in pushing clean-air regulations.51 Concerns over the potential impact on human health did play a large role in Germany’s 1972 restrictions that reduced by 33 percent the amount of lead in gasoline. But the far greater reductions Germany implemented four years later were motivated more by the presumed impact of sulfur dioxide and other pollutants on the health of its forests. Because the best tool for eliminating those everyday pollutants from auto emissions was the catalytic converter, which is quickly destroyed by the exhaust byproducts of TEL, the anti-lead activists had a powerful ally, which has been used to great effect. The lead industry’s response to all this troubling linkage between environmental lead emissions, human absorption, and governmental restrictions was sadly predictable, ramping up their customary denialism while marketing leaded gasoline more aggressively in developing nations with more pliable regulators. But the astounding link between falling TEL levels and average blood-lead levels in countries as they weaned themselves off leaded gasoline made industry’s denials seem desperate at best, and the accumulating evidence of the medical and social effects of lead absorption at ever-lower levels all but eliminated the very notion of threshold for harm, to which industry apologists still clung.52

Conclusion The adage that lead poisoning happens where you look suggests a darker corollary, and it follows from the assumption that in a just society, where you find harm, you will apply the levers of change. So, what was true of occupational and pediatric plumbism in the United States—that large lead using industries and poor people in “wellconnected” cities received the first notoriety and the earliest gains in remediation—seems to apply equally on the global stage. It seems likely that many contingencies led to the US population being more heavily leaded than much of the world, with consequences in terms of mortality and serious morbidity. But as America led the charge to cover the earth with lead, so did it lead in overturning the toxic “truths” that justified that environmental assault.53 Global lead consumption continued to rise all along, however, and the newly chastened lead-using industries of the “developed world” exported the dirtiest processes to

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places removed from the industrialized centers, and through the end of the twentieth century, much of the developing world continued to mix TEL in its petrol. Consequently, what was a defining problem of the industrial West in 1910 is seen today as one of a myriad of the health problems that developing societies “must” accept in their devil’s bargain to industrialize, of concern to the rest of the world only when lead-bearing toys manufactured in China make their way into American children’s toy boxes. There is a stark contrast between the low-level threat these finished products pose to their users, and the heavy toll in morbidity and mortality imposed on the workers who manufacture them or on the children who breathe the effluents of nearby factories and smelters. It is heartening that awareness of this contrast is growing and that transnational networks of activists, regulators, and business interests are evolving. But it is no longer sufficient to globalize yesteryear’s concern with high-level clinical and chronic assault. The goal for the nations that rushed headlong into the century of lead needs to be reinterpreted and act on Uncle Sam’s mission to repay the rest of the world “for any inconvenience” we visited on them “while bringing them into line and giving them their freedom.”54 In this post-Kehoe, Patterson-inspired world, we need to export the precautionary principle even as we need to more completely adopt it ourselves. Christian Warren is a historian of nineteenth- and twentieth-century America, studying the social dynamics of health, class, race, and the natural and built environment. He is Associate Professor of History at Brooklyn College of the City University of New York. His first book is Brush with Death: A Social History of Lead Poisoning (2000). He coedited a collection by historians and epidemiologists, Silent Victories: The History and Practice of Public Health in Twentieth Century America (2006). He is currently working on two related book projects, Starved for Light: How Rickets and Vitamin D Deficiency Shaped Modern America and From Haven to Hazard, a cultural history of Americans moving into the “great indoors.”

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Notes   1. NLC, “Uncle Sam’s Experience.”  2. BGS, World Mineral Production.   3. Lestel, this volume; Rainhorn, “Mouvement”; Rainhorn, “Interroger”; Fassin and Naudé, “Plumbism”; Uekötter, “Merits”; Rainhorn, “Banning”; Sellers, “Cross-Nationalizing.”  4. LIA, Useful Information.  5. Rom and Markowitz, Environmental, 955; Nriagu, Lead; Ruddock, “Lead Poisoning,” 1682.  6. Ramazzini, Diseases, 55.  7. Baker, Essay.   8. Eisinger, “Lead,” 296; Wedeen, Poison, 20–22.  9. Baker, Essay. 10. Gensel, “Medical World.” 11. Letter from Benjamin Franklin to Benjamin Vaughan, 31 July 1786, in Franklin, Writings, 530: “When I was in Paris with Sir John Pringle in 1767, he visited La Charité, a Hospital particularly famous for the Cure of that Malady, and brought from thence a Pamphlet, containing a List of the Names of Persons, specifying their Professions or Trades, who had been cured there. I had the Curiosity to examine that List, and found that all the Patients were of Trades that some way or other use or work in Lead.” 12. Tanquerel des Planches, Traité. 13. Rainhorn, “Banning”; Hepler, Women; Markowitz and Rosner, Deceit; Sellers, Hazards; Warren, Brush. 14. Sellers, Hazards, 89. 15. KKAAH, Bleivergiftungen. 16. Sellers, Hazards; Warren, Brush; Stern, Pottery Industry. 17. Asher, “Failure”; Keller, Regulating, 198–202. 18. “International Labor Conference at Geneva,” Monthly Labor Review 14, no. 1 (1922): 51–56. 19. Warren, Brush, 135–36. 20. Hirsch, “Tödliche Bleivergiftung.” 21. Friedberg, “Zur Klinik.” 22. “In Deutschland ist die Bleivergiftung im Kindesalter erfreulicherweise zu einer ausgesprochenen Seltenheit geworden, nachdem die gesetzlichen Schutzbestimmungen insbesondere Kinder vor dem Umgang mit Blei und dessen toxischen Verbindungen schützen.” Kramer and Schmöger, “Bleivergiftung,” 271. 23. This tendency has a long tradition in the history of lead poisoning—just consider the “Colic of Poitou” or the “Devonshire Colic”; Warren, Brush, 22–24. 24. This point was made about Paris in the context of French screening programs from 1995–2002. Canoui-Poitrine et al., “Childhood Lead Poisoning.” 25. USPHS, “Proceedings,” 62; Markowitz and Rosner, Deceit, 12–35.

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26. NLM, “Tetraethyl Lead.” 27. On the introduction of leaded gasoline, see Markowitz and Rosner, Deceit, 12–35; on Kehoe and the Kettering Lab, see Warren, Brush, 116–33. 28. Ashe, “Robert Arthur Kehoe,” 139; Campbell, “House.” 29. For a summary of the Kettering Institute’s control over lead research, see Graebner, “Hegemony.” 30. Bamberg, History, 196. 31. Uekötter, “Merits,” 128. 32. “Dozen Nations Ready to Scan Lead Gasoline / League’s Labor Office Undertakes Study of Industrial Peril,” Miami News, 8 June 1925; Zangger, “Gefährliche Verbesserung.” 33. Mosimann et al., “Vom Tiger.” 34. Warren, Brush, 130. 35. Sellers, Hazards, 214–16. 36. “U.S. v. Du Pont, General Motors et al.: Memorandum of Conference with Robert A. Kehoe,” 24 January 1952, typed manuscript, Robert A. Kehoe (MD) Papers, UCA. 37. Kehoe, “Harben Lectures.” 38. Patterson, “Contaminated”; Gilfillan, “Lead Poisoning.” 39. USCB, Vital Statistics 1944; the thesis of sudden deterioration of housing is associated with English, Old Paint; for an alternate explanation see Warren, Brush, 30–31. For a recent review of the history of childhood lead poisoning in the United States, see Markowitz, “Childhood Lead Poisoning.” 40. Other examples of accidental or “exotic” causes include Stewart, “Lead Convulsions”; Kato, “Lead Meningitis”; Gibson, “Plea.” 41. Conway, “Lead Poisoning,” 471. 42. Needleman et al., “Deficits”; Needleman et al., “Long-Term Effects.” 43. Florini et al., Legacy of Lead, 12. 44. Needleman et al., “Deficits”; Needleman et al., “Long-Term Effects.” 45. Pirkle et al., “Decline.” 46. Dignam et al., “High-Intensity”; for some of the complications of this renewed perception, see Rosner and Markowitz, Lead Wars. 47. Fassin and Naudé, “Plumbism”; for a closely analogous case study from New York in 1951, see Warren, Brush, 168–69. 48. Canoui-Poitrine et al., “Childhood Lead Poisoning.” 49. Bierkens et al., “Predicting.” 50. The graph first appeared in Annest, “Trends.” Some have likened its impact in mobilizing support for lead activism to Rachel Carson’s Silent Spring, or The Blue Marble photograph of Earth taken by astronauts on their way home from the moon. 51. Warren, Brush, 219–21. 52. Storch et al., “Four Decades.” 53. Wheeler and Brown, “Blood Lead Levels”; Bierkens et al., “Predicting.” 54. NLC, “Uncle Sam’s Experience.”

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Bibliography Archives UCA (University of Cincinnati Archives).

Publications Annest, J. L. “Trends in the Blood Lead Levels of the U.S. Population: The Second  National Health and Nutrition Examination Survey (NHANES II) 1976–1980.” In Lead versus Health: Sources and Effects of Low Level Lead Exposure, edited by Michael Rutter, and Robin Russell Jones, 33–58. New York, 1983. Ashe, William F. “Robert Arthur Kehoe, MD.” Archives of Environmental Health 13, no. 2 (1966): 138–42. Asher, Robert. “Failure and Fulfillment: Agitation for Employers’ Liability Legislation and the Origins of Workmen’s Compensation in New York State, 1876–1910.” Labor History 24, no. 2 (1983): 198–222. Baker, George. An Essay Concerning the Cause of the Endemial Colic of Devonshire. London, 1767. Bamberg, James H. The History of the British Petroleum Company, Vol. 2: The Anglo-Iranian Years, 1928–1954. Cambridge, 1994. BGS (British Geological Survey). World Mineral Production 2006–2010. Nottingham, 2012. Bierkens, Johan, Roel Smolders, Mirja van Holderbeke, and Christa Cornelis. “Predicting Blood Lead Levels from Current and Past Environmental Data in Europe.” Science of the Total Environment 23, no. 409 (2011): 5101–10. Campbell, Irene R. “The House That Robert A. Kehoe Built.” Archives of Environmental Health 13, no. 2 (1966): 143–51. Canouï-Poitrine, Florence, Patrick Harry, Daniel Poisot, Monique Mathieu-Nolf, Christine Cezard, Sabine Sabouraud, Jocelyne Arditti, et al. “Childhood Lead Poisoning Screening Activity in France between 1995 and 2002.” Epidemiology 17, no. S6 (2006): 121–22. Conway, Nell. “Lead Poisoning—from Unusual Causes.” Industrial Medicine 9 (1940): 471–76. Dignam, Timothy A., Anne Evens, Eduard Costagliola Eduardo, Shokufeh M. Ramirez, Kathleen L. Caldwell, Nikki Kilpatrick, Gary P. Noonan, et al. “HighIntensity Targeted Screening for Elevated Blood Lead Levels Among Children in 2 Inner-City Chicago Communities.” American Journal of Public Health 94, no. 11 (2004): 1945–51. Eisinger, Josef. “Lead and Wine: Eberhard Gockel and the Colica Pictonum.” Medical History 26, no. 3 (1982): 279–302. English, Peter C. Old Paint: A Medical History of Childhood Lead Poisoning in the United States to 1980. Piscataway, NJ, 2001.

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Fassin, Didier, and Anne-Jeanne Naudé. “Plumbism Reinvented: Childhood Lead Poisoning in France, 1985–1990.” American Journal of Public Health 94, no. 11 (2004): 1854–63. Florini, Karen L., George D. Krumbhaar, and Ellen K. Silbergeld. Legacy of Lead: America’s Continuing Epidemic of Childhood Lead Poisoning. Washington, DC, 1990. Friedberg, Eduard. “Zur Klinik der chronischen Bleivergiftung im Kindesalter.” Archiv für Kinderheilkunde 71 (1922): 25–30. Franklin, Benjamin. The Writings of Benjamin Franklin, Vol. 9: 1783–1788. Edited by Albert Henry Smyth. London, 1906. Gensel, Lisa. “The Medical World of Benjamin Franklin.” Journal of the Royal Society of Medicine 98, no. 12 (2005): 534–38. Gibson, J. Lockhart. “A Plea for Painted Railings and Painted Walls of Rooms as the Source of Lead Poisoning among Queensland Children.” Australasian Medical Gazette 23 (1904): 149–53. Gilfillan, S. Colum. “Lead Poisoning and the Fall of Rome.” Journal of Occupational Medicine 7, no. 2 (1965): 53–60. Graebner, William. “Hegemony through Science: Information Engineering and Lead Toxicology, 1925–1965.” In Dying for Work: Workers’ Safety and Health in Twentieth Century America, edited by David Rosner and Gerald Markowitz, 140–59. Bloomington, IN, 1987. Hepler, Allison L. Women in Labor: Mothers, Medicine, and Occupational Health in the United States, 1890–1980. Columbus, OH, 2000. Hirsch, Samson. “Tödliche Bleivergiftung eines zweijährigen Kindes, verursacht durch habituelles Lutschen an der Bettstelle.” Berliner Klinische Wochenschrift 47, no. 4 (1910): 1820–21. Kato, Katsuji. “Lead Meningitis in Infants: Résumé of Japanese Contributions on the Diagnosis of Lead Poisoning in Nurslings.” American Journal of Diseases of Children 44, no. 3 (1932): 569–91. Kehoe, Robert A. “The Harben Lectures, 1960: The Metabolism of Lead in Man in Health and Disease, Lecture 3—Present Hygienic Problems Relating to the Absorption of Lead.” Journal of the Royal Institute of Public Health and Hygiene 24, no. 8 (1961): 177–203. Keller, Morton. Regulating a New Society: Public Policy and Social Change in America, 1900–1933. Cambridge, MA, 1994. KKAAH (K. K. Arbeitsstatistisches Amt im Handelsministerium). Bleivergiftungen in hüttenmännischen und gewerblichen Betrieben: Ursachen und Bekämpfung. Vol. 1. Vienna, 1905. Kramer, H., and R. Schmöger. “Bleivergiftung im Kindesalter.” Archiv für Kinderheilkunde 66 (1962): 271–78. LIA (Lead Industries Association). Useful Information about Lead. New York, 1931. Markowitz, Gerald. “The Childhood Lead Poisoning Epidemic in Historical Perspective.” Endeavour 40, no. 2 (2016): 93–101.

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Markowitz, Gerald, and David Rosner. Deceit and Denial: The Deadly Politics of Industrial Pollution. Berkeley, CA, 2002. Mosimann, Matthias, Michael Breu, Tomás Vysusil, and Samuel Gerber. “Vom Tiger im Tank: Die Geschichte des Bleibenzins.” GAIA 11, no. 3 (2002): 203–12. NLC (National Lead Company). “Uncle Sam’s Experience with Paints.” Pamphlet. New York, 1900. NLM (National Library of Medicine). “Tetraethyl Lead.” Toxnet: Toxicology Data Network, last updated 8 December 2009. http://toxnet.nlm.nih.gov/cgi-bin/ sis/search/a?​dbs+hsdb:@term+@DOCNO+84. Needleman, Herbert L., Charles Gunnoe, Alan Leviton, Robert Reed, Henry Peresie, Cornelius Maher, and Peter Barrett. “Deficits in Psychological and Classroom Performance of Children with Elevated Dentine Lead Levels.” New England Journal of Medicine 300, no. 13 (1979): 689–95. Needleman, Herbert L., Alan Schell, David Bellinger, Alan Leviton, and Elizabeth Allred. “The Long-Term Effects of Exposure to Low Doses of Lead in Childhood: An 11-Year Follow-Up Report.” New England Journal of Medicine 322, no. 2 (1990): 83–88. Nriagu, Jerome O. Lead and Lead Poisoning in Antiquity. New York, 1983. Patterson, Clair C. “Contaminated and Natural Lead Environments.” Archives of Environmental Health 11, no. 3 (1965): 344–60. Pirkle, James L., Debra J. Brody, Elaine W. Gunter, Rachel A. Kramer, Daniel C. Paschal, Katherine M. Felgal, and Thomas D. Matte. “The Decline in Blood Lead Levels in the United States: The National Health and Nutrition Examination Surveys (NHANES).” Journal of the American Medical Association 272, no. 4 (1994): 284–92. Rainhorn, Judith. “The Banning of White Lead: French and American Experiences in a Comparative Perspective (Early Twentieth Century).” European Review of History / Revue Européenne d’Histoire 20, no. 2 (2013): 197–216. _____. “Interroger l’opacité d’une maladie: Le saturnisme professionnel comme enjeu sanitaire, scientifique et politique dans la France du XIXe siècle.” Histoire, Économie et Société 36, no. 1 (2017): 8–17. _____. “Le mouvement ouvrier contre la peinture au plomb. Stratégie syndicale, expérience locale et transgression du discours dominant au début du XXe siècle.” Politix 23, no. 3 (2010): 9–26. Ramazzini, Bernardino. De morbis artificum diatriba: Diseases of Workers. The Latin Text of 1713. Translated by Wilmer Cave Wright. Introduction by George Rosen. New York, 1964. Rom, William N., and Steven B. Markowitz. Environmental and Occupational Medicine. New York, 2007. Rosner, David, and Gerald Markowitz. Lead Wars: The Politics of Science and the Fate of America’s Children. Berkeley, CA, 2013. Ruddock, John C. “Lead Poisoning in Children with Special Reference to Pica.” Journal of the American Medical Association 82, no. 21 (1924): 1682–84.

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Sellers, Christopher C. “Cross-Nationalizing the History of Industrial Hazard.” In Environment Health and History, edited by Virginia Berridge and Martin Gorsky, 178–205. London, 2011. _____. Hazards of the Job: From Industrial Disease to Environmental Health Science. Chapel Hill, NC, 1997. Stern, Marc. The Pottery Industry of Trenton: A Skilled Trade in Transition, 1850– 1929. New Brunswick, NJ, 1994. Stewart, David Denison. “Lead Convulsions: A Study of Sixteen Cases.” American Journal of Medical Science 109, no. 3 (1895): 288–306. Storch, Hans von, Mariza Costa-Cabral, Charlotte Hagner, Frauke Feser, Jozef Pacyna, Elisabeth Pacyna, and Steffen Kolb. “Four Decades of Gasoline Lead Emissions and Control Policies in Europe: a Retrospective Assessment.” Science of the Total Environment 311, nos. 1–3 (2003): 151–76. Tanquerel des Planches, Louis. Traité des maladies de plomb ou saturnines. 2 vols. Paris, 1839. Uekötter, Frank. “The Merits of the Precautionary Principle: Controlling Automobile Exhausts in Germany and the United States before 1945.” In Smoke and Mirrors: The Politics and Culture of Air Pollution, edited by Erna Melanie DuPuis, 119–153. New York, 2004. USCB (US Bureau of the Census). Vital Statistics of the United States 1944. Washington, DC, 1946. USPHS (US Public Health Service). Proceedings of a Conference to Determine Whether or Not There Is a Public Health Question in the Manufacture, Distribution or Use of Tetraethyl Lead Gasoline. Washington, DC, 1925. Warren, Christian. Brush with Death: A Social History of Lead Poisoning. Baltimore, 2000. Wedeen, Richard P. Poison in the Pot: The Legacy of Lead. Carbondale, 1984. Wheeler, William, and Mary Jean Brown. “Blood Lead Levels in Children Aged 1–5 Years: United States, 1999–2010.” Morbidity and Mortality Weekly Report 62, no. 13 (2013): 245–48. Zangger, Heinrich. “Eine gefährliche Verbesserung des Automobilbenzins.” Schweizerische Medizinische Wochenschrift 55 (1925): 26–29.

/ PART II Discovering New Health Impacts Carcinogenesis, Mutagenesis, and More in Times of Uncertainty and Non-knowledge

/

CHAPTER 4

Discovering Chemical Carcinogenesis The Case of Aromatic Amines Heiko Stoff and Anthony S. Travis

In the first half of the twentieth century, many hundreds of work-

men at factories engaged in the manufacture of synthetic dyestuffs were afflicted with what had previously been a rare form of disease, namely bladder cancer. The search for the causes was confounded by several factors, including worker exposure to a wide variety of chemicals and long latency periods. The main suspects were intermediate products, with names hardly known outside factory walls and laboratories. However, they were all members of the class of organic chemicals known as aromatic amines, of which aniline is the earliest known and simplest member. The difficulty of identification of individual aromatic amines as likely culprits was hampered not only by the long latency period, from the time of exposure to onset of tumors, but also by lack of animal models with responses similar to those of humans, at least until the late 1930s. Even then, apart from one culprit, there were considerable uncertainties. This held back workable strategies for developing comprehensive regulatory measures. Moreover, by the 1930s, certain dyes manufactured from amine intermediates were found, by animal experiments, to induce tumors. This chapter focuses on relevant knowledge in confronting these concerns, on research into causative agents and on regulation of and concerns over both industrial and consumer products. The special case of the dyestuff butter yellow is used to emphasize the close relationship between human health issues, holistic body concepts, and the identification of toxins derived from aromatic amines as cancer-causing substances in Germany, both during and after the National Socialist era. As a debate that reached well into the general population and political

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arena, this is seen within the context of genuine concerns, scientific theories, racial purity (or at least contamination of the body), and, invariably, alarmism. By contrast, the issue of the toxicity of the dye intermediates was before the 1960s mainly confined to clusters of bladder cancer within a single industry, and investigated by communities of medical practitioners comprised of company physicians, pathologists, toxicologists and industrial hygienists, and external medical experts and other specialists. Since a large number of people were exposed to human hazards, often at high concentration, it is from their often-unfortunate experiences that the specialists were enabled to piece together some of the earliest knowledge about industrial cancers in humans. This culminated in the 1960s. T. S. Scott, medical officer at Clayton Aniline Company Ltd., of Manchester, in 1962 published Carcinogens and Chronic Toxic Hazards of Aromatic Amines. A year later, the cancer researcher Eric Boyland’s The Biochemistry of Bladder Cancer appeared, described by the British toxicologist Regina Schoental as complementary to Scott’s study, “which deals with industrial hazards of aromatic amines used in the dye industry.”1 Aniline will serve to introduce the aromatic amines, in part because this important intermediate gave its name to the first modern sciencebased chemical industry: that of aniline dyes. From the end of the nineteenth century, aniline and other aromatic amines were converted into pharmaceutical products, and in the twentieth century into polymers, rubber products, and agricultural chemicals. For many years, aniline also gave its name, as “aniline cancer,” or anilism, to the first industrial disease arising from the vast industry engaged in the manufacture of organic chemicals. Though occupational cancers had been observed since the last quarter of the eighteenth century (e.g., soot wart among chimney sweepers), the scale of production and widespread prevalence specifically of bladder cancer in the aniline dye industry, with aniline at first considered the major culprit, was to prefigure the study of all other industrial cancers, as well as bladder cancer from use of dyes and smoking. By the early 1950s, experimental and epidemiological investigations, as well as animal-to-human extrapolations, established causality relevant to cancer for several aromatic amines, particularly in cases where the latency period between exposure and the appearance of a recognizable tumor was known to be very long.2 The most potent carcinogens among the amines, and in fact among industrial synthetic chemicals,

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were found to be beta-naphthylamine and benzidine. By the early 1970s, manufacture and use of these two products in Western countries either had ceased or was reduced in scale. Stringent regulations on the handling and use of aromatic amines were enforced, notably in Britain, in the late 1960s, and in the United States after the creation of the Environmental Protection Agency in 1970. These moves stimulated investigations into toxic, mutagenic, and carcinogenic properties of amines of great utility; by the early 1980s, several comprehensive literature reviews had appeared.3 Since the history and nature of occupational exposure to aromatic amines has contributed to studies of the development of occupational and environmental carcinogenesis, as well as to the origins of other cancers, the historical approach is instructive for understanding developments in relevant aspects of toxicology and industrial hygiene, and for observing changes in societal attitudes and concerns. The three aromatic amines aniline, beta-naphthylamine, and benzidine together animate the first and last parts of this study. They sounded the alarm that led to concerns over the toxicity of their derivatives, the colorants, of which butter or aniline yellow, is the most prominent example.

Contaminated Water and Blue Lip From the late 1860s, Germany had emerged as the leading nation in the manufacture of synthetic dyestuffs, mainly the firms Agfa, BASF, Bayer, and Hoechst, as a result of monopolies based on clever strategies for protecting patents, high-quality products, and outstanding sales abilities—not to mention solid scientific achievements.4 Azo dyes are just one of several classes of novel colorants. Important members in the nineteenth century were those based on the intermediates betanaphthylamine and benzidine, as originally introduced by German firms. First, in 1879, was scarlet red (Biebrich scarlet of Kalle & Co.), that required beta-naphthylamine. Second, in the mid-1880s, was the so-called benzopurpurine class of fast cotton dyes, such as Congo red, that Bayer and Hoechst made from benzidine and its derivatives (fig. 4.1).5 From the first years of the aniline dye industry, waste disposal from use and manufacture of toxic reagents, intermediates, and dyes was a major issue. Following well-documented cases of poisoning from contaminated waters containing aromatic wastes, including amines and nitro compounds, and arsenic, laws, and regulations were introduced in

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Figure 4.1  Meister Lucius & Brüning (later Hoechst) advertisement (dated 1892) for textile colorants based on the intermediates aniline, naphthylamine (of which there were two isomers), benzidine, and other products (© Deutsches Museum).

Europe aimed at preventing contamination of surface and subsurface waters.6 Similar problems arose in the United States from the midtwentieth century on.7 Shop-floor discomfort among workers arising from exposure to aromatic intermediates was noted in the chemist A. W. Hofmann’s report as a juror for the 1862 International Exhibition in London.8 At that time, Hofmann observed, the effect appeared to be temporary, and good health was restored once workers left the manufacturing area. The

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cause was cyanosis, commonly known as blue lip, from acute exposure to aniline and its precursor, nitrobenzene, through skin contact, inhalation, and ingestion. Chronic cyanosis arises when the ability of blood cells to transport oxygen is destroyed, because hemoglobin in the blood is converted to methemoglobin. Symptoms include headaches and dizziness.9 In Germany, this condition was investigated, along with other ailments found among dye workers, at the Hoechst dyeworks, in the town of Höchst, near Frankfurt am Main, by Wilhelm Grandhomme, a medical consultant to the factory since 1867 and the full-time works hygienist from 1874. In his 1883 report, Grandhomme said he observed his first case of the impact of exposure to dye intermediates on the urinary tract in 1877.10 Cyanosis was prevalent until the 1930s, often because of poor working conditions in the manufacture and handling of aniline and other aromatic amines. In the early 1900s, Cecil Price Jones and Arthur Boycott had studied aniline at Guy’s Hospital in London and, based on experiments with rabbits, as well as observations of changes in blood and bone marrow, confirmed its toxic nature.11 It was examined instrumentally in the late 1930s at American Cyanamid Company’s Calco Chemical Division in Bound Brook, New Jersey, using the then new GE2 Hardy recording spectrophotometer, which provided a measure of the methemoglobin concentration of blood. Improved industrial hygiene, including changes in manufacture introduced between the 1930s and 1950s, reduced the dangers from cyanosis. Thus, for aniline and many other aromatic amines, inhalation and skin contact were, as far as possible, avoided by improved ventilation, and reactions were conducted in closed vessels with adequate exhaust ventilation. Workers were recommended to wear appropriate rubber footwear and be supplied with rubber gloves and aprons, goggles, and respirators.12

Bladder Cancer in Germany In the mid-1890s, cases of bladder cancer began to appear among German workmen whose duties brought them into contact with aromatic amines. Papillomatous disease of the bladder, originally called “aniline cancer,” was first reported to be present among workers at the Hoechst aniline dyeworks by the prominent physician Ludwig Rehn (1849–1930), a surgeon, since 1886, at the Frankfurt city hospital. From 1875 to 1885, Rehn, then a physician at Griesheim, had served

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as the factory physician at the Chemische Fabrik Griesheim, where he became familiar with workers suffering from industrial diseases related to intermediate and dye manufacture. His studies in subsequent decades contributed considerably to the development of urology as an established discipline in Germany. Rehn received data on the Hoechst workers from Heinrich Paul Schwerin, a works doctor since 1892 and the head of the Hoechst hospital. In his own clinic, Rehn undertook examinations with a cystoscope, a slender, cylindrical device introduced by physician Maximilian Nitze and employed in examining the inside of the urinary bladder. Bladder cancer was found among workers exposed to aromatic amines, including aniline, during the production of the aniline red dye known as fuchsine, or magenta. Rehn reported the results on 20 April 1895 at the German Society of Surgery (Deutsche Gesellschaft für Chirurgie, DGCH) congress held in Berlin. As a result of his ongoing study of the etiology of bladder cancer, Rehn suggested that liberation of aniline, when the crude red fuchsine dye (magenta) was heated, caused tumors.13 At this time, Grandhomme, the Hoechst works hygienist, was highly skeptical of Rehn’s findings. Grandhomme, in his 1896 report, opined that Rehn’s cohort of forty-five workers was hardly representative, since some four thousand workers in the factory were exposed to vapors from chemical reactions.14 At most, he opined, aniline irritated the bladder’s mucous membrane, but it did not bring on tumors. There was no mention of other manufacturing departments, where, for example, beta-naphthylamine and benzidine were made and used. In 1906, Rehn reported thirty-three cases of bladder cancer from seven German dye factories.15 In 1912, the Swiss urologist S. G. Leuenberger reported cases of bladder cancer among eighteen dye factory workers in Basel, where CIBA and Geigy were located. After reviewing the city’s death statistics for 1901 to 1910, Leuenberger concluded that mortalities due to tumors of the urinary passage were thirty-three times greater among dye factory workers than among workmen engaged in other activities. The archival records of the Basel Surgical Clinic from 1861 to 1900 supported Leuenberger’s findings on the risks to dye workers.16 One Hoechst physician, Schwerin, had by 1913 noted thirty-eight cases of bladder tumors in Germany. Statistical data and clinical research, based on studies in Germany and Switzerland, led to widespread acknowledgment early in the twentieth century of the new hazard to workers in dye factories. However, the long latency period, sometimes a decade or more before the tumor was observed, complicated early

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identification of the causative amines. Fritz Curschmann, the factory doctor at Agfa in Wolfen, also presented a report on bladder cancer at a 1913 conference of factory medical officers engaged in the larger German chemical works.17 Most cases had been observed in Germany and Switzerland because these countries were the leading dye manufacturers before 1914.18 In addition, both maintained generally careful record keeping, which has enabled modern historians to draw up comprehensive studies of the impact of toxic chemicals on dye industry workers. More recent interest has encouraged historical reviews of the global impact.19 Max Nassauer, a chemist at Hoechst, provides a significant example of ongoing concerns: he embarked on the study of medicine, leading to a 1919 thesis on “malignant bladder swelling.” He had since 1914 worked on “fighting against this awful illness” that reduced the life spans of workers once so inflicted to a “very few years.” Nassauer found that twenty-eight of thirty-two men he investigated at Hoechst had contracted the cancer. He believed aniline, inhaled over several years, was the causative agent. Other aromatic amines, in his opinion, did not bring on the disease, with the possible exception of the poorly soluble benzidine, used at Hoechst (and at Bayer) in producing benzopurpurine dyes, but even here the culprit, he surmised, was probably aniline formed as byproduct. To minimize risks, Nassauer recommended the urine of workers be checked every eight days and that they wear gas masks (or cover the face with a cloth soaked in vinegar), wear gloves, take showers before going home, and not spend more than three months in a manufacturing department where cases of bladder cancer had been found. If the leucocyte count of a worker fell, then he should leave the factory and live in the country. Nassauer found that 25 to 30 percent of all patients with bladder tumors who underwent surgery in the University Hospital Frankfurt had been engaged in the Hoechst factory. Nassauer’s study was widely reported in the specialist press, which must have done much at least to draw attention to the problem.20 He expressed concern over the effect on women who had worked in dye factories from 1914 to 1918, when men were called away for military service. The women were exposed to the same dangers as the men they replaced, particularly in departments for producing nitro compounds, required on a vast scale for explosives, and precursors of the aromatic amines. This would have sensitized a new works population to hazards. Franz Koelsch, the Bavarian state industrial hygienist since 1909, made

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an extensive study of problems, including bladder cancer, related to dye factories, particularly in departments where the aromatic nitro compounds were being produced on an unprecedented scale. He observed that the German Ministry of the Interior had issued regulations concerning the conditions in 1911 that should be adopted in factories where both aromatic nitro and amino compounds were produced.21 Two colleagues at Hoechst (Schwerin and Adolf Kuchenbecker) supported Nassauer’s focus on the “benzidine-naphthionic departments.” In contrast, Hans Engel, the BASF factory physician, based on his studies conducted between 1918 and 1920, believed beta-naphthylamine was a more likely cause of bladder cancer. This no doubt arose because, unlike Hoechst and Bayer, with their monopolies on the benzopurpurines, BASF was not a major user of benzidine.22 Of particular significance was that Engel was one of the first to investigate the effects of aromatic amines on animals. He discovered that dogs especially were a good choice for that purpose. No other animals were, before or after, found to be better suited to studying bladder cancer caused by betanaphthylamine and other aromatic amines.23 However, the use of dogs does not appear to have been taken up again until the mid-1930s, and then at Du Pont in the United States. In the 1920s, Rudolf Oppenheimer, the head urologist at the Frankfurt Red Cross Hospital, reported on bladder cancer found at three German dye factories. At one facility, of sixty workers, fifteen had contracted bladder cancer within twelve years of starting work; in another, of sixty workers, twenty-seven had bladder cancer, and in the third factory, of thirty workers examined, twenty-nine had bladder cancer within ten years of starting work. Though aniline and benzidine were suggested as the probable culprits, in line with Engel’s findings, beta-naphthylamine and other aromatic bases were now implicated. According to Oppenheimer, the latency period varied from 9.5 to 28 years.24 Engel and Oppenheimer suggested long-term exposure of the bladder epithelium to urine containing the carcinogen was responsible for tumor growth.

Chemical Carcinogenesis Becomes a New Field of Enquiry: International Research after World War I The hazards of the dye industry were investigated, including with visits to European factories, by the American industrial hygienist Alice

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Hamilton, associated since 1919 with Harvard Medical School. In 1921, she criticized German physicians’ methodologies and diagnostic accuracies. She even preferred to focus on the role of arsenic, once widely used in the manufacture of fuchsine.25 Nevertheless, the International Labour Office reviewed in the same year presumptive evidence for the role of beta-naphthylamine as a principal cause of bladder tumors.26 In his 1895 Berlin lecture before the DGCH, Ludwig Rehn suggested all interested parties take up research into “aniline cancer.” Nine years later, at the 1904 DGCH congress, a commission under Rehn was set up to investigate specifically bladder cancer. By 1923, Rehn reported ninety-four cases of bladder cancer in the dye industry. Though he then thought the commission’s work had faltered, the initiative no doubt contributed to an important regulation of 12 May 1925 to provide accident insurance to cover occupational diseases, including those arising from contact with aromatic amines and nitro compounds. Thus, by 1925, in Germany at least, regulations provided compensation to workmen suffering from a limited number of registered occupational diseases (meldepflichtige Berufskrankheiten). Claims were required to be supported by a works physician and an industrial hygienist. Significantly, in the mid-1920s, Wilhelm Hergt, a physician and Engel’s colleague at BASF, and Franz Koelsch, the Bavarian state industrial hygienist, had jointly conducted an exhaustive study on the toxicities of aromatic hydrocarbons, nitro compounds, and amines.27 In 1926, members of the British factory medical inspectorate described the first cases of bladder tumors in the country’s dye industry (following its expansion in World War I). Three years later, T. H. Wignall, a physician at the Imperial Chemical Industries Dyestuffs Division headquarters in Blackley, near Manchester, reported to the British Medical Association at its Manchester meeting the prevalence of bladder cancer among workers exposed to alpha-naphthylamine (isomer of the beta-derivative) and benzidine.28 At this time, experimental research into cancer was mainly treated as a branch of pathology. In London, the chemical pathologist Ernest Kennaway, at the Institute of Cancer Research, in 1931 reported, with S. A. Henry, the factories medical inspector, the apparent high incidence of cancers and deaths among coal tar and chemical industry workers.29 Kennaway’s own research moved away from the earlier emphasis on “morbid anatomy” to identifying carcinogens’ chemical specificity. This represented a major refocusing, on not only pure chemicals but also the manner in which they induced tumors. The medical researchers Isaac Berenblum

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and Georgiana M. Bonser investigated workplace carcinogenesis at the new Department of Experimental Pathology and Cancer Research at the University of Leeds. It was typical of similar departments, and research institutes, then opening in Europe and the United States. In August 1932, Berenblum published a comprehensive review of what was generally still called “aniline cancer” with the emphasis on bladder cancer.30 Though chemical carcinogenesis had now become an established field, identifying aromatic amine culprits was hindered by the very long latency period, generally measured in years, and sometimes decades; also, there was still the belief that aniline was as powerful a carcinogen as beta-naphthylamine.31 A major advance occurred in the United States during investigations conducted shortly after 1935 at Du Pont’s newly opened Haskell Laboratory of Industrial Toxicology. Du Pont, along with several other US firms, embarked on large-scale synthetic dye manufacture mainly after 1915, during severe wartime shortages. As a result, bladder cancer appeared later than in Europe, apparently around 1930. By this time, universities, such as Harvard, and government labs were studying issues related to industrial hygiene and poisons, which was one stimulus for the corporation to undertake its own studies. One motive for the Haskell Laboratory’s activities was Du Pont’s interest in identifying carcinogens to protect itself against claims for compensation from worker exposure to various chemicals. By 1933, twenty-five workers had contracted bladder cancer at its dye plant in Deepwater, New Jersey, and another plant acquired in 1931. Cystoscopical examination was undertaken of existing workers, and of potential new entrants to the industry, to exclude those showing symptoms of the disease. George H. Gehrmann, Du Pont’s medical director, visited German and Swiss dye factories in late 1933 to glean as much information as he could about awareness of the disease. A year later, he sent the Haskell Laboratory’s German-born and -educated Wolfgang F. von Oettingen to Europe to follow up investigations into bladder cancer caused by ­aromatic amine intermediates. At the Du Pont lab, the pathologist Wilhelm C. Hueper, also German born, and coworkers, probably drawing on Hans Engel’s 1920 study, found that dogs developed bladder cancer when administered pure beta-naphthylamine. Here at last was an experimental animal that offered the possibility for providing irrefutable evidence of the nature of at least one aromatic amine carcinogen. Hueper and coworkers injected and fed beta-naphthylamine to several dogs; after two years, bladder tumors were identified in  many  cases,

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either at autopsy or by cystoscopy. The Du Pont research workers in 1938 were thus the first to confirm by controlled experiment that beta-naphthylamine was responsible for the appearance of tumors in the urinary tract of dogs.32 Significantly, benzidine, aniline, and alphanaphthylamine were not found to induce bladder tumors in the Du Pont experiments or, apparently, experiments carried out elsewhere before 1950. Engel gathered statistical data retained at BASF (part of IG Farben since 1925) from 1903 to 1937 to support his belief that beta-­naphthylamine and benzidine were the main causes of bladder cancer, though he, as did his colleagues, also suspected aniline and its derivatives.33 Following earlier recommendations of Nassauer and Oppenheimer, respectively, microscopical examinations of urine for blood cells and pus cells were employed in Germany and Switzerland. In the 1930s, cystoscopy was adopted in Switzerland, Italy, and the United States. It was an uncomfortable procedure, and the workmen often objected. In Britain, early detection of bladder cancer in the 1940s relied on a urine smear test. However, the appearance of blood cells was not specific to cancer caused by aromatic amines, and where they did appear, cystoscopic examination was called for. In 1935, Franz Koelsch reported that just six months’ exposure to beta-naphthylamine was enough to develop a tumor.34 At the end of 1936, the third German regulation on the extension of accident insurance included cancer as an occupational disease, and referred to the role of aromatic amines in changing the mucous membrane of the urinary tract.35 Three years later, when writing on “chemical causes worthy of attention for accidents and sicknesses in the workplace,” H. Berger of the Verein deutscher Chemiker drew attention to the roles of both aniline and beta-naphthylamine as causes of bladder cancer, based on the studies of Koelsch, who recommended routine monthly checkups. Then, 90 percent of production in Germany of synthetic dyes and their amine intermediates was confined to the factories of IG Farben.36 By this time, many hundreds of pure chemicals had been tested for ­carcinogenic activity.

The Major Impact of Butter Yellow on Regulation in Germany From 1930 to 1960, the toxic natures of dyes derived from aromatic amines of the azo class were revealed.37 Among them was a brilliant

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yellow, first prepared in England around 1860. Its chemical constitution, p-dimethylaminoazobenzene, became available in 1875 when A. W. Hofmann established the basic structures of azo dyes. This yellow (methyl yellow, etc.), later produced by BASF and other firms, became better known under the name butter yellow, because it was used to give butter, as well as cheese and margarine, an attractive yellow that imitated the color of butter produced from cattle fed with grass in the summer. While azo dyes had been found to be toxic before the early 1930s, no evidence suggested they were carcinogenic until the Japanese pathologist Tomizo Yoshida, following German research, in 1934 demonstrated that liver tumors could be induced in rats fed or injected with the azo compound 2-amino-5-azotoluene, the active component of scarlet red (a dye closely related to butter yellow).38 From 1932 to 1937, another Japanese pathologist, Riojun Kinosita, orally administered either scarlet red or butter yellow to rats over three hundred days and found the oil-soluble butter yellow to be a highly carcinogenic substance. Those rodents, despite the toxicity of butter yellow, survived the first fifty days but without exception developed hepatic cancer after 150 days. Kinosita suggested butter yellow developed carcinogenic potency because of its chemical structure.39 The induction of liver tumors from aminoazo compounds was one of the main topics at the Second International Congress of the Scientific and Social Campaign against Cancer, held in Brussels in 1936. In 1940, a working group at the pharmacological institute of the Friedrich Wilhelm University in Berlin, consisting of the pharmacologist Hermann Druckrey and his collaborators Norbert Brock and Herwig Hamperl, confirmed Kinosita’s findings, thereby also rejecting the assumption that his results might have been induced by the Japanese rats’ genetic predisposition or diets different to those in Europe.40 For the first time, an experiment appeared to have proved that a substance coming from outside the organism provoked tumors in internal organs. Over the following years, several researchers, most notably Druckrey, continued work on butter yellow.41 In 1943, the chemist Richard Kuhn (the 1938 Nobel laureate in chemistry, the head of the Kaiser Wilhelm Institute for Medical Research in Heidelberg since 1937, and the principal figure in the organization of chemical research in National Socialist Germany) with Helmut Beinert declared butter yellow the most prominent representative among carcinogenic azo dyes.42 A year later, Eugene L. Opie reported, “Administration of butter yellow produces multiple foci of focal hyperplasia, cystic ducts, and cholangiofibrosis, and correspond-

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ing with these lesions, which are precursors of tumor growth, multiple tumors are formed.”43 Criticism of industrialized food production was common in all Western nations since the late nineteenth century. But while this controversy had focused mainly on adulteration, the highly influential interplay of diet reform (as part of the “life reform” movement) and new dietetics in Germany emphasized the need for a healthy diet based on natural and pure food. In the 1930s and 1940s, diet reformers like Werner Kollath denounced industrially produced food as unnatural and dangerous for the people’s health and vitality. In 1931, the elementary school teacher and journalist Curt Lenzner published Gift in der Nahrung (Poisoned food) in which he blamed the modern lifestyle and industrialization for contaminating essential or vital food substances with toxic foreign matter. A year later, Erwin Liek, an outspoken enemy of the Weimar Republic’s social and health security system, claimed a close connection between modern society and cancer, in which synthetic chemicals and mass food production were the most characteristic features. Food additives such as colorants and preservatives were seen as agents responsible for the statistical rise in cancer rates. The political discourse turned health reform into a science and nutrition research into an endeavor linked to lifestyle reform.44 The story of aniline yellow in National Socialist Germany took on a new urgency in 1939 when President of the Reich Health Office Hans Reiter proposed a new color law. This debate is of special interest because it was part of a more general health debate on “poisoned food.” It also transcended the political divide before and after 1945. The narrative of the pure and natural body threatened by foreign and artificial matter— the trope of “poisoned food”—fit well into National Socialist ideology. In the late 1930s and early 1940s, there was an open dispute between diet reformers and purists on the one side and those nutrition experts fulfilling the need of belligerent National Socialist Germany to secure an adequate standard of nutrition, with the aid of food technology, on the other.45 In 1941, German women’s organizations, which were deeply involved in the nation’s health and nutrition policies, pressured Reiter to prevent the production and use of azo dyes. As the historian Robert Proctor relates in his book on cancer research in National Socialist Germany, in 1941 a member of the Göttingen branch of the Deutsches Frauenwerk asked her superiors why “cancer-causing” substances were still allowed in butter and margarine. The regional women’s leader informed Reiter that while women were certainly ­willing to sacrifice for

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the war, accepting the presence of cancer-causing agents in food was a completely different matter. Reiter was now placed in an awkward situation, because any sudden removal of food dyes in the middle of the war might have been interpreted as the result of producing inferior foodstuffs. However, Reiter, who appreciated the women’s organization as allies in his efforts for maintaining wartime food security, successfully negotiated with the different groups producing and marketing synthetic coal tar dyes to reduce the use of these products. Even IG Farben ceased production of butter yellow. Presumably, butter and margarine were supposed to be colored with carotene, and not azo or similar dyes, since 1942. In the end, a coalition of scientists, politicians, life reformers, women’s organizations, and the chemical industry itself succeeded in the prohibition of butter yellow. Despite their different interests, all these actors could agree on a preventive strategy to ensure race hygiene and the need to secure the völkisch (people’s) body from invasion by foreign matter like butter yellow.46 The unlikely coalition broke up after the war in the spring of 1949 when Germany’s leading biochemist and the 1939 Nobel laureate Adolf Butenandt, then at the University of Tübingen, created a public scare by proclaiming butter yellow, despite its proven cancercausing effects, was still in use.47 As the news magazine Der Spiegel reminded readers four years later, Butenandt, who presented his findings at the Congress of the German Society for Internal Medicine in Wiesbaden, calculated that each person eating a pound of butter also consumed eighty milligrams of a highly carcinogenic substance called dimethylaminoazobenzene, better known to the public as butter yellow.48 Butenandt’s rather technical lecture, annotated with the demand for legislation that would ban synthetic dyes from food, created a stir, if not a panic, among ordinary Germans, who in general were consumers of considerable amounts of butter. In November 1949, the engineer Walter Hinnendahl of Nuremberg was one among many concerned citizens who appealed to German President Theodor Heuss to eliminate potentially cancer-causing food colorants, citing his shock from an article entitled “Todbringendes Buttergelb” (Deadly butter yellow) by Michael Morava in the weekly Echo der Woche. Hinnendahl argued that authorities who allowed the use of butter yellow as a food dye should be prosecuted for the involuntary manslaughter of millions of people and demanded measures to secure his own family from certain death from cancer; otherwise, he would seek prosecution.49 Around

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1950, a heated debate on the use of butter yellow written in militarylike language—the journalist Bettina Ewerbeck even used the phrase “Kesselschlacht um den Krebs” (cauldron battle about cancer)—filled the pages of popular newspapers and magazines.50 Butter yellow was not only a pars pro toto for the supposed evils of modern civilization but also a catalyst for addressing new risk policies. Whether butter yellow was still industrially produced and used as a food dye in 1950s West Germany was not even clear, but it nevertheless played a major role in establishing a new theory of carcinogen dose-response relations and fostering measures to control food additives on a West German and pan-European scale. Butenandt of course distanced himself from the media hype. Other congress participants praised his strictly scientific contribution. According to the physician Fritz Hartmann, Butenandt gave a perfect overview of the chemistry of cancer causation. While certain aromatic hydrocarbons were well-known cancer-inducing substances, the amino-containing butter yellow, as a product added to food, received special mention. Hartmann observed that Butenandt considered it a model compound for quantitative studies on the dose-time dependency of tumor formation through azo dyes. And, Hartmann said, this cancer-inducing substance was still present in foodstuffs for needless reasons, while the authorities did nothing to correct this grievance.51 Even though nutrition experts and representatives of the chemical and pharmaceutical industries immediately denied this accusation, a new debate was opened and shaped the risk policies on food additives in Germany throughout the 1950s. Bernhard Wurzschmitt from the BASF research lab, who, like Ulrich Haberland, the highly influential Bayer chairman, actually supported a strict policy on food additives, informed the public that butter yellow was no longer produced.52 S. Walter Souci, one of Germany’s leading food chemists and a former participant in drawing up the National Socialist nutrition policy, wrote in 1952 that German manufacturing companies had stopped producing butter yellow in 1939. According to Souci, butter, since November 1944, was permitted to be colored only in the winter and then only with carotene. In May 1949, right after Butenandt’s lecture, a directive for a general prohibition of chemical food coloring for dairy products and margarine was issued. In June 1951, an act prohibiting the coloring of butter with synthetic dyes was passed.53 But, despite claims and regulations, it remained uncertain as to what really happened between 1939 and 1949, and whether the informal arrangement over abandonment of butter

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yellow was just a temporary measure. Rumors on the use of butter yellow as a food dye circulated well into the 1950s.54 Butenandt, in his lecture, referred to the well-respected physician Karl Heinrich Bauer, who, in emphasizing the significance of exogenous agents, based a new cancer theory on that of azo dyes, thereby linking the assumed rise in cancer to modern lifestyles and civilization in general. According to Bauer, human cancer was mostly caused by industrially produced chemicals, “cancer noxa” (Krebsnoxen), a term first used by Ludwig Rehn concerning aniline. The main reasons for cancer were cell-altering noxa-like rays, namely, artificial colorants, roast products, preservatives, spices, and concentrated alcohol. In an article on cancer as “the disease of the era,” Der Spiegel drew attention to the body of scholarship that critiqued the exposure of consumers to synthetic chemicals and concluded by focusing on Bauer’s view that modern humankind had to escape from its self-made artificial, technical, and chemical environment. To radically fight cancer therefore meant a radical change in attitudes.55 Bauer introduced a new oncological theory, ignoring the role of genetics while emphasizing the significance of exogenous chemical and physical factors. In basing this on the case of azo dyes, and in taking up Lenzner’s and Liek’s arguments, he also recapitulated the thesis of a strong connection between modern civilization and an assumed rise in cancer. It was the pharmacologist Fritz Eichholtz, the director of the Institute of Pharmacology at the University of Heidelberg, who coined a poignant term for use in public discourse on the “toxic condition” of modern life and the perceived negative roles of the pharmaceutical and chemical industries. His toxische Gesamtsituation (toxic total situation) informed a far-reaching debate on the boundaries of risk assessment and the dangers of chemical substances, the result of the modern lifestyle and uncontrolled industrial productivity: modernity, civilization, and capitalism together seemed to be poisoning the German people.56

A New Scientific Basis for Regulation: The Cumulative Danger of Low Doses Butter yellow brought together the life reform discourse about diseases of civilization with production of scientific facts. Hermann Druckrey, born in 1904, and a member of the NSDAP Party and the SA as early as 1931, acquired a high rank in the latter, and was close to the SS; in the early postwar years, Adolf Butenandt’s support was required

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to officially denazify him. Though he never achieved an impressive academic career after 1945, he remained an internationally renowned expert on carcinogenic and toxic substances because of his new theory on the relationship between dose and effect, developed in 1948 with the electrical engineer Karl Küpfmüller while residing in the Hammelburg internment camp.57 According to Druckrey and Küpfmüller, cancer development was a chronological pharmacological process following mathematical regularities.58 They referred to animal tests with butter yellow that supported rejection of the pharmacological dogma of an ineffective dose-effect relation based on uptake of small amounts of a certain substance. Druckrey’s experiments in which he fed seven hundred rats with butter yellow showed that a certain total dose was necessary to produce tumors, irrespective of the period of intake, in his case between 35 and 365 days. There existed a simple relation of reciprocal proportionality between the amount of the daily administration of butter yellow and the necessary duration of treatment to bring about cancer: with a daily dose of three milligrams, the latency period was 350 days, but if the dosage was ten times higher and the daily amount thirty milligrams, the latency period would be just one-tenth, that is, 34 days. The latency period was inversely related to the daily dose. Whether given three or thirty milligrams daily, respectively, the total came to one thousand milligrams of butter yellow. Druckrey concluded that the cancer-causing effect of butter yellow was, even at the smallest doses, irreversible, right from the start of the experiment and throughout the entire life span of the animals. Once the critical total dose had been exceeded, tumors developed. A central conclusion of this study was that the ongoing consumption of even the smallest dosage of a carcinogenic substance like butter yellow could be lethal for consumers.59 Ironically, because of the latency period (the dose-effect and dose-time relation), it was nearly impossible in many cases to decide whether a certain substance was carcinogenic. Druckrey and Küpfmüller substantiated their thesis with an impressive mathematical methodology: in pharmacology, several substances exist whose effect is caused by the product of a constant concentration C of the toxin and the time of duration t. The effect of these Ct toxins, the occupancy of cellular receptors, must be irreversible if the effects sum up.60 If toxins were chemically bound to specific receptors of an organism, then this corresponded to the hit theory of the radiologist Friedrich Dessauer concerning the release of mutations through rays. Development of tumors therefore rested on irreversible

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effects of p ­ hysical and chemical agents. The common and particular characteristic is that they affect specific receptors that are unreplaceable functional units of the cell. This type of cumulative effect could be found in two highly important biological processes: the triggering of mutations through rays, and the release of cancer with dimethylaminoazobenzene.61 Thus, Druckrey concluded in his radical theory, later called “genotoxic,” that cancer-causing substances bring about irreversible alteration of inheritance.62 Crucial for the carcinogenic effect was, therefore, not so much the toxic concentration but the overall effect of concentration and duration. Since the late 1940s, three features of poisoning were invoked: concentration, accumulation, and their summation.63 Druckrey drew the then significant conclusion that scientists should both seek out such cancer-causing substances in the environment and encourage elimination as far as possible of those with which humans were in daily contact, even if they only occur in trace amounts.64 In 1949, at the first postwar DGCH congress in Frankfurt, this theory was translated into political demands and the need for legislative rulings. The surgeon Eduard Rehn, son of Ludwig Rehn, drafted a resolution with far-reaching health and political implications, including the preparation of “black” and “white” lists for synthetic dyes. The colorants in foodstuff should be printed on the packaging, while dye manufacturing and processing firms should require authorizations for various specific uses.65 Eduard Rehn based his resolution on ideas Karl Heinrich Bauer had already presented in six articles for a new food law. Bauer referred to the newly founded German Research Council (Deutscher Forschungsrat), a short-lived but nonetheless important forerunner of the German Research Foundation (Deutsche Forschungsgemeinschaft), which had decided to convene a special commission to consider the problem of colorants.66 Bauer, Druckrey, and Butenandt were allies in the ongoing war against cancer. The German Research Council, founded in 1949 by Werner Heisenberg mainly to advise the government on scientific problems, established a commission to investigate the problems of carcinogenic colorants led by Butenandt and Druckrey. This drew together all parties concerned with the production, distribution, and application of food dyes under the guidance of scientists. Over the following years, several commissions for colorants, foreign matter, whitening agents, and nutrition were established. When the German Research Council merged with the Provisional Association of German Science (Notgemeinschaft der Deutschen Wissenschaft) in 1951 to create the

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German Research Foundation, its only features that survived were these commissions, which included biochemists, pharmacologists and nutrition scientists, state representatives, and members of the pharmaceutical and food industries. Their remit was to decide on which additives could and could not be tolerated. The commissions functioned as influential instruments of policy advice.67 This policy on chemicals drawn up by scientists was supported by women’s organizations as main actors of consumer resistance in Germany. But there was also open criticism in the 1950s of the fact that consumers were not represented on the commissions. At this time, German consumers’ associations did not exist in a strict sense. Nevertheless, women’s organizations resumed their battle against “poisoned” food. In February 1950, the German Women’s Association (Deutscher Frauenring) demanded measures against the coloring of food. Catholic and Protestant women’s organizations wrote hundreds of letters to the ministries of health and interior demanding prohibition of food coloring. The information service for women’s questions, uniting eighty women’s groups, lobbied relevant political representatives to support the passage of a new food law based on a list of experimentally proven carcinogens.68 On 24 February 1956, the MPs Christian-Democrat Hedwig Jochmus, Liberal Marie-Elisabeth Lüders, Social-Democrat Käte Strobel (later to become the minister of health), and forty-three other women delegates presented a petition calling on the German Bundestag to request the federal government produce a draft for a new food law before 1 May 1956. Jochmus, Strobel, and Werner Gabel, undersecretary at the Ministry of the Interior, drew up the petition text. The United Front of Female Delegates (Einheitsfront der Weiblichen Abgeordneten) found strong support from the public and the media.69 The much stricter food law passed in 1958 was actually based on Druckrey’s dose-time-effect law and the debate on butter yellow as a poison of the German people. In the early 1950s, Butenandt (who was interested in the relationship between cancer and hormones) and Druckrey lobbied for their new carcinogenic theory to become accepted as a European norm. In May 1954, the commission on food colorants organized an international meeting for cancer prophylaxis, which resulted in the founding of the organization EUROTOX and the Godesberger decrees on food additives. The latter played a major role in establishing the Joint FAO/ WHO Expert Committee on Food Additives a year later.70 While the German scientists did not succeed in establishing rigid policies for food

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additives, a discourse of poisoning and contamination determined the agenda of both the European consumer and environmental movement of the 1960s and 1970s. Druckrey’s radical conclusions drawn from the case of butter yellow were politically manifest in the commission on food colorants, the new food law of 1958, and the Godesberger decrees. They were successively displaced by specific regulations based on the much more flexible and industry friendly concept of an acceptable daily intake in the late 1950s and the 1960s, which established zones of lesser or higher risk, as well as the conditional and unconditional acceptance of substances: a calculable risk.71 The essential tension between the axiom that there are no harmless substances and the pragmatic drawing up of a white list characterized the debate on food additives in the second half of the twentieth century. The history of butter yellow brings together the industrialization of food production, consumer and risk policies, a novel theory of cancer, and an innovative model of dose-time relationships. Butter yellow impacted public opinion on colorants and influenced legislative measures worldwide. Its outcome, far from being a success story, exemplifies the history of azo dyes as precarious substances—not only in food but also in textiles and leather—and risk management in the twentieth century. Butter yellow itself vanished from the debate on risk policies in the 1960s; it is still used, though not as food colorant. It comes within the technical regulations for azo compounds that release cancercausing aromatic amines by metabolic breakdown. Undoubtedly, no other chemical had such a major impact on consumer risk policies in the twentieth century.

New Views on Aniline: The Differentiation of Cancer Risks after 1945 While butter yellow highlighted human health concerns and the discourse on risk policies, the reports of workplace toxicity and cancer caused by aromatic amines were still not sufficient to stimulate factory regulations, or compensation, apart from those already noted in Germany. Improved working conditions were not always forthcoming, despite many recommendations. After World War II, German and Italian industrial chemists shared knowledge of beta-naphthylamine toxicity with British and American investigators. In particular, very high incidences of bladder cancer were found among German workers

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exposed to benzidine, as noted by the American pathologist Robert R. Kehoe, of the University of Cincinnati, when, as a member of the U.S. Army Field Investigation Unit, he visited the Bayer headquarters in Leverkusen in the mid-1940s. The cancer was found in almost every workman, often several years after the exposure period.72 German firms, until at least the 1940s, had taken advantage of the long latency period by employing only older men in the beta-naphthylamine and benzidine departments; the cancer would often appear long after the men had left the factory, a situation that would not incriminate the company. This practice was often followed elsewhere, including in Britain. Despite the increased understanding that beta-naphthylamine was a potent human carcinogen, even George Gehrmann and colleagues at Du Pont reported in the late 1940s that they found no tumors from animal experiments with benzidine, though they had expressed concerns over aniline, at least until 1948, when they concluded it was not a causative agent. It was hardly surprising that, in 1951, given the lack of consensus, the first edition of N. Irving Sax’s Handbook of Dangerous Materials, while stating that, for beta-naphthylamine, “there is no known safe concentration . . . safety engineers should aim at zero,” noted benzidine was a less clear-cut case but should remain “on the list of suspected materials, because it is a possible cause of bladder tumors.”73 A year earlier, Sophie Spitz and coworkers at New York’s Memorial Center for Cancer and Allied Diseases, in collaboration with Allied Dye & Chemical, had provided experimental evidence that benzidine induced tumors in rats and dogs. Their experiments with rats produced tumors similar to those found with butter yellow.74 Later editions of Sax’s handbook would include the confirmed dangers associated with benzidine. The dye industry took the initiative in modifying its working practices to consider new insights.75 In 1951, industrial hygiene specialists from dye-making firms attended an industry-sponsored symposium in Basel. Wilhelm Hergt, the then medical superintendent at Ludwigshafen, reviewed records of BASF workers going back to 1903. Hergt had conducted the joint survey with Koelsch in the 1920s. Notable was the shift in the attitude toward benzidine (much greater) and away from aniline (not a culprit) since the 1930s. Hergt in 1932 had reported eighty-five cases of bladder cancer, thirty-seven with beta-naphthylamine, three with benzidine, and thirty-nine with “aniline, toluidine, xylidine.” Considering the number of workers in the various departments, Hergt now emphasized the role of beta-naphthylamine more than did his colleague Hans

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Engel, who, based on the survey he conducted using data available until 1937, gave some prominence to aniline (more than seventy cases) and its derivatives, in addition to benzidine (twenty-five cases) and beta-naphthylamine (sixty-seven cases). Though the aniline department, as the biggest department, was found to produce the largest number of ill workers in absolute terms, in proportional terms it was obvious to all that even Engel’s figures caused beta-naphthylamine to stand out.76 Hergt in his 1951 presentation posited benzidine after beta-­naphthylamine as the second most potent carcinogen among the aromatic amines produced in bulk. Carcinoma had been detected in about one hundred cases at Ludwigshafen, with, now, just one case in almost half a century believed to have arisen from exposure to aniline. At Bayer’s beta-naphthylamine plant, “each man working for a few years in this plant contract[ed] a bladder tumor,” leading the firm to cease manufacture in 1943. Questions were raised about worker age, virility and libido, diet, and liquid intake. Excretion from the body of toxic amines through intake of suitable liquids, including carbonated water, was emphasized. Audience members were advised that, at Bayer’s Leverkusen works, “to increase the solubility of the carcinogenic substances and to effect [and] accelerate diuresis and excretion [respectively,] the workers daily are supplied with pure coffee. Furthermore, they receive milk.”77 The summary noted, “The latter however was considered not to have any prophylactic effect,” though it was “beneficial to the general constitution.”78 Undoubtedly, the most comprehensive survey of bladder tumors (“benign papillomata and infiltrating carcinoma”) resulting from exposure to aromatic amines was initiated in 1947 by the Association of British Chemical Manufacturers. This drew on a community of experts brought in from several specialist areas. Alexander Haddow, successor since 1946 to Ernest Kennaway at the Chester Beatty Research Institute, chaired the scientific committee “to guide research work into the cause, consider diagnostic methods, and examine preventive techniques.” N. Strafford chaired a subcommittee to “provide accurate methods for the analysis of suspected compounds.” Two medical officers in Manchester’s dye industry, T. S. Scott at Clayton Aniline and Michael H. C. Williams at the ICI Dyestuffs Division, were appointed members of the Papilloma Committee. In 1952, Scott noted that manufacture of beta-naphthylamine at Clayton Aniline had ceased in 1950. However, this was not the case for benzidine, “considered to be as dangerous a carcinogen, industrially,

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as beta-naphthylamine.” Since no alternative process was available (at least for benzidine intermediates), he recommended that “men under the age of 30 should not be employed in the manufacture or handling of substances known as suspected carcinogens and, when possible, healthy men over forty should be employed on these processes.”79 Though such advice would now be considered somewhat cavalier, the study did contribute to improved working conditions and later regulatory measures. Moreover, Scott also overcame any remaining doubts about the carcinogenic nature of benzidine when encountered in the industrial environment through studies on men whose work was confined to the plant area where this amine was made and handled. This was of course supported by Spitz’s lab results. Scott reported about seventy cases of bladder cancer at Clayton Aniline, where beta-naphthylamine and benzidine manufacture commenced after 1918.80 Another important contributor to the ABCM survey was Robert A.  M. Case, at the Chester Beatty Research Institute, who from 1948 led a five-year epidemiological investigation of bladder tumors in the synthetic dye industry, eventually covering the period from 1921, the first year in which death certificates were available for the research, until 1 February 1952.81 The induction times for cancers were found to vary from two years to more than a decade for workers exposed to naphthylamines and benzidine. The evidence was unequivocal. The probability of contracting cancer was stated to be about thirty times greater for workers engaged in manufacture and use of naphthylamines and benzidine than for the general population. There was no evidence for aniline as a cause of bladder cancer.82 The ABCM report was distributed to “managements, trades unions, and workmen” in 1953 and contributed to improved working practice and changes in industry. As a result, some twenty companies involved in the ABCM study discontinued manufacture of beta-naphthylamine in 1953, as reported in the chemical trade press, including in the United States.83 Scott’s own findings were included in the 455 cases known in the British chemical industry since 1921.84 With the cases admitted by Bayer and BASF in 1951, this amounted to around 650 known incidences, at just two German firms and throughout British industry, with most workers exposed to benzidine and naphthylamines. Then there was the United States, the largest dye manufacturer after 1945, with about two hundred cases by 1950; Switzerland, a major producer of dyes, with one hundred cases from one factory by 1954; the Soviet Union and Eastern European manufacturers; countries engaged in expanding their dye industry,

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such as Japan; and newer manufacturers such as India and in South America.85 Despite the growing consensus, Heinz Oettel, of the BASF Gewerbehygienisch-Pharmakologisches Institut, in 1958 drew attention to inconclusive evidence from animal studies when correlated with cancer in humans, and vice versa, and emphasized the role of cigarette smoking as a cause of tumors.86 In 1957, Scott and Williams, as members of the ABCM Papilloma Committee, cowrote a Code of Working Practice related to manufacture, handling, and use of aromatic amines, specifically in the dye industry. They suggested modifications of manufacturing plants to minimize exposure. Scott’s studies of aromatic amines became the standard works in the field.87 The strong correlation between the period and extent of exposure and a long latency period confirmed that carcinogenic amines caused chronic effects as the result of apparent prolonged intake at dose levels that showed no recognizable acute symptoms.

Regulation and New Dangers among Users of Chemicals Robert Case developed an epidemiological method for establishing the environmental risk of bladder tumors in other industries where aromatic amines were employed, including the rubber, paint, cable, and leather trades. Thus, incidences of bladder cancer in the British rubber industry, which employed aromatic amines as antioxidants, particularly the alpha-naphthylamine-containing Nonox S (until 1949), were revealed in 1953 and 1954 after analysis of records of case histories at hospitals in Birmingham, a city closely associated with the rubber industry. In his 1962 book, T. S. Scott reviewed the legal position on aromatic amines: In the United Kingdom, a specialized section of the Factories Act, the Chemical Works Regulations, contains regulations relating to the manufacture of nitro and amino derivatives of benzene and its homologues. Although special regulations concerning the manufacture of carcinogenic aromatic amines are rare it is a credit to the industries in many countries where they are manufactured that the precautions applied are rigidly observed. Nevertheless, in a few countries the standard of working practice is still deplorably low.88

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In 1953, bladder cancer was a prescribed disease for those engaged in any form of contact with naphthylamines, benzidine, and the dyes auramine and magenta, according to the British Ministry of Pensions and National Insurance (“Industrial Disease no. 39,” National Insurance (Industrial Injuries) Act). From 1957, bladder cancer was finally designated an industrial disease, with compensation under the Workmen’s Compensation Acts.89 The growing interest in industrial hygiene and cancer research from the early 1960s, public concern, and the emergence of environmental movements created new career opportunities for industrial and academic researchers, as well as greater acknowledgment of their scientific achievements: Scott in 1964 succeeded Ronald Lane as professor of occupational medicine at the University of Manchester; Eric Boyland was recognized for his contributions to the role of chemicals in the environment and the biochemistry of cancer; and aromatic amines, including azo compounds, featured prominently at international symposia and conferences dedicated to the mechanism of carcinogenesis.90 Nevertheless, and despite the widespread knowledge on sources of human carcinogenesis, making the best use of the scientific knowledge, detailed epidemiological surveillance, and guidelines in industry, received insufficient attention, particularly for the aromatic amino compounds whose carcinogenic action was restricted to a single organ, the bladder. Correspondence in The Lancet in the second half of 1964 injected a new urgency into the debate over aromatic amines in the workplace by pointing to serious lacunae in information on occupational tumors of the bladder among high-risk groups engaged in the rubber and cable industries. Through the columns of the journal, Case and colleagues said benzidine was still advertised for use in industry. The Lancet criticized limited cooperation from the rubber-processing industry in dealing with, and possibly ignoring, the hazards, even though bladder cancer in the industry was known for ten years.91 H. Guy Parkes, of the Health Research Unit at the Rubber Manufacturing Employers’ Association, later the British Rubber Manufacturers’ Association Ltd., based in Birmingham, revealed that benzidine had been used in the industry until 1956.92 The epidemiologist Case followed up by drawing attention to conflicting statements in industry pamphlets and elsewhere, particularly concerning naphthylamine used in rubber antioxidants. He expressed great disappointment that in 1954 the RMEA chairman had successfully lobbied Her Majesty’s Chief Inspector of Factories to redact his comments about carcinogenic

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aromatic amines, following studies of case histories at Birmingham hospitals.93 The polemical but ultimately valuable exchanges in The Lancet encouraged greater awareness, and action. Parkes, representing the RMEA, backed Case’s suggestion that the Medical Research Council statistical unit should undertake an independent investigation of bladder cancer in the rubber industry.94 Cable workers who had worked with the antioxidant Nonox S came under special attention. Though the product had been withdrawn in 1949, several cases of bladder cancer from workers at one site alone were confirmed by the 1960s. In February 1965, The Lancet drew attention to an inquest into the death of a cable worker caused by bladder cancer and circulation by the British Ministry of Labour to several interested parties of two draft statutory instruments related to the control of manufacture, use, or importation of known bladder carcinogens for comment. The cable worker had been employed at the former WT Henley (Telegraph Works) Company of North Woolwich. At the inquest into the death of the cable worker, J. T. Watts of ICI said Nonox S had been used from 1926 until 1949, and the naphthylamine content included 0.25 percent of the beta isomer. Case drew attention to the fact that alpha- and beta-naphthylamine and benzidine “were officially recognised as carcinogens in 1953, in that bladder tumour was prescribed as an industrial disease in relation to these substances at that date.” David M. Wallace reported seven cases of bladder cancer from workers at the Henley cable factory.95 However, not until 1967 did the UK carcinogenic substances regulations (which came into effect in 1969) place restrictions on the manufacture and use of the aromatic amines beta-naphthylamine, and benzidine, and their salts. Controls were also placed on alpha-naphthylamine, three other amines and their salts, and two dyes.96 As a result of the new regulations, the Department of Employment and Productivity Advisory Panel on Occupational Cancer in 1967 initiated a follow-up and survey of occupational cancers among rubber- and cable-making workers. The regulations stimulated more thorough investigations of causation, not just in government departments and labs but also in courts of law. The first death of a woman from bladder cancer following exposure to naphthylamines to come to inquest was recorded at Westminster Coroner’s Court on 27 May 1968. A former machine operator at the same factory, WT Henley, where the aforementioned cable worker was employed, she had been exposed to Nonox S since 1941, probably until the time its use was discontinued in 1949. The verdict was death from “the industrial

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disease of carcinoma,” due to exposure to beta-naphthylamine.97 By 1968, there were sixteen recorded cases of bladder cancer in workers formerly employed at this site, nine more than in 1965. Rubber industry problems were also reported elsewhere around the same time. Sidney Pell of Du Pont, who attended the June 1968 Boston Conference on the Epidemiology and Etiology of Human Bladder Cancer, in his summary drew colleagues’ attention to “some observations and points of view . . . that may be relevant to the bladder cancer problem in the Du Pont Company.” Thus, he noted, since 1965 the British rubber industry’s Papilloma Committee “found 49 cases compared with 45 expected. These studies use thorough case-finding methods and detailed occupational histories.” Moreover, “the incidence (of bladder cancer) has been increasing in the United States among males but not among females . . . In addition to dye workers, hairdressers and leather workers may have an increased risk . . . persons who smoke about one pack of cigarettes per day have twice the risk of developing bladder cancer than do non-smokers.”98

Health Risks after 1970: The United States and Britain In the United States, concerns over bladder cancer from aromatic amines and their derivatives brought them under even greater scrutiny after Congress passed the Occupational Safety and Health Act of 1970. There were strong calls for zero-tolerance levels of several known workplace carcinogens.99 In 1973, eight aromatic amines, including beta-­naphthylamine and benzidine, were among fourteen chemicals controlled by the second emergency standard issued by the Department of Labor’s Occupational Safety and Health Administration.100 US regulators erred on the side of caution, accepting extrapolations from animal bioassays to humans and adopting rulings based on zero tolerance. In many ways, this was a response to the tremendous impacts of Rachel Carson’s Silent Spring and the use of Agent Orange in the 1960s. In 1976, the EPA implemented the Toxic Substances Control Act. These various initiatives led to renewed screening and evaluation campaigns, as well as studies on threshold exposure that caused sensitization and on effective doses that interact with target organs. The US National Institute of Occupational Safety and Health chose fiftyeight potentially carcinogenic substances for review and recommended workplace standards.101 Of these substances, twenty-three were dyes

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and dye intermediates, and of nine classes of chemicals containing known carcinogens and mutagens, aromatic amines and azo dyes were listed as one class. The American “Dye Industry ad hoc Committee on NIOSH (carcinogen project)” was established, also in 1976, to determine the significance of the NIOSH project and the inclusion of the large number of dyes.102 The dye industry’s NIOSH committee and the Synthetic Organic Chemical Manufacturers’ Association established a joint “Ad Hoc Dyes Ecology Group” in December 1976. The Dyes Environmental and Toxicology Organization, founded in 1977, created a classification task force whose remit included evaluating the health risks posed by benzidine-derived azo dyes. Three intermediates, benzidine and its derivatives tolidine and dianisidine, tested positive in mutagenicity tests, as did many of their colorants. A similar study covered a wider range of azo dyes.103 After interest in exposure to benzidine had peaked in the early 1970s, the focus became aromatic amines either that were less potent carcinogens or about which there was some uncertainty regarding their abilities to induce tumors. Aniline came into the latter category, particularly since commercial production far exceeded that of other amines. Its known toxicity, allied with uncertainty about mutagenic-carcinogenic effects in humans, led to restrictions in handling and use, and research into the possible significance for the initiation of carcinogenesis. Because of the recognized toxicity of aromatic amines, the EPA enforced testing consent orders on manufacturers (including importers) of aniline and seven of its derivatives.104 In 1980, the British Association of Scientific and Managerial Staff complained that existing government guidelines were not as stringent as in the United States. 105 These complaints were supported by Samuel Epstein’s 1978 book The Politics of Cancer (which was heavily critical of the National Cancer Institute and the American Cancer Society) and findings of the report Estimates of the Fraction of Cancer in the United States Related to Occupational Factors, published by the NCI, the National Institute of Environmental Health Sciences, and the National Institute for Occupational Health and Safety. Cultural changes in society around 1980 favored individual claims for damages, often involving substantial sums. In Britain, the situation changed in 1982, when Nonox S came before the High Court of Justice. The court’s verdict, upheld on appeal and based on “contemporaneous documentation,” was that liability for worker exposure to a product containing about one percent of beta-naphthylamine lay with the manufacturer, ICI, which had been aware of the danger associated

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with the amine since the early 1940s, and to a lesser extent with the user, Dunlop, for lack of screening cystoscopy.106 As Guy Parkes of the British Rubber Manufacturers’ Association, and A. E. J. Evans of the ICI Dyestuffs Division observed in 1984, when discussing the implications: “A victim of industrial bladder cancer cannot be adequately compensated for the infliction of an injury that will in many cases cost him his life . . . .the threatened application of strict legal liability will certainly influence future manufacturing and marketing policies.”107 The case had set an important precedent for strict liability concerning the safety of a product on the parts of both manufacturers and users that went way beyond liabilities for aromatic amines alone.

Conclusion The aromatic amines as a group are the longest studied of synthetic organic chemicals, because they were the first to be manufactured on a large scale, and their toxic properties were established early on in working practice. The main acute impact associated with exposure to aniline is cyanosis. For several important industrial aromatic amines, mutagenic injury to humans by workplace exposure was established in the early 1900s, and decrees and laws that offered compensation were implemented in Germany in the 1920s and 1930s. Epidemiological approaches to seeking out carcinogens enabled identification of likely culprits. However, the nature of just one, beta-naphthylamine, was established only at the end of the 1930s. Questions remained regarding the other main culprit, benzidine. Thus, in 1938, while the dog was found to be the only animal that developed bladder cancer when fed pure beta-naphthylamine, benzidine did not then induce tumors under the same experimental conditions. Consensus, after further animal experiments, was reached only around 1950, though regulations in Britain and the United States were not immediately forthcoming. The problem of identification had been confounded by the long latency period (sometimes a decade or more), the long focus on aniline, and the nature of remotely acting carcinogenesis, as demonstrated by the amines. Laboratory findings had major impacts on occupational health, legislation, and regulation in both manufacturing industries and public spheres. Somewhat different is the case of butter yellow, which, because it concerned nutrition and diet reform, was seen as a symbol of the threat posed by a civilization gone wrong, promoting a new reformist

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lifestyle, highly important at least in mid-twentieth century Germany. Subsequently, an apparatus of new theories, legislative measures, and political actors emerged, deeply transforming risk policies in the second half of the twentieth century.

Acknowledgments Heiko Stoff thanks the Deutsche Forschungsgemeinschaft for supporting his research into food additives (foreign matter). Anthony Travis thanks the staff of the Wellcome Collection, and Ute Deichmann for discussing chemical and biochemical research in the National Socialist era. Heiko Stoff is Research Scholar at the Hannover Medical School. His work focuses on the history of science, medicine, and gender in the nineteenth and twentieth centuries. He recently edited, with Alexander von Schwerin, a special issue on food additives regulation in Technikgeschichte 81, no. 3 (2014). He also edited, with Alexander von Schwerin and Bettina Wahrig, Biologics: A History of Agents Made from Living Organisms in the Twentieth Century (2013) and wrote Gift in der Nahrung: Zur Genese der Verbraucherpolitik in Deutschland Mitte des 20. Jahrhunderts (2016), Wirkstoffe: Eine Wissenschaftsgeschichte der Hormone, Vitamine und Enzyme, 1920–1970 (2012), and Ewige Jugend: Konzepte der Verjüngung vom späten 19. Jahrhundert bis ins Dritte Reich (2004). Anthony S. Travis is Deputy Director of the Sidney M. Edelstein Center for the History and Philosophy of Science, Technology and Medicine at The Hebrew University of Jerusalem. He has published extensively on the history of chemical technology in the nineteenth and twentieth centuries and on aspects of chemical waste, including analytical techniques. Publications include The Rainbow Makers: The Origins of the Synthetic Dyestuffs Industry in Western Europe (1993), Heinrich Caro and the Creation of Modern Chemical Industry (with Carsten Reinhardt, 2000), Dyes Made in America, 1915–1980: The Calco Chemical Company, American Cyanamid, and the Raritan River (2004), and Nitrogen Capture: The Growth of an International Industry (1900–1940) (2018).

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Notes 1. Schoental, “Review.” 2. Parkes and Evans, “Epidemiology”; Josephy and Mannervik, Molecular Toxicology. 3. Travis, “Toxicological.” 4. Travis, Rainbow Makers. 5. Reinhardt and Travis, Heinrich Caro, 174–76, 275–85. 6. Travis, “Poisoned Groundwater.” 7. Fagin, Toms River; Michaels, “Colorfast Cancer”; Travis, Dyes. 8. Hofmann, “Colouring Derivatives,” 120. 9. EPA, “Testing Consent Orders.” 10. Grandhomme, Theerfarben-Fabriken, 118–21; Koelsch, Handbuch, 2:629–30. See also Grandhomme, Fabriken; Reinecke, “Zur Geschichte,” 22–25, 30–32. 11. Price Jones and Boycott, “Observations.” 12. American Cyanamid Company, “Safety Meeting for Week of June 17, 1950. Subject: Discourse on Cyanosis—Necessary Protective Equipment to Be Worn and Means of Prevention,” Bound Brook, NJ, RSA, Sidney M. Edelstein Center, The Hebrew University of Jerusalem, Jerusalem. 13. Rehn, “Blasengeschwülste,” 588–600; Thomann, “Ludwig Rehn”; Wagner, Innovation, 46–47. For more on Rehn, see Dietrich and Dietrich, “Ludwig Rehn”; Dietrich and Golka, “Bladder Tumours”; Reinecke, “Zur Geschichte,” 52–55; Werner et al., “Ludwig Rehn.” 14. See Grandhomme, Fabriken. 15. Rehn, “Über Blasenerkrankungen”; Rehn, “Harnblasengeschwülste”; Liech­ ten­stein, “Harnblasenentzündung.” 16. Leuenberger, “Unter dem Einfluss.” 17. Curschmann’s studies contributed to regulations introduced in Germany in 1925. Curschmann, “Statistische Erhebungen.” See also Curschmann, “Erkran­kungen,” 109–16; Andersen, “Auseinandersetzungen,” 205. 18. Travis, Rainbow Makers. 19. Important studies on the situation in Germany are Reinecke, “Zur Geschichte”; Hien, “Zur Geschichte”; Hien, Chemische Industrie. See also Dietrich and Golka, “Bladder Tumours.” 20. Nassauer, “Über bösartige Blasengeschwülste bei Arbeitern.” See also sum­ maries in Nassauer, “Über bösartige Blasengeschwülste bei den Arbeitern” (1919); Nassauer, “Bladder Swellings”; Nassauer, “Über bösartige Blasen­ geschwülste bei den Arbeitern” (1920); Reinecke, “Zur Geschichte,” 57–58. 21. Koelsch, “Giftigkeit,” 968; Koelsch, 25 Jahre, 41. On Koelsch, see Hall, “Franz Koelsch,” esp. 219; Bauer, “F. Koelsch.” 22. Reinhardt and Travis, Heinrich Caro, 275–86. 23. Engel, “Über das Schicksal.” 24. Oppenheimer, “Über die bei Arbeitern der chemischen Betriebe,”12–14. See also Reinecke, “Zur Geschichte,” 63–66.

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25. Alice Hamilton had investigated various workplace hazards since 1910. See her reports on bladder cancers caused by aromatic amines, based on mainly German publications: Hamilton, “Discussion”; Hamilton, “Industrial Poisoning.” These were based on visits to thirty-six US factories, from 1916 to 1919, and several factories in Europe in 1919. See also Hamilton, Industrial Poisoning. Hamilton, Industrial Toxicology, was published in 1934, and a second edition, with the industrial physician Harriet Hardy, in 1949. 26. ILO, Cancer of the Bladder, 6. 27. For the ordinance of 12 May 1925, see Brauns, “Verordnung”; Koelsch, Meldepflichtigen, 10–13, esp. 12; Koelsch, “Ärztliche Erfahrungen,” 33–41; Koelsch, Handbuch, 1:127–29, 443–45, 629–30; Koelsch, Lehrbuch, 205, 263–65. 28. Wignall, “Incidence of Disease.” 29. Henry et al., “Incidence of Cancer,” 125. 30. Berenblum, “Aniline Cancer.” 31. For aromatic amines that are toxic and carcinogenic, and the general background to the development of knowledge about synthetic carcinogens encountered in the workplace, see Searle, Chemical Carcinogens. Certain of these and other areas of concern for aromatic amines, including waste treatment, are reviewed in Travis, “Toxicological.” See also Penning, Chemical Carcinogenesis. 32. Hueper et al., “Experimental Production”; Hounshell and Smith, Science, 560–63. Hueper left Du Pont in 1938 and published Hueper, Occupational Tumors, in 1942. He was appointed first director of the Environmental Cancer Section of the National Cancer Institute in 1948. For other aspects of aromatic amine toxicity in the United States, see Travis, Dyes, 320–32. 33. Wilhelm Hergt, “Symposium on Industrial Hygiene, Basel, 11–12 October 1951,” report for Cincinnati Chemical Works, RSA, part 2, p. 9. 34. Koelsch, Handbuch, 1:621. 35. Seldte, “Dritte Verordnung,” 1119. See also Dietrich and Golka, “Bladder Tumours,” 282. 36. Berger, “Bemerkenswerte”; Koelsch, Handbuch, 2:970–74, 1136–37. 37. Weisburger and Weisburger, “Chemicals.” See also Garner et al., “Car­cino­genic.” 38. Bauer, “Über Chemie,” 26–28. 39. Ibid.; Kinosita, “Studies,” 287, 291–92. 40. Brock et al., “Erzeugung.” 41. Deichmann, Flüchten, 346–48. 42. Kuhn and Beinert, “Über das aus krebserregenden,” 904. On Kuhn, see Deichmann, “Duce”; Schmaltz, Kampfstoff-Forschung, 357–87. 43. Opie, “Pathogenesis,” 244. 44. Lenzner, Gift; Liek, Krebsverbreitung; Kollath, Ordnung; Melzer, Vollwerter­ nährung; Merta, Wege; Fritzen, Gesünder leben; Stoff, Gift; Treitel, Eating Nature.

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45. Stoff, Wirkstoffe, 253–79; Sperling, “Kampf.” 46. Proctor, Nazi War, 165–70. 47. Hartmann, “55. Tagung,” 247–48. 48. “Krebs/Medizin: Die Krankheit der Epoche,” Der Spiegel 7, no. 28 (1953): 22–30 (26). 49. Letter from Walter Hinnendahl to Theodor Heuss, 1 January 1950; see also letter from Paula Greeven to Theodor Heuss, 30 November 1949; letter from Eberhard von Campenhausen to Theodor Heuss, 22 January 1950, BArch, B 116/419. 50. Letter from S. Walter Souci to Bundesministerium für Landwirtschaft und Forsten, 30 November 1952; manuscript, 29 November 1952, BArch, B 116/420; Souci, “Sind gefärbte Lebensmittel.” 51. Hartmann, “55. Tagung,” 247–48. 52. See Wurzschmitt’s response to Druckrey, “Versuche,” 58–59. 53. Souci, “Sind gefärbte Lebensmittel”; manuscript, 29 November 1952. “Anord­ nung über das Färben von Milch- und Molkenerzeugnissen sowie Margarine mit chemischen Farbstoffen,” Amtsblatt für Ernährung, Landwirtschaft und Forsten 18 (1949): 11. 54. Souci, “Sind gefärbte Lebensmittel”; Druckrey and Küpfmüller, “Quanti­ tative,” 254. 55. “Krebs,” 26–27. 56. Eichholtz, Toxische Gesamtsituation. 57. Wunderlich, “Mit Papier”; Wunderlich, “Zur Entstehungsgeschichte,” 375–78, 388; Hubenstorf, “Medizinische Fakultät,” 262. 58. Hermann Druckrey, “Begründung für die Schaffung eines speziellen Institutes für die pharmakologische Lebensmittelforschung,” undated, MPG Archive, III. Abt., Rep. 84/1, Nr. 429; Wunderlich, “Zur Entstehungs­ geschichte,” 371. 59. Druckrey, “Versuche,” 46–47; Druckrey and Küpfmüller, “Quantitative,” 258–59; Druckrey, “Begründung.” 60. Druckrey and Küpfmüller, “Quantitative,” 259. 61. Druckrey and Küpfmüller, “Dosis,” 607–8. 62. Druckrey, “Versuche,” 47; Druckrey and Küpfmüller, “Quantitative,” 260. 63. Druckrey and Küpfmüller, “Dosis,” 514, 604–10, 643. 64. Druckrey and Küpfmüller, “Quantitative,” 254, 259. 65. Druckrey, “Versuche,” 56. 66. Bauer, “Über Chemie,” 39. 67. Stoff, “Hexa-Sabbat.” 68. Deutscher Frauenring, Ausschuss für Volks- und Heimwirtschaft an Bundes­ minister des Innern, Abtlg. Gesundheit, 14 February 1950, BArch B116/419. 69. Second Deutscher Bundestag, 149th meeting, Bonn, 8 June 1956, BArch, B 142/1528, 7901. 70. See Jas, “Adapting.”

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71. See Boudia and Jas, Toxicants; Pestre, “Regimes.” 72. Andrews, German Dyestuffs, 401. For Kehoe’s career, including his infamous role in the leaded gasoline scandal, see Sellers, Hazards. 73. Sax, Handbook, 42, 265. 74. Spitz et al., “Carcinogenic Action.” 75. Scott and Williams, “Control,” 150. 76. “Engel adds, as far as (his figures) are concerned, that the number of operators in the aniline group is considerably greater than the number of men working in the remaining amine plants. In regard to this, therefore beta-naphthylamine would be the most carcinogenic substance.” Hergt, “Symposium,” part 2, 9. 77. Ibid., part 2, 5. 78. Ibid., part 1, 5. 79. Scott, “Incidence.” 80. Scott, Carcinogens, 56–58. 81. Case et al., “Tumours.” 82. For Case, see Parkes and Evans, “Epidemiology,” 290–93. 83. Case, “Expected Frequency”; “Incidence of Bladder Tumors in British Dye Industry Studied,” Chemical & Engineering News 31, no. 51 (1953): 5392; ABCM, Papilloma. 84. Case et al., “Tumours.” 85. Scott, Carcinogens, 36–41. 86. Oettel, “Cancerogene Substanzen.” 87. Scott and Williams, “Control”; Scott, Carcinogens. 88. Scott, Carcinogens, 177. 89. “Occupational Bladder Tumours and the Control of Carcinogens,” The Lancet 285, no. 7380 (1965): 306–7. 90. Bergmann and Pullman, Physico-chemical Mechanisms. 91. “Cancer Research,” The Lancet 284, no. 7349 (1964): 25–26. 92. Parkes, “Cancer Research,” 254. 93. Case, “Cancer Research.” 94. Parkes, “Cancer Research,” 414. 95. “Occupational Bladder Tumours,” 306–7; “Industrial Cancer of the Bladder,” The Lancet, 285, no. 7380 (1965): 328–29. See also “Safety with the Naphthylamines,” Chemical Trade Journal and Chemical Engineer 157 (1965): 658. 96. The Carcinogenic Substances Regulations, Statutory Instruments no. 879 (London, 1967). 97. “Industrial Carcinoma of the Bladder,” The Lancet 291, no. 7544 (1968): 1257. 98. Letter from Sidney Pell to C. A. D’Alonzo, Du Pont medical director, 12 June 1968, RSA. 99. PCHRG and OCAW, “Petition.” 100. Travis, “Toxicological,” 859.

Discovering Chemical Carcinogenesis  171

101. NIOSH, Special Occupational Review. See also NIOSH, Preventing Bladder Cancer. 102. Boeniger, Carcinogenecity. 103. Burg and Charest, Evaluation; Burg and Charest, Azo Dyes. 104. EPA, “Testing Consent Orders”; see also EPA, “OOPT Chemical.” 105. Walgate, “United Kingdom.” 106. Parkes and Evans, “Epidemiology,” 294–97. 107. Ibid., 294, 296.

Bibliography Archives BArch (Bundesarchiv), Koblenz. MPG (Max-Planck-Gesellschaft) Archive, Berlin. RSA (Regina Schoental Archive), Sidney M. Edelstein Center, The Hebrew University of Jerusalem.

Publications ABCM (Association of British Chemical Manufacturers). Papilloma of the Bladder in the Chemical Industry. London, 1953. Andersen, Arne. “Auseinandersetzungen um den Arbeitsschutz.” In Arbeit Mensch Gesundheit, edited by Christina Bargholz, 200–211. Hamburg, 1990. Andrews, D. B. German Dyestuffs and Dyestuffs Intermediates, Including Manu­ facturing Processes, Plant Design, and Research Data. 3 vols. FIAT Final Report no. 1313 / PB no. 85172. Washington, DC, 1948. Bächi, Beat. “Zur Krise der westdeutschen Grenzwertpolitik in den 1970er Jahren: Die Verwandlung des Berufskrebses von einem toxikologischen in ein sozio­ ökonomisches Problem.” Berichte zur Wissenschaftsgeschichte 33, no. 4 (2010): 419–35. Bauer, Karl Heinrich. “Über Chemie und Krebs: Dargestellt am ‘Anilinkrebs.’” Langenbecks Archiv für Klinische Chirurgie 264, no. 1 (1950): 21–44. Bauer, M. “F. Koelsch zum 80. Geburtstag am 4. Juli 1956.” Zentralblatt für Arbeitsmedizin und Arbeitsschutz 6 (1950): 149–51. Berenblum, Isaac. “Aniline Cancer.” Cancer Review 6 (1932): 338–55. Berger, H. “Bemerkenswerte chemische Ursachen bei gewerblichen Unfällen und Erkrankungen.” Die Chemische Industrie /Gemeinschaftsausgabe 62 (1939): 221. Bergmann, Ernst David, and Bernard Pullman, eds. Physico-chemical Mechanisms of Carcinogenesis: Proceedings of an International Symposium Held in Jerusalem, 21–25 October 1968. Jerusalem, 1969. Boeniger, Mark. The Carcinogenecity and Metabolism of Azo Dyes, Especially Those Derived from Benzidine. NIOSH Technical Report no. 80-119. Cincinnati, OH, 1980.

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Boudia, Soraya, and Nathalie Jas, eds. Toxicants, Health and Regulation since 1945. London, 2013. Boyland, Eric. The Biochemistry of Bladder Cancer. Springfield, IL, 1963. Brauns, Heinrich. “Verordnung über Ausdehnung der Unfallversicherung auf gewerbliche Berufskrankheiten vom 12. Mai 1925.” Reichsgesetzblatt 1, no. 20 (1925): 69–70. Brock, Norbert, Hermann Druckrey, Hermann Herwig, and Herwig Hamperl. “Die Erzeugung von Leberkrebs durch den Farbstoff 4-Dimethylaminoazobenzol.” Zeitschrift für Krebsforschung 50, no. 6 (1940): 431–56. Burg, A. W., and M. C. Charest. Azo Dyes: Evaluation of Data Relevant to Human Health and Environmental Safety. Boston, 1980. _____. An Evaluation of the Literature Concerning the Potential for Carcinogenic Properties of Bisazobiphenyl Compounds Used as Dyes. Boston, 1979. Case, R. A. M. “Cancer Research.” The Lancet 284, no. 7454 (1964): 309–10. _____. “The Expected Frequency of Bladder Tumours in Works Populations.” British Journal of Industrial Medicine 10, no. 2 (1953): 114–20. Case, R. A. M., Marjorie E. Hosker, Drever B. McDonald, and Joan T Pearson. “Tumours of the Urinary Bladder in Workmen Engaged in the Manufacture and Use of Certain Dyestuff Intermediates in the British Chemical Industry, Part 1: The Role of Aniline, Benzidine, Alpha-Naphthylamine, and BetaNaphthylamine.” British Journal of Industrial Medicine 11, no. 2 (1954): 75–96. Curschmann, Fritz. “Die Erkrankungen durch Benzol oder seine Homologen durch Nitro- und Amidoverbindungen der aromatischen Reihe.” In Koelsch, Die meldepflichtigen Berufskrankheiten, 93–116. _____. “Statistische Erhebungen über Blasentumoren bei Arbeitern in der ­chemischen Industrie.” Zentralblatt für Gewerbehygiene 8 (1920): 145–49, 169–76. Deichmann, Ute. “‘Dem Duce, dem Tenno und unserem Führer ein dreifaches Sieg Heil!’ Die Deutsche Chemische Gesellschaft und der Verein deutscher Chemiker in der NS-Zeit.” In Physiker zwischen Autonomie und Anpassung: Die Deutsche Physikalische Gesellschaft im Dritten Reich, edited by Dieter Hoffmann and Mark Walker, 459–98. Weinheim, 2006. _____. Flüchten, Mitmachen, Vergessen: Chemiker und Biochemiker in der NS-Zeit. Weinheim, 2001. Dietrich, Holger G., and B. Dietrich. “Ludwig Rehn (1849–1930): Pioneering Findings on the Aetiology of Bladder Tumours.” World Journal of Urology 19, no. 2 (2001): 151–53. Dietrich, Holger G., and Klaus Golka. “Bladder Tumors and Aromatic Amines: Historical Milestones from Ludwig Rehn to Wilhelm Hueper.” Frontiers in Bioscience E4 (2012): 279–88. Druckrey, Hermann. “Versuche zur Krebserzeugung mit Anilin oder AnilinDerivaten.” Langenbecks Archiv für Klinische Chirurgie 264, no. 1 (1950): 45–60.

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Druckrey, Hermann, and Karl Küpfmüller. “Dosis und Wirkung: Beiträge zur theoretischen Pharmakologie.” Die Pharmazie 8, no. S1 (1949): 514–645. _____. “Quantitative Analyse der Krebsentstehung.” Zeitschrift für Naturforschung B 3 (1948): 254–66. Eichholtz, Fritz. Die toxische Gesamtsituation auf dem Gebiet der menschlichen Ernährung: Umrisse einer unbekannten Wissenschaft. Berlin, 1956. Engel, Hans. “Über das Schicksal des Betanaphthylamins im Organismus des Hundes.” Zentralblatt für Gewerbehygiene und Unfallverhütung 8 (1920): 81–86. EPA (Environmental Protection Agency). “OOPT Chemical Fact Sheets, Aniline Fact Sheet (CAS no. 62-53-3).” EPA 749-F-95-002. December 1994. https:// nepis.epa.gov/Exe/ZyPURL.cgi?​Dockey=​P1000IC7.txt. _____. “Testing Consent Orders on Aniline and Seven Substituted Anilines.” 40 CFR Part 799. Federal Register 53, no. 161 (1988): 31804. Fagin, Dan. Toms River: A Story of Science and Salvation. New York, 2013. Fritzen, Florentine. Gesünder leben: Die Lebensreformbewegung im 20. Jahrhundert. Stuttgart, 2006. Garner, R. C., C. N. Martin, and D. B. Clayson. “Carcinogenic Aromatic Amines and Related Compounds.” In Searle, Chemical Carcinogens, 1:174–276. Grandhomme, Wilhelm. Die Fabriken der Aktien-Gesellschaft Farbwerke vorm. Meister, Lucius und Brüning zu Höchst a. M. in sanitärer und socialer Bezie­ hung. Frankfurt, 1896. _____. Die Theerfarben-Fabriken der Actien-Gesellschaft Farbwerke vorm. Meister, Lucius und Brüning zu Höchst a. M. in sanitärer und socialer Beziehung. Heidelberg, 1883. Hall, Götz. “Franz Koelsch: Pionier des medizinischen Arbeitsschutzes.” Arbeits­ medizin, Sozialmedizin, Präventivmedizin 19 (1984): 218–22. Hamilton, Alice. “A Discussion of the Etiology of So-Called Aniline Tumours of the Bladder.” Journal of Industrial Hygiene 3 (1912): 16–28. _____. “Industrial Poisoning of Compounds of the Aromatic Series.” Journal of Industrial Hygiene 1 (1919): 200–212. _____. Industrial Poisoning in Making Coal-Tar Dyes and Dyes Intermediates. Washington, DC, 1921. _____. Industrial Toxicology. New York, 1934. Hartmann, Fritz. “55. Tagung der Deutschen Gesellschaft für innere Medizin.” Die Naturwissenschaften 36, no. 8 (1949): 245–49. Hartwell, Jonathan L. Survey of Compounds Which Have Been Tested for Carcinogenic Activity. Washington, DC, 1941. Henry, S. A., Nina Marion Kennaway, and Ernest L. Kennaway. “The Incidence of Cancer of the Bladder and Prostate in Certain Occupations.” Journal of Hygiene 31, no. 2 (1931): 125–37. Hergt, Wilhelm. “Ärztliche Erfahrungen bei der Durchführung der Verordnung über Ausdehnung der Unfallversicherung auf gewerbliche Berufskrankheiten.” Zeitschrift für Gewerbehygiene und Unfallverhütung 7 (1930): 33–41.

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Hien, Wolfgang. Chemische Industrie und Krebs: Zur Soziologie des wissenschaftlichen und sozialen Umgangs mit arbeitsbedingten Krebserkrankungen in Deutschland. Bremerhaven, 1994. _____. “Zur Geschichte des Anilinkrebses.” In Berufskrankheitenrecht: Beit­räge zur Geschichte und Gegenwart der Berufskrankheiten und des Berufskrank­ heitenrechts, edited by Detlev Jung, and Klaus-Dieter Thomann, 163–77. Stuttgart, 2002. Hofmann, August Wilhelm. “Colouring Derivatives of Organic Matter, Recent and Fossilised.” In International Exhibition, 1862: Reports by the Juries on the Subjects in the Thirty-Six Classes into Which the Exhibition Was Divided, edited by J. F. Iselin and Peter Le Neve Foster, 114–38. London, 1863. Hounshell, David A., and John K. Smith Jr. Science and Corporate Strategy: Du Pont R&D, 1902–1980. Cambridge, MA, 1988. Hubenstorf, Michael. “Medizinische Fakultät 1938–1945.” In Willfährige Wissen­ schaft: Die Universität Wien 1938 bis 1945, edited by Gernot Heiß, Siegfried Mattl, Edith Saurer, and Karl Stuhlpfarrer, 233–82. Vienna, 1988. Hueper, William C. Occupational Tumors and Allied Diseases. Springfield, IL, 1942. Hueper, William C., Frank H. Wiley, and Humphrey D. Wolfe. “Experimental Production of Bladder Tumors in Dogs by Administration of BetaNaphthylamine.” Journal of Industrial Toxicology 20 (1938): 46–84. ILO (International Labour Office). Cancer of the Bladder among Workers in Aniline Factories. Geneva, 1921. Jas, Nathalie. “Adapting to ‘Reality’: The Emergence of an International Expertise on Food Additives and Contaminants in the 1950s and early 1960s.” In Boudia and Jas, Toxicants, Health and Regulation, 47–69. Josephy, P. David, and Bengt Mannervik. Molecular Toxicology. 2nd ed. New York, 2006. Kinosita, Riojun. “Studies on the Cancerogenic Azo and Related Compounds.” Yale Journal of Biology and Medicine 12, no. 3 (1940): 287–300. Koelsch, Franz. 25 Jahre Bayerischer Landesgewerbearzt: Rückblicke und Ausblicke. Munich, 1935. _____.  “Die Giftigkeit der aromatischen Nitroverbindungen.” Münchener ­Medi­zin­ische Wochenschrift 30 (1917): 965–68. _____. Handbuch der Berufskrankheiten. 2 vols. Jena, 1935–1937. _____. Lehrbuch der Gewerbehygiene. Stuttgart, 1937. _____. Die meldepflichtigen Berufskrankheiten. Munich, 1926. Kollath, Werner. Die Ordnung unserer Nahrung. Stuttgart, 1942. Kuhn, Richard, and Helmut Beinert. “Über das aus krebserregenden Azofarbstoffen entstehende Fermentgift.” Berichte der deutschen chemischen Gesellschaft 76, no. 9 (1943): 904–9. Lenzner, Curt. Gift in der Nahrung. Leipzig, 1931. Leuenberger, S. G. “Die unter dem Einfluss der synthetischen Farbenindustrie beobachtete Geschwulstentwicklung.” Beiträge zur klinischen Chirurgie 80 (1912): 208–16.

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Liechtenstein, Otto Michael Ludwig. “Über Harnblasenentzündung und Harn­ blasengeschwülste bei Arbeitern in Farbfabriken.” Deutsche Medizinische Wochenschrift 45 (1898): 709–13. Liek, Erwin. Krebsverbreitung, Krebsbekämpfung, Krebsverhütung. Munich, 1932. Melzer, Jörg M. Vollwerternährung: Diätetik, Naturheilkunde, Nationalsozialismus, sozialer Anspruch. Stuttgart, 2003. Merta, Sabine. Wege und Irrwege zum modernen Schlankheitskult: Diätkost und Körperkultur als Suche nach neuen Lebensstilformen 1880–1930. Stuttgart, 2003. Michaels, David. “Colorfast Cancer: The Legacy of Corporate Malfeasance in the U.S. Dye Industry.” In Toxic Circles: Environmental Hazards from the Workplace into the Community, edited by Helen E. Sheehan and Richard P. Wedeen, 81–112. New Brunswick, NJ, 1993. Nassauer, Max. “Bladder Swellings: Malignant—among Workers in the Organic Chemical Industry.” Abstract. Journal of the Society of Chemical Industry 38, no. 23 (1919): 922A. _____.  “Über bösartige Blasengeschwülste bei Arbeitern der organisch-­chemischen Grossindustrie.” Zeitschrift für angewandte Chemie 32, no. 84 (1919): 333–35. _____. “Über bösartige Blasengeschwülste bei den Arbeitern der organisch-chemi­ schen Grossindustrie.” Münchener medizinische Wochenschrift 66 (1919): 1451. _____. “Über bösartige Blasengeschwülste bei den Arbeitern der organischchemischen Großindustrie.” Frankfurter Zeitschrift für Pathologie 22 (1920): 353–99. NIOSH (National Institute for Occuptional Safety and Health). Preventing Bladder Cancer from Exposure to o-Toluidine and Aniline. DHHS (NIOSH) Publication no. 90-116. Washington, DC, 1990. _____. Special Occupational Review for Benzidine-Based Dyes. HHEW (NIOSH) Publication no. 80-109. Washington, DC, 1980. Oettel, H. “Cancerogene Substanzen, Berufskrebs und Krebssterblichkeit.” Ange­ wandte Chemie 70, nos. 17–18 (1958): 532–39. Opie, Eugene L. “The Pathogenesis of Tumors of the Liver Produced by Butter Yellow.” Journal of Experimental Medicine 80, no. 3 (1944): 231–46. Oppenheimer, Rudolf. “Über die bei Arbeitern chemischer Betriebe beobachteten Geschwülste des Harnapparates und deren Beziehungen zur allgemeinen Geschwulstpathogenese.” Münchener medizinische Wochenschrift 67 (1920): 12–14. Parkes, H. Guy. “Cancer Research.” The Lancet 284, no. 7353 (1964): 254–55, 414. Parkes, H. Guy, and A. E. J. Evans. “Epidemiology of Aromatic Amine Cancers.” In Searle, Chemical Carcinogens, 1:277–301. PCHRG and OCAW (Public Citizen Health Research Group and Oil, Chemical, and Atomic Workers International Union). “Petition Requesting a Zero

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Wunderlich, Volker. “‘Mit Papier, Bleistift und Rechenschieber’: Der Krebsforscher Hermann Druckrey im Internierungslager Hammelburg (1946–1947).” Medi­zin­historisches Journal 43, nos. 3–4 (2008): 327–43. _____. “Zur Entstehungsgeschichte der Druckrey-Küpfmüller-Schriften (1948– 1949): Dosis und Wirkung bei krebserzeugenden Stoffen.” Medizinhistorisches Journal 40, nos. 3–4 (2005): 369–97.

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CHAPTER 5

Cyclamates A Tale of Uncertain Knowledge (1930s–1980s) Alexander von Schwerin

Salts of cyclohexanesulfamidic acid (sodium and calcium cyclamate)

were first marketed as artificial sweeteners in the 1950s. From the mid1960s to the 1980s, there was controversy about the possible toxic impacts of cyclamates and their metabolic intermediate cyclohexylamine. The story of cyclamates mirrors to some extent the story of the development of the food additives industry. “People seem to have an almost insatiable desire for sweet taste, but it is the hedonic delight of sweet-taste sensation that is being sought rather than the calories.”1 This statement, in a volume on the chemical, molecular, chemoreceptive, and psychophysical aspects of artificial sweeteners, reads like an advertising slogan for why people need sugar substitutes. It gives the flavor of a field that is at once subsidized science—with hundreds of compounds tested and today designed through molecular modeling approaches—as well as an omnipresent commercialism and contested regulatory politics. This chapter sketches the first stages in the life of cyclamates as a potential food additive within the context of a growing food industry in the era of mass consumption, the “Golden Age” in terms of wealth and welfare, lifestyle and health politics. The history of cyclamates can also be told as a comparative cultural history of consumption in the United States and Europe. The story of cyclamates reveals differences, particularly in terms of regulation and the genealogy of regulative measures, between markets and consumer politics in the United States and Europe. In this respect, this study takes advantage of the pathbreaking comparative study by Ronald Brickman, Sheila Jasanoff, and Thomas Ilgen on the regulation of chemicals.2 However, recent historical approaches have begun to tackle the history of so-called CMR (carcinogenic, mutagenic,

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or toxic for reproduction) substances and their regulation in a broader temporal framework.3 This case study tries to bring the comparative approach together with history, understanding national differences from the history. As the carcinogenic and mutagenic effects of synthetic chemicals such as food additives, pesticides, and active agents in medicines came to be better understood, the harmlessness of many common substances, including cyclamates, came into question. While carcinogens became the object of regulation in the 1950s, regulatory measures to prevent mutagenic harm to consumers’ and workers’ health were developed only in the 1970s and 1980s. The US Food and Drug Administration banned the sale of cyclamates in 1969, while other countries, including West Germany, were reluctant to follow the FDA in that decision. The debate is silent today, but a conclusion on the safety of cyclamates was never reached. This undetermined situation was not an exception but exemplifies the problems of mutagen and carcinogen regulation and reflects the characteristics of chemopolitics in the environmental age. For an answer to why the regulation of cyclamates differed in several countries, one must consider the national cultures of regulation: the specificities in terms of regulatory institutions and their relation to industry, of the regulatory body of laws and rules, as well as of health politics, public discourse, and science. Knowledge together with the way knowledge is produced is a key subject for the study of chemopolitics. Knowledge of the detrimental effects of sweeteners was communicated, debated, interpreted, criticized, taken for granted, and addressed in regulatory action. Cyclamates are a good case study to highlight the historic epistemology of this knowledge, that is, the rules and practices of research into health risks.4

Becoming Synthesized—and Tasted Today, molecular modeling plays an important role in sweetener design. In the past, the discovery of sweeteners was a matter of serendipity. Saccharin, cyclamates, and aspartame led the list. Their stories have been repeatedly told in historical approaches and can quickly be reviewed here.5 Saccharin’s sweet taste was discovered when Constantin Fahlberg, working at John Hopkins University with his supervisor, Ira Remsen, in 1879 accidentally spilled some of the substance on his hand. Similarly, Jim Schlatter was working on the

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synthesis of gastric peptides at G. D. Searle & Company when he in 1965 accidentally got some aspartame on his hand; later, as he licked his finger to pick up a piece of weighing paper, he noticed a sweet taste. The sweet taste of sucralose, a chemically modified saccharose (sucrose), was discovered in the 1970s when a foreign student at the Queen Elizabeth College of the University of London, S. P. Phadnis, misunderstood the request to test a compound as a request to taste the compound. Last but not least, in 1937, Michael Sveda, a graduate student working with Ludwig Frederick Audrieth at the University of Illinois, was preparing a series of compounds called sulfamates because they were expected to have interesting pharmacological properties. Sveda noticed the sweet taste on a cigarette he had temporarily laid down on his laboratory bench. He traced the source back to a substance he was preparing, which turned out to be sodium cyclo­ hexyl­sulfamate (sodium cyclamate).6 It is difficult to measure a substance’s degree of sweetness objectively. But relying on the taste of test subjects, saccharin is considered the most powerful of all known sweeteners at about three hundred times sweeter than natural sugar (saccharose, sucrose). Sodium and calcium cyclamates are about thirty times as sweet as sucrose. Though both these salts of cyclohexanesulfamidic acid are obviously significantly less sweet than saccharin, which meant they would need to be used in relatively high concentrations in food industry applications, they have some valuable properties saccharin could not offer: the cyclamates have no bitter aftertaste, even at higher concentrations, and their thermostability is remarkably higher than that of saccharin. These properties made a wide range of applications in the food industry feasible.

Becoming Commercial The introduction of artificial sweeteners was not a success story from the beginning—quite the opposite.7 For a long time, the only sweetener available to replace sugar was saccharin, which had appeared unknowingly to Americans in their carbonated beverages, selected deliberately because it was cheaper than sugar.8 When the substitution was revealed as part of the FDA’s indictments against the industry, Americans rejected the substance en masse. This changed in the early 1950s, when the first wave of “diet” products sweetened with saccharin and cyclamates entered the market. Cyclohexanesulfamidic acid, sodium

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cyclamate, and calcium cyclamate were produced commercially for the first time in the United States. Du Pont had purchased the patent for cyclamates and then sold it to Abbott Laboratories, the first commercial producer of cyclamates, which undertook the necessary studies and submitted a New Drug Application to the FDA in 1950.9 Two years later, after an initial rejection, the FDA approved cyclamates for use as non­ nutritive sweetening agents.10 In the same year, Abbott released sodium cyclamate onto the market, followed by calcium cyclamate, which was considered more pleasant in taste and thus the better dietetic option. As a tabletop sweetener, sodium cyclamate was marketed under the trade name Sucaryl and promoted for use by the obese and diabetics. Sucaryl was actually a mixture of ten parts cyclamate and one part saccharin, which until then had been the most popular sweetener. In contrast to saccharin, cyclamate—because of its great ­thermostability—retained its sweetness even when cooked or baked. As cyclamates cut the bitter aftertaste of saccharin, mixtures of these two sweeteners replaced the one-substance products.11 The advent of cyclamates, which had no undesirable aftertaste, marked a new era in artificial sweeteners and led to the development of a host of artificially sweetened commercial products ranging from canned fruit and chewing gum to toothpaste and mouthwash and other foods—not only in the United States but worldwide. Cyclamates were sold under many trade names, including Asugryn, Dulzor-Etas, HachiSugar, Ibiosuc, Sucaryl Sodium and Sucaryl Calcium, Sucrosa, Sucrun 7, Suestamin, Sugarin, Sugaron, Cyclan, Cylan, Dietil, Natreen, and Succaril (with the latter two containing saccharin) and in several forms: crystalline powders, aqueous solutions, and tablets. In 1963, when the Federal Ministry of Economics (Bundesministerium für Wirtschaft) approved cyclamates for the West German market, they were marketed—with a big initial advertising campaign—as Assugrin feinsüß (the “friendly Swiss cube”) and vollsüß (also containing saccharin), Ilgonetten, Natreen Diätsüße, Süssette, and others.12 In the 1960s, several companies were involved in cyclamate production worldwide, with most of them in the United States (Abbott, the Pillsbury Company, Pfizer, and Miles Laboratories), and others in West Germany, Spain, Taiwan, and Brazil. At the end of the 1960s, annual cyclamate production was estimated at 7,400,000 kilograms, compared with 770,000 kilograms in 1957.13 In the 1950s, artificial sweeteners had been introduced as sugar surrogates for diabetics,14 but cyclamate use boomed with the “diet

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beverage craze.” By the end of the 1950s, cyclamate had become both a sweetener for use by people on special diets and a substance that was added in generally unrestricted quantities to any food—although in some countries such as West Germany cyclamate use was restricted to dietetic food.15 As the fear of heart attacks and the fight against obesity ramped up in the early 1960s, the market for artificial sweeteners increased considerably.16 It was also argued that artificial sweeteners could be preventative against dental caries. The US consumption of cyclamates in 1965 was 53 percent in soft drinks, 17 percent in dry beverage bases, 13 percent in diet foods, and 12 percent in sweetener formulations (e.g., pharmaceutical products).17 Consumption patterns changed over the years as the industry worked hard to include in the market not only elderly people at risk of diabetic complications but also middle-aged adults.18 The German media was especially keen to present superlatives when reporting on US consumption trends, for example, that Americans “swallowed 10,000 tons of cyclamate.”19 Press reports stated that, by the end of the 1960s, 30 percent of US households had used artificial sweeteners versus 10 percent of West German households.20 In consequence, the sugar industry became embroiled in an advertising and promotion race with the diet beverage industry.21 Actually, there was another reason why the food industry used cyclamates more and more as a surrogate for sugar: it was cheaper.22 All this stopped when questions about the safety and cancer-causing potential of cyclamates emerged.

Becoming Questioned and Banned: The United States The Food Additives Amendment of 1958 to the US Federal Food, Drug, and Cosmetic Act included the so-called Delaney clause,23 which said “any chemical additive found to induce cancer in man, or, after tests, found to induce cancer in animals” shall not be approved for use in food. The regulation exempted certain substances, including cyclamates, under the category “generally recognized as safe,” that is, owing to their long-term and widespread use in food, they were considered safe.24 Nevertheless, in the 1960s, the private Food and Drug Research Laboratory began to investigate the effects of cyclamates in rats fed with high doses of a cyclamate-saccharin mixture.25 Some of the results suggested the test rats showed higher incidences of bladder tumors. Pending confirmation of these results, cyclamates continued to be used.

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However, because of concerns about gastrointestinal effects, it was ­suggested in the United States that cyclamate use should be limited to 70 mg/kg body weight per day for adults.26 Around the same time, in 1967, the Joint FAO/WHO Expert Committee on Food Additives set a temporary acceptable daily intake of 50 mg/kg body weight for all cyclamates.27 In 1968, the National Research Council established an ad hoc committee on nonnutritive sweeteners to review the FDRL data. The committee concluded that the cyclamate-saccharin mixture was carcinogenic in the tests conducted.28 The impact of saccharin in the mixtures investigated was not clear at that point. According to an FDA officer, there was a lot of pressure on the FDA at that time, for example, by the consumer protection activist Ralph Nader.29 At that point, Secretary of Health, Education, and Welfare Robert F. Finch decided to restrict the commercial sale and distribution of cyclamates.30 On 21 October 1969, the FDA, citing the Delaney clause, announced it was removing cyclamates from the GRAS list and banning their use in common food and nonprescription drugs.31 It also required cyclamates intended for use in the dietary management of human disease be relabeled to comply with drug provisions of the law; existing stocks had to be withdrawn from the market by 1 January 1970.32 Also, in his “consumer message,” President Richard Nixon ordered the FDA to review the GRAS list to assure the American public that other substances were not subject to safety concerns.33 As with the case of DDT, when the FDA stood almost alone against industry lobbyists, scientists, farmers associations, the Department of Agriculture, and even the Public Health Service, the FDA was strict in basing its cyclamate decision on the Delaney clause.34 The Delaney clause proved to be a pathbreaking regulatory tool the FDA could rely on. Though the law allowed a more relaxed regulation for all noncarcinogenic toxins—setting limit values rather than banning them outright—for carcinogens, evidence from animal studies was sufficient to ban a substance: “No one needed to prove that the quantities in question caused cancer; no one needed to prove that animal studies applied to humans.” The Delaney clause was a “legal expression of precaution” that contrasted with common regulatory models at that time, such as the ADI value, which was based on calculations of tolerable quantities of substances in question to be consumed per day.35 Actually, the ADI was introduced to avoid strict regulatory measures and the total ban of economically useful substances.36

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But still, the FDA’s application of the Delaney clause’s principle of precaution was not unambiguous, since the FDA was not really prompt in banning cyclamates, although there had been hints of their harmful effects for some years.37 Only in 1970 were cyclamates completely taken off the market, after the Medical Advisory Group of the Department of Health, Education, and Welfare concluded they had no therapeutic value in the treatment of obesity or diabetes.38 The FDA determined the continued sale of cyclamate-containing products with drug labeling would not be permitted after August 1970. Cyclamates, once the basis for a billion-dollar industry, would disappear; the artificial sweetener market in the United States belonged once again to saccharin.

Becoming Questioned and Not Banned: West Germany West Germans were familiar with the US debates on food additives from the start. When the German Food Law (Lebensmittelgesetz) was being revised in 1958, the FFDCA revision had some influence on the German discussion.39 The revised food law represented a significant change in German regulatory politics, as all food additives (fremde Stoffe) were banned unless they received special approval as specified in directives following the law—one of them being the Directive on Dietary Substances (Diät-Fremdstoff-Verordnung).40 The legal situation of artificial sweeteners remained unclear, however, since relevant legislation introducing the first legal regulations of food additives dating back to 1939 was still on the books; the Sweetener Law (Süßstoffgesetz) and the Directive on the Marketing of Sweeteners (Verordnung für den Verkehr mit Süßstoffen) became an ongoing point of conflict between federal departments.41 For example, while saccharin was approved immediately, the artificial sweetener dulcin was taken off the list of approved substances, since animal studies revealed carcinogenic risks. However, dulcin’s use in food production was not completely banned because of its earlier approval in the Sweetener Law. The crucial point was that the Food Law did not regulate the use of sweeteners in pharmaceuticals as the Sweetener Law did. Thus, when the German Federal Ministry of Health (Bundesministerium für Gesundheit) reluctantly took steps in 1960 toward an approval of cyclamates for use in special foods and pharmaceuticals only, this fell under the Sweetener Law.42 The German industry had been waiting for approval of cyclamates for years. In fact, the BMWi pressed for a speedy approval in accordance

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with the Food Law and for the abolition of the Sweetener Law, which only complicated the approval processes.43 Thus, arguments in favor of stricter or looser regulation became intermingled with constitutional conflicts within the German government—a common but tiresome situation in West German politics owing to the transition of the former law of the Reich into federal law, which slowed down decisions and legal processes.44 The public debate on cyclamates started in 1968. The German political magazine Der Spiegel reported alarming results derived from studies done by scientists in Austria, Japan, and France.45 Immediately and in reaction, proponents of more liberal regulation accused the sugar industry of steering the discussion to generate public hysteria and protect sugar beet farmers.46 Similarly, in the United States, an alliance between consumer activists and Senator Warren Magnuson from Washington State, with its numerous sugar factories, was suspected.47 Critics of the German sugar industry included physicians and the German Green Cross, the main public relations organization of the pharmaceutical industry.48 Interestingly, both proponents and critics of a more liberal regulation claimed to speak on behalf of consumers: proponents of cyclamate argued that diabetics needed a sugar surrogate, while opponents emphasized the potential danger for the consumer. In 1969, German Federal Minister of Health Käte Strobel, a Social Democrat, moved to restrict the sale and distribution of pure cyclamates (not combined with other sweeteners) to drugstores and restricted the addition of cyclamates to dietetic food; relevant advertisements were banned too.49 At the same time, Strobel insisted no clear evidence revealed carcinogenic effects of cyclamates. Thus, Strobel’s initiative, which was a reaction to public concerns, was in keeping with the precautionary principle. From a legal perspective, however, there was no clear basis for her action. As politicians decided on regulatory action on a caseby-case basis, the decisions were open to backroom negotiations that were corporatist in nature and often ended in more or less reliable “self-restraint” by the industry. Accordingly, Strobel emphasized the recent measures had been taken “together with the manufacturers and distributors of cyclamates.”50 The media criticized the “calculated risk” of the existing situation, since, although cyclamates might help diabetics, it could also endanger their health.51 Not long after the partial sales moratorium was put in place, Strobel attended a lecture by Frederick Coulston, the director of the Institute of Experimental Pathology and Toxicology at the Albany Medical College

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of Union University, who was visiting West Germany. The toxicologist Coulston explained why the precautionary principle was not appropriate for guiding these kinds of decisions. If the principle were applied in this manner, the United States would soon face food shortages and famine because ubiquitous toxins such as aflatoxins or DDT would have contaminated the food supply indirectly.52 Also, the BMG concluded based on an expert report from the Deutsches Krebsforschungszentrum (German Cancer Research Center) in Heidelberg that the carcinogenic studies did not support extensive regulatory actions.53 In consequence, Strobel ultimately abolished the strict restrictions on cyclamates.54 She took the stance that the scientific evidence did not show serious cause for concern. The use of cyclamates in diabetic food became generally allowed. Her contemporaries such as Coulston predicted a similar turn of events for the United States: nobody would renounce the right to use cyclamates when such additives could be shown to serve the public interest, for instance, in the case of diabetics.55 However, Coulston would be proved wrong.

From Carcinogenesis to Mutagenesis The main focus of anxiety about artificial sweeteners was carcinogenicity, although embryotoxic or teratogenic effects were also considered. These concerns reflected recent drug scandals. In the early 1960s, the FDA began to require testing of new substances for effects on reproduction, fertility, and teratogenicity.56 The background was the thalidomide scandal that had hit West Germany severely, whereas the number of affected children was limited in the United States thanks to the courage of an FDA officer who resisted industry pressure.57 The thalidomide scandal was quite present in public consciousness when the debate on cyclamates emerged. The German media immediately raised concerns that cyclamates might be teratogenic.58 In the 1960s, another problem emerged in the scientific and public discourse: the possibility of genetic damage. Cyclamates appear to have been the first chemicals whose potential mutagenic effects became the subject of public concern.59 Of the earliest voices to suggest cyclamates could be mutagenic were Chief of the Genetic Toxicology Branch of the FDA Marvin S. Legator and his coworkers in 1968.60 They injected cyclohexylamine, an intermediate substance in the industrial production of herbicides, antioxidants, accelerators in vulcanization, anticorrosion agents, and other chemical

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substances, into male rats and found damaged chromosomes in their germ cells.61 Cyclohexylamine was considered a likely intermediate of cyclamate catabolism when it was detected in dogs and humans after cyclamate consumption.62 Legator’s work must have served as a valuable support for the agenda of the Environmental Mutagen Society, which was founded in early 1969.63 As one of his first actions, the EMS President Alexander Hollaender, the founder and former director of the Biology Division of Oak Ridge National Laboratory, appointed a committee to review and evaluate existing studies on the mutagenicity of cyclamates (similar committees later studied other substances including mercury, caffeine, the antischistosomal drug hycanthone, and nitrosamines).64 Still, in the same year, the committee pleaded for a cyclamate ban and applied for government funding to hold a conference on cyclamates.65 Also, cyclamates turned out to be the hot topic at the First Annual Meeting of the EMS in March 1970 in Washington, DC.66 Although the mutagenicity data were not a factor in the FDA’s decision to ban cyclamates in late 1970,67 the EMS quickly became a scientific pressure group to foster legal efforts to control environmental mutagens. The “scientist-­activists,” as the historian Scott Frickel describes them (mostly geneticists and toxicologists), who were active in the EMS successfully translated the problems of genetic toxicology into the framework of ongoing toxicological debates. “The most committed scientist-activists promoted their concerns ‘abroad’ in forums devoted to medicine, toxicology, cancer research, radiation research, and reproductive biology and in the NAS.”68 The EMS’s main effort, however, was to push for an epistemic transformation in cancer research and elaborate the interrelationships between mutagenesis and carcinogenesis. This new kind of problematizing of harmful agents becomes obvious in Legator’s words: “Aflatoxin [a toxin from a fungus] is teratogenic, carcinogenic and mutagenic; cyclamate has been shown to induce bladder tumors in addition to its cytogenetic effects; [. . . Consequently,] there are similarities among agents that produce hereditary alterations in the information content or distribution of hereditary material whether the final expression is mutagenic, teratogenic, or carcinogenic.”69 After the EMS was founded, similar efforts were made in other countries. In 1971, the European Environmental Mutagen Society was formed at a scientists meeting in Munich. German geneticists and toxicologists had been discussing the rising threats from mutagens since the late 1950s. Internationally,

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the Deutsche Forschungsgemeinschaft (German Research Foundation) was one of the first science organizations to tackle these threats and, as a result, founded the Central Laboratory for Mutagenicity Testing (Zentrallaboratorium für Mutagenitätsprüfung) in 1969.70 Notably, however, mutagenic threats of cyclamates, despite their prevalence in media reports, were not among the first topics undertaken.71 Only in the mid-1970s did the BMG ask the toxicogeneticists to reevaluate the case of cyclamates in light of evidence from mutagenicity studies.72 This demand was a direct reaction to pathbreaking developments that crossed the Atlantic Ocean to Europe. In 1973, Bruce N. Ames, a biochemistry professor at the University of California, Berkeley, introduced a new assay linking mutagenicity to carcinogenicity. The test relied on four mutant strains of salmonella that Ames’s group had customized for the detection of mutagenicity. Ames showed his test could identify nearly all known chemical carcinogens, and he advocated its use in assessing the cancer risks posed by new substances. Companies immediately adopted the Ames test as a less expensive way to undertake routine chemical screening. For similar reasons, environmental groups were equally enthusiastic: this new generation of “short-term tests” had the advantage of taking less time than carcinogenicity studies relying on mammals.73 However, the value of the Ames test relied on two assumptions. First, as Ames put it, a carcinogen is a mutagen; human cancer, in this view, is caused principally by exposure to environmental mutagens. Second, Ames assumed a microbe was a suitable model organism for assaying mutagenicity, as it occurred in human cells. The success of the Ames test obviously reflected a “convergence of new ideas about genetic damage and cancer” that the EMS scientist-activists promoted.74

The Trickiness of Test Systems As carcinogenicity and mutagenicity came to be equated, there was increasing discussion about the empirical basis of regulatory decisions. Up to then, carcinogenic hazards had been regulated using bans, restrictions, and limit values based on epidemiological data and loose extrapolations from experimental studies. In 1971, when the International Agency for Research on Cancer began a series of monographs on evaluating the carcinogenic risk of chemicals to humans, the assessments of carcinogenicity in humans and experimental animals

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were made separately. No attempt was made to quantitatively estimate carcinogenic risks to humans based on data from experimental animals. Only in 1977 did the IARC begin to change its practice, as human data were available for only forty-eight chemicals at that time. An ad hoc working group drafted guidelines for standardizing the evaluations of carcinogenicity studies in both humans and animals. According to the guidelines, it was reasonable, “for practical purposes,” to regard chemicals for which there was “sufficient evidence” of carcinogenicity in animals as presenting a carcinogenic risk for humans, although the group admitted there was no “scientific basis” for this correlation.75 Obviously, this point of view was questionable. The big promise of Ames’s short-term bacterial test system was that it would provide a simple procedure to detect carcinogens via mutagenicity testing. Though, as the historian Angela Creager showed, the Ames test was established within a few years as a short-term test to distinguish quickly carcinogens and noncarcinogens, its reliability to detect human carcinogens and estimate their potency was not accepted without question.76 With its potential to shape government regulation and policy, critics raised doubts about the test’s basic premise that cancer should be regarded as a disease induced by mutagens.77 To cast doubt on such links and generate contradictory facts was, of course, a focus of the industry and trade associations in those years.78 But toxicologists and cancer biologists also objected to the simplistic assumptions of the new generation of short-term tests, as their endpoints were mutations in bacteria and not tumors in human cells. Saccharin—cyclamate’s “­competitor”— became one of the “best studied and most credible examples” of nongenotoxic carcinogens: substances found to be carcinogens but not mutagens. Even geneticists were skeptical and argued that only mammalian test systems could generate relevant results of a human threat.79 German geneticists in particular doubted the short-term approach, although their own test results on cyclamates could not rule out the possibility that cyclamates were mutagenic and carcinogenic.80 In the following years, more than two hundred different assays for genotoxicity were published.81 National and international agencies became occupied with evaluating and establishing standard test systems. From its establishment, the EMS had focused on this task and organized special committees to recommend standard protocols for mutagenicity testing. In 1970, a methods committee was appointed “to critically assess recommended methodologies and also to recommend and evaluate future research and method development.” A cytogenet-

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ics committee was established the following year to focus on in vitro human cell tests that could be used to screen for chromosome aberrations in humans. This was a response to increasing doubts about the “correlation between human genetic risk and positive mutagenicity in bioassays relying on sub-mammalian systems.”82 Moreover, the question of the effect of low doses exacerbated the genetic testing dilemma. The main problem of the chemical age of mass consumption was chronic intoxication by consuming low doses of hidden toxicants. The common premise of toxicology was that toxins were not dangerous below a certain threshold, but genetics contradicted this premise because ­mutagens—radiation as well as chemicals—could induce mutations even at low doses.83 Hence, unanswered questions about the risks of low doses and chronic intoxication became the obstacles of regulation, even more so when mutagenesis was linked to carcinogenesis. In March 1979, the IARC Working Group on the Evaluation of the Carcinogenic Risk of Chemicals to Humans discussed the evidence concerning cyclamates and saccharin published to date and was “unimpressed” by the relatively large number of experimental studies, most of which were “inadequate” for one reason or another. In general, it found “acceptable criteria of adequacy of experiments for determining carcinogenicity, especially for compounds that are of only moderate or low potency,” lacking.84 This was a reminder that experiments that had shown mutagenic or carcinogenic activity of test substances often required several grams per kilogram body weight to produce visible toxic effects in an acceptable timeframe. Hence, critics turned this fact against the alarmists and pointed out that positive tests required ridiculously high quantities of cyclamates and saccharin, quantities nobody usually would consume.

Evaluation in the Age of Uncertainty: Risk-Benefit Assessment At the end of the 1970s, the regulatory status of cyclamates had not changed significantly. The use of cyclamates as additives in foods and beverages was still banned in most nations, including many European countries such as the United Kingdom, the Netherlands, France, Sweden, Spain, Austria, and communist Eastern Europe. The only countries that did not restrict cyclamates were West Germany, Italy, Norway, Finland,

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Iceland, Ireland, Switzerland, Mexico, Argentina and Brazil, although most of these restricted the use to dietetic products, and some mandated special labeling or specific governmental approval.85 However, cyclamates were reevaluated again and again, since the food additives industry claimed there wasn’t sufficient evidence to justify the ban. In 1973, Abbott Laboratories petitioned the FDA to reapprove cyclamates based on its own studies done in animals.86 To assess these studies, FDA committee members visited key laboratories to validate the experimental methods. Also, in March 1976, the FDA received a report from the National Cancer Institute that said Abbott’s evidence was not sufficient to change cyclamate’s status and did not demonstrate “to a reasonable certainty” that cyclamates were safe for human consumption.87 The FDA asked Abbott to drop its petition, but the company refused. Abbott officials themselves referred to the NCI report, as it also concluded that the evidence so far had not demonstrated cyclamates were carcinogenic.88 In the following years, Abbott pressed its case at hearings before an administrative law judge and in federal courts. A formal FDA hearing was held in 1977, and in 1978, after written and oral testimony, the administrative law judge issued an initial decision that cyclamates remained banned. Another hearing was initiated after that. The final decision on this series of hearings was published in September 1980 when the FDA formally denied Abbott’s 1973 petition for the reapproval of cyclamates. The FDA commissioner concluded: “Cyclamate has not been shown not to cause cancer; and . . . cyclamate has not been shown not to cause heritable genetic damage.”89 This statement sounded long-winded and weak, yet the conclusion was in favor of the enacted ban. As the FDA Consumer commented, the wording of the decision was particularly important because the decision, in essence, conclusively established not that cyclamates were carcinogenic but only that Abbott had failed to demonstrate its safety “adequately.”90 Especially notable about this decision was that, while the question of the cancer-causing potential of cyclamates was the principal reason for the denial, the Delaney clause was explicitly not invoked. Instead, the FDA relied on a new and expansive interpretation of the general safety clause of the FFDCA.91 William Havender, a geneticist and self-designated consultant on environmental carcinogens who notoriously complained about “hysterias” concerning carcinogens, noted this shift of focus with feelings of doom.92 He had been a critic of the Delaney clause and now complained the FDA’s recent move worsened the situation, as it

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turned the burden of proof upside down and placed it entirely on the petitioner: Those who have been urging Delaney’s repeal have been outmaneuvered: For under the Delaney clause, the burden of proof at least was on those who made an affirmative declaration that a substance did cause cancer in animals. This needs no longer be done. All that is needed now is a small reason to raise a suspicion that a substance might cause cancer, and then the burden of proof is on the petitioner to demonstrate that it does not. It is possible that one day we will look back on the Delaney clause with nostalgia.93

This comment and the FDA’s maneuver must be understood in the context of successful criticisms of the Delaney clause. As the challenges of finding adequate systems to test for low-dose and chronic effects became obvious in the 1970s, critics of the Delaney clause became more encouraged to start a new attack on this regulatory edifice. The whole discussion centered on the value and meaning of scientific evidence, especially the meaning of knowledge that is uncertain. From a skeptical viewpoint, one might object that all knowledge is uncertain, but to specifically mark knowledge as uncertain makes a difference. The latter was the case in the times of regulatory crises and with the risk concept grasping for cultural hegemony in the 1970s.94 The ongoing problems with carcinogenicity testing called the established approval regime into question: the lesson of all the radiation and toxicogenetic studies was that it is very hard to be certain whether low doses of radiation or toxins induce mutations or cancer. Those who wished to be extra cautious would favor the general extension of the Delaney clause and the precautionary principle that had guided the regulation of carcinogenic substances in the United States since the late 1950s. The EMS, for example, argued the Delaney clause should be extended to cover mutagens and teratogens.95 In contrast, the industry went all out to revise it. Its solution was to reframe the knowledge problem within the language of risk and risk-benefit assessment, as this reframing was the technical condition to weigh health risks and economic benefits. Those wishing to avoid strict regulations—as the industry preferred—would favor a regime of risk-benefit assessment. In the industry’s calculus, this assessment would settle the debates: “Industry lawyers argued that qualitative judgments of potential harm from chemicals known to cause cancer in animals were ‘unscientific’

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and ‘unbalanced,’ for they failed to account for benefits from economic growth.”96 The historian Nancy Langston has emphasized the major impact of a US Supreme Court decision made in the year the FDA rejected Abbott’s petition. In 1980, qualitative methods such as those implicit in the Delaney clause, which assumed any dose of an animal carcinogen was probably also a human carcinogen, were ruled insufficient to support regulation. In other words, the decision demanded quantitative risk assessment become the legal basis of regulatory action. How risk assessment would be used in regulatory discourse, however, was ambiguous. Not only the industry but also toxicologists and even some environmentalists favored quantitative risk assessment, although for different reasons.97 Yet, the FDA seemed to make an effective maneuver in the case of cyclamates when it deliberately avoided using the Delaney clause to elude the problems arising from the Supreme Court decision and instead referred to the safety clause, demanding the industry come up with clearer evidence that cyclamates were not carcinogenic. Havender said this “change in policy” would allow “the agency leeway to weigh benefits against risks, and to take the exaggerated conditions of animal cancer tests into consideration when estimating human risks— that has permitted the FDA unexpectedly to revise its application of this provision in a much more stringent and unreasonable manner.”98 This critique was certainly right in one point: reframing regulation based on risk and risk assessment solved the problem of evidence but not by making knowledge certain again. The great mutation researcher Charlotte Auerbach, who, in the 1940s, was of the first to demonstrate the mutagenic impacts of chemicals, expressed the difficulty arising from this situation: estimating “risk is a dangerous procedure, because it will create the impression that our conclusions are meaningful, whereas in reality they are so full of uncertainties as to be practically meaningless.”99

Reevaluation in the Age of Risk: Promoters of Cancer The next round of regulatory reevaluation of cyclamates was not long in coming. During the process, it became clear how genetic data had grown in importance for assessing carcinogenicity over the years, although its actual value for regulation remained somewhat uncertain.100 Whether the Supreme Court decision on the precautionary principle served to

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encourage Abbott is unclear, but in 1982, the company once more petitioned the FDA for approval of cyclamates as a food additive. Again, Abbott argued that new results from animal tests strengthened the claim that cyclamates were not carcinogenic. Hence, Abbott cast doubt on a crucial reason for the ban on cyclamates: its alleged mutagenicity and the evidence that mutagenic studies would prove carcinogenicity. In the Ames test and similar short-term tests, cyclamates had been shown to be inactive as a gene mutagen. Only tests for chromosome anomalies in mammalian cells could be regarded as positive, but these were difficult to interpret in terms of carcinogenicity. An internal FDA cancer assessment committee reviewed the data and drew a conclusion different from that reached by the FDA commissioner in 1980: “The collective weight of many experiments . . . indicates that cyclamate is not carcinogenic.”101 At this point, in November 1983, the FDA requested the NRC, the action arm of the National Academy of Sciences, to reevaluate the data.102 In 1984, the NRC committee held a public meeting at the NAS in Washington, DC, to obtain the views of scientists, the food industry, and agencies responsible for regulation. The subsequent report published in 1985 acknowledged the conclusions of the former assessments but introduced a new, important aspect into the considerations. First, the NRC committee pointed out the FDA had asked it to focus exclusively on carcinogenicity, although it had observed other adverse effects such as testicular atrophy that would need to be considered in detail in the overall evaluation of cyclamates for widespread use. Second, the NRC committee concluded no clear epidemiological or experimental evidence proved cyclamates or cyclamate-saccharin mixtures increased the risk of cancer, confirming the FDA cancer committee’s most recent assessment; however, the NRC emphasized two studies with rodents that suggested cyclamates possessed tumorpromoting and cocarcinogenic activity, that is, cyclamates might intensify the effects of other carcinogens in the production of cancer, data that could be consistent with negative results for cytogenetic activity in short-term tests and hinted at more complex mechanisms of carcinogenicity.103 The NRC’s conclusion referred to arguments that some agencies had brought forward since the late 1970s as they struggled with the criteria for assessing carcinogenicity testing and animal bioassays. The IARC, especially, warned that caution must be used in using short-term tests. Even when negative results were obtained, it argued, it was “not clear

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that they could be used reliably to predict the relative potencies of compounds as carcinogens,” since the available tests “do not detect all classes of agents that are active in the carcinogenic processes (e.g., hormones, promoters).” Hence, IARC experts suggested the need to consider the possible importance of cancer promoters, which may not cause tumors but instead promote their development, when analyzing the role chemicals play in causing human cancer.104 Also, they recommended the extension of tests to include all tissues and organs from test animals. Up to then, the most widely used test technique was the surgical insertion of a test substance into the bladder of mice. Obviously, the IARC’s suggestions did not support a quick and simple methodology, namely short-term tests, but instead argued for a comprehensive approach. As such, they marked a shift in carcinogenicity testing as well as in cancer research to “multiple factors,” each of which might play a different role in initiating or facilitating a particular step or steps in the carcinogenic process.105 This shift was clear to the actors in the cyclamate case, the NRC itself, Abbott Laboratories, and the media, which reported on the panel held in June 1985. The New York Times headline read: “Panel Suggests Role of Cyclamate in Cancer May Be an Indirect One.”106 The NRC committee chairman said its members “spent a lot of time” examining studies suggesting a role of cyclamates in cancer promotion: “We felt these were studies we can’t fault scientifically that do indicate that cyclamates can be a promoter of bladder cancer in rats. You cannot ignore those studies.” Abbott’s vice president was pleased with the NRC’s conclusions, except the findings that cyclamate could act as a cancer “promoter” or “cocarcinogen.” According to the Los Angeles Times, he said it was “speculation,” adding that committee members “didn’t know what they were talking about.”107 The shift toward promotion processes and complex factors of carcinogenesis was not only significant in how concepts of carcinogenesis changed rapidly in the 1970s and 1980s. It also gives a clue as to how regulation and risk knowledge might have adapted to each other. The introduction of “multiple factors” affecting carcinogenesis could be traced to the introduction of the rationale of risk to regulation. Hence, the approach of risk assessment simply involves quantifying several risk factors that would describe a situation in terms of probability. Likewise, to redirect cancer research to the detection of factors of carcinogenesis meant abandoning the search for the cause of cancer and instead describing the process of carcinogenesis as a set of facilitating events.

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This shift was not the final act in the history of carcinogenesis testing, but it was the last decisive one in the story of cyclamates. After the NRC report, all sides claimed victory, although nothing seemed certain. Organizations such as the Calorie Control Council representing the low-calorie food and beverage industry continued to claim this and subsequent evaluations, including by the FAO/WHO Joint Expert Committee on Food Additives and the EU Scientific Committee for Foods, concluded that cyclamates are not carcinogens.108 From the perspective of regulatory agencies, however, these studies reveal that the case is still open. “Cyclamate does not have a clean bill of health with respect to the cancer issue, in our opinion,” the NRC committee chairman concluded before the microphones of the media in 1985. The committee called for the replication of animal studies that suggested the sweetener could promote cancer in the presence of known cancercausing substances. It also noted other adverse health effects had been associated with cyclamates, such as gene damage and testicular atrophy, and said these problems “would need to be considered in detail in the overall evaluation of cyclamates for widespread use.”109 Likewise, the FDA announced that further studies were under way and that no decision on cyclamates was likely before 1986. In the end, cyclamates never received a final judgment and remain banned from food products in the United States. Currently, the Abbott Laboratories petition is held in abeyance and not under active consideration.110 However, the international map of cyclamate bans changed after the last big reevaluations of the 1980s. In contrast to the 1970s, most countries came to permit cyclamate use, although in Germany and the rest of the European Union, some restrictions applied: cyclamates cannot be used to sweeten ice cream, bonbons, or chewing gum.

Summary of a Story with an Open End The story of cyclamates is also the story of the development of mass consumption societies and their problems: the commercial boom of artificial, nonnutritive sweeteners was connected to the unprecedented rise of the food industry and food additives. The industry developed new products, invented new methods of distribution, and envisioned new consumer habits. Artificial sweeteners became a product between the pharmaceutical market for diabetics and the general market for low-calorie food. Quite a number of actors were involved in the debates

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on the benefits and risks of these new products: industry, associations, agencies, media, politicians, and scientists, all claiming to speak for the interests of the consumer. As such, the cyclamates story mirrors quite well the growing concerns about health hazards from the late 1950s on and adds a more food-centered perspective, since our collective memory seems to highlight pollutants such as DDT and adverse drug effects. In general, this development was similar in the two countries compared in this case study, the United States and West Germany, although there were differences in the most prominent problems: DDT in the United States and thalidomide in West Germany. Nevertheless, these debates touched on similar problems at a more fundamental level, as all these substances called into question common principles of toxicology and hence characterized a major, long-ranging shift in the risk episteme. Scientists became convinced that even low doses of radiation and chemicals would result in genetic mutations, teratological effects, or carcinogenesis; moreover, chronic intoxication and intake would allow adverse effects to accumulate. As scientists drew attention to the dangers of genetic toxicity, they warned of the “dysgenic” impact of chemical mutagens, which implied the accumulation and perpetuation of defective or disadvantageous genes and traits in offspring of a particular population so, in short, would cause genetic degeneration. Some even became scientist-activists. “Similarities, however, are overshadowed by differences in the legal frameworks and cultural styles for regulating.”111 This conclusion, a reference to the comparison of drug regulations in the United States and West Germany, applies as well to the regulation of food additives. In Germany, the debate on cyclamates and sweeteners occurred within neo-corporatist arrangements among organized interest groups.112 Since German consensus-based politics protected regulatory authorities from public criticism and sheltered expert opinion behind closed doors, the public cyclamate debate ended quickly and never forcefully reappeared. West German consumer organizations also seemed to change their focus over the decades, turning more in the 1970s and 1980s to environmental pollution than to food additives. The striking difference in this story lies in the legal regulations. The 1969–1970 FDA ban on cyclamates was a disaster for cyclamate producers, since only a minority of countries worldwide, among them West Germany, continued to permit cyclamates. One explanation for the different regulatory results could be that the sugar industry lobby was more powerful in Washington, while the pharmaceutical industry

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was more powerful in Bonn. Still, the legal framework was likely the cause here, not the effect. The FFDCA and the German Food Law were both revised in the 1950s, but the German law did not incorporate the precautionary principle in any way comparable to the Delaney clause. This difference in legal recognition explains why the BMG was reluctant to act on carcinogenic risks while the FDA became the trustee of the precautionary principle—at least in those years. Owing to this legal difference and to a cultural bias, German scientists and civil servants were more concerned with the dysgenic impact of mutagens rather than carcinogenic effects. This problematization was a reminder of eugenic concerns—although they were difficult to address in public. In the US context, the genetic problem became absorbed by concerns about carcinogenesis in the 1970s. Interestingly, US consumer groups began to refer to the dysgenic impact of cyclamates when it proved unlikely that cyclamates are carcinogenic. These national differences were not unusual and remind us that the internationalization of chemical regulation was in its infancy. Consumers keen for foods or pharmaceuticals containing cyclamates had only to cross the border from the United States into cyclamateliberal Canada. However, the situation was just the other way around for the artificial sweetener saccharin, whose troubles began in 1977, when a Canadian scientist first identified it as a possible carcinogen. The Canadian Ministry of Health reported the data to the WHO and moved unequivocally for a ban on saccharin. The FDA decided the study results met the criteria mentioned in the Delaney clause and proposed banning saccharin.113 This plan generated a public outcry, the “saccharin rebellion,” as the historian Carolyn de la Peña has referred to it.114 “In a compromise,” the Saccharin Study and Labeling Act prevented the ban but listed saccharin on the US National Toxicology Program’s Report on Carcinogens.115 Consequently, saccharin was banned in Canada but permitted in the United States, although a warning label was required: “Use of this product may be hazardous to your health. This product contains saccharin which has been determined to cause cancer in laboratory animals.”116 The cyclamate story is also an example of the epistemic and regulatory impact of test systems.117 One toxicologist said the ongoing debate on the FDA cyclamate ban “is the most extreme divergence of views on a single set of evidence.”118 The comment sheds some light on the huge problems of carcinogenicity testing and regulation. Actually, the assessment of carcinogenic activity turned out to be a story of ­scientific

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crises. Toxicological studies originally designed to provide yes-no answers could not provide certain results and became controversial the more the Delaney clause was applied.119 Also, the low-dose paradigm called for new solutions.120 The Ames test was such an attempt to rescue certainty in the fiercely contested field of carcinogenesis. The Ames test’s boundary work made it feasible to use mutagenicity testing for the experimental assessment of carcinogenicity. However, the approach of short-term tests became controversial and was eventually superseded by models of quantitative assessment that would permit conclusions on the real dangers for humans that are more exact. Though the risk assessment approach still reflected a technocratic dream of control, it produced subversive effects on the regulatory system.121 In fact, the enduring uncertainty about low-dose effects was in striking contrast to the promises of risk assessment. This became even more problematic in times of growing public distrust in science. The new question was who should actually decide what risks are acceptable. Scientists themselves pledged more and more to delegate ultimate responsibility to society and to risk-benefit assessment. This was especially the case where the regulatory regime had been based on closed-door negotiations, as in West Germany. Thus, politically, different interests supported the move toward quantitative risk assessment but primarily those opposed to the precautionary principle of the Delaney clause. They argued that quantification of risks would show the carcinogenic potency of some chemicals is so low that it has no real significance in the human population (the principle of negligible harm or the de minimis principle).122 Altogether, the scientific and political uncertainties resulted in a dynamic of ongoing reevaluation and reinterpretation of data, as well as of transformation of regulatory principles and methods.123 Those involved were driven to look repeatedly for new evidence or more data that are relevant. The rationale of risk assessment was quite productive in this respect, as it aimed to distinguish an ever-increasing number of risk factors. Hence, in the late 1970s and the 1980s, carcinogenesis was redefined to include cancer-promoting effects. This redefinition opened up a new field of evidence and testing practice. It remains an open question, though, whether this redefined regulatory language resulted from cancer research or, vice versa, whether regulation determined a new era in the epistemology of carcinogenesis.

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Acknowledgments Special thanks for numerous helpful comments and suggestions go to Angela Creager. The German Research Foundation supported part of the research for this chapter under the project “Mutations and Mutagens: Biological and Risky Things in the Analytics of Biopolitics.” Alexander von Schwerin is Research Scholar at the Max Planck Institute for the History of Science. His work addresses many aspects of the history of the life sciences and biomedicine and historical epistemology, focusing on the genealogy of risk and the history of regulation and, recently, on science activism within the environmental movement. His most recent book, Strahlenforschung (2015), is on risk regulation and radiation biology in Germany. On these subjects, he also edited, with Heiko Stoff, a special issue on the regulation of food additives in Technikgeschichte 81, no. 3 (2014) and wrote the article “Low Dose Intoxication and a Crisis of Regulatory Models” (Berichte zur Wissenschaftsgeschichte, 2010) and the chapter “From Agriculture to Genomics: The Animal Side of Human Genetics and the Organization of Model Organisms in the Longue Durée,” in Human Heredity in the Twentieth Century (2013). Notes 1. Walters et al., Sweeteners, ix. 2. Brickman et al., Controlling Chemicals. 3. See, e.g., Stoff, Gift; Boudia and Jas, Toxicants; Boudia and Jas, Powerless Science; Frickel, Chemical Consequences. 4. For the concept of risk episteme, see Schwerin, “Low Dose,” 403–4. 5. See Roberts, Serendipity, 150–52; Walters et al., Sweeteners, ix; Walters, “Rational Discovery,” 1–2. For a different perspective on “serendipity” that focuses on the dispute on who could claim for patents, see Warner, “Ira Remsen,” 52–54. 6. Roberts, Serendipity, 151. 7. For an early history of the commercialization of saccharin, see Warner, “Ira Remsen.” 8. Peña, “Just Like a Peach,” 214. For this early story, see Peña, Empty Pleasures, 19. 9. For the commercial history, see NRC, Evaluation, 4. 10. Pines, “Cyclamate Story,” 20; Packard, Processed Foods, 33.

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11. Kreutzig, “Cyclamate,” 413, 415. 12. “Freundliche Würfel,” Der Spiegel, 10 June 1968, 126; Wirtschaftliche Vereini­ gung Zucker e.V. to BMWi, 30 June 1965, BArch, B 189, 1172, pp. 104–7. 13. IARC, Sweetening Agents, 62. 14. Pines, “Cyclamate Story,” 20. 15. Lecos, “Sweet and Sour,” 8. 16. NRC, Evaluation, 12. 17. IARC, Sweetening Agents, 63. 18. In the 1980s, scientific reports emphasized that there was no “racial” difference in consumption, but a strong gender component, with women being far ahead in the consumption of artificially sweetened soft drinks. NRC, Evaluation, 13–15. 19. “Bedenkliche Süße,” Der Spiegel, 27 October 1969, 223. 20. “Freundliche Würfel,” 126. 21. Pines, “Cyclamate Story,” 20. 22. Randow, “Cyclamat.” For an early history of the use of artificial sweeteners, see Peña, Empty Pleasures, chaps. 3–4. 23. For the Delaney committee and its outcomes, see Davis, Banned, 116–52. 24. IARC, Sweetening Agents, 63; cf. Pines, “Cyclamate Story,” 20; Hutt, “Regu­ lation,” 200–204; Packard, Processed Foods, 50–53. 25. NRC, Evaluation, 10. For a detailed chronology of the debate, see Pines, “Cyclamate Story” (FDA perspective); Packard, Processed Foods, 332–36 (industry perspective). 26. NRC, Evaluation, 4; Pines, “Cyclamate Story,” 25. 27. This recommendation was repeatedly lowered in the following years to an ADI of 4 mg/kg body weight. IARC, Sweetening Agents, 63. 28. Pines, “Cyclamate Story,” 25. 29. Ley, “History,” 20. 30. FDA Officer Herbert L. Ley recalls this personal decision. Ibid., 21; see also Pines, “Cyclamate Story,” 26. 31. Havender, “Science,” 19. 32. IARC, Sweetening Agents, 63. 33. Hutt, “Regulation,” 203. 34. For DDT, see Böschen, Risikogenese, 153; Davis, Banned. 35. Langston, Toxic Bodies, 82. 36. Jas, “Adapting,” 58–62. 37. Böschen, Risikogenese, 155n; cf. Packard, Processed Foods, 190. As was the case for diethylstilbestrol, the FDA was reluctant to pursue regulation. Langston, Toxic Bodies, 106–208. 38. NRC, Evaluation, 11. 39. Stoff, “Hexa-Sabbat,” 67. 40. Sperling, Kampf, 296. 41. Verordnung zur Veränderung der Verordnung über den Verkehr mit Süßstoffen: Begründung, BArch, B 142/4386, f 176; BMG to other federal

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ministries, 6 August 1962, BArch, B 142/4387, f 11; for preservative regulation since the 1930s, see Sperling, Kampf. 42. BMG, BArch, B 142/4387, f 9, 19. 43. BMWi to BMG, 3 September 1962, BArch, B 142/4387, f 22–23. 44. Cf. Bundesministerium des Innern to BMG, 20 September 1962, BArch, B 142/4387. 45. “Freundliche Würfel.” 46. Zöllner to Manger-Koenig, BMG, 19 December 1968, BArch, B 189/1175, p. 1. 47. Jungmann, “Zyklamat-Alarm,” 175–76. 48. Randow, “Bittere Kunde.” 49. BMG, Mitteilung für die Presse, 22 October 1969, BArch, B 189/1175, p. 2. 50. Extract from protocol: Deutscher Bundestag – 6. Wahlperiode – 9. Sitzung, 6. November 1969, Antworten erarbeitet von Referent Neussel (II B 4), BArch, B 189/1175, pp. 288–89. 51. Rainer Flöhl, “Das kalkulierte Risiko,” Frankfurter Allgemeine Zeitung, 27 October 1969, BArch, B 189/1175, p. 297. 52. Coulston, “Verantwortung,” 18. 53. Neussel to MP Gerhard Jungmann, 3 December 1970, BArch, B 189/1175, p. 3. It has been suggested that the differences in the toxicological test results were due to differences in the manufacturing processes of the involved companies. An intermediate (2-cyclo-hexen-1-on), which emerged only in the “American,” not the “German,” manufacturing process, was suggested to be responsible. Leitenberger, Was Sie schon immer, 117. However, I could not confirm this hint. 54. Randow, “Bittere Kunde.” 55. Coulston, “Verantwortung,” 18. 56. NRC, Evaluation, 10. 57. For the United States, see Langston, Toxic Bodies, 90–95. The West German government was more reluctant in its reaction and in demanding concrete testing. Daemmrich and Krücken, “Risk,” 510; Daemmrich, Pharmacopolitics, 39; Kirk, Contergan-Fall, 179–82. 58. Neussel, BMG: remark, 21 June 1968, BArch, B 189/1175, p. 1; “Bedenkliche Süße.” 59. Prival and Dellarco, “Evolution,” 47. 60. Pines, “Cyclamate Story,” 26. 61. Randow, “Cyclamat.” 62. Pines, “Cyclamate Story,” 25. Today, cyclohexylamine is listed as a very toxic substance. NCBI, “Cyclohexylamine.” 63. For the EMS, see Frickel, Chemical Consequences, 2. 64. Ibid., 127. 65. Epstein et al., “Wisdom”; Wassom et al., “Reflections,” 751. 66. Röhrborn und Schoeller: Bericht über das “First Annual Meeting” der Environmental Mutagen Society in Washington D.O., 22.–25. March 1970, DFG, Az 6037, Sonderkommission Mutagenität, Ordner 5, pp. 2–5.

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67. Prival and Dellarco, “Evolution,” 47. Whether and how the competition between Ames and Legator affected the FDA’s decision not to use mutagenicity data when it banned cyclamate is unclear. Angela Creager, personal communication. 68. Frickel, Chemical Consequences, 68, 94. 69. Legator 1970, cited in ibid., 95. 70. Schwerin, “Low Dose,” 404–6; for the West German early toxicogenetics, see also Schwerin, “Vom Gift”; Schwerin, “Mutagene Umweltstoffe.” 71. Flöhl, “Kalkulierte Risiko”; “Bedenkliche Süße.” 72. Anlage cited in in Maier-Leibnitz an Mitglieder des Hauptausschusses, 5 January 1977, HUA, Acc 12 95-40, 12. 73. Creager, “Political Life.” 74. Ibid., 53. 75. IARC, Chemicals and Industrial Processes, 3. 76. Cf. Creager, “Political Life,” 54–55. 77. Creager, “Making Mutations,” 13–22. 78. Proctor, Cancer Wars, 101–3; Langston, Toxic Bodies, 15. 79. Ashby, “Origins,” 55. Mammalian test systems were also controversial as in the case of experiments showing carcinogenic activity of artificial sweetener in the bladder of rats. There was some evidence that the formation of crystals was responsible for the bladder cancer in rats. Cohen and Ellwein, “Cell Growth,” 130–31. However, as the bladder metabolism of rats is quite different from that of humans, doubts arose that the results could be transferred to the digestion of sweeteners in humans. 80. “Erbschäden,” 251; see also Schwerin, “Low Dose,” 407–9. 81. Ashby, “Origins,” 54. 82. Frickel, Chemical Consequences, 127. 83. Boudia, “From Threshold,” 85–86. 84. IARC, Sweetening Agents, 33. 85. Ibid., 39–50. 86. Havender, “Science,” 20. 87. Lecos, “Sweet and Sour,” 9. 88. NRC, Evaluation, 11. 89. Ibid., 4. 90. Lecos, “Sweet and Sour,” 10. 91. Havender, “Science,” 18. 92. Cf. Havender, “EDB,” 13. 93. Havender, “Science,” 30. 94. Cf. Bächi, “Zur Krise,” 430–32; Schwerin, “Low Dose,” 409–11; Boudia, “From Threshold,” 83–85. 95. Frickel, Chemical Consequences, 127. 96. Langston, Toxic Bodies, 113. 97. Ibid., 114. 98. Havender, “Science,” 31.

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99. Auerbach, “Effects,” 8. 100. The evaluation of saccharin is another example. An IARC report emphasized that “any evidence of its interaction with cellular macromolecules such as DNA and protein, either by itself or after suitable metabolism” was absent. Actually, the new IARC guiding criteria established to evaluate “carcinogenic risk” of chemicals to humans included mutagenicity from 1978 on. The IARC admitted, however, that mutagenicity testing was not yet ripe to guide final decisions as the present state of knowledge did not permit the selection of a specific (short-term) test as the most appropriate. IARC, Sweetening Agents, 34, 23–24. 101. NRC, Evaluation, 12. 102. Ibid., vii, 4–5, 12. 103. Ibid., 2, 3. 104. IARC, Chemicals, Industrial Processes and Industries, 10. 105. IARC, Sweetening Agents, 33. 106. Boffey, “Panel.” 107. Cimons, “Cyclamate.” 108. Ibid.; Takayama et al. “Toxicity,” 38; CCC, “International Regulatory Status.” 109. Cimons, “Cyclamate.” This was in line with claims of the consumer organization, the Community Nutrition Institute, Ralph Nader’s Health Research Group, and the National Consumers League. Boffey, “Experts”; Boffey, “Diet Sweetener”; Boffey, “Panel.” 110. FDA, “High-Intensity Sweeteners.” 111. Daemmrich, Pharmacopolitics, 20. 112. Cf. Daemmrich and Krücken, “Risk,” 507. 113. Kamrin, “Toxicology,” 74–75. 114. Peña, Empty Pleasures; Peña, “Just Like a Peach,” 218–19. 115. Stolberg, “Panel.” 116. Roth and Lück, “Saccharin-Saga,” 420. In 2010, saccharin’s delisting from the Report on Carcinogens led to legislation repealing the warning label requirement. NIH, “Artificial Sweeteners and Cancer.” 117. For the impact of monitoring systems on DDT research and regulation, see Böschen, Risikogenese, 105–92. 118. Boffey, “Diet Sweetener Risk.” 119. The GRAS regime included the definition of safety as “reasonable certainty in the minds of competent scientists that the substance is not harmful.” Packard, Processed Foods, 53. 120. Boudia, “From Threshold,” 86. 121. Though there is a vast literature on the history of the risk concept, the invention of risk assessment as a method to compare and evaluate risks and benefits has not been well studied that thoroughly yet. See, e.g., Steel, “Extrapolation”; Langston, Toxic Bodies; Boudia, “From Threshold”; Davis, Banned. 122. Kamrin, Toxicology, 78.

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123. Cf. Creager, “Making Mutations.” The role of uncertainty in this story reminds science and technology studies (STS) and history of science of its omissions: “The vast majority of published STS research is about knowledge production, not the non-production of knowledge.” Frickel, “Absences,” 87.

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Cohen, Samuel M., and Leon B. Ellwein. “Cell Growth Dynamics and DNA Alterations in Carcinogenesis.” In Suresh H. Moolgavkar, ed., Scientific Issues in Quantitative Cancer Risk Assessment. Boston, 1990, 118–35. Coulston, Frederick. “Verantwortung von Wissenschaft, Wirtschaft und Regierung bei der Beurteilung der Sicherheit von Chemikalien und Arzneimitteln erläutert an den Beispielen Thalidomid, Cyclamat, Glutamat, Pestizide u. a.” Pharma International 2 (1970): 12–23. Creager, Angela N. H. “Making Mutations Useful: The Development of In Vitro Tests for Carcinogens in the 1970s.” Presented at the workshop “The Making of Useful Knowledge,” Max Planck Institute for History of Science, 30–31 October 2014. _____. “The Political Life of Mutagens: A History of the Ames Test.” In Powerless Science?​Science and Politics in a Toxic World, edited by Soraya Boudia and Nathalie Jas, 46–64. New York, 2014. Daemmrich, Arthur A. Pharmacopolitics: Drug Regulation in the United States and Germany. Chapel Hill, NC, 2004. Daemmrich, Arthur A., and Georg Krücken. “Risk versus Risk: Decision-Making Dilemmas of Drug Regulation in the United States and Germany.” Science as Culture 9, no. 4 (2000): 505–34. Davis, Frederick Rowe. Banned: A History of Pesticides and the Science of Toxicology. New Haven, CT, 2014. Epstein, Samuel S., Joshua Lederberg, Marvin Legator, Arthur H. Wolff, and Alexander Hollaender. “Wisdom of Cyclamate Ban.” Science 166, no. 3913 (1969): 1575. “Erbschäden und Krebs durch Chemikalien: Ein Bericht aus dem Zentrallabor für Mutagenitätsprüfung.” Umschau 77 (1977): 250–52. FDA (US Food and Drug Administration). “High-Intensity Sweeteners.” Last updated 11 January 2018. Frickel, Scott. “Absences: Methodological Note about Nothing, in Particular.” Social Epistemology 28, no. 1 (2014): 86–95. _____. Chemical Consequences: Environmental Mutagens, Scientist Activism, and the Rise of Genetic Toxicology. New Brunswick, NJ, 2004. Havender, William R. “EDB and the Marigold Option.” Regulation, January/ February 1984, 13–17. _____. “The Science and Politics of Cyclamate.” Public Interest 71 (1983): 17–32. Hutt, Peter Barton. “Regulation of Food Additives in the United States.” In Food Additives, edited by Alfred Larry Branen, P. Michael Davidson, Seppo Salminen, and John A. Thorngate, 198–226. New York, 2002. IARC (International Agency for Research on Cancer), ed. Chemicals and Industrial Processes Associated with Cancer in Humans. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans S1. Lyon, 1979. _____. Chemicals, Industrial Processes and Industries Associated with Cancer in Humans. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans S4. Lyon, 1982.

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_____. Some Non-nutritive Sweetening Agents. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans 22. Lyon, 1980. Jas, Nathalie. “Adapting to ‘Reality’: The Emergence of an International Expertise on Food Additives and Contaminants in the 1950s and the Early 1960s.” In Toxicants, Health and Regulation since 1945, edited by Soraya Boudia and Nathalie Jas, 47–69. London, 2013. Jungmann, Gerhard. “Zyklamat-Alarm im Zwielicht wirtschaftlicher Interessen.” Der Diabetiker 5 (1970): 175–76. Kamrin, Michael A. Toxicology: A Primer on Toxicology Principles and Applications. Chelsea, MI, 1988. Kirk, Beate. Der Contergan-Fall: Eine unvermeidbare Katastrophe?​Zur Geschichte des Arzneistoffs Thalidomid. Stuttgart, 2004. Kreutzig, Lothar. “Cyclamate.” In Handbuch Süßungsmittel: Eigenschaften und Anwen­dung, edited by Gert-Wolfhard von Rymon-Lipinski and Hubert Schiweck, 413–24. Hamburg, 1991. Langston, Nancy. Toxic Bodies: Hormone Disruptors and the Legacy of DES. New Haven, CT, 2010. Lecos, Chris. “The Sweet and Sour History of Saccharin, Cyclamate, and Aspar­ tame.” FDA Consumer 15, no. 7 (1981): 8–11. Leitenberger, Bernd. Was Sie schon immer über Lebensmittel und Ernährung wissen wollten. Norderstedt, 2013. Ley, Herbert L. “History of the U.S. Food and Drug Administration.” Interview by Ronald T. Ottes and Robert A. Tucker, Rockville, MD, 15 December 1999. https://www.fda.gov/media/80939/download. NCBI (National Center for Biotechnology Information). “Cyclohexylamine.” PubChem Compound Database, accessed 15 February 2019. http://pubchem. ncbi.nlm.nih.gov/compound/7965. NIH (National Cancer Institute). “Artificial Sweeteners and Cancer.” Reviewed 10 August 2016. https://www.cancer.gov/about-cancer/causes-prevention/risk/ diet/artificial-sweeteners-fact-sheet. NRC (National Research Council). Evaluation of Cyclamate for Carcinogenicity. Washington, DC, 1985. Packard, Vernal S, Jr. Processed Foods and the Consumer: Additives, Labeling, Standards, and Nutrition. Minneapolis, MN, 1976. Peña, Carolyn de la. Empty Pleasures: The Story of Artificial Sweeteners from Saccharin to Splenda. Chapel Hill, NC, 2010. _____. “Just Like a Peach: Visions of Nature in U.S. NutraSweet Marketing.” Technikgeschichte 78, no. 3 (2011): 211–30. Pines, Wayne L. “The Cyclamate Story.” FDA Consumer 8, no. 10 (1974): 19–27. Prival, Michael J., and Vicki L. Dellarco. “Evolution of Social Concerns and Environ­mental Policies for Chemical Mutagens.” Environmental and Mole­ cular Mutagenesis 14, no. S16 (1989): 46–50.

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Proctor, Robert N. Cancer Wars: How Politics Shapes What We Know and Don’t Know about Cancer. New York, 1995. Randow, Thomas von. “Bittere Kunde für Süßstoff-Hersteller.” Die Zeit, 4 September 1970, 47. _____. “Ist Cyclamat gefährlich?​” Die Zeit, 13 December 1968, 31. Roberts, Royston M. Serendipity: Accidental Discoveries in Science. New York, 1989. Roth, Klaus, and Erich Lück. “Die Saccharin-Saga.” Chemie in unserer Zeit 45, no. 6 (2011): 406–23. Schwerin, Alexander von. “Low Dose Intoxication and a Crisis of Regulatory Models. Chemical Mutagens in the Deutsche Forschungsgemeinschaft (DFG), 1963–1973.” Berichte zur Wissenschaftsgeschichte 33, no. 4 (2010): 401–18. _____. “Mutagene Umweltstoffe: Gunter Röhrborn und eine vermeintlich neue eugenische Bedrohung.” In Das Heidelberger Institut für Humangenetik: Vorgeschichte und Ausbau (1962–2012), edited by Anne Cottebrune and Wolfgang U. Eckart, 106–29. Heidelberg, 2012. _____. “Vom Gift im Essen zu chronischen Umweltgefahren. Lebensmittel­ zusatzstoffe und die risikopolitische Institutionalisierung der Toxikogenetik in  der Bundesrepublik, 1955–1964.” Technikgeschichte 81, no. 3 (2014): 251–74. Sperling, Frank. “Kampf dem Verderb” mit allen Mitteln?​Der Umgang mit ernährungsbezogenen Gesundheitsrisiken im “Dritten Reich” am Beispiel der chemischen Lebensmittelkonservierung. Stuttgart, 2011. Steel, Daniel. “Extrapolation, Uncertainty Factors, and the Precautionary Principle.” Studies in History and Philosophy of Biological and Biomedical Sciences 42, no. 3 (2011): 356–64. Stoff, Heiko. Gift in der Nahrung: Zur Genese der Verbraucherpolitik Mitte des 20. Jahrhunderts. Stuttgart, 2015. _____. “Hexa-Sabbat: Fremdstoffe und Vitalstoffe, Experten und der kritische Verbraucher in der BRD der 1950er und 1960er Jahre.” NTM: Zeitschrift für  Geschichte der Wissenschaften, Technik und Medizin 17, no. 1 (2009): 55–83. Stolberg, Sheryl Gay. “Panel of Experts Rebuffs Effort to Absolve Saccharin.” New York Times, 1 November 1997. Takayama, Shozo, Andrew G. Renwick, Sonny L. Johansson, Unnur P. Thorgeirsson, Massahiro Tsutsumi, Dan W. Dalgard, and Susan M. Sieber. “Long-Term Toxicity and Carcinogenicity Study of Cyclamate in Nonhuman Primates.” Toxicological Sciences 53, no. 1 (2000): 33–39. Walters, D. Eric. “The Rational Discovery of Sweeteners.” In Walters et al., Sweeteners, 1–11. Walters, D. Eric, Frank T. Orthoefer, and Grant E. DuBois, eds. Sweeteners: Discovery, Molecular Design, and Chemoreception. Washington, DC, 1991. Warner, Deborah J. “Ira Remsen, Saccharin, and the Linear Model.” Ambix 55, no. 1 (2008): 50–61.

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Wassom, John S., Heinrich V. Malling, K. Sankaranarayanan, and Po-Yung Lu. “Reflections on the Origins and Evolution of Genetic Toxicology and the Environmental Mutagen Society.” Environmental and Molecular Mutagenesis 51, nos. 8–9 (2010): 746–60.

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CHAPTER 6

Cadmium Poisoning in Japan Itai-itai Disease and Beyond Masanori Kaji†

Cadmium-containing ores are rare in nature, with greenocite (cad-

mium sulfide) being the only major cadmium mineral.1 This mineral is almost always associated with sphalerite (zinc sulfide), the main zinc ore in Japan.2 Cadmium is located just below zinc in the periodic table, and its properties are similar to those of zinc. Most cadmium in nature occurs as atomic substitution for zinc in zinc minerals and is produced as an associate product when zinc ores are reduced.3 The Kamioka mine, one of Japan’s richest zinc mines, is located in the upstream region of the Jinzū River, a major river running through the Toyama Plain (fig. 6.1).4 The basin, located in central Honshu, Japan’s main island, has been one of the most fertile rice-producing areas since the Middle Ages. Kamioka was first developed in the seventeenth century as a silver, copper, and lead mine (fig. 6.2).5 After the Meiji Restoration in 1868, which marked the beginning of the Westernization of Japan, the Mitsui Group purchased it.6 By 1889, Mitsui had purchased all the pits and the operation rights of the Kamioka mine and at first continued to mine for silver, copper, and lead. When Japan finally adopted a gold standard system instead of traditional bimetallism in 1897, the price of silver dropped dramatically. Many silver mines, including Kamioka, were in financial crisis. During the Russo-Japanese War (1904–1905), the import of zinc metal for iron-alloy production, especially for military use, started to increase. In 1905, Mitsui began to mine zinc in Kamioka.7 At first, Japan exported zinc ore (sphalerite) and imported zinc metal, because the country had no smelting facilities. Zinc ore was initially separated based on density differences, but after 1909, zinc minerals began to be separated using surfactants and wetting agents

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Figure 6.1  Map of the polluted area in the Jinzū River basin of the Toyama Plain, used with permission from the annual inspection group to which the author belonged.

(froth flotation).8 To produce zinc metal in Japan, Mitsui decided to introduce German zinc-ore smelting processes in 1910. In 1912, in Ōmuta (Fukuoka Prefecture), Mitsui built zinc-ore smelting facilities and started producing zinc metal for export the next year—the first

Cadmium Poisoning in Japan  213

Figure 6.2  The Jinzū River basin and the location of the Kamioka mine, used with permission from the annual inspection group to which the author belonged.

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company in Japan to do so.9 When World War I started, demand from abroad for zinc as a military material increased dramatically, as did the demand from the shipbuilding industry inside Japan, so smelting facilities in Ōmuta were expanded until 1917. Zinc-ore roasting (i.e., the conversion of sulfide minerals into oxide) started in Kamioka in 1913 and was greatly expanded during World War I.10 In the 1920s, the Kamioka mine became one of the largest zinc producers in Japan.11 The introduction of improved froth flotation processes helped increase zinc production, but some of the fine, powdered, cadmium-containing mineral particles produced in the frothing process escaped and floated down the river. These fine particles were then easily oxidized into ions, which were in turn readily absorbed by plants and humans.12 The waste from the Kamioka mine increased sharply during the 1930s, when the war with China created a significant demand for zinc production. Farmers and peasants who used the water of the Jinzū River for agriculture, and anglers who fished those same waters, noticed a decrease in crop yields and fish catches so established an association for fighting mining pollution in 1932. During World War II, unskilled workers replaced the skilled miners who had been drafted. The result was a decrease in yield along with an increase in waste, which was dumped into the Jinzū River. Damages to rice production and the fishery industry rose noticeably. After the discovery of cadmium by Friedrich Stromeyer in Germany in 1817, it remained an important producer of this metal. By World War I, Belgium, England, and the United States had also started producing it.13 In Japan, some mines tried producing cadmium from zinc ore around 1917 and 1918 but stopped because of the low demand. Cadmium was at first used for pigments and as a component in low-melting alloys. The first cadmium production for industrial use in Japan began in 1929 in a zinc smelting work in Aizu (Fukushima Prefecture) by Nippon Soda Co. Several zinc smelters followed.14 At the Kamioka mine, cadmium was simply discarded as waste into the Jinzū River. Mitsui started extracting cadmium as part of the zinc production process in the Kamioka mine only after 1947. Since Kamioka was one of the richest zinc mines in Japan until its closure in 2001, it also became one of the largest cadmium producers, producing 10 to 15 percent of cadmium in Japan in the first half of the 1980s.15 In the 1960s and 1970s, Japan enjoyed a period of very high economic growth but suffered from various forms of pollution such as air, water, noise, and mining. Pollution-related diseases became a matter of public

Cadmium Poisoning in Japan  215

concern. Itai-itai disease, caused by a severe type of cadmium poisoning resulting from the pollution of rice fields, was one such disease. The liquid waste of the Kamioka mine of the Mitsui Mining & Smelting Co. (hereinafter Mitsui Kinzoku) was eventually identified as the cadmium source. The number of patients suffering from itai-itai between 1910 and 2007 has been estimated at four hundred.16 Notably, most of them were women, most likely because of their generally lower body weight, less dense bones, and physiology, which specifically amplifies the uptake of cadmium and therefore the amount of damage it causes.17 The affected residents, and the victims, began suing polluters in an attempt to make their complaints public and receive compensation for the damages. This was one of several important lawsuits in the 1970s known as the “four major pollution-related lawsuits”: itai-itai disease, Minamata disease, Niigata Minamata disease, and Yokkaichi asthma.18 All victims, including those of itai-itai, filed and won a suit against the companies that caused the damages. However, only in the case of itaiitai disease did the victims succeed in making the polluting company bring the pollution almost completely under control, which was rare in Japan.19

The Discovery of Itai-itai Disease and Its Causes: The Roles of Three Experts Even though itai-itai disease was named and identified in the 1950s, the Ministry of Health and Welfare (MHW) announced on 8 May 1968 that its first patients are estimated to have appeared as early as the 1910s in the Jinzū River basin in Toyama Prefecture.20 Shigejiro Hagino (1885–1943), a local physician, was one of the first to notice this unfamiliar disease, characterized by severe pain in all parts of the body, around 1935 and correctly suggested mining pollution was its cause. The Hagino family were prestigious and influential local landholders and, for generations, had been physicians.21 Noboru Hagino (1915–1990), Shigejiro’s son, served in the army as a doctor soon after graduating in 1940 from the national Kanazawa Medical University, not far from Toyama. He returned to his home village in March 1946 from China, where he had served as an army doctor. He inherited a local clinic from his father, who had passed away in 1943, before his return. Soon after World War II, Kanazawa Medical University researchers reported itai-itai disease, initially thought to be a rheumatic disease

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with no connection to mining waste problems, in a medical journal. The forty-four patients studied, mostly women, averaged 57.7 years of age. A group of doctors from a Tokyo rheumatology institute conducted a more thorough medical study of the disease in 1955, in which Noboru Hagino participated as a local doctor, unaware of his father’s earlier observations and not anticipating any connection with pollution from the mine. The Toyama Shimbun, a local newspaper, named the syndrome itai-itai (“it hurts, it hurts”), since it was very painful, and the patients, mostly women over thirty-five years, often cried out. The study concluded the disease was not rheumatic but rather a kind of osteomalacia.22 Nobuo Hagino, like other physicians, at first thought overwork and malnutrition caused the disease but soon realized all the patients lived and worked near the midstream region of the Jinzū River, in an area irrigated by river water. Therefore, he began to consider mining pollution from the Kamioka mine located upstream as a potential cause. In 1957, Hagino reported to an academic society that heavy metals, especially zinc, caused the disease, basing his conclusions on experimental work on the cause of diabetes by Kozo Okamoto (1908–1993) of Kyoto University in 1952.23 Okamoto had proved that zinc-chelating agents such as oxine (8-hydroxyquinoline) caused diabetes, but Hagino thought Okamoto had proved that zinc caused diabetes. Since most itai-itai patients showed proteinuria (presence of an excess of proteins in the urine) or glycosuria (excretion of glucose into the urine), Hagino guessed that zinc caused itai-itai disease. This was wrong, because Okamoto had proved that oxine, not zinc, caused diabetes. Oxine prevents zinc from binding to insulin, which plays an important role in sugar metabolism. Naturally, other researchers heavily criticized his report. Hagino’s guess that mining pollution was a possible cause of the illness was right, but he could not show sufficient evidence to persuade researchers, who believed the disease was caused by malnutrition, overwork, and lack of sunshine in the winter. Kin-ichi Yoshioka (1902–1990), an agronomist, developed Hagino’s hypothesis into well-founded arguments and proposed that cadmium was the causative agent of the disease.24 In 1948, two organizations with the same name, the Jinzū Mining Pollution Prevention Council (JMPPC), were established: one led by heads of local administrations, and the other by heads of agriculture cooperatives. Japan has a history of conflict between large mining companies and groups of farmers and fishermen from the early twentieth century in various parts of the

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country.25 It was not unusual for companies to financially compensate complaining groups in damaged areas. After negotiating with residents issuing complaints, the Kamioka mine compensated them every year from 1949 to 1954.26 Meanwhile, the two mining pollution prevention councils merged in 1951, and the new organization demanded compensation from Kamioka. In 1955, the three parties (the JMPPC, Toyama Prefecture, and the Kamioka mine) agreed on the amount of compensation, which was to be revised every five years.27 In 1960, the next compensation agreement was concluded, with less money being issued. In September 1958, Yoshioka, a well-known expert on agricultural flood damage, had happened to visit the Jinzū River to conduct research on flood and agricultural damage caused by mining pollution. In August 1960, the Fuchū-machi branch of the JMPPC commissioned him to carry out a full survey of the agricultural damage, aiming to find stronger evidence against the Kamioka mine, which had tried to reduce compensation to the victims in every possible way. Yoshioka decided to extend his study to include other forms of possible biological damage, including itai-itai, which was still a local disease of unknown cause. Using an epidemiological study, he, with Hagino’s help, plotted the locations of known itai-itai patients on a map, clearly demonstrating the disease appeared in those places irrigated by the Jinzū River. He asked Jun Kobayashi (1909–2001), an analytical chemist at Okayama University, to analyze the metal content of the water, soil, vegetables, and animals, as well as the patients’ organs; the results showed an unusual abundance of cadmium.28 Kobayashi noticed a correlation between the annual increase in the number of patients and the increased production of zinc ore at the Kamioka mine. He also surveyed medical papers to find similar cases of chronic cadmium poisoning in various countries.29 In June 1961, in his report to the head of the Fuchū-machi branch of the JMPPC, Yoshioka concluded that itai-itai disease was caused by cadmium discarded by the Kamioka mine.30 At the same time, he reported these results, with Hagino, at a medical society’s scientific meeting.31 Kobayashi helped detect cadmium in the samples sent by Yoshioka and Hagino. He developed specific heavy metal analysis techniques, using spectroscopy and polarography to advance the study of itai-itai disease.32 These three experts—Hagino, Yoshioka, and Kobayashi—with their different backgrounds, played decisive roles in identifying the cause of itai-itai disease.

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Central and Local Administrations and Itai-itai Disease: “Inventing” the Precautionary Principle The central government and local authorities were not very responsive to the itai-itai disease victims. At the end of 1961, Toyama Prefecture set up a special committee for the prevention of local diseases, the first of this kind on itai-itai disease by a local authority. The committee made a list of patients and surveyed them by questionnaires to reinforce the malnutrition theory of the disease and dispel the idea that mining pollution was the cause. The Toyama Prefecture administration was trying to promote industrialization in the middle of the Jinzū River basin in the late 1950s and feared the presence of a pollution-related disease like itai-itai disease would deter enterprises from coming to the region. In 1963, government-funded research groups were established under the auspices of the MHW and the Ministry of Education to look into the matter. In January 1967, one such joint research group admitted cadmium was a cause of the disease but claimed other causes were possible.33 Victims were disappointed by this unclear conclusion and in March 1968 filed a case against the government and the responsible company, Mitsui Kinzoku. However, on 8 May 1968, the MHW announced the disease was caused by cadmium poisoning and that the only possible source of it was the effluent coming from the Kamioka mine owned by Mitsui Kinzoku This was the first time a government ministry mentioned the mine as the source of pollution. Michio Hashimoto (1924–2008) played a key role in changing the ministry’s attitude. Hashimoto belonged to the first generation that was aware of new approaches in public health. He was born in Osaka, graduated in 1948 from Osaka University’s medical school, and worked as a doctor in the Osaka Prefecture Public Health Center. He was sent first to study for a year at the MHW National Institute of Public Health (which ended up recruiting him in 1957) and then, in 1954, to study public hygiene (a master’s course) for a year at the Harvard School of Public Health. The MHW was beginning to realize the need for a new approach to industrialization and urbanization, so it created a pollution department and appointed Hashimoto as its first head.34 In the spring of 1967, a Kanazawa Medical University research group showed a correlation between the condition of patients and their use of the Jinzū River water, as well as the degree of cadmium pollution of the soil. As head of the MHW pollution department, Hashimoto insisted

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the public administration act based on available scientific evidence but not wait for conclusive scientific proof to avoid taking action too late to prevent or fix a problem.35 Minister of Health and Welfare Sunao Sonoda (1913–1984) accepted his opinion and announced the Kamioka mine’s responsibility as the source of cadmium pollution. This could be considered one of earliest government decisions in Japan based on what later became known as the precautionary principle.

The Resident Movement and the Itai-itai Disease Trials: Cadmium vs. Nutrition Mining damage to agriculture occurred much earlier than human health damage as manifested in itai-itai disease. As early as 1890, sulfur dioxide gas from roasting furnaces (used to reduce sulfur content and heavy metal powder dust) caused damage in the area surrounding the Kamioka mine. From 1896, agricultural and fishery damage became a problem in the midstream and downstream areas of the Jinzū River. The Jinzū River Mining Pollution Prevention Union, established around 1932, asked the prefectural administration to analyze the river water and demanded Mitsui Kinzoku build facilities to prevent mine waste from polluting the river.36 As mentioned, the JMPPC was established soon after World War II to counter the pollution in the villages downstream of the Jinzū River. Although the council paid attention to agricultural damages, it did not look at the effects of pollution on humans.37 After Hagino and Yoshioka reported at a 1961 academic meeting that well-founded research had shown the cause of itai-itai disease to be cadmium discarded by the Kamioka mine, the prefectural and central governments established several research groups. The locals, including Hagino, expected the authorities to provide justice.38 However, the MHW and Ministry of Education joint research group presented inconclusive evidence and mentioned the possibility of cadmium as the cause of the disease only in passing, which disappointed the patients, who expected conclusive results from governmental research. Young, local leaders in the polluted areas, together with Hagino, realized they had to act themselves to solve the problem. In November 1966, the Itai-itai Disease Residents’ Association (IDRA) was established in the Kumano district of Fuchū-machi (Toyama Prefecture), the most-polluted area with a high concentration of patients. The IDRA aimed to obtain relief for patients, a free supply of clean water, remediation of polluted soil,

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and clarification of the company’s responsibility for the disease.39 The association members tried to negotiate directly with the Kamioka mine several times in the summer of 1967 on the issue of compensation for dumping the polluted effluent, but the company denied the charge, saying there was no scientific proof of any causal relationship between the company’s activity and the disease. A Kamioka mine representative even said the company would willingly compensate every incident of damage if official institutions would confirm the responsibility of the “world-renowned” large company, Mitsui, for the disease.40 In the 1960s, several acute cases of pollution-related disease appeared in Japan and attracted nationwide attention. Minamata disease, a neurological syndrome caused by severe mercury poisoning, was the most famous. The disease was first discovered in Minamata (Kumamoto Prefecture, southern Japan) in 1956 and was caused by methylmercury found in the industrial waste from the Chisso Corporation chemical factory in Minamata. In June 1965, patients with a similar mercury poisoning syndrome, referred to as the second (Niigata) Minamata disease, were found in near the Showa Denko chemical plant in Niigata Prefecture (neighboring Toyama Prefecture). The victims and residents organized an association in August, as they were unhappy with the government’s belated action. The association filed a suit against Showa Denko in June 1967, as the first of four major pollution-related lawsuits.41 Some IDRA members participated in the site inspection in October 1967 and identified the need for a lawsuit. At the end of 1967, the IDRA held a meeting in Fuchū-machi to discuss a lawsuit. Two young lawyers from Toyama Prefecture, Tatsuru Shimabayashi (1933–2016) and Jun-ichi Matsunami (*1930), attended.42 After vacillating for some time, the IDRA, with the help of these lawyers, decided to file a lawsuit against the Mitsui Kinzoku in January 1968. Shimabayashi asked for the help of his fellow lawyers in the large, liberal Japan Young Lawyers Association. Matsunami gained the support of local lawyers, not only those with leftist or liberal tenets but also those with conservative beliefs, including the respected and influential Kinosuke Shoriki (1904–1980), whose uncle Matsutaro Shoriki (1885–1969) was the president of Yomiuri Shimbun, a conservative, national newspaper with the largest circulation in Japan. This connection would prove helpful for winning the lawsuit, as it brought on board conservative and respected persons like Kinosuke Shoriki to counterbalance the largely antigovernment and leftist activist leanings of the other members.

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On 9 March 1968, fourteen victims, as well as fourteen family members of deceased victims, filed a suit against Mitsui demanding 61 million yen for pain and suffering. This group was the first to represent patients and the bereaved from polluted towns. If this court fight went well, other victims would follow suit. In all, 236 lawyers, mostly young and inexperienced but passionate and hardworking, were involved in the suit. Twenty worked on the suit full-time and attended every session of the court; Shoriki became the head of this group of lawyers. One of these lawyers, Chuko Kondo (1932–2013), moved to Toyama from Tokyo and set up his permanent office in front of the Toyama railway station, which became a center for the court fight. Some lawyers, including Shimabayashi, followed him and moved to Toyama. These moves helped gain local support. The suit was one of the largest pollution lawsuits in Japan’s history. Mitsui, one of Japan’s largest monopoly capital groups, employed the most prestigious lawyers and even once tried to hire Kinosuke Shoriki. When Shoriki declined, Mitsui asked him not to engage in the suit.43 After thirty-six pleadings and four on-site examinations of the mine, the itai-itai disease plaintiffs won their first case in June 1971. In the lawsuit, four experts attested in support of the plaintiffs: Noboru Hagino and Jun Kobayashi, two of the main discoverers of the cause of the disease, as well as Arinobu Ishizaki, a Kanazawa Medical University professor, and Saburo Fukai, a geologist and professor at the University of Toyama. Only the director of the Kamioka mine hospital testified for Mitsui as an expert. Particularly notable is that the court concluded, based on the epidemiological evidence, a causal relationship existed between the disease and the liquid waste of the Kamioka mine of the Mitsui Kinzoku—the first judicial decision based on epidemiological evidence in Japan.44 In March 1970, one year before the court’s verdict, the Supreme Court of Japan gathered judges who had been engaged in pollution-related lawsuits, and they studied the causal relationships in such lawsuits.45 They decided proof based on epidemiological evidence was adequate in principle and that if an offending company was unable to disprove the plaintiff’s claims, a court should decide in favor of the plaintiff.46 One must also note that mining law, which permits liability without fault, was applied in the case of itai-itai disease. Therefore, the plaintiffs did not have to prove the company’s fault and intent—only that the Kamioka mine discarded waste polluted with cadmium into the Jinzū River.47 In contrast, civil law was valid in the case of Minamata

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­ isease, which meant the plaintiffs had to prove the defendant company d purposely caused the damage, making the case very difficult to win. Mitsui appealed to a higher court, with Jugoro Takeuchi (1922–1998), a Kanazawa Medical University professor, testifying for Mitsui. Takeuchi had once explained the function of cadmium in causing itai-itai disease. He now denied his own theory and claimed vitamin D deficiency was the cause. His former theory was crucial for the plaintiffs’ victory in the suit, and persuading the judges he had been wrong would be a fatal blow for the victims. However, Matsunami, one of two young lawyers who played a key role in starting the lawsuit, cross-examined Takeuchi and disproved his new argument.48 Interestingly, Takeuchi later wrote an evaluation on the relative merits of the cadmium hypothesis and the vitamin D deficiency hypothesis in a 1978 collection on itai-itai disease.49 Naturally, he sided with the latter and criticized the former, saying there is no epidemiological basis for the cadmium hypothesis. The Japanese researchers in the collection were members of a government-funded committee for reinvestigating the causes of the disease, most of whom supported the non-cadmium hypothesis and one of whom explained the cadmium hypothesis as follows: “Based on findings of proteinuria (an excess of serum proteins in the urine), glucosuria (that of glucose), aminoaciduria (that of amino acids), and the manifestation of osteomalacia (softening of the bones) in the itai-itai disease patient, it is claimed that tubular impairment (of kidney) is first caused by cadmium and then the bone change is manifested as an adult form of the Fanconi syndrome” (a disease of the kidney in which proteins, glucose, and amino acids pass into the urine instead of being reabsorbed).50 We do not know why Takeuchi denied his own theory in favor of Mitsui. One possible explanation would be Mitsui’s pressure and inducement. Even though his deficiency theory did not change the court’s decision, it played a certain role in the mining industry’s later resistance to the ruling, including the creation of the reinvestigation committee.51 Takeuchi was one of many whose “expertise” was used to maintain the status quo of the ruling system and who were rewarded with a high position.52 The Kanazawa branch of the Nagoya High Court did not admit any further witnesses Mitsui proposed, and it dismissed the appeal on 9 August 1972 after only twelve pleadings. The case ended in favor of the plaintiffs. The Mitsui Group did not appeal further. The court’s final decision was that itai-itai disease was caused by cadmium discarded by the Kamioka mine and that Mitsui was responsible for compensat-

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ing the victims for all the damages, as well as for remediation of the contaminated soil. By the morning of 10 August 1972, the day after the court’s decision, negotiations between the itai-itai disease victims and the company started in Mitsui’s headquarters in Tokyo. After an eleven-hour confrontation, the company admitted the disease was caused by cadmium and other heavy metals discarded by the Kamioka mine owned by Mitsui and thereafter pledged to refrain from disputing the court’s judgment. Mitsui also admitted its responsibility in the six other itai-itai lawsuits by other groups of patients. The company also agreed to compensate not only all the plaintiffs of the litigating groups but also all the sufferers of the disease, including those who were under medical observation pending diagnosis of the disease. Mitsui also agreed to compensate for all agricultural damage and restore the polluted soil.53 One of the most important victories was a pollution control agreement (PCA) between Mitsui and the victims.54 Under the terms, the victims (the IDRA), with experts, had the right to enter and inspect the mines and factories at the company’s expense at any time and whenever the association considered it necessary. Mitsui was obligated to release data on pollution at the association’s request and do its best to fulfill the IDRA requirements to improve its facilities to prevent further pollution. Soon after the IDRA was first organized, association representatives had gone to the Kamioka mine to demand inspections had always been denied entrance. The mine did not allow inspection until the court ordered it to do so in November 1968. Even then, association representatives and their experts were not able to complete their inspection of the mine because Mitsui refused to cooperate.55 Therefore, the right to enter and inspect the factory was the one of the most important victories resulting from the lawsuit.

A Post-trial Pollution Prevention Program: Collaboration between Experts and Citizens On 16 November 1972, a group that included representatives of the victims’ group, lawyers, and scientists inspected the Kamioka mine for the first time under the PCA. Even though the company’s employees were more cooperative than before, some tension remained between the victims and the company.56 The second annual inspection (6–8 August 1973) was carried out more systematically. The inspection group made

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a list of items that would be investigated for each facility in the mine and demanded the company prepare the necessary data beforehand. The group was divided into five subgroups, each in charge of the inspection of a certain part of the mine. Subsequent annual inspections followed the model set by this second inspection.57 For the first several years, constant antagonism existed between the IDRA and the company. Each year, the association carried out a full inspection of the mine and always in a strained atmosphere. The company broke its promise to improve its facilities more than once. Local residents from polluted areas and environment-conscious people from all over Japan with various backgrounds, including researchers, university professors, schoolteachers, and students, participated in the inspections.58 Based on the PCA, a full inspection of the mine has been conducted every year since 1972. I participated in the twenty-eighth annual inspection of the mine in August 1999. By 2011, when the fortieth annual inspection was held, the number of residents who had participated totaled six thousand, and experts two thousand.59 The Mitsui Group paid 280 million yen for residential inspections and additional research by outside experts from 1972 to 2010. The company also invested 21.3 billion yen for pollution preventive measures based on advice by IDRA experts in the same years.60 From 1974 to 1978, at the IDRA’s request, a research project on the mine and the river was carried out with the cooperation of many universities in Japan and produced comprehensive reports on reducing pollution.61 The reports proposed some measures by which Mitsui’s management could prevent pollution, and the company started to issue an annual report on the preventive measures undertaken at Kamioka mine against mining pollution. After an annual residential inspection of the mine, the meeting between the mine representatives and participants of the inspection is held, during which the residents ask questions and demand various measures to prevent further pollution. In earlier days, the meeting was held under a tense atmosphere and always lasted until almost midnight. However, after a few years, the atmosphere of the post-inspection meetings became more friendly and sympathetic, and a constructive relationship with the company was formed. The company’s attitude has gradually changed, for several reasons. For one thing, the IDRA experts, who were lawyers, university professors, and researchers in public institutions, cooperated with residents in the polluted areas and gained more expertise in pollution control than was possessed by the company’s own mining engineers. They were thus

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able to give appropriate advice on improving the facilities. For example, a special inspection in 1977, conducted by the experts with IDRA members, found a source of cadmium pollution leading from the zinc smelting plant to the underground drains.62 These continuous efforts of outside experts helped the residents trust the company. The second factor in the company’s changing attitude toward inspections was a change in Japanese society itself. In the 1980s and especially the 1990s, people became more environmentally conscious. Companies that were not “green” could not survive: environmental consciousness appealed to the public and could even be profitable for companies.63 Kamioka was, until recently, one of the few mines in Japan large and wealthy enough to continue its operations. Only in June 2001 did it finally close. Today, the company continues to refine and smelt imported ores from overseas mines, using the remaining facilities at Kamioka. The continuous inspections of forty years resulted not only in greatly reduced pollution outflow and improved mining facilities but also in the development of an unprecedented cooperative relationship between victims and the company. The total amount of cadmium discarded decreased from 35 kg/month in 1972 to 5 kg/month in 1997 and to 3.8 kg/month in 2010, and the mean concentration of cadmium in the mine effluent fell from 9 ppb in 1972 to 1.5 ppb in 1996 and 1.2 ppb in 2010. Improved dust collection reduced the total amount of cadmium discharged in smoke from more than 5 kg/month in 1972 to 0.4 kg/ month in 1997 and 0.17 kg/month in 2010.64 To prevent further pollution of the once polluted but now restored agricultural land, the mean concentration of cadmium was limited to 0.1 ppb, the background level. This aim was finally attained in 1996 and resulted in almost negligible cadmium outflow.65 In May 1998, the International Conference on Itai-itai Disease, Environmental Cadmium Pollution and Countermeasures was held in Toyama, in which well-known cadmium-poisoning researchers from abroad participated and presented their papers,66 including Lars Friberg, who had been working on the health effects of cadmium for fifty years.67 In the first edition of Cadmium in the Environment (1971), Friberg, of the Karolinska Institute, had already discussed itaiitai disease, concluding: “We have no doubts that the Itai-itai disease is a manifestation of chronic cadmium poisoning.”68 This conference gave an opportunity for foreign scholars to increase their knowledge about cadmium poisoning, especially itai-itai disease, in Japan and for Japanese researchers to see it in international comparative perspectives.

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Post-trial Cadmium Production and Use in 1960s Japan: Environmental Problems Continued As mentioned earlier, Mitsui started to extract cadmium as part of the zinc production process in the Kamioka mine only after 1947 for production of cadmium yellow (cadmium sulfide). In the next year, the Kamioka mine started to produce cadmium for other uses, including alloy components, electroplating, plastic stabilizer, and batteries.69 Around 1970, the general industrial use of cadmium dropped sharply in Japan, because the industry realized its danger after the four major pollution-related lawsuits, including the one on itai-itai disease. Since then, cadmium has been used mainly in (especially nick-cadmium) batteries.70 The source of cadmium also changed from domestic production to import.71 After the 1980s, the major source of cadmium contamination changed from mines or factories to city waste, which contained discarded batteries (especially NiCd batteries, because they are only partly recycled in Japan). One researcher on environmental problems in Kamioka estimated the amount of cadmium flown out of the mine from 1889 to 1972 to be 854 metric tons but that the cadmium in city waste could have been about 1,206 tons a year at the end of the 1990s.72 Even though the cadmium-poisoning problem in mines was basically solved, problems remained in the form of city pollution. Another concern is cadmium in rice, since rice is the staple diet for the Japanese.73

Conclusion This chapter has described the production and poisoning problem of cadmium in Japan, focusing mainly on itai-itai disease, caused by pollution from the Kamioka mine, the richest zinc mine in Japan, which produced cadmium as a byproduct. Itai-itai disease was first noticed in the Jinzū River basin in Toyama Prefecture in central Japan around the 1930s. However, it was not identified as a cadmium poisoning disease until the 1960s. A local physician, with cooperation from outside experts, confirmed the disease was caused by pollution from the Kamioka mine of Mitsui Kinzoku, located in the upstream region of the river. In the mid-1960s, the victims of itai-itai disease filed a suit against the company; they won their case in 1972. The victims received com-

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pensation and signed a pollution control agreement with the company. The case of itai-itai disease is a rare example of successful pollution control in Japan, because the ensuing forty years of annual inspections, based on the PCA, now show a reduction in cadmium concentrations in the river to natural levels. This case study not only described cadmium production and poisoning in Japan but also, by analyzing the roles of various experts involved, has contributed substantially to understanding the nature of expertise and the significance of public participation in resolving environmental problems. Cadmium poisoning is not an issue of the past, however. New patients with itai-itai disease continue to be found even now. After exposure to cadmium in their youth, patients develop the disease as they age.74 Cadmium poisoning caused by mining pollution has been brought under control, but the metal is still present, now in the form of city waste, and the cadmium content of rice is still higher than normal. Masanori Kaji† was Professor of the History of Science at the Tokyo Institute of Technology. His research interests included history of chemistry in Russia and in Japan, and environmental history. He wrote, in Japanese, Mendeleev’s Discovery of the Periodic Law of Chemical Elements (1997) and Mendeleev: The Discoverer of the Periodic Law of Elements (2007). He also contributed “Riko Majima and the Formation of Research Tradition in Organic Chemistry in Japan” (in Japanese) to Essais d’histoire de la pensée scientifique au Japon moderne (2011). The American Chemical Society Division of the History of Chemistry awarded his article “D. I. Mendeleev’s Concept of Chemical Elements and the Principles of Chemistry” (Bulletin for the History of Chemistry, 2002) the 2005 Outstanding Paper Award. His last book, Early Responses to the Periodic System (edited with Helge Kragh and Gabor Pallo, 2015), was published shortly before he passed away on 18 July 2016 at the age of sixty. See Yasu Furukawa, Ernst Homburg, and Elena Zaitseva, “Obituary: Professor Masanori Kaji (1956–2016),” Chemical Intelligence: The Newsletter of the Society for the History of Alchemy and Chemistry 17 (2017): 22–25.

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Notes   1. This is a revised and extended version of Kaji, “Role.”   2. Nakanishi et al., Kadomiumu, 45.  3. Daintith, Oxford Dictionary, 91.   4. Iwamoto, “Restoration,” 180.   5. Kurachi, “General Research.”   6. The Mitsui family of merchants founded Mitsui in the seventeenth century. After the Meiji Restoration, the family established the Mitsui Group in 1872, which was reorganized into Mitsui Bank, Japan’s first private bank, and Mitsui Bussan, a trading company, in 1876. These two companies, with Mitsui Mining, established in 1888, became the core enterprises of one of the largest corporate conglomerates (zaibatsu) in modern Japan. “Mitsui,” in Japan: An Illustrated Encyclopedia (Tokyo, 1993).   7. Kurachi et al., Mitsui, 41.  8. Matsunami, Kadomiumu, 85–87. This is the most comprehensive and ­readable book that analyzes every aspect of itai-itai disease and related ­cadmium poisonings in Japan. It was first published in 2002 as Itai-itai byo  no kioku [The memory of itai-itai disease] with about 230 pages. However, the book was revised and expanded, eventually becoming a 600page encyclopedia. Matsunami lists 195 officially designated victims of itai-itai disease between 1967 and 2007 and says about 200 victims must have died before 1967, when the official system of certification of victims was initiated.  9. The Ōmuta refinery was later renamed Miike. Kurachi et al., Mitsui, 45–46. 10. Ibid., 62–63. 11. Japan took advantage of the absence of European powers in Asia during World War I to expand its influence in Asia and the Pacific. It enjoyed an economic boom and unprecedented prosperity, and 1910 to 1920 marked a turning point for the Japanese economy. Mitsui produced about 48 percent of Japan’s zinc metal after 1925. Matsunami, Kadomiumu, 88. The Kamioka mine produced 57 percent of all zinc ore mined in Japan in the first half of 1950. Yamada, “On the Lead Mining,” 46. 12. Kurachi et al., Mitsui, 81. 13. Ullmann, Enzyklopädie, 169. 14. Matsunami, Kadomiumu, 126; Nakanishi et al., Kadomiumu, 47. 15. Matsunami, Kadomiumu, 128n19. 16. Ibid., 44–48, 537. 17. Ibid., 451–61. Only 3 of the 195 (1.5 percent) officially recognized victims from 1967 to 2008 were men. Ibid., 453. 18. “Yondai kogai saiban no kyokun” [Lessons of the four major pollution-related lawsuits] describes each lawsuit and emphasizes the importance of antipollution measures by private Japanese companies. Kankyo-cho, Showa, chap. 2,

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sec. 1. Yokkaichi asthma was an air pollution disease caused by sulfur oxide released by petrochemical companies in Yokkaichi (Mie Prefecture). I will discuss the Minamata diseases later in this chapter. 19. See also Walker, Toxic Archipelago. 20. Matsunami, Kadomiumu, 40–48. 21. Hatta, Shi no kawa, 22. 22. Matsunami, Kadomiumu, 9–14. 23. Hagino, Itai itai, 53. 24. Yoshioka was born in Okayama Prefecture and graduated from Kyoto Imperial University’s agricultural department. After working at the Institute for Science of Labor and the Ohara Institute for Agricultural Research, both in Okayama Prefecture, he became a professor at Doho University in Nagoya and then at Okayama University of Science. Later, he became president of Kanazawa University. 25. Shozo Tanaka (1841–1913), a statesman and a member of the Japanese House of Representatives, was famous as a protest movement leader against the Ashio Copper Mine (Tochigi Prefecture) that caused the agricultural and fishery damage in the area downstream. See, e.g., Yui, Tanaka Sozo; Dehn, Tanaka Shōzō. 26. Matsunami, Kadomiumu, 153–54. 27. The compensation was only for the agricultural and fishery damages, not for the pollution-related disease. The connection between itai-itai disease and mining pollution was beginning to be noticed in the mid-1950s and was proved in the early 1960s. 28. Kobayashi was born in Kurashiki (Okayama Prefecture) and graduated from Tokyo Imperial University’s agricultural department. After working at agricultural experimental stations of the Ministry of Agriculture and Forestry, he was as a research associate at the Ohara Institute for Agricultural Research. After World War II, he became a faculty member of Okayama University. He retired in 1975. 29. His survey report, “Jinzu gawa suikei kogai kenkyu hokokusho” [Jinzū River system mining pollution scientific report] to the Fuchū-machi branch of the JMPPC (later published in Yoshioka, Kogai kenkyu, 5–95) cites Wilson et al., “Effects,” 222–35; Nicaud et al., “Troubles”; Baader, “Chronische Cadmium­ vergiftung”; Friberg and Nyström, “Synpunkter.” 30. Yoshioka later published the conclusion in a local medical journal. Yoshioka, “Itai-itai.” 31. Hagino and Yoshioka, “Itai itai.” 32. Kobayashi, Mizu, 70–103. The Rockefeller Foundation and the National Insti­ tutes of Health in the financed his analytical study on cadmium of itai-itai disease. When he applied for the NIH funding, he received copies of articles including Nicaud et al., “Troubles”; and Harrison, “Fanconi Syndrome.” Kobayashi, Mizu, 15. 33. Matsunami, Kadomiumu, 30–35.

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34. Hashimoto, Shi-shi, 19–66. In 1972, he moved to the Environmental Agency, established the previous year. After an early retirement in 1978, he became a professor of public health at the national, newly established Tsukuba University. 35. Ibid., 136. Hashimoto referred to the case of Minamata disease as such a belated decision. Ibid., 145. 36. Kurachi, Mitsui, 109–11. 37. Fujikawa, “Kogai higai houchi,” 108–10. 38. Hagino was much criticized and pressured not to work on itai-itai. He even once almost gave up studying the disease, and he traveled to the United States and Europe to escape the embattled situation in 1963 and 1964. Matsunami, Kadomiumu, 158–59. 39. Ibid., 162–71. 40. Ibid., 172; IBSB, Itai-itai, 585. 41. Yokkaichi pollution disease patients followed in September 1967. Finally, after the itai-itai disease case, Minamata disease victims filed a suit against Chisso Corporation, the source of pollution, in June 1969. 42. Matsunami and Shimabayashi were in their thirties and had only one or two years of law experience at the time. Shimabayashi was born in Fuchū-machi and happened to visit Toyama to help a friend from Tokyo, and he started working as a lawyer there. While staying at his parents’ house in Fuchū-machi, he met with Hagino and the IDRA leaders and got to know the details of the disease and the resident movement. Matsunami was born in Himi and started working as a lawyer in Takaoka (both in Toyama Prefecture). In 1967, he had a chance to listen to a lecture by a lawyer who had helped the Niigata Minamata disease victims file a suit. The lawyer suggested he investigate itai-itai disease in Toyama. Matsunami first met Shimabayashi at a meeting organized by Shimabayashi and the IRDA to discuss the lawsuit and decided to help him with a lawsuit against Mitsui. Matsunami Kadomiumu, 185–88. 43. Ibid., 213–14. 44. Even though the Jinzū River flows through the Toyama Plain, the only area ridden with the disease relied on river water for not only agricultural irrigation but also human consumption. 45. Ibid., 257. 46. There was discussion on this matter even in the National Diet (Japan’s bicameral legislature) in 1970. See NDL, “63rd Session”; NDL, “64th Session.” 47. Matsunami, Kadomiumu, 112–13. 48. Matsunami, Aru Hantai Jinmon, 55–131. Matsunami played an important role in various pollution-related lawsuits, including the subacute myelo-optico neuropathy (SMON, a drug-induced disease) and Minamata disease lawsuits, until his retirement in 2001. 49. Takeuch, “Cadmium,” 283–86. 50. Kajikawa, “Pathogenesis,” 292. 51. For details of the pressure exerted by industry and politics to change this position, see Kaji, “Role,” 107–8.

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52. The itai-itai suit did not seem to damage Takeuchi’s career. Takeuchi was born in Chiba Prefecture and graduated from Tokyo Imperial University’s medical school in 1944. In 1974, he became a professor at the prestigious Tokyo Medical and Dental University and later the director of its hospital. He was even elected president of the Japanese Society of Internal Medicine, one of the oldest and most prestigious medical societies. 53. Matsunami, Kadomiumu, 299–303. 54. Isono, “Itai-itai Disease,” 213–14. 55. Matsunami, Kadomiumu, 168, 223–33. 56. Yomiuri Shimbun (Toyama edition), 17 November 1972, 12–13; Toyama Shimbun, 17 November 1972, 15. 57. Matsunami, Kadomiumu, 344–46. The annual inspection group is now divided into seven subgroups. In August 2010, the thirty-ninth annual inspection was held with about 110 participants in seven subgroups, including, for the first time, four officials from Toyama Prefecture. Kitanihon Broadcasting, a local Toyama Prefecture broadcast, reported about the visit on 10 August 2010. 58. According to the Pollution Protection Agreement, the IDRA can invite anyone it considers necessary to participate in the inspection. Outside participants, including researchers and ordinary citizens, belong to this category. 59. According to Akio Hata, who has long been studying environmental problems in the Kamioka mine and participating in various inspections of the mine, the number of residents who had participated came to more than 5,000 by 1998, and the number of experts to 1,700. Hata, “Itai-itai,” 2. By 2010, the former reached 6,000. Hata, “Kamioka.” The number of “experts” by 2011 was 1,000, but this number did not include lawyers. Otherwise, it would have been about 2,000. Hata, personal communication. 60. Hata, “Kamioka.” 61. The project organized groups on (1) effluent from the Kamioka mine and refinery (Kyoto University); (2) smoke emissions from the Kamioka refinery (Nagoya University); (3) the cadmium balance of the Kamioka refinery (University of Tokyo); (4) sedimentation and outflow of heavy metals into the Jinzū River (University of Toyama); (5) the structural stability of the tailing dams at the Kamioka mine (Kanazawa University). For a project outline, see Yoshida et al., “Itai-itai,” 219. On several occasions, thanks to these experts’ inspection, an unknown pollution source was identified and appropriate countermeasures were proposed. Kurachi et al., Mitsui, 246–51. 62. Besides the annual inspection, about ten others on specific themes such as drainage, ventilation, pits, abandoned mines, and planting are held. Hata, “Kamioka.” 63. “Environment” is an important keyword in Mitsui Kinzoku, “Message.” 64. Hata, “Itai-itai,” 3; Hata, “Kamioka.” 65. Hata, “Itai-itai,” 7. 66. In the conference proceedings, one can also see the following names: Alfred Bernard (Catholic University of Louvain); Marie Vahter and Marika Berglund;

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Monica Nordberg; Lars Järup; T. Alfvén, D. Carlsson, L. Hellström, B. Persson, C. Pettersson, G. Spång, and C. G. Elinder (Karolinska Institute); Erkki Vuori (University of Helsinki); Robert A Goyer (University of Western Ontario); Manfred Anke, Michael Glei, M. Müller, M. Seifert, Sabine Anke, G. Gunstheimer, Oluyemisi Latunde-Dada, Winfried Arnhold, and Esther Hartmann (Friedrich Schiller University); Taiyi Jin (Shanghai Medical University); Gunnar Nordberg (Umeå University); Tord Kjellström (University of Auckland). Nogawa et al., Advances. 67. See the dedication to Lars Friberg in Järup et al., “Health Effects,” 5. 68. Friberg, Cadmium, 111–35 (quote on 135). Friberg also mentioned the role of nutrition such as a low calcium and vitamin D intake. 69. Matsunami, Kadomiumu, 126. 70. Ibid., 508. 71. Nakanishi et al., Kadomiumu, 35–36. 72. Matsunami Kadomiumu, 124, 511. 73. Ibid., 513–24; Asami, Kadomium, 71–112. 74. Fujikawa, “Kogai higai houchi,” 112–13; Aoshima, “Jinzu-gawa ryuiki jumin,” 6–23.

Bibliography Aoshima, Keiko. “Jinzu-gawa ryuiki jumin no kadomiumu bakuro to jin-shogai: Genjo to korekara” [Cadmium exposure and kidney disorder of Jinzū River residents: Present and future]. Itai-itai byo seminar koen-shu 22 (2004): 6–23. Asami, Teruo. Kadomium to Tsuchi to Kome [Cadmium pollution of soil and rice]. Tokyo, 2005. Baader, E. W. “Die chronische Cadmiumvergiftung.” Deutsche Medizinische Wochen­schrift 76 (1951): 484–87. Daintith, John, ed. Oxford Dictionary of Chemistry. 6th ed. Oxford, 2008. Dehn, Ulrich. Tanaka Shōzō: ein Vorkämpfer für Menschenrechte und Umweltschutz. Tokyo, 1995. Friberg, Lars, and Åke Nyström . “Synpunkter på den kroniska kadmiumförgiftningens prognos” [Aspects on the prognosis of chronic cadmium poisoning]. Svenska läkartidningen 49, no. 43 (1952): 2629–38. Friberg, Lars, ed. Cadmium in the Environment. Cleveland, OH, 1971. Fujikawa, Ken. “Kogai higai houchi no sho-yoin” [Various factors for negligence to pollution]. Kankyo-shakai-gaku Kenkyu 11 (2005): 103–16. Hagino, Noboru. Itai itai byo tono tatakai [Fight against itai-itai disease]. Tokyo, 1968. Hagino, Noboru, and Kin-ichi Yoshioka. “Itai itai byo no gen-in ni kansuru kenkyu ni tsuite” [On the cause of itai-itai disease]. Nihon Seikei Geka Gakkai-shi 35 (1961): 812–15. Hashimoto, Michio. Shi-shi Kankyo Gyosei [Memoirs on Japanese environmental administration]. Tokyo, 1988.

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Harrison, Harold E. “The Fanconi Syndrome.” Journal of Chronic Diseases 7, no. 4 (1958): 346–55. Hata, Akio. “Itai-itai byo saiban go no jumin-sanka ni yoru hassei-gen-kisei to kigyo-joho-kokai no yakuwari” [The control of a pollution source by the participation of local residents and the role of access to the involved company’s information after the itai-itai disease lawsuit]. Mizu-shigen Kankyo Kenkyu 11 (1998): 1–10. _____. “Kamioka kozan no haisui taisaku no totatsuten to kongo no kadai” [Accom­ plishment and further problems in the drainage measures in Kamioka mine]. In Proceedings of the Symposium to Commemorate the 40th Annual Inspection of the Kamioka Mine, Toyama, Japan, 6 August 2011, 5–9. Toyama, 2011. Hatta, Seishin. Shi no kawa to tatakau: Itai-itai byo wo otte [Fighting against Death River: Following itai-itai disease]. Tokyo, 1983. IBSB (Itai-itai byo Sosho Bengo-dan) [Defense counsel of the itai-itai disease suit], ed. Itai-itai byo saibain [Itai-itai disease lawsuit]. Vol. 3. Tokyo, 1972. Isono, Yayoi. “Itai-itai Disease and the Pollution Control Agreement.” In Nogawa et al., Advances, 213–14. Iwamoto, Akihisa. “Restoration of Cd-Polluted Paddy Fields in the Jinzū River Basin.” In Nogawa et al., Advances, 179–83. Järup, Lars, Marika Berglund, Carl Gustaf Elinder, Gunnar Nordberg, and Marie Vahter. “Health Effects of Cadmium Exposure: A Review of Literature and A Risk Estimate.” Scandinavian Journal of Work, Environment and Health 24, no. S1 (1998): 1–50. Kaji, Masanori. “Role of Experts and Public Participation in Pollution Control: The Case of Itai-itai Disease in Japan.” Ethics in Science and Environmental Politics 12, no. 2 (2012): 99–111. Kajikawa, Kin-ichiro. “Pathogenesis of Itai-itai Disease Based on Post-mortem Studies.” In Tsuchiya, Cadmium Studies, 286–95. Kankyo-cho [Environmental Agency]. Showa 48 nen ban Kankyo Haku-sho [White paper on the environment in Japan for 1973]. Tokyo, 1973. Kobayashi, Jun. Mizu no Kenko Shindan [A “checkup” of water]. Tokyo, 1971. Kurachi, Mitsuo. “General Research into Cadmium Poisoning Prevention in the Jinzū River Basin and the Worldwide Significance of Pollution-Free Mining.” In Nogawa et al., Advances, 149–54. Kurachi, Mitsuo, Haruo Tonegawa, and Akio Hata. Mitsui Shihon to Itai-itai Byo [Mitsui capital and itai-itai disease]. Tokyo, 1979. Matsunami, Jun-ichi. Aru Hantai Jinmon [Cross-examinations]. Tokyo, 1998. _____. Kadomiumu higai hyaku nen: Kaiko to tenbo [One hundred years of cadmium poisoning: Recollection and prospect]. Toyama, 2010. Mitsui Kinzoku (Mitsui Mining & Smelting Co.). “Message from Management.” Accessed 15 February 2019. https://www.mitsui-kinzoku.co.jp/en/company/ c_​message. Nakanishi, Junko, Kyoko Ono, Masashi Gamo, and Ken-ichi Miyamoto, eds. Kadomiumu [Cadmium]. Tokyo, 2007.

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NDL (National Diet Library). “The 63rd Session of the Diet: Industrial Pollution Measures Special Committee No. 6.” [In Japanese.] 1 April 1970. http:// kokkai.ndl.go.jp/SENTAKU/syugiin/063/0620/06304010620006c.html. _____. “The 64th Session of the Diet: Law Committee No. 4.” 8 December. http:// kokkai.ndl.go.jp/SENTAKU/syugiin/064/0080/06412080080004c.html. Nicaud, P., A. Lafitte, and A. Gros. “Les troubles de l’intoxication chronique par le cadmium.” Archives des maladies professionnelles, hygiène et toxicologie industrielle 4 (1942): 192–202. Nogawa, Koji, Mitsuo Kurachi, and Minoru Kasuya, eds. Advances in the Prevention of Environmental Cadmium Pollution and Countermeasures: Proceedings of the International Conference on Itai-itai Disease, Environmental Cadmium Pollution and Countermeasures, Toyama, Japan, May 13–16, 1998. Kanazawa, 1999. Takeuch, Juguro. “Cadmium vs. Nutrition in Itai-itai Disease.” In Tsuchiya, Cadmium Studies, 283–86. Tsuchiya, Kenzaburo, ed. Cadmium Studies in Japan: A Review. Tokyo, 1978. Ullmann, Fritz, ed. Enzyklopädie der technischen Chemie. Vol. 3. Berlin, 1916. Walker, Brett L. Toxic Archipelago: A History of Industrial Disease in Japan. Seattle, WA, 2010. Wilson, Robert H., Floyd Deeds, and Alvin J. Cox Jr. “Effects of Continued Cadmium Feeding.” Journal of Pharmacology and Experimental Therapeutics 71 (1941): 222–35. Yamada, Yoshio. “On the Lead Mining and Metallurgy of Japan.” [In Japanese.] Nihon Kogyo Kaishi 67, no. 753 (1951): 46–51. Yoshida, Fumikazu, Akio Hata, and Haruo Tonegawa. “Itai-itai Disease and the Countermeasures against Cadmium Pollution by the Kamioka Mine.” Environmental Economics and Policy Studies 2, no. 3 (1999): 215–29. Yoshioka, Kin-ichi. “Itai-itai byo to kogai tono kanrensei ni tsuite no eikigaku teki kenkyu” [Epidemiological study on relationship between itai-itai disease and mining pollution]. Yomaguchi Igaku 3 (1964): 146–70. _____. Kogai kenkyu: Itai-itai byo kenkyu [Pollution study: Itai-itai disease study]. Yonago, 1970. Yui, Masaomi. Tanaka Sozo. Tokyo, 1984.

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CHAPTER 7

Dioxins The “Total Poison” Stefan Böschen

Dioxins are absolutely toxic. Dioxins are ubiquitous. Dioxins are

inevitable. Not surprisingly, the public debate about chemicals and their regulation in the late 1970s and early 1980s often focused on these substances. Constant attention was given to the side effects of industrial chemicals and their production processes—even though dioxins themselves are not products. They are byproducts of chemical synthesis and diverse combustion processes (industrial as well as natural). Against this background, dioxins achieved the status of a “collective symbol.”1 But this dynamic of the formation of a collective symbol must be seen with all its ambivalent consequences. On the one hand, the debate about dioxins offered the chance for a discussion about the use and regulation of chemicals in general. In this regard, dioxins are “tracers” to structure the field of chemical policy. On the other hand, the debate was often restricted to topics related to the problem of dioxins. This might have been necessary to reduce complexity, given the heterogeneity of the production and use of chemicals. But the consequences are dramatic. Different chemicals have very different characteristics and hence must be regulated in different ways.2 These dynamics of an “economy of attention” are quite common in the field of environmental protection: there is a reason the action-mobilizing symbols in nature protection are not earthworms—although they have a vital importance for the ecological system—but tigers and gorillas.3 They have much more potential to serve as a collective symbol. It is decisive for risk policy debates to focus on specific objects capable of forming a collective symbol to initiate and form a public debate, as well as the implementation of risk management procedures. But such a focus may lead to un-intended reductions.

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An example for such dynamics is the classic analysis of the consequences of massive use of insecticides: Silent Spring by Rachel Carson.4 Carson offers a comprehensive view on the problems resulting from the use of organochlorine insecticides; her descriptions show the complexity of the environmental effects of such insecticides. Yet, her study depicts an erroneous scenario concerning the importance of the cancer problem. DDT was finally banned in the United States in 1972—but based on the incorrect assessment that DDT would cause cancer. Mainly responsible for this outcome of the debate was the “marriage” of a symbol of a “wrong” type of agriculture (DDT) and the most important “collective symbol” of health problems (cancer). But regarding dioxins, we deal with a crucial difference: DDT is a product used for different processes (not only in pest management but also in health care management), whereas dioxins are an unwanted byproduct. Therefore, substitution or change cannot be implemented without great effort. Also, in many cases, a policy of avoiding dioxins is a policy without concrete reasons. Therefore, the debate about dioxins is more incidentdriven than other debates in the arena of chemical policy. The most important dioxin-linked incident took place on 10 July 1976: the accident in the Italian city Seveso. The warning “Seveso is everywhere” echoed throughout Europe, symbolizing the hazards of the chemical production system and its products.5 Various types of hazards were aggregated to the symbol of TCDD, the super poison or the “Seveso dioxin.”6 The effects could be seen not only in poisoning effects on workers and children but also in irregular practices of production and waste disposal. The “dioxin drums” haunting Europe helped leave a “dioxin trace” in the chemical policy landscape. In terms of regulation, this process ended with the Stockholm Convention on Persistent Organic Pollutants (2001). And so, the “dirty dozen” were banned: DDT, PCBs, dioxins, and other organochlorine compounds were regulated on a global scale. The convention intended to eliminate sources of dioxins. Inventories on national and regional level were compiled to obtain an overview about dioxin sources and their character.7 However, the conflict about the relevant sources is not finished but has entered a new phase. What about the hundreds of industrial waste disposals in which dioxins can be detected as inheritance of industrial production from the nineteenth century?​8 This chapter has a double focus: first, the processes regarded as decisive for the formation of the collective symbol “dioxins” as a total poison are analyzed. Second, I will explore how this collective symbol and

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its formation processes influenced concrete chemical policy conflicts. Therefore, different contexts of debating dioxins must be discussed. These contexts are important to show how the different actors tried to use the symbol “dioxins”—its sources and impacts—for their specific strategies of knowledge politics. Different actors told different stories about chemicals, their importance, and unhealthy impacts. These stories use narratives to underpin the importance or unimportance of dioxins regarding the regulation of chemicals. The crucial point here is that the formation of dioxins as a collective symbol of the total poison was mainly influenced by the emergence of a multifaceted “network of experimentation” for the analysis of the (non)hazardousness of dioxins. To underline this, my argumentation follows the different phases of collective experimentation with the risks of dioxins. The first phase is characterized by the fact that dioxins themselves, as well as phenomena that could be related to dioxins, were discovered in the context of occupational medicine. The second phase, which could be seen as passage phase to a public debate about dioxins, is mainly characterized by two events: the Vietnam War with the use of Agent Orange by the US military and the Seveso disaster. In many cases, incidents trigger certain developments, and the concurrence of several, unrelated incidents results in the establishment of structures of risk regulation. In the third phase, finally, the phenomenon of the ubiquity of dioxins generated a key issue for risk policy in general and environmental protection policies in particular. These different phases can be characterized as the evolution of a “network of experimentation.”

Stories about Dioxins: Historical Prologue The story begins at industrial workplaces. Since the early days of the chemical industry, the workplace was the site for industrial intoxication and therefore for more or less unintended experiments. Not by accident, much research was done on this aspect of “chemicalization” of the social and natural environments.9 Looking at dioxins, we can say they were unknown as a cause of diseases for a long time. Initially, only few effects on workers at specific plants could be detected. Dioxins became known in the context of occupational medicine—but first not as dioxins themselves. The problem was that specific symptoms of poisoning could be connected to a large number of substances subsumed under the group of chlorinated cyclic hydrocarbons. Hence,

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not only the precise number of harmful substances but also the exact form and structure of the diseases were unknown.10 The starting point was the introduction in 1890 of chlor-alkali electrolysis for chlorine production at the chemical plant of the Chemische Fabrik Griesheim (later Griesheim-Elektron) near Frankfurt, Germany. At that stage, the process was realized with carbon electrodes. And it was so successful that it was installed in many factories. Griesheim built plants at its subsidiary companies in Bitterfeld and Rheinfelden in 1893; BASF used the process since 1897. Since the implementation of this process, two curious observations could be made. First, a new form of poisoning was diagnosed. Karl Herxheimer, consultant at the dermatological department of the municipal clinic in Frankfurt, was confronted with the first cases in Griesheim and depicted an early description of this disease. Herxheimer described it as “chloracne” because the main symptom is a disfiguring facial rash. Second, no plant using this process had been spared from the so-called chloracne.11 Given these facts, strategies had to be implemented to solve the problem. One strategy was the replacement of workers who felt sick by workers who were assumed to have a more solid constitution.12 Another strategy involved an extension of hygiene procedures, the use of showers, and the cleaning of work clothes. Nevertheless, occupational physicians with a broader view on the general problem were aware the solution could not be to fit humans into illness-supporting working conditions. They criticized the established chemical-technical production processes. Supporting this argument, the physician Siegfried Bettmann from the Heidelberg University Hospital wrote: “The better prophylaxis would be the elimination of harmfulness as such; in any case, the workers must be seen as victims of their industrial plants, and therefore their illness may claim a general hygienic interest.”13 Surprisingly, the problem solved itself—not by taking prophylactic measures but by a change in technical procedures. Regarding the further debate, the metaphor of chloracne turned out to be misguiding. Herxheimer supposed chlorine to be the causal agent.14 However, large numbers of production processes involving chlorine were not causing chloracne.15 Bettmann, who examined workers from a hydrochloride acid plant, concluded correctly that the cause of chloracne must be seen in the substance group of “chlorinated derivatives of coal tar.”16 By analyzing the occurrence of chloracne in different chemical plants, the scope of causal agents could be narrowed down and specified: chlorinated cyclic hydrocarbons.17 For some time,

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products of coal tar were experienced as an occupational problem. Very interesting is a conclusion that can be interpreted as a first articulation of a general suspicion against this group of substances: “Such derivatives of coal tar formed by the addition of chlorine are able to produce phenomena which must be seen, so to speak, as the tip of a series of diseases that are caused by substances of the coal tar group.”18 An incident at a Bayer production plant in 1911 could have given hints to identify dioxins as main suspects, because chloracne was observed after a dioxin leakage.19 However, the pieces of the puzzle were not put together; the exact action pathways and the potential scope of poisoning remained unknown. Was chloracne caused by inhalation of the noxa or by transfer through the skin?​Was chloracne the most important effect, or were there other long-term effects to the human body (such as cancer)?​However, the debate about the risks remained limited and was narrowed to the symptoms of chloracne. This perspective was so well established that, in the course of elucidating phenomena of chloracne, symptoms of chronic intoxication were systematically overlooked. Obviously, such end points (like chloracne) are important for the understanding of risks. Yet, they turn out to be barriers for the expansion of risk knowledge by narrowing the perspective, as can be shown by the example of animal experiments conducted at that time to reproduce chloracne. The reproduction of phenomena of chloracne failed—but the animals suffered from symptoms of chronic intoxication.20 Although these effects were striking, they were not taken seriously, and new experiments were not conducted. To be fair, the case was complex and confusing, so it was difficult to arrive at a concise set of risk hypotheses. The plants in which the disease was observed were quite different. For example, in the production of polychlorinated naphthalene, which was used in gas mask filters during World War I and thereafter for primer production in the mining industry, phenomena of chloracne were observed. Against the background of the multitude of diseases, occupational physician Ludwig Teleky drew the wide-ranging conclusion: “The desirable goal is therefore to abandon the use of chlorinated hydrocarbons for the production of primers.”21 Nevertheless, the triumphal prevalence of the PCN substance group continued, although there have been signs of chronic effects caused by PCN as early as 1936.22 Though the search heuristics for negative effects were extended from acute toxic effects (chloracne) to effects of chronic poisoning, it remained unclear if the different symptoms were correlated or if they had to be seen as independent.23

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In the 1950s, because of a series of accidents in the chemical industry related to the production of pentachlorophenol, the group of substances causing chloracne could be identified, and the most toxic substance of synthetic chemistry was discovered: tetrachlorodibenzodioxin (“Seveso dioxin”). To be specific, the accidents in question happened at Monsanto in 1949, at Boehringer in 1952, and at BASF in 1953.24 After a change in trichlorophenol production, the whole staff of the Boehringer department concerned had to be treated in a dermatological clinic. The responsible physician, Karl Heinz Schulz, was supported by fortunate circumstances: At the same time, the chemist Wilhelm Sandermann and colleagues carried out experiments to study the pyrolysis of PCP. In the course of an involuntary self-experiment, they discovered TCDD as a powerful agent to cause chloracne.25 A reanalysis of Boehringer’s plant procedure by Schulz and the responsible chemist, Georg Sorge, showed that, in the process of transforming tetra chlorobenzene to 2,4,5-trichlorophenol, TCDD could be produced as a byproduct. In this case, TCDD was identified as causal agent for chloracne.26 Subsequent experiments showed TCDD was extremely toxic even at low dosages. Nevertheless, Ernst Boehringer, patriarch and company boss, actively tried to prevent these findings from being published.27 But finally, the work, “Occupational Acne (So-Called Chloracne) Caused by Chlorinated Cyclic Ethers,” was published and reported in Chemical Abstracts and Chemisches Zentralblatt.28 A striking difference can be shown between the reports in Chemisches Zentralblatt (most important for chemistry) and Chemical Abstracts. The former addressed the negative toxic effects on humans directly, whereas the latter focused on the enormous effects of TCDD as insecticide or fungicide. Further, the latter publication was listed under the keyword “pentachlorophenol,” so the reference to “dioxin” did not play a central role. Sandermann himself later explained that this unusual way of handling was ordered by the superior of his department (the German Federal Ministry of Food, Agriculture, and Forests).29 Many others supported the strategy of silencing set by Boehringer, although the boundary conditions for pursuing this strategy changed. Otherwise, a big market (herbicide production) would have been at risk. One important aspect of the change of boundary conditions was the establishment of a new context. So far, the problem of dioxins was mainly discussed within the horizon of production safety. But with the use of pentachlorophenol and analogous substances as herbicides, the context of agricultural production became (at least implicitly) a hori-

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zon for reflecting negative unanticipated consequences. However, the problem of pentachlorophenol herbicides was at first defined as a problem of occupational safety only. The main actors were convinced risks would be manageable by technological innovation—a strategy proved successful in many cases. Accordingly, process innovations were implemented, and the cases of chloracne decreased. But chloracne was just the most perceptible and most acute symptom of the problem—what about chronic intoxication?​However, the “cartel of silencing” could be maintained until the incidents in Vietnam and the Seveso accident made the public an important reference point in the risk debate.

Passages: The Emergence of Real-World Experimental Settings The history of trichlorophenol production started during World War II. The US military searched for a war-ending weapon not only in Los Alamos (the atomic bomb) but also in Fort Detrick, the center of the military’s chemical department. The underlying strategy was to destroy the Japanese rice harvest to force them into capitulation. This kind of weapon was discovered in the search for chemical substances to regulate the growth of crops.30 During this research, it was observed that some crops were growing to death if they were exposed to an overdose of specific herbicides. The weapon constructed in Los Alamos finally decided World War II. But the techniques discovered in Fort Detrick initiated the civil production of herbicides immediately afterward. At the forefront: Monsanto, Du Pont, and Dow Chemical. But with this specific form of herbicides, a complex mixture of various chemical substances, including dioxins, was released into the environment. This does not mean plans of using such substances as military weapons were relinquished. In 1959, when he had read about it in the latest publications, the chief officer of the unit of active substances at the chemical department in Fort Detrick traveled to Germany to explore the usability of TCDD as a chemical weapon. His statement was a bit surprising for a member of the army: “Dioxin must not be used for chemical warfare as it is too lethal.”31 The argument was that this substance was not manageable for the soldiers and would expose them to heavy risks. Therefore, the search for chemical weapons was carried on with chlorophenol herbicides—unaware that dioxins as a byproduct were an important ingredient of such herbicides. Finally, during the

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Vietnam War (under the code name Operation Hades), these weapons were frequently used and demonstrated their strategic importance.32 The strategic goals were to destroy the rice harvest and defoliate the rain forest protecting the Vietcong against the US military. The chemical warfare was conducted with furious cruelty. Before the end of the war, studies showed the problems of herbicides containing dioxins.33 Nevertheless, the situation remained unclear and complex regarding possible causal agents and action pathways. What was the toxic agent— dioxin or the herbicide 2,4,5-T?​It was known the US military spread about 170 kilograms of dioxins along with the herbicides used from 1962 to 1970.34 Two groups were especially exposed to these herbicides and therefore most affected by side effects of the chemical war: the Vietnamese people and US soldiers. Initially, only a few critical publications reviewed the negative side effects of the herbicide war, which concluded a correlation between the herbicide war and an increased rate of malformations and Down syndrome among newborn children.35 At the same time, a National Academy of Sciences (NAS) study came to a different conclusion: it confirmed the fact of acute toxicity but did not arrive at an unambiguous evaluation regarding chronic effects or reproductive toxicity.36 Anyhow, the debate about damages caused to Vietnamese people was quite small compared to the public outcry about the chemically induced damages to US soldiers, particularly after a soldier announced on television in 1978, “I died in Vietnam, but I did not know.”37 The biggest compensation lawsuit so far ended with a settlement: the chemical industry had to pay $180 million. However, the firms were assured Agent Orange had not caused the damages. The data the US military had collected in Vietnam with painstaking precision was the starting point of a heated debate and a vast number of analyses. Because of a precise protocol of sprayings (9,495 in total) and the availability of knowledge about troop movements, there was a good chance to study the relationship between dose and effect. It could be learned in particular that specific toxic end points exist: non-Hodgkin lymphoma and soft tissue sarcoma. This seems to confirm the metaphor of “society as a laboratory.”38 However, it is necessary to notice that the systematic of an “experiment” can only be seen from an ex-post perspective. It is not plausible to allege the military was running an experiment to analyze the self-endangerment of troops by chemical warfare agents: this seems far too cynical, even for the military. Only with the beginning of the next war (Gulf War) and the Agent Orange

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Act of 1991 did veterans suffering from specific diseases receive pensions as a vested right. Afterward, the NAS initiated a broad-based study about the relation between exposure to herbicides and/or other toxic agents in Vietnam and the observed toxic effects.39 It confirmed the causal relationship between exposure in Vietnam and toxic effects. Not until twenty years after the incident was this study initiated, illustrating that it is more or less impossible to prove a risk hypothesis with high symbolic value in a highly politicized situation. The other incident that promoted dioxins as a key issue for the environmental movement was the accident at Seveso, where the ICMESA—a subsidiary of Hoffmann-La Roche—produced trichlorophenol, a compound important for herbicide production. The plant was put into operation in 1971 and produced at maximum five tons per month with 1.2 kilograms of dioxins as byproduct. On 10 July 1976, the production plant broke down. To enable the pressure balancing of the overheated reactor, a safety valve opened, and the greater part of the reaction mixture was released into the environment, including one to five kilograms of dioxins. The damages were to be seen immediately: white dust, dead animals, and, most important, chloracne in the face of a child.40 It took up to ten days to initiate security procedures for the inhabitants. Seveso was divided into three zones: zone A with a concentration of 50 to 5,400 micrograms of TCDD per square meter, zone B with a concentration up to 50 micrograms TCDD per square meter, and zone R with a concentration of at least 5 micrograms TCDD per square meter or a positive evidence of dead animals or chloracne on humans. Overnight, the potential dangers of chlorophenol-herbicide production became visible for the public. In retrospect, it seemed obvious that the chemical production firms intentionally played down the negative side effects and enormous risks accompanying such herbicide use. A reaction to this interpretation is in an article in the industry-friendly journal Europa Chemie: The damage, not only the economical one for the affected region and firms, is bad enough. One should not add journalistic damage by stirring up emotions with a misguiding wording like “poison gas plant” and “defoliation agent.” Trichlorophenol is not a “poison” but a chemical intermediate product which contains impurities—like many others, too—and which should not be released uncontrolled into the environment.41

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Yet, in Seveso, these substances found their way into the environment— uncontrolled (except one wants to understand the opening of a safety valve as a controlled release). Moreover, the management concealed the involvement of dioxins from the local Italian government. Particularly interesting in this quotation is the formal style of the argument, which can be interpreted as an attempt to reconstruct the normality of things and of control options with a context-neutralizing language. Most important, it seems like an attempt to leave the power of definition not only to the media. Seveso became a metaphor for the risks of the chemical industry, as expressed in the metaphor “Seveso is everywhere.” Besides, it also developed into a laboratory of risk analysis. The Milan physician Paolo Mocarelli saw Seveso as an “open field laboratory.”42 However, other scientists have stated that, in light of Seveso, fieldwork had to be organized differently because different methodological rules apply in such cases: A different policy of research in defining priorities and allocating resources to experimental, clinical, and epidemiological work seems to be needed to produce not only better data, but a new cultural attitude. People trained for and involved in a laboratory and/or hospital-based work where “controlled” conditions are the rule and the prerequisite, will then become more ready to adapt their methodology and instruments to the real needs of field work where often confounding factors are prevalent.43

This statement can be seen as an early vote for a reflective context orientation. Which risks were considered, and how were they addressed?​ At the end of the Vietnam War, several new research fields had been established to analyze consequences and damages more deeply. They increased in importance with the Seveso disaster, especially effects of reproductive toxicity.44 Of course, “classic” issues like the increase in cancer cases were also addressed. This was important for risk analysis, particularly as new theoretical approaches and empirical test strategies, like the Ames test to detect the potential for mutagenesis, had been established.45 The health effects on the affected population comprised the core of research interests. Committees were convened and registers compiled (among others registers for malformation and for cancer) to collect phenomena of damage and interpret changes in human health. Nevertheless, the studies were of complex design as a vast number of

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known effects had to be considered: chloracne; organic dysfunctions; increase of spontaneous miscarriage, infectious diseases, and mortality rate; malformations; growth disorders; cell transformations; immunological malfunctions; and decrease of birth rate.46 An enormous increase of cancer cases and miscarriages was predicted, but only the effects concerning the hereditary disposition could be verified significantly. In their review article, Pier Bertazzi and Alessandro di Domenico concluded: “Chloracne was the only effect consistently established. Other health outcomes known to be possibly associated with dioxin exposure were investigated. For none of them could an unusual pattern, either for frequency or for the type of outcome concerned, attributable to TCDD be firmly established.”47 In the course of recent decades, the effects on the hormone system and the immune system have received increasing attention. Because the predicted indicators (like increase of cancer rate) did not signal a problem, the problem shift that took place must be seen against the general background of risk debates of those days. In the late 1980s and early 1990s, the endocrine-disrupter debate pushed the focus of risk debates to effects on the hormone system. Conspicuously, the deepening of Seveso accident analyses was justified by the argument that these insights would be necessary to improve risk management. But, obviously, these studies were undertaken mainly based on scientific interests: they might be of interest as such, but they seem to be of less importance for risk regulation. These dynamics of delinking scientific risk analysis and political risk management were possible because dioxins had become a collective symbol of chemical-induced risks and the need for their regulation.

Transformations: The Takeoff of the General Risk Debate Mary Douglas in 1966 characterized waste as “matter out of place.” The debate about dioxins is mainly fueled by the fact that dioxins often turn up at places where they should not be: in rivers, food, or breast milk. For the establishment of dioxins as a collective symbol of the risks of the chemical industry in general and synthetic chemicals in particular, a series of transformations was necessary. The passage phase with the two important incidents, chemical warfare in Vietnam and the Seveso disaster, opened up an opportunity to debate the risks of dioxins. Heinrich von Lersner, the former president of the German Federal

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Environment Agency, coined “dioxins” as a symbol for the “failure of environmental politics.”48 In this context, the public debate about dioxins as a total poison and a symbol of risky production processes was formative for the environmental movement, as well as the emergence of a critical public opinion about the chemical industry. This does not come as a surprise: the field of chemistry is frighteningly complex and arcane. Even the deceptively simple question of which aspects should be debated—specific substances, synthetic chemistry, chlorine chemistry, or specific pathways of the chemical industry—was not easy to answer and confirmed the public opinion of the hazardousness of chemistry and its products.49 This situation was amplified because a large number of environmental chemical analyses and measurements proved dioxins virtually ubiquitous.50 Thus, the problem gained a downright incredible dimension, especially for a substance known as very stable, fat soluble, absolutely persistent, and accumulative—in other words, everything that qualifies for an environmental toxin. The knowledge of its ubiquity was mainly held by the industry. One important reason is the highly complex process of measuring dioxins. The other reason is that the chemical industry, after administrators limited landfill capacities, invested in waste incineration plants. From monitoring the exhaust air of such incinerators, it was observed that dioxins are created in virtually all incineration processes—although mostly only in marginal amounts. Dioxins Produced by Incineration Plants Until the late 1970s, different sources for dioxins were detected. Especially emissions by municipal waste incineration plants were discussed in a lively debate after this connection was discovered in 1977.51 Waste incineration plants were seen as an important source for diffuse emission of dioxins into the environment. Though a limit value was established, it also meant, on the other hand, a permission to release these substances into the environment.52 This reinforced the debate about the ubiquity of dioxins, and various broad-scoped screening analyses were conducted after the Seveso accident. Consequently, the ubiquity of dioxins was an established fact in the early 1980s.53 This can be seen as an ironic twist of fate: waste incinerator plants were constructed to face the environmental problem of rising levels of waste and to prevent uncontrolled waste disposal. They were considered necessary to solve the problem of decreasing capacities of landfills. In this

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sense, the debate about incineration plants as a source of dioxins led to a debate about a failed environmental policy and its orientation toward end-of-pipe strategies. Such strategies will necessarily remain provisional arrangements. In many cases, recycling procedures work only inefficiently, are energy consuming and often economically unprofitable, and generate environmental problems themselves.54 Dioxins in Biocides A second important point of criticism: different biocides were accused of containing dioxins in measurable amounts. The most important biocides were herbicides and fungicides used in not only agriculture but also private households. The biocide pentachlorophenol played a prominent role in this debate. In most cases, it contained dioxins as contaminant.55 In March 1985, Horst Neidhard (dioxins expert of the Federal Environment Agency) testified in the Bundestag: “We have seen that PCP is currently one of the most important, if not the most important, sources of dioxins in Germany.”56 As PCP was used in wood preservatives, a commission was established in 1978 within the German Federal Health Agency to investigate the problem of residential wood preservatives (especially concerning PCP). In 1981, the first data presented did not indicate a causal relationship between the presence of PCP in living spaces and health problems.57 Nevertheless, an interest group of people affected by wood preservatives filed a charge against Desowag employees in 1984, which was taken up by the public prosecutor’s office in Frankfurt five years later.58 The state of evidence turned out to be fragmentary and scanty, but in the end, the defendants were condemned to fines and suspended sentences. Finally, in 1989, PCP was the first substance to be banned from all use. The German Federal Ministry for the Environment, Nature Conservation, and Nuclear Safety, founded in 1986, could score its first major victory, which was crucial for the still poorly established ministry, but the problem of dioxins in biocides remained important. Even though the use of these substances in domestic spaces decreased, organochlorine pesticides (with their contaminant dioxins) are still used in agriculture. Dioxins in Food The third line of debate made the dioxin problem obvious—and, at the same time, highly problematic—to everyone: dioxins in food, especially

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in the food, mother’s milk. In 1984, dioxins were first detected in breast milk. A year later, it was shown that breast milk exceeded the limit values for cow’s milk in many cases. Therefore, it was recommended to breastfeed babies for only half a year. The debate about dioxin-contaminated breast milk demonstrated the phenomenon of ubiquity quite plainly to the public. The contamination of breast milk mirrored the problems of general environmental pollution.59 The special sensibility to the question of dioxins in food is highlighted by the many scandals when dioxins were detected in things where they should not be, even not as a contaminant. Dioxin is “matter in the wrong place” in the strongest sense of this phrase. Not surprisingly, debates are quite heated, even though the actual potential for damage might be rather low. This fact is often hard to understand for risk administration officers. In this sense, Andreas Hensel, the president of the German Federal Institute for Risk Assessment, argued: “Our risk perception is very selective. No matter what we are doing, which hobbies we have: we live in a fun society. People are crashing down the hills on snowboards—but they fear dioxins.”60 To be fair, rules of comparison are not simple in this case. Dioxins on Waste Dumps There is a specific set of problems resulting from the fact that the disposal of industrial waste (mostly production waste) was only systematically organized with the beginning of environmental politics in the 1970s. Until then, the largest part of chemical production waste was simply dumped in landfills or can be found as toxic remnants in the soil of production sites. These can be addressed as focal points of a specific industrialization policy. In this case, dioxins symbolize a chemical production policy that utterly failed, because it dramatically underestimated the negative side effects of the industrial production of substances. At Boehringer’s production site in Hamburg, a total of 377 kilograms I-TEQ of dioxins is estimated.61 Another aspect: the uncontrolled waste dumps. The debate about the cleanup of the Bonfol waste dump in Switzerland demonstrates how the strategies of various actors differ and collide, not only at the time of usage but also, nowadays, while elaborating cleanup strategies. Greenpeace Switzerland showed how the industry tried to narrow the focus and underestimated environmental risks. The Swiss chemical industry, on the other side, criticized the specific form of scaremongering over problems resulting from past dioxin use. Nevertheless, the government urged the industry

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to pay the bill for the cleanup of this waste dump, an estimated sum of 1 billion Swiss francs. Networks of Experimentation From considering the insights collected in the previous sections, it becomes obvious the case of dioxins represents not just one but a multitude of real-world experiments. The debate about dioxins can be reconstructed as a “network of experimentation.” Insights generated in highly different contexts must be aggregated and put together like a mosaic—but without a blueprint existing. So, an assessment of this complex situation is challenging—as much as opening up the situation for strategies of knowledge politics. The main issues are options for knowledge politics by debating non-knowledge. The process of defining scope and importance of a phenomenon unknown or not yet known offers the chance to narrow down the number of relevant aspects or raise the standards of evidence to prove harm caused by a certain product. Robert Proctor characterized such strategies as “agnotological.” Analyzing the history of smoking and cancer, he concluded the knowledge about the correlation between smoking and cancer could not result in regulatory effects for such a long time because the tobacco industry was successfully playing the “joker” of non-knowledge. Their strategy was not to deny a potential relation but to spearhead an uncompromising analysis of all unknown aspects and call for strong evidence.62 The point was to demand strict proof and a high threshold of evidence, which is unlikely to be met in situations with open-ended contexts. In the debate about dioxins, one can also observe a whole spectrum of such strategies that served to limit the activity of regulatory bodies. But science also used this situation to promote its own interests. With a link to dioxins, it was quite easy to get research funds so that scientists could position all kinds of research programs by claiming involvement of dioxins. This dynamic of acceleration was supported by the fact that dioxins are not simply a product but a contaminant or tracer. Therefore, the field was not structured by a limited number of actors but rather by various actors that served as “provider of non-knowledge.” After decades of occupational research and after identifying dioxins as a key agent causing chloracne, the problem situation was reframed by the fact that dioxins are not limited to occupational settings but can be detected in various environmental contexts. Especially the instrumental analytics of dioxins had to be further developed, as dioxins occur only in

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small amounts. The development of instrumental analytics was mainly the job of industry researchers.63 During the 1970s, the detection limit could be lowered from one part per million (1969) to one part per billion (1980).64 In the same time, the scope of exposure situations and potential pathways to damage humans or the environment was broadened. In the aftermath of Seveso, but also because of the “permanent incidents” of waste incinerator plants or the use of organochlorine biocides, a new debate about the set of evidence was initiated and shifted the focus back on the ways and forms of dioxin-induced damage on humans and the environment. In a first wave (in the 1980s), effects of chronic intoxication (e.g., carcinogenicity, mutagenicity, reproductive toxicity) were studied without any connection to the symptom of chloracne. And in a second wave (in the 1990s), effects on the immune and hormone system were considered.65 In this way, dioxins achieved the importance of a paradigmatic substance of environmental chemistry and human toxicity. At the same time, as these substances could be detected in diverse sites and contexts, it was possible to define and redefine evernew experimental settings. A “network of experimentation” developed with increasing speed and diversity (see fig. 7.1). The development of this network of experimentation also brought a multitude of methodological and practical problems. One was the production and analysis of epidemiological information. The interrelation between incidents (e.g., accidents) and their adverse effects was difficult to prove because of historical (the incidents happened years ago) or systematic reasons (the concentration of dioxins was below detection limit). Finally, certain methodological problems were connected with the specific form of epidemiological knowledge. Important for epidemiology as a science is not only the statistical construction of correlations between agent and effect. On top of that, criteria of causality—first

Figure 7.1  Diagram of stages in the evolution of the “network of experimentation.” Diagram created by the author.

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formulated by Sir Bradford Hill in the 1950s—are decisive. Hence, a significant statistical correlation can only be the conditio sine qua non, but the sufficient condition is bound to biological plausibility of the assumed interrelation. Without any idea about the causal mechanisms, the statistical argument is simply not evident enough. Despite the clarity of this statement, it is difficult to proceed in this manner. In many cases, knowledge about biological mechanisms is rather poor—in some cases, even misguiding. Furthermore, the designing of such studies faces various practical problems. Even analyses of the same phenomena and known collectives (e.g., BASF workers) can lead to surprisingly different insights. Therefore, reassessment of such accidents by means of studies in the field of occupational medicine was and is very important to strengthen evidence. Additionally, these cases provide an opportunity to analyze the importance of agnotological strategies while defining the boundary conditions for these “experiments.” Well known, for example, is the accident at the Monsanto trichlorophenol plant in 1949. In 1980, Raymond R. Suskind of the University in Cincinnati and the Monsanto company doctor, Judith Zack, wrote a medical report: in the previous twenty years, a strong increase of cancer cases among affected workers was observable.66 In 1983, Zack published another study as a reassessment of the first one and aroused a debate that finally ended in a lawsuit, because the later study presented the group of affected workers in a different way, the result being that neither effects nor relations between the accident and the increase in cancer cases could be found.67 Evidently, the second study described people who had been described as exposed in the first one as nonexposed. In a reassessment of Zack’s report, the scientists Alastair Hay and Ellen Silbergeld concluded there is indeed a statistically significant relation between the accident and the rate of cancer (especially of lung and bladder cancer).68 The 1953 accident at BASF in Ludwigshafen, Germany, can also be seen as an instructive case within the context of epidemiological analyses, showing specific problematic aspects of this kind of analysis. From 1955 to 1982, four different studies about this accident and its effects on workers were conducted. It is significant, first, that each study is centered on another group of people and, second, that only the latest study focused on cancer diseases. The occupational physicians Gerhard Lehnert and Dieter Szadkowski conducted a study on behalf of the industrial injuries corporation of the Chemical Industry (Berufsgenossenschaft Chemie) to elucidate the relation between

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e­ xposure due to the ­accident and harmful effects on the workers, especially cancer.69 Their conclusion: there are no such effects. They built their conclusion on the argument that there are no dose-response relationships; therefore, there could not be a causal relationship between dioxins and cancer. This study was heavily criticized.70 The occupational physicians, both epistemologically trained in the paradigm of toxicology, denied the validity of epidemiological analyses and said the accident insurance law necessarily requires proven causal relationships between exposure and effect. Finally, a study by the BASF company doctor, Andreas Zober, concluded there is indeed a relationship between highly exposed workers and the occurrence of cancer.71 So the question here is, what can actually be regarded as a proven causal relationship?​ Obviously, no single study can conclusively prove or disprove such correlations. Only a set of (complementary) studies can substantiate first hypotheses of potential interrelations between exposure and effect. In the context of occupational medicine, even though methodological aspects turn out to be rather complex, networks of experimentation are characterized by their clear arrangement. But with the broadening of scope and form of the included contexts, the structure of such networks of experimentation diversifies. I showed this earlier with the discussion on the effects of chemical warfare in Vietnam and the lawsuit concerning wood preservatives in Germany. But, regarding environmental effects in general, a relationship between a certain emission and a connected damage is difficult to reconstruct. In the case of dioxins, these difficulties multiply because of the inherent complexity of the interactions between these substances and living organisms. The vast number of situations and contexts brings about a high variety of aspects to be addressed within the network of experimentation. If the proof of harm from tobacco was extremely difficult, then what are the chances to prove toxicological effects of low doses of dioxins released into the social and natural environment?​In the oscillating networks of experimentation, it is easier to produce contradictions and delegitimize proof. Therefore, the boundary conditions for the construction of evidence must be maintained while the network is emerging. This aspect highlights the problem that there is much leeway in setting up and using agnotological strategies. The variety of observed contexts, the complexity of the biological structures, the diversity of possible effects—all these aspects form part of the quest for the assessment of risks, as well as their accessibility in general. These considerations can be illustrated by concrete examples.

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One strategy, helpful in many cases, is to compare the toxicity of dioxins with that of other toxins. The result is a scale of toxicity— and the insight that natural toxins are often far more poisonous than chemical ones. This strategy must be interpreted as a strategy of naturalization, and it is successful when dioxins occur in marginal amounts. Another strategy is to ask for the origins of dioxins as trace substance. The questions: Are dioxins mostly of anthropogenic origin?​If so, do they originate from industrial sources?​Or can dioxins also be produced naturally?​A prime example is the “trace chemistry of fire” hypothesis elaborated by Dow Chemical. Its core argument is that every single combustion process—whether industrial or natural—produces dioxins.72 Thus, important sources of dioxins are not only waste incineration plants. Under specific conditions, every simple fireplace could become a source of dioxins. What was the background of the development of this hypothesis?​At that time, Dow Chemical cooperated with federal agencies to improve the water quality of the Tittabawassee River in Michigan. In this context, Dow conducted a study that, on one side, showed this kind of analysis is necessarily based on a deep understanding of the complex methodology. On the other side, the study cited in minute detail its own limitations, as well as why it was, nevertheless, a valid document.73 The main findings: first, dioxins are ubiquitous.74 Second, dioxins are produced in almost every combustion process: industrial, individual (automobiles), natural. Third, the pesticide production facilities are not measurable sources of the chlorinated dioxins found in fish taken from the Tittabawassee River.75 In sum, this argumentation allows Dow to normalize—moreover, to naturalize dioxin production. Other chemical plant managers observed this strategy with admiration: “When Dow Chemical reported two years ago that dioxins can be found all over the globe whenever organic matter (wood, coal, waste) is decomposed by combustion, this message caused not only amazement. Moreover, off the record, people said: ‘Look, how clever Dow is selling this fact!’”76 But the “trace chemistry of fire” hypothesis also provoked opposition. Some scientists analyzed sediments and mummies to study whether the level of dioxin contamination had changed over time. They concluded the level of environmental dioxin contamination had increased since the beginning of industrialization.77 Interestingly enough, this hypothesis itself generated a network of experimentation. Furthermore, this debate is as lively as ever. To give but one example, debates about the sources of dioxins and the factors that lead to high

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concentrations exist within the context of the UNEP Toolkit for identifying environmental hazards. In these debates, “targeted” positions try to relate high rates of dioxins to natural processes.78 In this way, they try to frame dioxins as a natural problem that should not be seen as dramatic as it often is.

Conclusions Mainly regarding these fuzzy networks of experimentation, the substance group of dioxins is an instructive case to study the topic of “hazardous chemicals.” By their example, qualities and characteristics regarding the constitution and communication of “hazardousness” can be shown systematically. First, the way in which risk analysis and risk policy addressed dioxins can be seen as a paradigmatic example of blurring boundaries between (scientifically defined) risks and (public) risk perception. Not only does hype-oriented media induce this: almost every group involved in this debate follows its own strategies and therefore promotes the blurring of boundaries. The general toxicity of dioxins is nowadays an established fact—but their concrete toxicity in specific situational contexts remains uncertain, if not unknown. Second, so to speak, the “worst aspects of both worlds” merge in this case: the public hype-oriented focus on dioxins on the one hand and the economic-industrial ignorance and silencing strategies on the other. Through their specific relationship and interplay, both aspects boosted the public-political debate. Third, specific agnotological ­strategies of science and industry manifest in the discourse about dioxins can be identified. Scientists learned quickly to exploit the debate about dioxins for their own research agenda—without any increase in value for risk management procedures. Industry, on the other hand, tried to dominate the discourse by sowing doubt about the effects of dioxins and fostering arguments that sought to normalize and naturalize potential risks of dioxins. But these insights should not lead to the misjudgment that only a hysterical public and greedy scientists searching for research funds fueled the debate. On the contrary, the debate about dioxins established a collective symbol for the dangers of synthetic toxins. Dioxins as “total poison” serve as an alarm signal and warn collectives about industrial and societal malformations.

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Stefan Böschen is Professor of Technology and Society at the Human Technology Centre of RWTH Aachen University. He studied chemical engineering, philosophy, and sociology and holds a degree in chemical engineering, a doctorate in sociology, and Habilitation in sociology. His current research focuses on the sociology of science, modernity, and risk and on environmental research, with special emphasis on transdisciplinary and problem-oriented research, technology assessment, the analysis of risk politics, and risk communication. He has published numerous books and articles on these themes. Recent publications include “TA at the Crossroads: Politics of TA from the Viewpoint of Societal Problem Solving” (Technological Forecasting and Social Change, 2019) and (with Sophie Elixhauser and Katrin Vogel) “Meshworks and the Making of Climate Places in the European Alps: A Framework for Ethnographic Research on the Perceptions of Climate Change” (Nature and Culture, 2018). Notes   1. Parr and Thiele, Link(s); Parr, “Interdiskursivität und Medialität.”  2. A former critic of the chemical industry wrote: “I consider the narrowing of the debate about pollution loads in highly different contexts to the term dioxins a problem. Sure, the symbolic character of the Seveso-toxin is a useful initiator to problematize the risks of chemical production. But sometimes I get the impression that an environmental scandal is only acknowledged when captioned with the headline of dioxins. Instead of chlorinated hydrocarbons: dioxins in gunnysacks. Instead of pentachlorophenol: dioxins in bedrooms.” Vahrenholt, “Beseitigung,” 223. All translations from German are mine.  3. Radkau, Ära der Ökologie, 231.  4. Carson, Silent Spring.   5. Koch and Vahrenholt, Seveso ist überall.   6. In sum, about two hundred different halogenated dioxins are known, differing in structure and toxicity. In many cases, furanes, an analogous group of substances is at the center of attention. Their structure is slightly different, and in many cases, they are not as toxic as dioxins. Against this background, the amount of dioxin is measured in international toxicity equivalents (I-TEQs), a scale based on the most toxic dioxin, TCDD.   7. Fiedler, “National PCDD/PCDF.” Generally, this Convention organized new classifications of purity, see Douglas, Purity and Danger.   8. Balzer et al., “Remediation Measures.”   9. This development can be substantiated by the fact that occupational medicine emerged quite early as a reaction to these developments. Chemicals hazards in the workplace were a ubiquitous phenomenon in quite different areas of application. Bluma and Rainhorn, History; Markowitz and Rosen, Deceit and

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Denial. Therefore, regulation has been a relevant question since then. Boudia and Jas, Toxicants. 10. At the beginning, there is an unclear observation, just a first idea, groping for insight. In many cases, it takes some time to develop an understanding of an issue’s full shape. Fleck, Entstehung und Entwicklung. 11. See Herxheimer, “Über Chlorakne”; Dohmeier and Janson, Zum Töten, 11. 12. The occupational physician Karl Bernhard Lehmann (Kurzes Lehrbuch, 156–57) recommended “to replace workers showing even the slightest sign of chloracne after a certain time of employment by those with a more robust skin.” 13. Bettmann, “‘Chlor-Akne,’” 440. 14. Herxheimer, “Über Chlorakne.” 15. K. Lehmann, Kurzes Lehrbuch, 155. 16. Bettmann, “‘Chlor-Akne,’” 437. 17. K. Lehmann, “Experimentelle Studien,” 324. 18. W. Lehmann, “Über Chlorakne,” 331. 19. K. Lehmann, Kurzes Lehrbuch, 156. 20. W. Lehmann, “Über Chlorakne,” 324. 21. Teleky, “Pernakrankheit,” 899. 22. In this year, PCN was described as a cause of the chronic “yellow liver atrophy.” Since this is a very rare disease, it could be related to specific noxa. During World War II, PCN was used to protect warships against sea mines, and workers in many plants resisted working with it because of health effects. In a study among workers of plants handling PCN, pathological analyses showed that almost none of the workers had a liver functioning normally (7 of 2,500 workers). See Cotter, “Pentachlorinated Naphthalenes.” 23. However, studies showing these interrelations already existed at that time. Teleky, “Über neuere Forschungsmethoden,” 253. Unfortunately, the focus remained on the indicator chloracne. Even in 1985, Raymond R. Suskind (“Health Effects,” 235), an expert on occupational medicine and dermatology at the University of Cincinnati who had been hired by Monsanto to carry out a study on their workers, characterized chloracne as “the hallmark of absorption and biological response,” although the knowledge on chronic intoxication was already well elaborated. But the broad range of phenomena offered the chance to play down the risks. 24. Sandermann, “Dioxin.” 25. Sandermann et al., “Über die Pyrolyse.” On the tradition of self-experimenting in science and medicine, see Hunter, “Saints and Martyrs.” 26. Kimmig and Schulz, “Berufliche Akne.” 27. First, Boehringer wrote a letter to the plant physicians to stop the diffusion of these insights. Second, he tried to influence Schulz’s superior to prevent any publication on this topic. Schnibben, “Das war der Tod”; Schnibben, “Tod aus Ingelheim.” This tactic is an example of the policies of silencing well established in the chemical industry (Markowitz and Rosen, Deceit and Denial) or of the specific public health hazard cancer (Proctor, Cancer Wars).

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28. Chemisches Zentralblatt 129 (1958): 7542. 29. Sandermann, “Dioxin,” 173. 30. Trost, Elements of Risk, 17. 31. Quoted in Paul, “Zu tödlich,” 111. The characterization “Dioxin-Gift Agent Orange” is interesting, as it frames the connection of dioxins and Agent Orange. In this phrase, it remains unclear if dioxins are Agent Orange or a (bigger or smaller) part of Agent Orange. 32. See Martini, Agent Orange; Pfeiffer and Orians, “Military Uses,” 117–76; Reggiani, “Historical Overview,” 31–76. A color code was used to label different mixtures: Agent White, Agent Blue, and Agent Orange. Agent Orange contains a 50/50 mixture of 2,4-D and 2,3,4-T. It was the most powerful and therefore most used herbicide in Vietnam. 33. An American Institute for Cancer Research study based on animal laboratory tests concluded such herbicides cause malformations and miscarriages. This study seemed to have influenced US President Richard Nixon to stop chemical warfare in Vietnam. Firestone, “2,3,7,8,-Tetrachlorodibenzo-para-dioxin,” 45. 34. Dioxins are fatal in doses of micrograms. 35. Tung et al., “Clinical Effects”; Tung, “Le cancer primaire.” 36. NAS, Effects of Herbicides, 33. 37. IOM, Veterans and Agent Orange, 33. 38. Krohn and Weyer, “Gesellschaft als Labor.” 39. IOM, Veterans and Agent Orange: Update. For an overview of this story, see Scott, Politics. See also Smith, Toxic Exposures. 40. This picture was a keystone for building up the collective symbol of dioxins. Children themselves are a collective symbol of pure and innocent life and therefore must be protected unconditionally. For an overview of this industrial disaster, see Silei, “Technological Hazards.” 41. “Das Trichlorphenol-Unglück von Seveso,” Eurpoa Chemie 15 (1976): 253. 42. “This is the only place on earth, where we can study dose and effect of dioxins in detail.” Quoted in Kohl, “Oase der Frische,” 167. 43. Bonaccorsi et al., “In the Wake,” 239. 44. For an overview, see Hay, “Tetrachlorodibenzo-p-dioxin.” 45. Webster and Commoner, “Overview,” 2–3. 46. Reggiani, “Historical Overview.” 47. Bertazzi and Domenico, “Chemical,” 621. 48. Quoted in “‘Auffallend, diese Parallele mit Seveso,’” Der Spiegel 28, no. 25 (1984): 69. 49. Radkau, Ära der Ökologie, 249. How the chemical industry handled the problem of dioxins (“cartel of silencing”) was not inspiring confidence either. 50. Luhmann, “Entdeckung der Gefahr.” 51. Olie et al., “Chloro-p-dioxins.” 52. This is a general problem of limit values: they limit by allowing something risky. The German Bundes-Immissionsschutzverordnung (23 November 1990) established the limit value of dioxins at 0.1 ng I-TEQ/Nm3.

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53. See Degler and Uentzelmann, Supergift Dioxin, 53. 54. Radkau, Ära der Ökologie, 253. 55. See Sandermann et al., “Über die Pyrolyse.” 56. Quoted in Schäfer, Dioxin, 52. 57. Aurand et al., “Pentachlorphenolhaltige Holzschutzmittel.” 58. See Schöndorf, Von Menschen. 59. See Schlumpf and Lichtensteiger, Humanmilch. 60. Hensel, “Nach der Krise.” But this view can also be criticized, as the relations between industry, food production, media, and government in many cases turns out to be complicated. Jacob et al., “Government Management.” 61. See Weber et al., “Dioxin,” 98–99. 62. See Proctor, Cancer Wars; Proctor, Golden Holocaust; Proctor and Schiebinger, Agnotology. 63. Blair, Chlorodioxins. 64. Tucker et al., Human and Environmental, 773. 65. See Safe et al., “2,3,7,8-Tetrachlorodibenzo-p-dioxin.” 66. Zack and Suskind, “Mortality Experience.” 67. Zack and Gaffey, “Mortality Study.” 68. Hay and Silbergeld, “Assessing the Risk.” 69. Lehnert and Szadkowski, “Zur Humankanzerogenität.” 70. For an overview, see Karmaus, Zusammenspiel, 89–205. 71. Zober et al., “Thirty-Four-Year Mortality Follow-Up.” In the same way, a study on the accident at Boehringer had the same findings: TCDD shows carcinogenic potency. Workers who started at Boehringer before 1954 and worked there for more than twenty years showed a cancer rate twice as high as those of the comparison group. Manz et al., “Cancer Mortality.” 72. Somers and Douglas, “Dioxins and Related Compounds.” For an overview of the different strategies and policies Dow used to pursue its interests, see Doyle, Trespass against Us. 73. Dow Chemical, Trace Chemistries, 2. The findings reported here are not offered as comprehensive or exhaustive results. Limiting factors include the small number of scientists specifically trained in the required methodology and the highly sophisticated instruments needed to conduct the work. In addition, the subject involves a large number of variables over which the investigators had no control. Due to the press of time, it was necessary to use the approach of a detective trying to identify suspects. Samples were not taken by statistical design and results are not intended to represent anything other than the sample analyzed. The analytical methodology is so very new that it has not always been validated and not yet corroborated by other scientists. In fact, the analytical methodology developed so rapidly during this investigation that later results cannot always be directly compared to earlier ones. Nevertheless, the total results are convincing and verify scientific observations that are now emerging worldwide.

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74. Under “Discovery”: “Chlorinated dioxins are ubiquitous. We have concluded their presence is due to the existence of a natural phenomenon, trace chemistry of fire. Trace chemistries of fire consist of numerous chemical reactions occurring during combustion at very low concentrations, parts per million and lower. The measurable yields of the trace chemical reactions can be low as 0.0000000001 percent. The trace chemistries of fire follow two pathways— chemicals reacting at very low yields and low concentration chemicals reacting at high yields.” Ibid., 3. 75. Their findings were reported as being absolutely surprising, but note, the Dow scientists searched for dioxins nearly everywhere with their highly sensitive methods: In explaining these surprising results the following facts must be recognized as very significant: 1. Refuse and fossil fuels are an extremely complex mixturew of many chemical elements and compounds. An enormous number of these chemical elements and compounds are present in refuse and fossil fuels at low concentrations. 2. Conditions in a flame favor the occurrence of every conceivable type of chemical reaction. 3. Chemical reactions which occur at part per million and part per billion levels have gone unreported because the measurement techniques to study them have not been available. 4. Modern analytical techniques are so incredibly sensitive and specific that results of chemical reactions occurring with very low yields, 0.0000000001 percent, can now be identified and determined. Therefore, it can be shown that chemicals at part per billion levels can produce measurable amounts of other chemicals. 5. Combustion processes must be greater than 99.9 percent efficient in order to insure the reduction of the concentration of a chemical from 1 part per million to 1 part per billion. Common combustion processes are not nearly this efficient. (Ibid., 5–6)

76. Memorandum Dr. Werner Krum, Boehringer-Werk Hamburg, 29 October 1980, quoted in Ernst et al., Gift-Grün, 150. 77. Schecter et al., “Sources of Dioxin.” 78. Martin Scheringer, personal email communication, 22 March 2012.

Bibliography Aurand, Karl, Norbert Englert, Christian Krause, D. Ulrich, and R. Walter. “Pentachlorphenolhaltige Holzschutzmittel in Wohnräumen.” Schriftenreihe des Vereins für Wasser-, Boden- und Lufthygiene 52 (1981): 293–313. Balzer, Wolfgang, H.-M. Gaus, Caroline Gaus, Roland Weber, Birgit SchmittBiegel, and Ulrich Urban. “Remediation Measures in a Residential Area Highly Contaminated with PCDD/PCDF, Arsenic and Heavy Metals as a Result of Industrial Production in the Early 19th Century.” Organohalogen Compounds 69 (2007): 857–60.

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Bertazzi, Pier Alberto, and Alessandro di Domenico. “Chemical, Environmental and Health Aspects of the Seveso, Italy, Accident.” In Schecter, Dioxins and Health, 587–632. Bettmann, Siegfried. “‘Chlor-Akne,’ eine besondere Form von professioneller Hauterkrankung.” Deutsche Medicinische Wochenschrift 27 (1901): 437–40. Blair, Etcyl H., ed. Chlorodioxins: Origin and Fate. Washington, DC, 1973. Bluma, Lars, and Judith Rainhorn, eds. History of the Workplace: Environment and Health at Stake. London, 2015. Bonaccorsi, Aurora, Roberto Fanelli, and Gianni Tognoni. “In the Wake of Seveso.” Ambio 7 (1978): 234–39. Boudia, Souraya, and Nathalie Jas, eds. Toxicants, Health and Regulation since 1945. London, 2013. Carson, Rachel. Silent Spring. Boston, 1962. Cotter, Lawrence H. “Pentachlorinated Naphthalenes in Industry.” Journal of the American Medical Association 125, no. 4 (1944): 273–74. Degler, Hans-Dieter, and Dieter Uentzelmann, eds. Supergift Dioxin: Der unheimliche Killer. Reinbek, 1984. Dohmeier, Hans-Joachim, and Erich Janson. Zum Töten von Fliegen und Menschen: Dioxin—Das Gift von Seveso und Vietnam, und wie wir täglich damit in Berührung kommen. Reinbek, 1983. Douglas, Mary. Purity and Danger: An Analysis of the Concepts of Pollution and Taboo. London, 1966. Dow Chemical. The Trace Chemistries of Fire: A Source of and Routes for the Entry of Chlorinated Dioxins into the Environment. Midland, MI, 1978. Doyle, Jack. Trespass against Us: Dow Chemical and the Toxic Century. Monroe, ME, 2004. Ernst, Andrea, Kurt Langbein, and Hans Weiss. Gift-Grün: Chemie in der Landwirtschaft und die Folgen. Köln, 1986. Fiedler, Heidelore. “National PCDD/PCDF Release Inventories under the Stockholm Convention on Persistent Organic Pollutants.” Chemosphere 67, no. 9 (2007): 96–108. Firestone, David. “The 2,3,7,8-Tetrachlorodibenzo-para-dioxin Problem: A Review.” In Chlorinated Phenoxy Acids and Their Dioxins: Mode of Action, Health Risks and Environmental Effects, edited by Claës Ramel, 39–52. Stockholm, 1978. Fleck, Ludwik. Entstehung und Entwicklung einer wissenschaftlichen Tatsache. Frankfurt, 1993. First published in 1935 (Frankfurt). Hay, Alastair. “Tetrachlorodibenzo-p-dioxin Release at Seveso.” Desasters 1 (1977): 289–308. Hay, Alastair, and Ellen Silbergeld. “Assessing the Risk of Dioxin Exposure.” Nature 315, no. 6015 (1985): 102–3. Hensel, Andreas. “Nach der Krise ist vor der Krise: Lebensmittelsicherheit zwischen Weltanschauung und globalisiertem Handel.” Presentation at the Bund für Lebensmittelrecht und Lebensmittelkunde annual meeting, Berlin, 14 April 2011.

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Herxheimer, Karl. “Über Chlorakne.” Münchner Medizinische Wochenschrift 46 (1899): 278. Hunter, Donald. “Saints and Martyrs.” The Lancet 228, no. 5906 (1936): 1131–34. IOM (Institute of Medicine). Veterans and Agent Orange: Health Effects of Herbicides Used in Vietnam. Washington, DC, 1994. _____. Veterans and Agent Orange: Update 1996. Washington, DC, 1996. Jacob, Casey, Corie Lok, Katija Morley, and Douglas A. Powell. “Government Management of Two Media-Facilitated Crises Involving Dioxin Contamination of Food.” Public Understanding of Science 20, no. 2 (2011): 261–69. Karmaus, Wilfried. “Das Zusammenspiel von Wissenschaft, Behörden und Industrie dargestellt am Fall der Risiko-Beurteilung und Risiko-Bewältigung von Dioxinen.” Forschungsgruppe Gesundheitsrisiken und Präventionspolitik WZB Discussion Paper. Berlin, 1989. Kimmig, Joseph, and Karl Heinz Schulz. “Berufliche Akne (sog. Chlorakne) durch chlorierte zyklische Äther.” Dermatologica 115 (1975): 540–46. Koch, Egmont R., and Fritz Vahrenholt. Seveso ist überall: Die tödlichen Risiken der Chemie. Köln, 1978. Kohl, Christiane. “Oase der Frische.” Der Spiegel 50, no. 28 (1996): 166–67. Krohn, Wolfgang, and Johannes Weyer. “Die Gesellschaft als Labor: Risiko­trans­ formation und Risikokonstitution durch moderne Forschung.” In Riskante Entscheidungen und Katastrophenpotentiale, edited by Jost Halfmann and Klaus Peter Japp, 89–122. Opladen, 1990. Lehmann, Karl Bernhard. “Experimentelle Studien über den Einfluß technisch und hygienisch wichtiger Gase und Dämpfe auf den Organismus: XI. Studien über ‘Chlorakne.’” Archiv für Hygiene 46 (1903): 322–36. _____. Kurzes Lehrbuch der Arbeits- und Gewerbehygiene. Leipzig, 1919. Lehmann, Wilhelm. “Über Chlorakne.” Archiv für Dermatologie und Syphilis 77 (1905): 265–88, 323–44. Lehnert, Gerhard, and Dieter Szadkowski. “Zur Humankanzerogenität von 2,3,7,8-TCDD: Unfallversicherungsrechtliche Beurteilung.” Arbeitsmedizin Sozialmedizin Präventivmedizin 20 (1985): 225–32. Luhmann, Hans-Jochen. “Die Entdeckung der Gefahr einer ubiquitären DioxinVerbreitung: Ein Beispiel einer latenten schleichenden Katastrophe?​ ” In Jahrbuch Ökologie 1993, 215–27. Munich, 1992. Manz, Alfred, Jürgen Berger, James H. Dwyer, Dieter Flesch-Janys, Sibylle Nagel,  and Hiltraud Waltsgott. “Cancer Mortality among Workers in Chemical Plant Contaminated with Dioxin.” The Lancet 338, no. 8773 (1991): 959–64. Markowitz, Gerald, and David Rosner. Deceit and Denial: The Deadly Politics of Industrial Pollution. Berkeley, CA, 2002. Martini, Edwin A. Agent Orange: History, Science, and the Politics of Uncertainty. Amherst, MA, 2012. NAS (National Academy of Sciences). The Effects of Herbicides in Vietnam. Washington, DC, 1974.

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Olie, K., P. L. Vermeulen, and Otto Hutzinger. “Chloro-p-dioxins and Chlorodi­ benzo­ furans Are Trace Compounds of Fly Ash and Flue Gas of Some Municipal Waste Incinerators in the Netherlands.” Chemosphere 6 (1977): 455–59. Parr, Rolf. “Interdiskursivität und Medialität.” In Medien des Wissens: Inter­ disziplinäre Aspekte von Medialität, edited by Georg Mein and Heinz Sieburg, 23–42. Bielefeld, 2011. Parr, Rolf, and Matthias Thiele, eds. Link(s): Eine Bibliografie zu den Konzepten “Interdiskurs,” “Kollektivsymbolik” und “Normalismus” sowie einigen weiteren Fluchtlinien. Heidelberg, 2010. Paul, Rainer. “‘Zu tödlich für die Kriegsführung’: Das Dioxin-Gift Agent Orange als chemische Waffe in Vietnam.” In Degler and Uentzelmann, Supergift Dioxin, 99–124. Pfeiffer, E. W., and Gordon H. Orians. “The Military Uses of Herbicides in Vietnam.” In Harvest of Death: Chemical Warfare in Vietnam and Cambodia, edited by John B. Neilands, Gordon H. Orians, E. W. Pfeiffer, Alje Vennema, and Arthur H. Westing, 117–76. New York, 1972. Proctor, Robert N. Cancer Wars: How Politics Shapes What We Know and Don’t Know About Cancer. New York, 1996. _____. Golden Holocaust: Origins of the Cigarette Catastrophe and the Case of Abolition, Berkeley, 2011. Proctor, Robert N., and Londa Schiebinger, eds. Agnotology: The Making and Unmaking of Ignorance. Stanford, CA, 2008. Radkau, Joachim. Die Ära der Ökologie: Eine Weltgeschichte. Munich, 2011. Reggiani, Guiseppi. “Historical Overview of the Controversy surrounding Agent Orange.” In Agent Orange and its Associated Dioxin: Assessment of a Controversy, edited by Alvin L. Young and Guiseppi Reggiani, 31–76. Amsterdam, 1988. Safe, Stephen, B. Astroff, M. Harris, T. Zacharewski, R. Dickerson, M. Romkes, and L. Biegel. “2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds as Antiestrogens: Characterization and Mechanisms of Action.” Pharmacology and Toxicology 69, no. 6 (1991): 400–409. Sandermann, Wilhelm. “Dioxin: Die Entdeckungsgeschichte des 2,3,7,8-Tetra­ chloro-dibenzo-p-dioxins (TCDD, Dioxin, Sevesogift).” Naturwissenschaftliche Rundschau 37 (1984): 173–78. Sandermann, Wilhelm, Hans Stockmann, and Reinhard Casten. “Über die Pyrolyse des Pentachlorphenols.” Chemische Berichte 90 (1957): 690–92. Schäfer, Herbert. Dioxin auf dem Holzweg: Giftige Farben und Lasuren— Verbraucherreport. Bergisch Gladbach, 1987. Schecter, Arnold, ed. Dioxins and Health. New York, 1994. Schecter, Arnold, Albert Dekin, N. C. A. Weerasinghe, Saleh Arghestani, and Michael L. Gross. “Sources of Dioxin in the Environment: A Study of PCDDs and PCDFs in Ancient, Frozen Eskimo Tissue.” Chemosphere 17, no. 4 (1988): 627–31.

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Schlumpf, Margret, and Walter Lichtensteiger, eds. Humanmilch: Daten zur Belastung mit PCB, Dioxinen, Pestiziden und Moschus-Xylol. Zürich, 1993. Schnibben, Cordt. “‘Das war der Tod persönlich.’” Der Spiegel 45, no. 31 (1991): 102–14. _____. “Der Tod aus Ingelheim.” Der Spiegel 45, no. 32 (1991): 106–20. Schöndorf, Erich. Von Menschen und Ratten. Göttingen, 1998. Scott, Wilbur J. The Politics of Readjustment: Vietnam Veterans since the War. Milton Park, 2017. Silei, Gianni. “Technological Hazards, Disasters and Accidents.” In The Basic Environmental History, vol. 4, edited by Mauro Agnoletti and Simone Neri Serneri, 227–53. Cham, 2014. Smith, Susan L. Toxic Exposures: Mustard Gas and the Health Consequences of World War II in the United States. New Brunswick, NJ, 2017. Somers, E., and V. M. Douglas. “Dioxins and Related Compounds as Issues of International Concern.” In Tucker et al., Human and Environmental Risks, 33–41. Suskind, Raymond R. “The Health Effects of 2,4,5-T and Its Toxic Contaminants.” In Dioxins in the Environment, edited by Michael A. Kamrin and Paul W. Rodgers, 231–35. Washington, DC, 1985. Teleky, Ludwig. “Die Pernakrankheit (Chloracne).” Klinische Wochenschrift 6 (1927): 845–48; 897–901. _____. “Über neuere Forschungsmethoden und Forschungen auf dem Gebiet der Gewerbekrankheiten.” Klinische Wochenschrift 27 (1949): 249–57. Trost, Cathy. Elements of Risk: The Chemical Industry and Its Threat to America. New York, 1984. Tucker, Richard E., Alvin L. Young, and Allan P. Gray, eds. Human and Environmental Risks of Chlorinated Dioxins and Related Compounds. New York, 1983. Tung, Ton That. “Le cancer primaire du foie au Vietnam.” Chirurgie 99, no. 7 (1973): 427–36. Tung, Ton That, T. K. Anh, B. Q. Tuyen, D. X. Tra, and N. X. Hugen. “Clinical Effects of Massive and Continuous Utilization of Defoliants on Civilians.” Vietnamese Studies 21 (1971): 53–81. Vahrenholt, Fritz. “Beseitigung von dioxinhaltigen Abfällen aus der Sicht der Verwaltung.” In Dioxine: Entstehung—Wirkungen—Beseitigung, edited by Fortbildungszentrum Gesundheits- und Umweltschutz, 223–33. Berlin, 1985. Weber, Roland, Mats Tysklind, and Caroline Gaus. “Dioxin: Contemporary and Future Challenges of Historical Legacies.” Environmental Science and Pollution Research 15, no. 2 (2008): 96–100. Webster, Thomas, and Barry Commoner. “Overview: The Dioxin Debate.” In Schechter, Dioxins and Health, 1–50. Zack, Judith A., and William R. Gaffey. “A Mortality Study of Workers Employed at the Monsanto Company Plant in Nitro, West Virgina.” In Tucker et al., Human and Environmental Risks, 575–91.

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Zack, Judith A., and Raymond R. Suskind. “The Mortality Experience of Workers Exposed to Tetrachlorodibenzodioxin in a Trichlorophenol Process Accident.” Journal of Occupational Medicine 22, no. 1 (1980): 11–14. Zober, Andreas, Peter Messerer, and Peter Huber. “Thirty-Four-Year Mortality Follow-Up of BASF Employees Exposed to 2,3,7,8-TCDD after the 1953 Accident.” International Archive of Occupational Environmental Health 62, no. 2 (1990): 139–57.

/ PART III New Products, New Effects The Discovery of the Environment and the Long Shadow of the 1960s

/

CHAPTER 8

Organophosphates Frederick Rowe Davis

Near the end of 1972, William Ruckelshaus, the first head of the US

Environmental Protection Agency, canceled the registration for DDT, thereby terminating most uses in the United States. This action closed the curtain on nearly a decade of rancorous debate on the indiscriminate use of DDT and other chemical insecticides that was first brought to public awareness with the publication of Silent Spring in 1962. However, the history of pesticides and toxicology reveals a tragic irony in pesticides regulation in the years following Silent Spring. In her wellknown book, Rachel Carson recommended reducing the use of DDT and all chemical insecticides, yet legislators focused inordinate attention on DDT and other chlorinated hydrocarbons. In celebrating the EPA ban on DDT and other chlorinated hydrocarbons, widely cited as a crowning achievement of the nascent US environmental movement, legislators failed to regulate other highly toxic insecticides. In a similar vein, many historians have studied the history of DDT and reified the significance of its ban to the environmental movement. However, neither legislators nor historians fully captured Carson’s broad recommendations. Moreover, reading Silent Spring simply as an indictment of DDT posed ongoing risks to farmworkers, wildlife, and consumers. Ignoring the risks of other pesticides had global implications. More specifically, the DDT ban in 1972 left farmers and public health officials scrambling for alternatives; farmers in particular soon adopted organophosphate insecticides, some of the most toxic chemicals in existence. Organophosphates were originally developed during the same era as DDT and other chlorinated hydrocarbons, but commercial distribution of these chemicals was delayed until after World War

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II. Despite toxicities of several orders of magnitude greater than DDT, farmers preferred organophosphates in certain circumstances for their efficacy and their effect on organisms like aphids that t­olerated DDT. But the irony of this story reaches full form in the decades after the DDT ban. Thus, a biography of organophosphates—or, more a­ ccurately, a “family history” of this large and diverse class of c­ hemicals—begins with their synthesis and proceeds to toxicological analysis and widespread adoption in agricultural and concludes with bans in the United States and Europe.1

Synthesizing Organophosphate Chemicals Organic phosphate (later called organophosphate) insecticides—most of them esters of phosphorous acid—were developed by German chemists who had since 1936 studied them in the plant protection laboratory of Farbenfabriken Bayer in Wuppertal-Elberfeld. Their task was to develop synthetic insecticides that could make Germany economically independent from the use of insecticides extracted from plants, such as nicotine, rotenone, or pyrethrum. All these insecticides had to be imported. Gerhard Schrader, a leading chemist at Farbenfabriken Bayer, had the task to develop insecticides based on domestic (German) resources that could be used as ersatz for natural pesticides that Germany had to import. Schrader’s task was part of the economic policy to make Germany self-sufficient and independent from foreign imports. Schrader concentrated his research on organophosphates. As the first examined organophosphorus compounds proved extremely toxic, it very quickly became clear they were far too toxic for warm-blooded animals, including humans. Thus, they were obviously unsuited for the use as plant protection agents. However, as soon as the organophosphorus compounds tabun and sarin were discovered in 1937 and 1938, respectively, these extremely toxic compounds clearly could be used as chemical warfare agents instead. Leading Bayer chemists informed the German chemical warfare department about the properties of these newly discovered substances. Shortly before World War II, this information sparked the interest of the relevant military institutions. Because of laboratory accidents, Schrader had direct experience with the toxic effects of these substances, which had strong physiological effects on the human body, particularly sight. After the war, Schrader’s observation led to the development of a medicament based on organo-

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phosphorus compounds, the German Mintacol, which has been used in ophthalmology to treat glaucoma and myasthenia gravis. Since 1938, Bayer toxicologists and physiologists were particularly interested in studying the biological mode of action of tabun and sarin, because the German military had meanwhile decided to use both these organophosphorus compounds as possible chemical weapons. However, though tabun and sarin were produced in large quantities in Germany, they were fortunately never deployed during World War II.2 The first commercial organic phosphate insecticide, hexaethyl tetraphosphate (HETP), was developed in Schrader’s lab in 1942; Bayer started producing it in Leverkusen in 1943. The compound that could be synthesized from resources easily available in Germany entered the market in 1944. It was named Bladan (derived from the German Blattlaus for “aphid”) and replaced nicotine, which Germany hitherto had to import to fight aphids. The Germans already knew HETP was very toxic for warmblooded animals. In 1938, Schrader also synthesized tetraethyl pyro­ phos­phate (TEPP), one of the first pyrophosphoric esters developed as an insecticide and thus one of the oldest organophosphates, though its commercial development was delayed. After the British Intelligence Objectives Sub-Committee (BIOS, Final Report, no.714) interrogated Schrader and his coworkers in the war’s immediate aftermath, the German knowledge about the properties of organophosphorus compounds reached the United States.3 There, one of the first groups to gain access to organic phosphates was the University of Chicago Toxicity Laboratory and, specifically, Kenneth DuBois, a young toxicologist who had joined the Tox Lab after receiving his doctorate in biochemistry and physiology at the University of Wisconsin. DuBois and his associates recognized cholinergic symptoms produced by the new chemicals and found atropine would be an effective antidote.4 In the United States, there was considerable interest in the new insecticides because organic phosphates could allegedly control aphids, against which DDT was proving ineffective. The Tox Lab assumed the responsibility for testing the toxicity of the new chemicals largely because the University of Chicago was near a major chemical firm, Chemagro, where organic phosphates were synthesized. Tox Lab researchers could not find any references to HETP’s mechanism of action other than the possible nicotinic effects. Several researchers noted during routine testing that animals showed symptoms such as muscular twitching, tonic and tonic-clonic convulsions, involuntary defecation, micturition (urination), and salivation, which prompted

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DuBois to consider HETP’s possible effects on cholinesterase. Through a series of in vitro and in vivo tests, DuBois and George Mangun (also a Tox Lab researcher and its director from 1946 to 1953) investigated HETP’s effect on cholinesterase. The in vivo results verified the in vitro experiments, revealing cholinesterase inhibition in all the tissues.5 This research definitively connected the new insecticides with cholinesterase inhibition. DuBois and other Tox Lab researchers examined the toxicity of other organic phosphate insecticides as well. The toxicologist John Doull, who earned his PhD and MD from the Tox Lab in 1950 and 1953, respectively, joined DuBois for much of this research. Doull later recalled he had initially contributed to the analysis of the toxicity of organic phosphate chemicals.6 One of the most important chemicals investigated at the Tox Lab was parathion. Although Schrader had already synthesized this compound in 1944, the Germans, who had called the same compound E605, could not release it to the market before the end of the war. As they were required to divulge all information about the synthesis and possible applications of that newly developed organophosphorus compound to the British and Americans, the knowledge about this and related organophosphate compounds reached the United States in August 1945.7 Thus, a US company— American Cyanamid—could release parathion to the market earlier than the Germans could. Parathion appeared to be particularly effective against plant insects; its potential use stimulated researchers to examine its toxicity and pharmacologic action in mammals. Their approach to the analysis of parathion shared many similarities with the toxicological analyses of DDT. Along with Paul R. Salerno and Julius M. Coon, DuBois and Doull conducted the standard toxicological assessment and evaluated the acute and subacute toxicity of parathion. They also tested its inhibitory action on cholinesterase. The initial task was to determine the LD50 (lethal dose 50, or median lethal dose), the dosage that would kill 50 percent of an experimental population. They determined LD50 values were low (less than 20 mg/kg) in all species (rats, mice, cats, and dogs) whether parathion was administered intraperitoneally (by injection) or orally. A low LD50 corresponds to a very high toxicity. When sublethal doses of parathion were administered daily, its toxic action was cumulative. DuBois and his team also noted the parathionproduced symptoms were similar in all species tested. These symptoms were typical of parasympathomimetic drugs. The Tox Lab researchers showed parathion, like HETP, was a strong inhibitor of cholinesterase.

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A picture of consistency within the class of organic phosphate insecticides gradually emerged from toxicological assessments. DuBois and his team also conducted the first toxicological evaluation of octamethyl pyrophosphoramide. Schrader, too, had already synthesized this compound, in 1941. In the United States, it entered the market under the name Pestox, whereas the German name, Schradan, was in honor of its discoverer. Also, the Bayer researchers had already studied the interesting insecticidal properties of OMPA in 1941. At that time, they recognized OMPA acted as systemic insecticide, which means the relevant insecticide, once applied, circulated within the plants that absorbed the chemical through the roots and/or leaves. In this way, the tissues of the plants themselves became insecticidal. Systemic insecticides promised to simplify insect control, but they also threatened nontarget insects such as bees. In his OMPA assessment, DuBois also noted OMPA’s systemic action.8 Most organophosphates (e.g., HETP, TEPP, parathion) acted as “contact” poisons, which meant they killed target insects on contact. In the Tox Lab, DuBois mainly studied the toxicity of organic phosphates to animals, while other labs assessed the risks posed to humans from information gained through occupational accidents. The staff scientist David Grob and other researchers at the Johns Hopkins University School of Medicine reviewed the toxic effects of parathion in thirty-two men and eight women following accidental exposure. As in the Tox Lab, the medical division of the US Army Chemical Corps supported the Johns Hopkins research. Grob and his colleagues revealed parathion could be absorbed through the skin without inflammation, which would limit detection before symptomology.9

Arnold Lehman, the FDA, and Organophosphate Insecticides Officials at the US Food and Drug Administration also studied the new chemicals. From 1946 on, Arnold J. Lehman served as the chief of the FDA Division of Pharmacology, which was responsible for the analysis and regulation of insecticides. That year, a reorganization of the FDA established specialized sections. Under the new arrangement, the division of toxicology division encompassed the acute, chronic, and dermal toxicity sections. Lehman assumed his post at the FDA after a distinguished career in research and academia.10 In June 1948, Lehman addressed the Association of Food and Drug Officials of the United States in Portland, Maine, on the subject of “The Toxicology of

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the Newer Agricultural Chemicals.” He compared the toxicities of two dozen insecticides including chlorinated hydrocarbons (DDT, chlordane, and heptachlor), organic phosphates (TEPP, parathion, HETP), and a plant-derived insecticide, nicotine. Using DDT as a reference standard for insecticide toxicology, he listed the insecticides according to their acute oral toxicities. In this hierarchy, DDT had a mean lethal dose of 250 mg/kg. In comparison, the lethal dose of TEPP was only 2 mg/kg (or 125 times more toxic than DDT); of parathion, 3.5 mg/kg (70 times more toxic); and of HETP, 7 mg/kg (35 times more toxic). Lehman’s hierarchy highlighted the relatively low acute toxicity of DDT and, in contrast, the high acute toxicity of organic phosphates. Lehman anticipated some of the most significant problems associated with the newer organophosphorus chemical insecticides. First, he undercut one of the fundamental beliefs behind the expanding pesticide use: “It is a fairly safe assumption that chemicals which are toxic to insects are also toxic to man and animals. The great emphasis that has been placed on the specificity of DDT for insects loses its importance when fatal doses are compared on a body-weight basis with warm-blooded animals. On this basis the quantities required are practically identical.”11 Although he was extrapolating from limited data, Lehman’s statement drew on his vast experience in pharmacology. He also expressed concern that the body stored certain insecticides like DDT in fat. Even more disturbing was the secretion of DDT and other chlorinated hydrocarbons in milk: “This is especially important in cases of infants, where the chief diet is milk.” Lehman’s concern was not limited to DDT and chlorinated hydrocarbons. Parathion was known to have a cumulative action, which pointed to its storage in tissues, but Lehman found evidence of translocation in plants more troubling given its high toxicity; he worried the dangers of parathion could transfer from one plant to another, increasing risks for consumers. Moreover, no one knew the dangers of using such chemicals in aerosol form. This point deserves emphasis. Most of these chemicals were slated to be aerosolized and deployed in agriculture and public health, but a leading expert on the toxicology of these chemicals warned that no one knew their toxicity in this form. This information was available only for DDT, which had a safety factor several hundred times greater in such conditions. Lehman effectively outlined a comparison of the toxicology of the new agricultural chemicals and from this review identified some of the significant concerns about their widespread utilization.12

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In 1949, Lehman returned to the new insecticides. He noted TEPP remained the most dangerous insecticide from the standpoint of acute and dermal toxicity, although its hydrolytic products posed little risk. The chronic feeding experiments for parathion had been extended to fifty-two weeks on rats and dogs, he reported, and the lowest level at which gross symptoms became apparent remained 25 ppm in the diet. Along with mg/kg, ppm was the benchmark notation for concentration. Correcting one of his earlier statements, he now noted parathion was not stored in the body tissues. Lehman attempted to list the insecticides in descending order of potential harmfulness to the public health, emphasizing risks other than those related to the spray residue on foods. He arranged the toxicity of insecticides as follows: “TEPP > Parathion > Compound 497 [later called Dieldrin] > Nicotine > Compound 118 (later Aldrin) > Chlordane > Toxaphene > DDT > Rotenone.”13 On the important issue of spray residues, he noted the values established as safe by the current experimental evidence were subject to change and applied only to a single item of food. According to this table, the most toxic of organic phosphates was also the most rapidly decomposed into harmless, nontoxic products. So quickly would TEPP decay that Lehman and other scientists saw no need to set a residue level. Because of its slower rate of decay, parathion’s residue limit was 2 ppm. DDT, the subject of the most scrutiny, received the lowest residue level. But, because specific chemical methods for isolating many chlorinated hydrocarbon insecticides had not been developed, Lehman acknowledged the detection of their presence in foods depended on organic chloride determinations.14 A committee on pesticides of the American Medical Association Council on Pharmacy and Chemistry reviewed the available information on the known organic phosphates in 1950. After a general description of TEPP, HETP, and parathion, DuBois and Grob summarized their pharmacology and toxicity (both were recapitulations of earlier papers). Two doctors from American Cyanamid (a chief producer of organic phosphate chemicals) and another from the California Department of Health discussed clinical experience, briefly presenting eight fatal cases (mostly occupational exposure of various sorts resulting from lack of protective clothing), but included accidental deaths. Such accounts set organic phosphates sharply apart from chlorinated hydrocarbons like DDT. In the final section of the CPC report, Arnold Lehman of the FDA and J. C. Ward of the US Department of Agriculture reported on the effects of organophosphates on beneficial forms of life, crops, and

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soil, as well as residue hazards. Lehman and Ward noted that while HETP and TEPP had little effect on beneficial plants, parathion damaged certain varieties of apples, pears, cucumbers, squash, and tomatoes, as well as dormant plants. The rapid hydrolyzation (disintegration in water) of most organic phosphates appeared to reduce their risk in soil, but Lehman and his collaborators said the relatively slower rate of hydrolyzation of parathion posed a health hazard when it was used on turf. They also introduced evidence from lifetime animal feeding studies that indicated no detectable cumulative effects below 25 ppm. From this data, Lehman extrapolated the risk to humans and set the safe residue level at 2 ppm. Even as he proposed a safe residue level, Lehman cautioned that normal weathering would reduce parathion residues to this level of safety only if parathion was applied strictly in accordance with the recommendations of the USDA Bureau of Entomology and Plant Quarantine with “particular reference to the time between the last spraying and the harvesting of the fruit.” Lehman also asked whether a fruit peel would be used in preparing a particular foodstuff. Even at the lowest effective spray concentrations, the peel of a fruit taken alone could carry a load of two to three parts per million of parathion, while this same concentration constituted 0.16 part per million extended to the entire fruit. This distinction was crucial: peeling the fruit before use, utilizing the whole fruit, or the peel alone could change the level of exposure to parathion by an order of magnitude. In light of these variables, Lehman’s conclusion seemed rather incongruous: “If spray schedules recommended by qualified entomologists are followed, it is quite unlikely that a parathion spray residue problem will become serious.”15 DuBois also addressed the issue of food residues and food contamination by insecticides such as DDT, organic phosphates, and, in particular, organophosphates that were new systemic insecticides. He succinctly reviewed the state of knowledge in 1950 on the acute and chronic toxicity of each of the insecticides. Chlorinated hydrocarbons had been a problem of major concern since their introduction. They were stable toward hydrolysis, and spray residues could remain on fruits and vegetables for a long time. In addition, they were fat soluble, and dairy cattle’s ingestion of contaminated forage resulted in the appearance of insecticides in the milk where they were concentrated in the fat. All these factors associated with chlorinated hydrocarbons contributed to the significant risk of chronic toxicity. DuBois cited

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one of the few studies of chronic dietary exposure to DDT, which showed DDT levels of 100 mg/kg of food-produced chronic poisoning (in the form of liver damage) in rats during the two-year study. Like Lehman, DuBois urged caution in the face of scientific uncertainty. In contrast to chlorinated hydrocarbons, food contamination had not been a problem with organic phosphate chemicals such as HETP and TEPP because of their rapid hydrolysis when in contact with moisture. Consequently, spray residues on fruits and vegetables would lose their toxicity before the foods were consumed. Even parathion, DuBois explained, although more stable toward hydrolysis than were other organic phosphates, was still rendered nontoxic before foods were harvested. DuBois drew a distinction between typical contact organic phosphates and the systemic insecticides such as OMPA. What did this mean for possible food contamination?​DuBois noted the insecticidal agent formed within plants from OMPA rapidly lost its toxicity, rendering plants nontoxic to insects by the time the plants reached maturity. He wondered, however, about the potential risk from plants harvested before they finished growing. Because those plants could be dangerously contaminated, he advised restraint in the application of systemic insecticides to plants not used as food or food crops that were never harvested before maturity.16 Thus, in 1950, DuBois underscored the fundamental differences between chlorinated hydrocarbons and organophosphates. Chlorinated hydrocarbons like DDT did not typically cause acute poisoning after a single dose. Research had demonstrated, however, that animals ingesting the new synthetic insecticides for a long time could be poisoned. In contrast, acute toxicity posed the most significant risk with organic phosphate insecticides, while their rapid hydrolysis greatly limited the threat of chronic toxicity and food contamination. Finally, DuBois noted that organophosphates used as systemic insecticides presented greater risk than contact organophosphates because of their ability to be absorbed by plants. His simple taxonomy of the risks associated with the three new classes of insecticides captured their essential differences. Most of the research activity on organophosphates discussed thus far was concentrated in two locations in the United States: the University of Chicago Tox Lab under the supervision of DuBois, and the FDA Division of Pharmacology with Lehman as its chief. Of course, there were similar research programs in Germany and the Soviet Union. Both DuBois and Lehman presented hierarchies of the risks posed by

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the various new insecticides within the broad categories chlorinated ­hydrocarbons, organophosphates, and systemic insecticides. Although the various groups seemed to work independently without direct collaboration, DuBois, Doull, and other Tox Lab researchers worked closely with Dan MacDougall and Dallas Nelson, the scientific staff at Chemagro in Kansas City to plan and execute studies and eventually to defend new insecticides before the FDA. Doull recalled meetings with the FDA and industry representatives as brief, informal, and focused on science.17 In 1952, DuBois and Julius M. Coon, a Tox Lab doctor, returned to the toxicology of organic phosphorous-containing insecticides to mammals. Organic phosphates were classified into three groups based on their chemical formula: alkyl pyrophosphates, alkyl thiophosphates, and phosphor amides, which gained importance in this very order. Among the alkyl pyrophosphates, TEPP was the most important, and DuBois and Coon reconfirmed TEPP’s considerable toxicology, particularly cholinesterase inhibition. In an analysis of additional alkyl pyrophosphates, they all exhibited cholinergic properties similar to TEPP. Several important organophosphates including parathion, malathion, and systox appeared among the alkyl thiophosphates. DuBois and Coon attributed the interest to the extensive use of parathion as an agricultural insecticide. Their goal in reviewing this group was to find a compound as toxic as parathion to insects but less toxic to mammals. The parathion LD50 for rats was 5.5 mg/kg, while that for malathon (which after 1953 was called malathion) was much higher, at 750 mg/kg. This was one of the first references to the toxicity of this important insecticide American Cyanamid had developed in 1950. DuBois and Coon urged these results be interpreted cautiously, however, in that lower toxicity to mammals generally correlated to lower toxicity to insects, which would require higher concentrations in formulations for insect control.18 Embedded within this statement is a clear expression of one of the challenges of insecticide development: insecticides of a lower toxicity to mammals often necessitated higher concentrations or quantities to produce the same measure of insect control. Raising the concentration or quantity undermined the advantage in toxicity, and this presents a paradox for economic entomologists. The reference to malathion indicates that, in the Tox Lab, DuBois and Coon had access to the newest insecticides, even those still in development stages. The first complete review of the toxicity of mala-

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thion did not appear until 1953, when Lloyd W. Hazleton and Emily G. Holland of Hazleton Laboratories in Falls Church, Virginia, summarized mammalian investigations of the new chemical. In collaboration with American Cyanamid, which produced malathion, Hazleton Laboratories selected from a coordinated screening program. From entomological data, Hazleton and Holland believed malathion would find wide use as an insecticide, which might lead to appreciable human exposure. Because their preliminary data suggested considerable variation between insect and mammalian toxicity, they conducted further experiments on the acute toxicity of the substance to several different kinds of animals, suggesting the possibility of a threshold for the effects of cholinesterase inhibition. In time, malathion would emerge as unique among organophosphates: it was the only chemical in the class to exhibit low toxicity for warm-blooded animals while simultaneously destroying aphids and other insects. The high toxicity of malathion to bees would also emerge over time. The results of the experiments conducted at Hazleton Laboratories demonstrated that malathion not only was much less toxic to mammals than parathion but also seemed to be the least toxic of all organophosphate insecticides. Hazleton and Holland used their results with to question DuBois and Coon’s opinion on organophosphorus insecticides: “These data suggest that it would be timely to reconsider the view expressed by DuBois and Coon that those materials which have a low toxicity for mammals generally exhibit a low toxicity for insects.” Hazleton and Holland argued that while parathion was approximately 100 times as potent in vitro and 135 times as toxic to rats as malathion, “under usage conditions, no more than two to three times as much as parathion is recommended.” They believed they had discovered an insecticide that was highly toxic to insects but minimally toxic to mammals. To determine whether that was the case required significantly more experimentation on both target and nontarget organisms. Would malathion control insects effectively at nontoxic levels?​They harbored even greater hopes for the new chemical. Beyond its specific value as an insecticide, they expected it to transform thinking about insecticide toxicity calling into question the “dogma” that anticholinesterase activity in vitro is necessarily an index to mammalian toxicity.19 These findings seem tainted, however, because American Cyanamid funded research at Hazleton Laboratories. The Hazleton researchers failed to place a convincing distance between their objective findings and their chief source of support.

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Continued Research at the FDA Research on the toxicity of organophosphate insecticides also continued at the FDA. In many respects, the FDA research complemented DuBois’s numerous studies on the toxicity of organic phosphates. J. William Cook, a biochemist in the FDA Division of Food from 1951 to 1972 who also served as the director of the Division of Pesticide Chemistry and Toxicology, realized one of the best applications of his enzyme research would be the analysis of organophosphorus compounds, as they were toxic because they inhibited cholinesterase. Learning from a colleague that the sulfur in thiophosphates might be sensitive to bromine, he developed from this tip a spot test for organic phosphates, which also contained sulfur. The bromination technique converted the non-cholinesterase in vitro inhibitors to in vitro inhibitors of cholinesterase. With this knowledge, Cook could visualize some of the general chemical characteristics of these compounds. Using this approach, he learned to look for many useful signs when petitions came in for new organophosphate compounds. He was thus able to accept or reject the data companies submitted in their petitions based on the bromination technique.20 Cook combined two tests (the anticholinesterase method of analysis with paper chromatography, and his newly devised brominated spot test technique) to analyze numerous organophosphate chemicals, including parathion. The literature indicated parathion was highly toxic to dogs (exposures as low as 1 ppm depressed cholinesterase). In contrast, large quantities fed to cows did not inhibit cholinesterase or cause it to appear in the cow’s milk. Cook believed something was happening to the parathion before it reached the bloodstream of the cow, because parathion fed at toxic levels in most mammals moved from the bloodstream into the milk and meat. He fed parathion to a cow with an opening in its rumen (where he assumed the cow would break down the parathion). By the time he returned to his lab, the parathion had disappeared from the samples. In a review of the literature, he discovered parathion had been reduced to a compound containing the far less toxic amino group. From his own experimental data and his literature review, Cook felt confident he could approve using parathion on plants fed to dairy cows, because he knew it would not be transferred to their milk.21 In addition to the paper chromatography test and the test for anticholinesterase activity, Cook and his colleague D. F. McCaulley

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resurrected Edwin P. Laug’s fly bioassay for the determination of organophosphate pesticides. Laug was a pharmacologist in the FDA Division of Pharmacology who developed a biological assay for the determination of DDT in animal tissues and excreta based on the toxic response of housefly (Musca domestica). The great sensitivity of the housefly to DDT (and other chemicals) provided an excellent indicator.22 While other researchers had developed bioassays using flies, most of them were based on mortality induced by graded amounts of pesticides. Such bioassays were very sensitive but unspecific. McCaulley and Cook felt that, by linking a measurement of in vivo depression of fly cholinesterase to a fly mortality count, group specificity might be added to the assay’s sensitivity. This procedure demonstrated the presence of any chemicals from the group of organophosphate pesticides with legal tolerances for food residues: parathion, systox, methyl parathion, malathion, OMPA, guthion (azinphos-methyl), phosdrin (mevinphos), trithion, and diazinon (a thiophosphoric acid ester developed by Ciba-Geigy in 1953).23 The fly bioassay was effective as a screening procedure. Those samples showing significant mortality could be checked later for cholinesterase inhibition. Cholinesterase inhibition roughly equal to mortality indicated a phosphate as the main toxic factor; a mortality figure much higher than inhibition indicated the presence of a combination of toxicants, not all organophosphate; and the absence of inhibition in the presence of considerable mortality would reveal a toxic factor other than an organophosphate.24 A technique that had been abandoned in favor of chemical methods was revived and effectively redeployed for use in a new context (detection of pesticide residues on foods). Refining such techniques ultimately led to the development and publication of the Pesticide Analytical Manual, which became the standard reference for testing the toxicity of pesticides.

Potentiation of Organophosphates A team of FDA pharmacologists led by John P. Frawley analyzed the additive toxicity resulting from simultaneous administration of two anticholinesterase compounds, which was essentially a study of joint toxicity. After reviewing the rather sparse literature on the toxicity of organophosphate insecticides, Frawley and his colleagues noted: “In all these studies, the observations have been based on the continued

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administration of a single compound. In practice a worker may be exposed to two or more compounds on the same or alternating days, and the average consumer may ingest at the same meal several different food products each containing a different insecticide.” Unlike the joint toxicity of antimalarial drugs previously studied at the Tox Lab, which required a prescription, individuals could be exposed to two organophosphates inadvertently through occupational exposure and possibly even normal daily consumption. Frawley and his team chose two organophosphates, EPN, and malathion because they were each less toxic than other organophosphates. Du Pont introduced EPN, the first phosphonic ester used as an insecticide, in 1949. Frawley and his colleagues first determined the acute toxicity (LD50) of each chemical for rats and dogs and then established the toxicity of the two chemicals in combination. In dogs, EPN and malathion administered simultaneously caused up to fifty times the potentiation (additive toxic effects) of separate exposures. And they noted potentiation in rats. The FDA group also investigated the joint toxicity of malathion and EPN combined in several ratios, to houseflies, using Laug’s fly bioassay, but found no indication of potentiation. This finding suggested potentiation involved complex chemical reactions between the two organophosphates and the biological system.25 Certainly, the fact that farmers used malathion (so effective against aphids) in combination with other organophosphates prompted interest in potentiation among toxicologists. DuBois also addressed the potentiation of organophosphates. He reasoned the simplest method for detecting potentiation by acute toxicity tests would be to administer half the LD50 of each of two organophosphates. If mortality due to the combination of the two compounds was additive (50 percent) or less than additive, no potentiation had occurred. DuBois used this approach to test for potentiation in several organophosphates and found most showed additive or less than additive acute toxic effects. This meant the combination of half the LD50 of the two chemicals produced a toxic effect equal to or less than the full LD50 dose for either chemical. DuBois anticipated these results when the compounds had the same mode of action, parallel dosage-mortality responses, and a similar time of onset of toxic effects. From the results of the tests of acute toxicity, DuBois realized he had to clarify the mechanism of toxicity for each organophosphate involved in potentiation to fully explore subacute effects. Such research revealed some agents inhibited hydrolytic detoxification reactions. DuBois thought this discovery was

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potentially valuable for basic research into normal metabolism, but it left unresolved the implications for food residues and occupational exposure.26 Organophosphate insecticides demanded novel toxicological techniques and strategies. After World War II, the University of Chicago Tox Lab responded to this considerable need. In particular, DuBois and his research group recognized the major toxicological effects of organophosphates: cholinesterase inhibition. They developed toxicological profiles for many of the new insecticides. In addition to research conducted at the Tox Lab, Lehman at the FDA considered the risks of organophosphates, particularly compared to other insecticides like chlorinated hydrocarbons. Like DuBois, Lehman constructed hierarchies of toxicity for the new chemicals. In general, organophosphate insecticides had a greater acute toxicity (because of cholinesterase inhibition) but considerably reduced chronic toxicity compared with chlorinated hydrocarbons. One possible exception to this developing rule was malathion, as American Cyanamid and scientists associated with it argued.

Toxicology for the Public The studies on organophosphates and other pesticides remained cloistered in the halls of the Tox Lab and the FDA save for the technical articles in professional journals. That is, until Rachel Carson, a biologist and science writer, published Silent Spring initially as a series of New Yorker articles, spread across three issues, and in book form later in 1962. In Silent Spring, Carson also established a hierarchy of dangerous insecticides. She first addressed chlorinated hydrocarbons, starting with DDT, and progressively described other chemicals in the class, including chlordane, heptachlor, dieldrin, aldrin, and endrin. Carson wove details about their toxicity to mammals, birds, and fish into her descriptions of chlorinated hydrocarbons. In just a few pages, Carson introduced concepts such as bioaccumulation, lipophilicity (the bonding of chemicals to fats), the passage of chemicals from mother to offspring via breast milk, food residues, and liver toxicity even at the residual levels found in food. Among chlorinated hydrocarbons, endrin stood out as highly toxic.27 Nevertheless, Carson did not believe chlorinated hydrocarbons posed the greatest threat to humans and wildlife: she had yet to address organic phosphates.

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Carson left no doubt as to where organic phosphates stood in the hierarchy of insecticides: “The second major group of insecticides, the alkyl or organic phosphates, are among the most poisonous chemicals in the world.” She proceeded to describe ironically the development of organic phosphates as nerve gases during World War II and the incidental discovery of insecticidal properties (a common misconception among American toxicologists); but it is her powerful description of the major effect of organic phosphates on organisms that set her account apart from previous reports: “The organic phosphorous insecticides act on the living organism in a peculiar way. They have the ability to destroy enzymes, enzymes that perform necessary functions in the body. Their target is the nervous system, whether the victim is an insect or a warm-blooded animal.”28 Aware that her subject demanded precision, Carson described the normal function of the central nervous system in detail, noting that excess acetylcholine presented a real threat to organisms. Her elegant description of cholinesterase inhibition was both vivid and technically precise. Carson elucidated the relation between the symptomology of cholinesterase inhibition and the normal function of the nervous system, and suggested repeated exposure could lower someone’s cholinesterase level and leave them vulnerable to acute poisoning.29 But what was the risk to people who were not exposed on a regular basis?​Carson answered this question with additional data showing that seven million pounds of parathion were applied in the United States, and the amount used on California farms alone could “provide a lethal dose for 5 to 10 times the whole world’s population.” What saved the people of the world was the rate at which organic phosphorous chemicals decomposed. When in contact with water or moisture, they broke down into harmless components rapidly compared with chlorinated hydrocarbons, and their residues did not remain as long, yet even relatively small quantities remaining posed a real threat: “The grove had been sprayed with parathion some two and a half weeks earlier; the residues that reduced (eleven out of thirty men picking oranges) to retching, half-blind, semi-conscious misery were sixteen to nineteen days old.”30 Carson noted similar residues had been found in orange peels six months after the trees had been treated with standard doses. Not even malathion, the least toxic of organophosphate insecticides, escaped Carson’s perceptive analysis. Malathion, according to her, was almost as familiar to the public as DDT. It was used in gardens, household insecticides, and mosquito spraying. Carson revealed nearly a

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­ illion acres of Florida communities had been sprayed with malathion m in an attempt to control the Mediterranean fruit fly. She questioned the assumption of many people that they could use malathion freely and without harm: “Malathion is ‘safe’ only because the mammalian liver, an organ with extraordinary protective powers, renders it relatively harmless. The detoxification is accomplished by one of the enzymes of the liver. If, however, something destroys this enzyme or interferes with its action, the person exposed to malathion receives the full force of the poison.”31 Citing research on potentiation by the FDA and DuBois, Carson explained the synergy between two organophosphorus chemicals could significantly exacerbate the effects of either or both. Moreover, Carson cited evidence that potentiation was not limited to organic phosphates. Parathion and malathion intensified the toxicity of certain muscle relaxants, and others (malathion included) dramatically increased the effect of barbiturates. Carson stressed that the advantages organophosphates possessed over chlorinated hydrocarbons, such as rapid decomposition, were significantly offset by the dangers of cholinesterase inhibition and potentiation. Her remarks on the acute toxicity of the various pesticides were only a preamble to her larger case: namely, the long-term risks of pesticides (particularly, chlorinated hydrocarbons) to landscapes, wildlife, and humans. In the remainder of Silent Spring, organic phosphate insecticides recede to the background. Although Carson thoroughly documented and dramatized the lingering damage to soil, water, flora, and fauna associated with chlorinated hydrocarbons, her research revealed few such problems with organic phosphates. Her one example of the effects of organophosphates on wildlife was typically dramatic. In an attempt to control flocks of blackbirds that fed on cornfields, a group of farmers engaged a spray plane to spray a river bottomland with parathion. More than sixty-five thousand birds died, and Carson wondered how many other animals perished from the acute effects of this universally toxic substance. Had rabbits, raccoons, and opossums succumbed as well?​Carson was most concerned, however, about unintended effects on humans such as farmworkers and children. Carson clearly believed organophosphates posed an equivalent if not greater risk to wildlife and humans than did chlorinated hydrocarbons. No chemical insecticide offered a genuine solution. Historians and biographers have analyzed the dramatic response to Silent Spring from consumers, scientists, industry representatives, and legislators.32 For the most part, the response split along predictable lines. Carson found

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her greatest support from environmental activists like Roland Clement, who presented the book’s chief arguments in many presentations to the public and various branches of government. Predictably, chemical companies mounted a savage campaign to discredit Carson and her claims in Silent Spring. One even threatened to sue the New Yorker after Carson’s articles appeared. William Shawn, the longtime editor, apparently relished the possibility of unexpected publicity for the magazine. Still, some environmental scientists who were apparently impartial distanced themselves and criticized some of Carson’s interpretations of the evidence of environmental and human health hazard. One wrote Silent Spring was “filled with truths, half-truths, and untruths.”33 But it would be an understatement to say the public was roused from its complacency about chemical insecticides. With Silent Spring and subsequent publicity including a nationally aired news program, the public discovered the risks of DDT and other synthetic insecticides, as well as the science of toxicology. Silent Spring and the public outcry inspired further study at the highest office in federal government, first when President John F. Kennedy directed his Office of Science and Technology to review hazards of pesticides and then by a congressional committee on interagency coordination in environmental hazards. As in other hearings, few questioned the considerable benefits of pesticides, and most witnesses couched evaluations of risks in light of benefits. Most witnesses, including Carson herself, acknowledged the considerable dangers associated with organophosphates. A familiar cast of scientists from the USDA, FDA, and Tox Lab presented their findings on organophosphates, the no-effect level, and potentiation (which was most common among organophosphates). In an attempt to defend their safety record, several representatives of the chemical industry presented the multistage and multiyear process through which a company identified, tested, and marketed a new insecticide, which involved literally thousands of chemicals. With a sharper picture of toxicological risk presented in simple language in Silent Spring and thoroughly analyzed by the executive branch and Congress, the pathway to further regulation appeared clear. However, neither the passage of the National Environmental Policy Act (1970) nor the establishment of the EPA in October 1970 ended the battle against DDT. The Environmental Defense Fund returned to court, suing the EPA in EDF v. Ruckelshaus, in which the EDF sought review of the failure to cancel the registration of DDT and stop its use during cancellation hearings. During this case, the EDF strength-

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ened its case sufficiently so that the EPA had to take significant action against DDT. The judge in this new case and two colleagues ordered EPA Administrator William Ruckelshaus to end all uses of DDT immediately. After complying initially, Ruckelshaus refused to suspend registrations after a sixty-day review. In June 1972, after yet another lengthy hearing, Ruckelshaus banned the remaining uses of DDT on crops. However, he did allow it to be used in cases of urgent public health such as emergency quarantine. He also allowed it to be manufactured for exportation. At the same time, the EPA suspended most uses of dieldrin, but more than two years (and the passage of the Federal Environmental Pesticide Control Act in 1972) went by before the agency announced a ban on the manufacture of dieldrin and aldrin.34

Replacing DDT: Discovering New Dangers to Humans and Wildlife More than a dozen years had passed since Rachel Carson alerted Americans to the environmental and health risks of synthetic insecticides. Most of the legislative effort in the years leading up to the DDT ban was concentrated on the persistent chlorinated hydrocarbons. The extensive toxicological research on organophosphates, Carson’s significant concern about wildlife and human effects, and extensive testimony in hearings at the federal level would naturally lead one to expect comparable legislative scrutiny for these highly toxic chemicals. However, such examination was delayed because the chemical industry could not yet provide suitable alternatives to replace organophosphorus compounds at that time. In 1988, the American Medical Association Council on Scientific Affairs reviewed the link between pesticides and cancer. After acknowledging the challenges of establishing such a link and the problems with animal models, the authors concluded acute toxicity was the primary hazard of pesticide exposure and that no pesticides had been proved carcinogenic, despite evidence of carcinogenicity in animals.35 Such a statement called into question the EPA and FDA’s preoccupation with cancer as the predominant toxicological concern of risk assessment of pesticides. For the most part, organophosphate insecticides were not associated with carcinogenicity, so they passed through the screen that was the regulatory emphasis on cancer. Since they t­ ypically did not bioaccumulate in the environment and were not persistent,

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they avoided a chief drawback of organochlorines. Lost in these toxicological analyses was the damage organophosphate insecticides posed to humans and wildlife directly in the form of acute toxicity. With the exception of malathion, organophosphates were moderately to highly toxic to humans and wildlife, especially birds, fish, aquatic organisms, and nontarget insects including bees. Thus, to a degree that would have shocked and disappointed Carson, the “road traveled” was flooded with highly toxic organophosphate insecticides, which she had identified as some of the most toxic chemicals known to humanity. In the mid-1990s, Theo Colborn, a World Wildlife Fund research scientist, pieced together evidence that pointed to a strikingly different concern. Drawing on hundreds of published studies, Colborn argued environmental chemicals caused endocrine disruption in a wide range of animals and humans.36 Such a finding squared well with one of Carson’s greatest concerns in Silent Spring, namely the decline of topline predators as a result of eggshell thinning due to the bioaccumulation of chlorinated hydrocarbons like DDT (and, for that matter, PCBs). Endocrine disruption was a neglected element of risk assessment, with serious consequences.37 With the DDT ban, DuBois at the Tox Lab worried farmers and public health officials would turn to organophosphates to control insects, thereby exposing farmworkers and others to extremely toxic chemicals. DDT was banned, as were other chlorinated hydrocarbons, but many years passed before any organophosphates underwent the kind of scrutiny that could support a move to phase them out. In fact, most organophosphates were still in use by 1996. As DuBois and others feared, organophosphate insecticides replaced DDT for many general uses. From 1964 to 1994, US pesticide use doubled from five hundred million to more than one billion pounds.38 Most pesticides in use through the 1990s were organophosphates. Wildlife continued to perish at phenomenal rates largely because of exposure to organophosphates. In 1997, Audubon magazine reported more than sixty-seven million birds were dying annually because of pesticide poisoning in the United States.39 Monocrotophos is one example of an organophosphate particularly toxic to birds. It was initially registered in the United States in 1965. Certain scientists believe monocrotophos has been responsible for more avian mortality incidents than any other pesticide since 1965. The EPA canceled all registered use of this chemical in 1991, and the largest US manufacturer voluntarily began to phase out its production, but monocrotophos and many other organophosphates are still in use internationally, where

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they pose significant risks to humans and wildlife. For example, up to twenty thousand Swainson’s hawks died in 1996 at their core wintering site after monocrotophos spraying.40 As DuBois predicted, urban and suburban pesticide use put humans and wildlife seriously at risk. Until its ban took effect in 2001, Americans annually used six million pounds of the organophosphorus insecticide diazinon, 70 percent of it used by homeowners and professional applicators for structural and lawn pest control around residences and public buildings. Diazinon applications have caused large numbers of bird deaths of numerous species.41 In addition to birds, populations of mammals, fish, reptiles, and amphibians, as well as beneficial and nontarget insects, all suffered from exposure to various pesticides, herbicides, and fungicides. As Linda Nash argued, farmworkers regularly faced exposure to these substances, in violation of state and federal regulations and at levels that can inhibit cholinesterase.42 John Wargo noted the other group most at risk was children who consumed more of the liquids, fruits, and vegetables that may have carried organophosphates. Children may also have encountered organophosphates applied indoors. Animal studies continue to sharpen scientists’ understanding of the risks posed by organophosphates.43 For example, substantial toxicological evidence shows repeated low-level exposure to organophosphate pesticides may affect neurodevelopment and growth in developing animals.44 In the 1980s and 1990s, as many as ten thousand cases of organophosphate poisoning occurred annually in the United States alone. Yet another factor adding to the danger of accidental poisoning as a result of exposure to organophosphates is the association of the chemicals with suicide cases.45 In 1996, President Bill Clinton signed the Food Quality Protection Act, which amended the Federal Insecticide, Fungicide, and Rodenticide Act (1947) and the Federal Food, Drug, and Cosmetic Act (1938) and required the EPA to reassess all food tolerances established before 3 August 1996, prioritizing those pesticides posing the greatest risk. This act compelled the EPA to conduct an extensive cumulative risk assessment (CRA) of organophosphates. The more than forty different organophosphates in use were among the first chemicals the EPA reviewed, followed by the other group of chemicals that induce cholinesterase inhibition: carbamate insecticides. The deadline for the EPA to complete its review of all tolerances was August 2006.46 Although progress was slow, the EPA completed its preliminary risk assessment in 2001 and a revised CRA the next year. Out of forty-nine organophosphates used widely in agriculture and residential settings in

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1996, the revised assessment announced registration cancellations for fourteen, including methyl parathion, ethyl parathion, diazinon, and chlorpyrifos.47 In 1999, the methyl parathion registrants voluntarily canceled many uses that contributed most to children’s diets, including apples, peaches, pears, grapes, nectarines, cherries, and plums, succulent peas, succulent beans, and tomatoes. Remaining uses of ethyl parathion (nine agricultural crops), highly restricted even before 2000, were to be phased out. Similarly, the CRA announced the cancellation of chlorpyrifos of nearly all indoor and outdoor uses, as well as food crops that contributed to dietary exposure of children. Likewise, in 2000, all indoor uses of diazinon were terminated, with outdoor residential and agricultural uses to be phased out over the next several years.48 In 2006, at the close of the CRA, the EPA announced the cancellation of the registrations for many other organophosphates. Global insecticide use tends to be much more difficult to track. Producers are not necessarily obligated to divide use by country, many of which lack governmental regulation. In 1990, a World Health Organization report on pesticides in agriculture predicted organophosphate use would increase: The organophosphorus compounds seem likely to continue to be the most important type of insecticide used in the developing countries and demand for them will probably more than double over the next ten years, but the more toxic of these chemicals will probably be phased out. Use of carbamates and pyrethroids is likely to increase substantially, while chlorinated hydrocarbons use should decrease considerably.49

In fact, recent trends in research suggest chlorinated hydrocarbons use has increased mainly as a result of residual (household) spraying in Southeast Asia and, to a lesser extent, Africa. Although organophosphates dominated agriculture and vector control in the 1990s, the use of these chemicals dropped considerably after the EPA’s CRA. According to a 2011 WHO report, from 2000 to 2001, organophosphate use fell by more than an order of magnitude (5,792 to 477 tons).

Conclusion This “family history” of the diverse class of insecticides known collectively as organophosphates has revealed several trends. From the outset

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of their development and introduction as insecticides, most organophosphates were characterized by high acute toxicity. Malathion stands apart as one of the few exceptions to this general rule. Toxicologists identified organophosphates as extremely toxic to mammals and other vertebrates, as well as to target and nontarget insects. They worried about potential exposure after organophosphates were released for agricultural use. In this regard, organophosphates differed from chlorinated hydrocarbons like DDT, which mostly showed lower acute toxicities. However, the persistence of chlorinated hydrocarbons in the environment, initially regarded by economic entomologists as a significant strength, created unintended consequences as the chemicals bioaccumulated in ecosystems, wildlife, and even humans. In contrast, organophosphates quickly broke down into relatively harmless components. When Carson published Silent Spring in 1962, she presented a clear hierarchy of the dangers of synthetic insecticides. She underscored risks associated with organophosphate use, which she believed posed an equivalent if not greater risk than did chlorinated hydrocarbons. Yet, in the aftermath of Silent Spring, US legislators—pushed by public opinion and the interests of the chemical industry that was willing to give up organochlorine pesticides but wanted to continue selling their organophosphorus insecticides—focused on DDT and its environmental effects as the most dangerous insecticide. Though the 1972 ban on DDT and other chlorinated hydrocarbons reassured people the food supply and wildlife were once again safe from persistent chemicals, farmers turned to the far more toxic organophosphates to control insects. As chlorinated hydrocarbons were phased out in the 1970s, organophosphate use rose dramatically, reaching astounding levels in the 1980s and 1990s in the United States and around the world. Only the passage of the FQPA in 1996 called into question widespread organophosphate use. With the act’s mandate, the EPA conducted a comprehensive risk assessment of organophosphates, which led to voluntarily withdrawals of several of the most toxic organophosphates from 1999 to 2001, with most organophosphates drastically restricted or banned by the completion of the EPA’s comprehensive risk assessment in 2006, more than three decades after the US ban on DDT took effect. More than forty years had passed since Carson revealed the risks of organophosphates in Silent Spring.

290  Frederick Rowe Davis

Frederick Rowe Davis is the R. Mark Lubbers Chair in the History of Science and Professor of History at Purdue University, where he teaches the history of science and environmental history. He is also Head of the Department of History. His research lies at the intersection of the history of environmental sciences and environmental history. He recently published Banned: A History of Pesticides and the Science of Toxicology (2014). Notes   1. This chapter expands on Davis, Banned.  2. Schrader, Development of Insecticides. On I. G. Farben, see Tucker, War of Nerves, 24–41.  3. Schrader, Development of Insecticides.   4. Doull, “Toxicology,” 2–3.   5. DuBois and Mangun, “Effect,” 139.   6. Doull, “Toxicology,” 3.   7. See Schrader, Development of Insecticides.   8. DuBois et al., “Studies on the Toxicity.”   9. Grob et al., “Toxic Effects in Man,” 107. 10. Hays, “Obituary”; “About the Authors: Arnold J. Lehman,” Food Drug Cosmetic Law Journal 8, no. 7 (1953): 403. 11. Lehman, “Toxicity,” 87. 12. Ibid., 88. 13. Lehman, “Pharmacological Considerations,” 68. Compound 497 (or dieldrin), compound 118 (or aldrin), and toxaphene were all chlorinated hydrocarbon insecticides. Rotenone was a naturally derived insecticide. 14. Ibid., 70. 15. CPC, “Pharmacology and Toxicology,” 107–8. 16. DuBois, “Food Contamination,” 326, 328. 17. Doull, “Toxicology,” 3–4. 18. DuBois and Coon, “Toxicology.” 19. Hazleton and Holland, “Toxicity of Malathon,” 401. 20. Cook et al., “Interview,” 1–2, 17–22. 21. Ibid., 31–32; Cook, “In Vitro Destruction.” 22. Laug, “Biological Assay.” 23. Guthion, phosdrin, trithion, and diazinon were all organophosphates developed in the 1950s. 24. McCaulley and Cook, “Fly Bioassay,” 206. 25. Frawley et al., “Marked Potentiation,” 96. 26. DuBois, “Potentiation,” 490–96. 27. Carson, Silent Spring, 26–27. 28. Ibid., 27, 28.

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29. Ibid., 28–29. 30. Ibid., 30. 31. Ibid., 31. 32. Lear, Rachel Carson; Lytle, Gentle Subversive; Dunlap, DDT: Scientists; Dunlap, DDT, Silent Spring; Hazlett, “Story of Silent Spring”; Hazlett, “Woman vs. Man,” 701–29; Kinkela, DDT and the American Century; Mart, Pesticides, Russell, War and Nature. 33. Cited in Dunlap, DDT, Silent Spring, 82. 34. Dunlap, DDT: Scientists. 35. CSA, “Cancer Risk.” 36. See Colborn et al., Our Stolen Future. 37. See Langston, Toxic Bodies. 38. See Wargo, Our Children’s Toxic Legacy. 39. Bourne, “Buggin Out,” 73. 40. ABC, “Solutions.” 41. Beyond Pesticides, “Diazinon.” 42. Nash, Inescapable Ecologies. 43. Schettler et al., Generations at Risk. 44. Eskenazi et al., “Exposures of Children,” 409. 45. Freire and Koifman, “Pesticides, Depression and Suicide.” 46. EPA, Organophosphate Pesticides, 1. 47. Chlorpyrifos is an organophosphate registered by Dow Chemical in 1965. 48. EPA, Organophosphate Pesticides, 9–10. 49. WHO, Public Health Impact.

Bibliography ABC (American Bird Conservancy). “Solutions.” Accessed on 11 February 2019. https://abcbirds.org/program/pesticides. Beyond Pesticides, “Diazinon,” ChemicalWATCH Factsheet, 2000. Accessed on 5 March 2019. https://www.beyondpesticides.org/assets/media/documents/ pesticides/factsheets/Diazinon.pdf. Bourne, Joel. “Buggin Out: Integrated Pest Management Uses Natural Solutions Both Old and New to Help Farmers Kick the Chemical Habit.” Audubon 101, no. 2 (1999): 73. Carson, Rachel. Silent Spring. Boston, 1962. Colborn, Theo, Dianne Dumanoski, and John Peterson Myers. Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival?​A Scientific Detective Story. New York, 1996. Cook, J. William. “In Vitro Destruction of Some Organophosphate Pesticides by Bovine Rumen Fluid.” Agricultural and Food Chemistry 5, no. 11 (1957): 859–63. Cook, J. William, Fred L. Lofsvold, and James Harvey Young. “Interview between: J. William Cook, Retired Director, Division of Pesticide Chemistry and

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Toxicology and Fred L. Lofsvold, FDA and James Harvey Young, Emory University.” In History of the U.S. Food and Drug Administration, 1–42. Rockville, MD, 1980. CPC (Council on Pharmacy and Chemistry). “Pharmacology and Toxicology of Certain Organic Phosphorous Insecticides.” Journal of the American Medical Association 144, no. 2 (1950): 104–8. CSA (Council on Scientific Affairs). “Cancer Risk of Pesticides in Agricultural Workers.” Journal of the American Medical Association 260, no. 7 (1988): 959–66. Davis, Frederick Rowe. Banned: A History of Pesticides and the Science of Toxi­ cology. New Haven, CT, 2014. Doull, John. “Toxicology Comes of Age.” Annual Review of Pharmacology and Toxicology 41 (2001): 1–21. DuBois, Kenneth P. “Food Contamination from the New Insecticides.” Journal of the American Dietetic Association 26, no. 5 (1950): 325–28. _____. “Potentiation of the Toxicity of Insecticidal Organic Phosphates.” A.M.A. Archives of Industrial Health 18, no. 6 (1958): 488–96. DuBois, Kenneth P., and Julius M. Coon. “Toxicology of Organic PhosphorusContaining Insecticides to Mammals.” Archives of Industrial Hygiene and Occupational Medicine 6, no. 1 (1952): 9–13. DuBois, Kenneth P., John Doull, and Julius M. Coon. “Studies on the Toxicity and Pharmacological Action of Octamethyl Pyrophosphoramide (OMPA; Pestox III).” Journal of Pharmacology and Experimental Therapeutics 99, no. 3 (1950): 376–93. DuBois, Kenneth P., and George H. Mangun. “Effect of Hexaethyl Tetraphosphate on Choline Esterase in Vitro and in Vivo.” Proceedings of the Society for Experimental Biology and Medicine 64 (1947): 137–39. Dunlap, Thomas R. DDT: Scientists, Citizens, and Public Policy. Princeton, NJ, 1981. _____. DDT, Silent Spring, and the Rise of Environmentalism: Classic Texts. Seattle, WA, 2008. EPA (Environmental Protection Agency). Organophosphate Pesticides in Food: A Primer on Reassessment of Residue Limits. Washington, DC, 1999. _____. Organophosphate Pesticides: Revised Cumulative Risk Assessment. Washington, DC, 2002. Eskenazi, Brenda, Asa Bradman, and Rosemary Castorina. “Exposures of Children to Organophosphate Pesticides and Their Potential Adverse Health Effects.” Environmental Health Perspectives 107, no. S3 (1999): 409–19. Frawley, John P., Henry N. Fuyat, Ernest C. Hagan, Jane R. Blake, and O. Garth Fitzhugh. “Marked Potentiation in Mammalian Toxicity from Simultaneous Administration of Two Anticholinesterase Compounds.” Journal of Pharma­ cology and Experimental Therapeutics 121, no. 1 (1957): 96–106. Freire, Carmen, and Sergio Koifman. “Pesticides, Depression and Suicide: A Systematic Review of the Epidemiological Evidence.” International Journal of Hygiene and Environmental Health 216, no. 4 (2013): 445–60.

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Grob, David, William L. Garlick, and A. McGehee Harvey. “The Toxic Effects in Man of the Anticholinesterase Insecticide Parathion (P-nitrophenyl Diethyl Thionophosphate).” Johns Hopkins Hospital Bulletin 87, no. 2 (1950): 106–29. Hays, Harry W. “Obituary: Arnold J. Lehman (September 2, 1900–July 10, 1979).” Toxicology and Applied Pharmacology 51, no. 3 (1979): 549–51. Hazlett, Maril. “The Story of Silent Spring and the Ecological Turn.” PhD diss., University of Kansas, 2003. _____. “‘Woman vs. Man vs. Bugs:’ Gender and Popular Ecology in Early Reactions to Silent Spring.” Environmental History 9, no. 4 (2004): 701–29. Hazleton, Lloyd W., and Emily G. Holland. “Toxicity of Malathon: Summary of mammalian investigations.” A.M.A. Archives of Industrial and Occupational Medicine 8, no. 5 (1953): 399–405. Kinkela, David. DDT and the American Century: Global Health, Environmental Politics, and the Pesticide that Changed the World. Chapel Hill, NC, 2011. Langston, Nancy. Toxic Bodies: Hormone Disruptors and the Legacy of DES. New Haven, CT, 2010. Laug, Edwin P. “A Biological Assay Method for Determining 2,2 Bis (P-chloro­ phenyl)-1,1,1 Trichloroethane (DDT).” Journal of Pharmacology and Experi­ mental Therapeutics 86, no. 4 (1946): 324–31. Lear, Linda. Rachel Carson: Witness for Nature. New York, 1998. Lehman, Arnold J. “Pharmacological Considerations of Insecticides.” Quarterly Bulletin of the Association of Food and Drug Officials of the United States 13 (1949): 65–70. _____. “The Toxicity of the Newer Agricultural Chemicals.” Quarterly Bulletin of the Association of Food and Drug Officials of the United States 12, no. 3 (1948): 83–85. Lytle, Mark Hamilton. The Gentle Subversive: Rachel Carson, Silent Spring, and the Rise of the Environmental Movement. Oxford, 2007. Mart, Michelle. Pesticides, A Love Story: America’s Enduring Embrace of Dangerous Chemicals. Lawrence, KS, 2015. McCaulley, D. F., and J. William Cook. “A Fly Bioassay for the Determination of Organic Phosphate Pesticides.” Journal of the Association of Official Agri­ cultural Chemists 42, no. 1 (1959): 200–207. Nash, L. L. Inescapable Ecologies: A History of Environment, Disease, and Knowledge. Berkeley, CA, 2006. Russell, Edmund. War and Nature: Fighting Humans and Insects with Chemicals from World War I to Silent Spring. Cambridge, 2001. Schettler, Ted Gina Solomon, Maria Valenti, and Annette Huddle. Generations at Risk: Reproductive Health and the Environment. Cambridge, MA, 1999. Schrader, Gerhard. The Development of New Insecticides. London, 1946. Tucker, Jonathan B. War of Nerves: Chemical Warfare from World War I to Al-Quaeda. New York, 2006. Wargo, John. Our Children’s Toxic Legacy. New Haven, CT, 1996. WHO (World Health Organization). Public Health Impact of Pesticides Used in Agriculture. Geneva, 1990.

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CHAPTER 9

A Tale of Two Nations DDT in the United States and the United Kingdom Peter J. T. Morris

The history of DDT use and regulation in the United States and the

United Kingdom—and, indeed, the public reaction to DDT—were very different. Comparing DDT regulation in the two countries between 1945 and the present will therefore offer some interesting insights in the social history of DDT.1 Moreover, after 1972, the United Kingdom was part of the European Economic Community (now the European Union) and hence was increasingly subject to European legislations and controls, so there is also an interesting story here about the gradual replacement of local controls by transnational regulations.

The Birth of DDT What were the origins of DDT?​By 1940, well over a million organic compounds had been synthesized, the biological and toxicological effects of which were rarely known well or even at all. Some of these compounds had been made several times, others only a few times and then forgotten. One such latter compound was a condensation product of chloral and chlorobenzene that we now know by the initials DDT. Why was it prepared in the first place, and how was its insecticidal properties discovered after six decades of complete obscurity?​This now infamous compound was prepared by one of Adolf von Baeyer’s students, Othmar Zeidler (1850–1911), during a wide-ranging study of aromatic condensations. Zeidler was given the task of condensing various halobenzenes with the well-known chemical (and soporific drug) chloral.2 One cannot emphasize sufficiently the obscurity of DDT, even

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in his paper. Zeidler was clearly more interested in the bromo analogue and the unsaturated compound produced by its dehydrobromination. DDT occupies only a few lines and is easily missed. Contrary to at least one account of his work, Zeidler even called it not dichlorodiphenyltrichloroethane but rather dimonochlorphenyltrichloräthan.3 In popular accounts, DDT is almost invariably presented as a laboratory chemical that was lying around without any apparent use. This was not the case: DDT hardly existed at all beyond Zeidler’s original samples. The only other chemist to make DDT was Walter Bausch at the University of Giessen in 1929, who used DDT (made according to Zeidler’s paper) as an intermediate in the synthesis of a butadiene compound.4 Zeidler himself returned to Vienna and eventually became a pharmacist. He died before DDT came to prominence. So why did Paul Müller at the Swiss company Geigy synthesize DDT in September 1939 to test its insecticide properties?​He explains the background in his Nobel Prize lecture, and there seems to be no reason to doubt his account.5 Müller was looking for a powerful contact insecticide for use in agriculture. A desideratum lacking in many existing insecticides was persistence, and, strikingly, if persistence, which would hardly be welcomed today, is removed from this list, then pyrethrum insecticides clearly would fit the bill but of course be of little interest to a chemical firm. Based on earlier work by Paul Läuger’s group at Geigy on moth killers derived from triphenylmethane dyes, Müller was aware of the potential value of dichlorophenyl compounds, that is, Cl

—X—

Cl  X=​ SO2, SO, S, O, etc.

From his own work, he knew the grouping -CH2Cl was biologically active.6 He then came across a paper by Frederick Chattaway and Roland John Kerr Muir of Oxford University, who revisited Baeyer’s work on condensations during a research program into carbinols and produced the condensation product of chloral and benzene.7 This paper was probably a result of Muir’s course “Chemistry Part II,” a one-year thesis written by Oxford chemistry undergraduates as part of the BA (Hons) degree, often based on a simple piece of chemical research. Muir’s synthesis of diphenyltrichloroethane certainly falls into this category. Müller prepared this compound and found it had good contact insecticidal properties. He then combined the ChattawayMuir compound with the chlorophenyl units of Geigy’s moth killer, Mitin FF, to arrive at DDT. He did not need to ­consult Zeidler’s

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paper, as he was able to make DDT using the method described in Chattaway and Muir’s paper. However, he later made the stronger claim that he was unaware of Zeidler’s paper when he first synthesized DDT, which is surprising, as Chattaway and Muir cited Zeidler’s paper, which was published in Berichte—hardly an obscure journal. One suspects Müller was anxious to avoid any patent problems caused by this paper. Muir himself became a Lieutenant-Colonel in the Royal Engineers in World War II and the director of personnel at the textile and chemicals firm Courtaulds in the 1960s.8 He died in 1974. I am not sure if he was ever aware of the important role he played in the development of DDT. DDT turned out to be a fantastic contact insecticide. It was lethal to a wide spectrum of insects while possessing a low mammalian toxicity, at least in terms of its acute toxicity.9 One can sense the amazement that greeted the effects of DDT on common insects such as houseflies. A British army officer in North Africa was astounded to see heaps of dead flies when he sprayed DDT on a window and then lamented the unwitting window cleaning by a German POW. Yet, to his amazement, the window continued to be lethal to flies for some time afterward.10 Its only drawback was that it did not always work immediately, but it was always lethal. Later research showed DDT could remain active in this way for up to six months. It was also very cheap, although cost does not seem to have been a major consideration in its early development. Chlorine was both cheap and abundant thanks to the development of the electrolysis process for caustic soda. Chlorobenzene was a cheap staple of aromatic chemistry, and chloral was well known as a pharmaceutical product. Furthermore, the production process was simple, involving heating with sulfuric acid, and the product was a crystalline solid easy to extract from the reaction mixture. The final product was a mixture of isomers and related compounds, but as the activity of the para/para isomer was extraordinarily high, this was not a problem. Geigy had a strong patent position, holding patents for DDT in Switzerland, the United States, United Kingdom, and Germany, but also a liberal licensing policy, as it did not want to be seen to be favoring either side in World War II.11 While this gesture was almost certainly made in the interest of public health and Swiss neutrality, a tighter patent policy might have prevented later excesses. As it was, enthusiasm for DDT was unbounded in the early postwar years. DDT-impregnated wallpaper was sold in the United States as a natural progression to the original advice to paint a DDT solution on existing wallpaper, probably

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to combat silverfish and flies.12 The wallpaper was said to be effective up to two years—hence, its use as children’s wallpaper (e.g., Trimz “Jack and Jill” and “Disney Favorites”), which is usually changed more frequently. DDT was developed for agricultural use, specifically against the Colorado beetle, but its immediate impact outside Switzerland was in the field of public health. By 1944, refugees were on the move across Europe, concentration camps were being liberated one by one, and the number of POWs increased. This created a major public health crisis in the form of typhus, a fatal disease spread by body lice. In December 1943, there was an outbreak in Naples, which had just been liberated by the US and British armies. A massive program of DDT dusting of the population a month later prevented a major epidemic.13 This outbreak demonstrated the major benefits of DDT: it was cheap; it had a low mammalian toxicity; as it was persistent, only one treatment was needed; and as a very stable solid, it could be easily made into a dusting powder. While the US authorities favored DDT, the British had previously used pyrethrum insecticides, which were, however, in short supply, not persistent, and thus unsuitable for typhus prophylaxis. DDT was also in demand for the control of malaria by eliminating the mosquito vector, an application pioneered by the Germans in the Balkans.14 Soon it was in use around Rome with its Pontine Marshes, only partly drained by Mussolini, and in Southeast Asia, where the Allies were pushing back the Japanese. In French West Africa, DDT nipped an outbreak of bubonic plague in the bud. DDT was seen as an almost miraculous weapon in public health during and immediately after the war. It was therefore not surprising Paul Müller was awarded the Nobel Prize in Physiology or Medicine in 1948. He continued to work for Geigy and died in 1965.15

DDT in the United States When the war ended in 1945, there was a continuing public health need for DDT in the US zones of occupation, but the military demand for DDT was winding down. Nonetheless, the United States was the ideal market for the new insecticide. As “Goodbye Mrs Ant,” the brilliant documentary by Adam Curtis, showed in 1992, the public was very concerned about insects in a country that sometimes seemed overrun by insects such as houseflies, ants of various kinds, and cockroaches.

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DDT persistence was very useful in this respect: one application, and your home remained insect-free for months afterward. DDT was also a powerful weapon against head lice. US farmers had even more reason to be grateful for the arrival of DDT. The Colorado beetle threatened the potato industry, and the boll weevil had plagued the cotton industry since the beginning of the century. These major pests were to meet their nemesis in the new Swiss wonder powder. Clearly, however, DDT was overused almost uniquely in the United States in the late 1940s and early 1950s. As experts realized even then, misplaced or excessive use of an insecticide can backfire. In California, it was used in citrus orchards in 1946 to control the citricola scale insect but also killed the ladybirds, leading to an explosion in the population of the hitherto rare cottony scale insect, which the ladybirds had previously kept under control.16 It is easy to see why DDT was overused: it was very cheap and, compared with earlier insecticides such as lead arsenate or even derris root, considered nontoxic.17 Furthermore, DDT was used to eliminate insects in nonagricultural areas either to eliminate malaria and other insect-borne diseases such as yellow fever or simply to remove pesky insects. This meant DDT penetrated the wider environment much more than earlier pesticides did. One unfortunate example was Clear Lake, a popular outdoor and camping resort north of San Francisco.18 This area suffered from swarms of the Clear Lake gnat, which was as unpopular with visitors as the better-known midge in Scotland. Biologists tried using DDD, a chemical relative of DDT, in a very cautious way in 1949 and during the 1950s. At first, the anti-gnat campaign seemed to be a complete success; the gnat was controlled without harming other wildlife. Unfortunately, the western grebe, a fish-eating bird at the top of the food chain, suffered from rapidly falling reproductive rates and almost disappeared. And as the gnat itself soon became DDD/DDT resistant, the whole campaign was ultimately in vain. Geigy had been the first DDT manufacturer in the United States in May 1943 at its Cincinnati factory, followed by Du Pont, and when even the combined production of Geigy and Du Pont fell short of the increasing demand from the military, Merck and Hercules took up its manufacture.19 While they were keen at the time, all these firms—except Geigy—had stopped manufacturing DDT by the late 1950s. After a slight dip in 1948, DDT production soared from 30,535 tons in 1950 to 52,488 tons in 1952. After another slight fall, it remained above 100,000 pounds (45,360 tons) per year until 1970, when it fell sharply to 26,905

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tons. Peak production was 85,176 tons in 1963.20 Although this may sound large, it was small relative to established organic chemicals such as its starting material chlorobenzene, which had a production level of 235,331 tons in 1963.21 It must also be kept in mind that US consumption was generally much lower than production. Average annual consumption from 1951 to 1960 was 31,000 tons, with a peak of 35,690 tons in 1959. As US consumption fell to a low of 13,724 tons in 1969, exports became increasingly important. They reached a peak of 51,600 tons in 1963 and of 49,509 tons as late as 1968. Thanks to the annual US Tariff Commission reports, we know all the US producers of DDT for any given year. 22 In 1953, for example, there were twelve producers including such well-known firms as Du Pont, Rohm and Haas, FMC Corporation, and Pennsalt Corporation. However, by 1958, the number had fallen to seven, and we can regard this group as the core manufacturers of DDT. The leading producer was a rather obscure firm, Montrose Chemical Corporation of California, which manufactured DDT in Los Angeles from 1947 to 1982. Pincus and Benjamin Rothberg ran the business, which apparently stemmed from the former’s New Jersey business that manufactured tricresyl phosphate, among other products, around the time of World War I.23 Having made DDT at its Newark plant in World War II, Montrose Chemical established a DDT factory in Torrance, Los Angeles. This was set up in collaboration with Stauffer Chemical, which owned 50 percent of Montrose. 24 Montrose also seems to have made plastics and plasticizers, but only at its Newark plant. It merged with Baldwin Rubber, probably at Stauffer’s prompting, in 1960. In addition to Geigy’s DDT plant in McIntosh, Alabama,25 the other major producers were mostly chlorine producers, namely Olin Mathieson Chemicals, Diamond Alkali (Organic Chemicals Division), Allied Chemicals (General Chemicals Division) and Michigan Alkali (part of Wyandotte Chemical Corporation, now BASF Wyandotte). Less well known was Lebanon Chemicals, based in Lebanon, Pennsylvania, where Vernon Bishop made chemical fertilizers but also produced DDT for UN malaria eradication projects. It is now called Lebanon Seaboard Corporation and is unconnected to the current Lebanon Chemicals based in Lebanon, Tennessee.26 By 1970, Geigy and Michigan Alkali had dropped out of DDT production, but the other five firms were still in the business. They then quickly departed, Lebanon Chemicals being the last one around 1972, leaving Montrose as the only manufacturer of DDT in the United States.

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Public concern about the impact of DDT on wildlife and the natural environment was slow to grow, mainly because of the slow timescale of DDT’s environmental impact, as Clear Lake demonstrates. Only after DDT and its metabolites accumulated in the water and soil, and in living organisms, did concern grow: at first, DDT seemed to be an unqualified success. By the mid-1950s, major pesticide producers such as Shell were developing methods to measure DDT and its chemical relatives at very low levels to monitor residues on food crops, as well as its impact on wildlife. As a result of the Clear Lake fiasco and concerns raised by organizations such as the National Audubon Society, the National Wildlife Federation, and the Izaak Walton League, the federal government, from 1957 onward, began to restrict DDT use on government lands, first in aquatic areas and then, in 1964, on all Department of Interior property unless no substitutes were available.27 This latter step came, of course, after Silent Spring, first serialized in the New Yorker in June 1962 and then published as a book in September.28 In this famous book, the marine biologist Rachel Carson highlighted the impact of persistent pesticides, notably DDT, on raptors, marine life, and human health. However, the most important impact came from neither the New Yorker articles nor the book but rather a television interview of Carson by the journalist Eric Sevareid, aired by CBS on 3 April 1963.29 The run-up to the airing was intense: CBS received an unprecedented thousand letters protesting the program, but the channel decided lobbyists working for pesticide producers had written most of them. The three largest sponsors of the series withdrew their sponsorships just before the program aired, but CBS pressed ahead. Ten to fifteen million people viewed the program, far more than would ever read the book, event though the program was competing with the US spacecraft Faith 7 orbiting the earth. The day after the program aired, Senator Hubert Humphrey ordered a congressional review of pesticides, to which Carson was invited to give evidence.

Growing Opposition to DDT Despite the impact of Carson’s book and her television interview, she did not have an immediate effect on the use and manufacture of DDT—the June 1963 congressional hearings simply suggested more studies of the ecological impact of pesticides were needed—and died of a heart attack and cancer in April 1964.30 It was another US woman

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who set the ball rolling on the banning of DDT two years later. Carol Yannacone, a teacher, had been reared on Yaphank Lake in the middle of Long Island and was concerned about the dead fish she was finding on the lakeshore.31 In early 1966, she discovered the Suffolk County Mosquito Control Commission was planning to spray the lake again to kill mosquito larvae (Yaphank Lake is in a built-up area, and the mosquitoes were presumably both a malaria risk and a nuisance). Her husband, Victor Yannacone, was a lawyer, and, significantly, both had a strong trade union background (his father had been a union leader).32 He suggested they sue the commission on the grounds that residents were entitled to a clean environment. This was a revolutionary idea at the time but was to become the main weapon of the US environmentalists against DDT and other environmental pollutants. It was also novel in that he was claiming damage not to an individual or even a group but to the environment. The case was filed in April 1966 and heard in November. In fighting the case, Yannacone had the support of the Brookhaven Town Natural Resources Committee and other concerned local biologists. As a rural area just outside New York City and on the path of many migrating birds, Long Island attracted professional biologists interested in the environment and other wildlife enthusiasts. The base for their discussions was the Brookhaven National Laboratory— hence, the setting up of the Brookhaven Town group. The most important of these biologists was Charles Wurster Jr., a chemist and biologist at the State University of New York at Stony Brook, where he studied Long Island osprey. Perhaps crucially to his future success as an expert witness, he had a PhD in organic chemistry and had worked at Monsanto for three years. In his testimony in the Yaphank Lake case, he said using DDT was like using atom bombs against street crimes in New York City.33 The result was a partial success for the Yannacones: the judge temporarily banned the spraying but said a permanent ban was a matter for the legislature. In the event, the commission simply switched to other methods of mosquito control. In the wake of the Long Island case, local activists formed the Environmental Defense Fund (EDF) dedicated to the strategy of opposing DDT use through similar legal means in 1967.34 This strategy combined knowledgeable biologists who would give the expert evidence with a flamboyant and combative lawyer, Yannacone. Yannacone later fell out with the EDF and has largely been written out of its history, but from the work of Thomas Dunlap, he clearly was crucial to its early successes. One EDF founder, Lewis Batts, from Michigan (in fact, the only member

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outside Long Island) was keen to ban DDT and related pesticides in his home state. A case to ban dieldrin use in the countryside floundered on a legal technicality, but a parallel case to ban DDT use to combat Dutch elm disease was more successful. None of the nine towns planning to use DDT contested the suit, and the EDF extended the suit to another fifty-six towns. But the EDF had still not found the high-profile case they were seeking that would enable them to try DDT at the bar of public opinion. The failed dieldrin case provided the breakthrough. The EDF tried to bring the case in Wisconsin on the grounds that the state shared a common ecosystem with the Michigan county in which the spraying was taking place. This case failed as well but brought the EDF into contact with the local Citizens Natural Resources Association of Wisconsin. The activists in Wisconsin wanted to ban DDT use for Dutch elm disease in Wisconsin, and the EDF agreed to help. The EDF was successful, and the matter was effectively settled out of court: as in the Michigan case, the towns would no longer use DDT. Ironically, the activists were upset they had been denied a public hearing. Crucially, the bemused examiner (judge) Maurice Van Susteren, who was sympathetic to their cause, suggested a Wisconsin citizen seek a declaratory ruling from the Wisconsin Department of Natural Resources. 35 In October 1968, the CNRA applied for a declaratory ruling that DDT was “a highly toxic persistent chemical, that its use be restricted in such way that it cannot enter the biosphere and that its existence in the biosphere constitutes pollution,” and Van Susteren took the case himself. The so-called Wisconsin hearings in the winter of 1968–1969 turned out to be crucial to the fate of DDT in the United States and of the EDF itself. By the time Van Susteren delivered his ruling that “DDT and its analogs are therefore environmental pollutants . . . by contaminating and rendering unclean and impure the air, land and waters of the state and making the same injurious to public health and deleterious to fish, bird and animal life” in May 1970, the debate had moved to Washington. The wide publicity the hearings had given to the EDF’s argument that DDT was an environmental poison, rather than the final ruling itself, had been the most important, although it was favorable to the environmentalists’ case. As the Wisconsin case has been well covered by Dunlap, I will restrict myself to drawing out the key elements of the EDF’s success. First and foremost, the EDF called well-qualified and articulate biologists as expert witnesses, which gave its case cred-

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ibility, while the dramatic nature of much of this evidence yielded much desired exposure in the media. It was assisted by the weakness of the opposition. Initially, just one pro-DDT advocate—Louis McLean, a former lawyer for the pesticide manufacturer Velsicol Chemical Corporation—attended the hearings on his own initiative. By the time the National Agricultural Chemicals Association pitched in to help him a month later, “much of the damage had been done.”36 The good impression made by a later pro-DDT witness, Wayland J. Hayes, the former head of the US Public Health Service toxicology section, was immediately undone by the poor showing of Harry Hays, the director of pesticide registration in the US Department of Agriculture. The EDF was also helped by the clear sympathy of Van Susteren, who had suggested this legal route and gave the EDF good opportunities to put its case forward during the hearings. Another crucial factor was the growing public support for the EDF and, in particular, the public donations that kept the expensive campaign afloat. Without this financial support, EDF’s ability to make its case would have been severely compromised. This is the real legacy of Silent Spring: the growing distrust of DDT and other pesticides in the broader public, which enabled environmental campaigns to flourish. It is also worth adding that Apollo 8’s dramatic photograph of Earth from the moon (now known as Earthrise), which became a symbol of “Spaceship Earth,” was taken on Christmas Eve 1968, during the Wisconsin hearings. The spotlight now turned to the human health aspects of DDT, an area of concern the EDF brought up in the Wisconsin hearings. The possible connection between cancer and chemicals had already become a major concern in the 1950s. Senator James Delaney had moved the Food Additives Amendment of 1958 to the Food, Drug, and Cosmetic Act of 1938, forbidding the use of any food additive that caused cancer in humans or test animals, which only indirectly applied to pesticide residues in a complex manner. Nonetheless, it signaled that allowing any chemical pollutant that could cause cancer was politically unacceptable. In the decade since the Delaney clause, the situation had been complicated by vast improvements in the chemical analysis of pesticide residues, which had raised the detection level from parts per million at best to parts per quadrillion.37 This huge leap in sensitivity made a mockery of Delaney’s much-vaulted “zero tolerance.” When chemists could only detect parts per million, zero tolerance effectively set a limit of 1 part per million, or thereabouts, which made some kind of sense. When the electron capture detector could find parts per quadrillion,

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it was debatable if such low levels had any significance.38 At the same time, the Delaney clause had created an expectation from the American public of zero tolerance, and hence zero risk, which was superficially attractive but impossible to implement.39 These new chemical techniques inevitably showed DDT was everywhere, including the body fat of Inuit people and, most emotively, in American mothers’ milk. If DDT were shown to cause cancer in humans, then it would forfeit all public support even from those sectors of the US public largely unconcerned about the effects on wildlife.

Banning DDT in the United States In the wake of the Wisconsin hearings and damning General Accounting Office reports on pesticide control by the USDA and, in particular, the increasingly hapless Harry Hays, the new Nixon administration, in April 1969, moved to limit the political damage by setting up a commission chaired by the food scientist Emil Mrak—under the auspices of the Department of Health, Education, and Welfare—to look at the risks and benefits of pesticides.40 HEW Secretary Robert Finch announced the commission’s conclusions in November. The complete report, issued just before Christmas, has been described as being unusually objective.41 One might suspect the full report was delayed and eventually published on the eve of the holidays because it was more evenhanded than its conclusions. Like the British experts (see below), the commission found it difficult to find hard evidence either way on the effect of pesticides. However, while the commission was deliberating, the National Cancer Institute published seemingly damning results in June, showing that mice exposed to DDT for long periods showed an increased incidence of liver tumors.42 It was impossible to extrapolate these results to humans, and three decades later, the International Agency for Research on Cancer still classifies DDT as only 2B (i.e., possibly carcinogenic to humans).43 But the Delaney clause had taken increased cancer rates in humans or test animals as the benchmark. Consequentially, the Mrak Commission concluded persistent pesticides such as DDT affected the environment, and called for interagency control of pesticides, effectively putting pesticide regulation out of the USDA’s hands. Subsequently, the USDA banned the residential use of DDT and its controversial use on shade trees while promising to phase it out altogether in the future.44 Somewhat to the USDA’s surprise,

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the industry accepted these new restrictions as it had accepted earlier local bans. Finally, the Nixon administration moved the responsibility for pesticides from the USDA to the new Environmental Protection Agency, which was set up in December 1970. The EDF immediately sued the EPA to cancel all the remaining registered uses of DDT, effectively a ban, and, as a result of the court order, the EPA agreed. Montrose Chemical called for an independent scientific review of the data used to justify the ban, which it was entitled to do under the Federal Insecticide, Fungicide, and Rodenticide Act of 1947. James G. Hilton, a University of Texas professor of pharmacology, chaired the committee. In its final report in September 1971, the Hilton committee concluded DDT persisted for long periods in the environment and hence would still pose a problem for a long time after any ban. However, it pointed out DDT use in the US was declining. In conclusion, the committee said there was no immediate threat to human health but that DDT presented “an imminent hazard to human welfare in terms of maintaining healthy desirable flora and fauna in man’s environment.”45 The FIFRA required this use of “imminent,” as the registration of a pesticide could only be canceled if it posed an imminent hazard to the public. Nonetheless, the committee felt either an immediate ban or a rapid decline in DDT use would achieve the desired result. It thus left the door open for the EPA to phase out DDT over several years. From August 1971 to March 1972, Edmund Sweeney from the Department of the Interior heard the “consolidated hearings” in Washington to appeal the cancellation of DDT’s registration, which were attended by the thirty-one formulators of DDT products who had requested the hearings, the USDA, the EDF, and the EPA.46 Essentially, the issue was one of timing rather than principle. The formulators wanted more time to phase out DDT, while the environmentalists sought an immediate ban. But these hearings were very different from those in Wisconsin. The pesticide industry was better organized, and a wider range of expert evidence was given, with 125 witnesses appearing. In essence, the debate had shifted from whether DDT was bad to how bad it was. Furthermore, as with the Mrak and Hilton reports, the focus had shifted from the impact on wildlife to the effect on human health. In some respects, both these shifts actually favored the pro-DDT side. It was easier to argue DDT was more useful, despite its drawbacks, than an unalloyed good, and long-term effects on human health are almost impossible to establish. When Sweeney produced his report on

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25 April 1972, he stressed the value of DDT for public health and, to a lesser extent, food production. By contrast, he believed the evidence of human harm was lacking, and the extrapolation from animal tests unconvincing. As far as the damage to ecosystems was concerned, he believed the evidence was often weak, conflicting, or even irrelevant. He also pointed out that the replacements could well be more harmful than DDT itself, concluding “there is a present need for the essential uses of DDT; that efforts are being made to provide a satisfactory replacement for DDT; and that a co-operative program of surveillance and review can result in a continued lessening in the risks involved.”47 In other words, an immediate ban was not justified. Despite Sweeney’s positive report on DDT, the new head of the EPA, William D. Ruckelshaus, produced his own report in June 1972, which damned DDT on several counts: notably its effect on marine life and avian raptors, and its potential effect on human health, including possible carcinogenicity.48 This was completely at odds with Sweeney’s report, which had considered all these factors and decided there was no compelling case. However, Sweeney was also at odds with the Hilton and Mrak reports, at least in terms of his level of concern, although none of the reports called for an immediate ban. It would be fair to say Ruckelshaus and the EPA produced the report they wished Sweeney had delivered. Ruckelshaus proceeded to ban the use of DDT in the United States, but to allow the continuation of limited production for vector control elsewhere. As we have seen, only one producer took full advantage of this concession. The (partial) ban took effect in December 1973 after the Court of Appeals for the District of Columbia turned down both the pesticide manufacturers’ appeal against Ruckelshaus’s ruling and the EDF’s appeal for a total ban.49 Why did Ruckelshaus overrule Sweeney, and did President Richard Nixon support the ban?​ On one level, Nixon appeared keen to ban DDT. He had moved the responsibility for DDT from the pro-pesticide USDA to the EPA and appointed the idealistic Ruckelshaus, a lawyer and a member of the National Audubon Society, as its head. Clearly, Nixon did not have any strong personal views on pesticides but sought a balance between the two sides.50 Toward the end of his vice presidency, he had been caught up in a scare over the spraying of cranberries just before Thanksgiving in 1959, and he may have felt this incident was one reason for his defeat in 1960. He was certainly aware the environment was one area in which he could lose votes to the Democrats in the forthcoming presidential election.

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It is interesting to note that Philip Abelson, then the editor of Science, had said a year earlier, in June 1971: “The realities of politics are that President Nixon cannot concede to Senator Muskie unchallenged leadership in the environmental field. Indeed the President must appear to be at least as effective in that arena as his potential contender.”51 Ruckelshaus himself has stated that Nixon had no real interest in DDT and was driven by public opinion, despite attempts by the agriculturalist Norman Borlaug to get Nixon’s support for DDT.52 Furthermore, the UN “Stockholm” Conference on the Human Environment opened on 5 June, and Ruckelshaus signed his recommendation for a ban just before leaving for the conference. As Sweden had banned DDT two years earlier and the United States prepared for a torrid time at the conference for various reasons including the Vietnam War, it would have been terrible PR for the United States to announce it was continuing to allow the use of DDT. In fact, Ruckelshaus announced his ban at the conference. Fearful of losing farmers’ support, Nixon was initially furious about the ban.53 However, he was more concerned about other environmental issues such as the Clean Air Act (1963), which threatened to affect his relationship with the Ford Motor Company.54 Nonetheless, the ban helped establish his socially progressive credentials with swing voters and the world at large. Fixing the Vietnam War was difficult; banning DDT was easy.55 In any event, he could not afford to give the impression of an administration in disarray by disagreeing with Ruckelshaus publicly.56 Following the ban, production appears to have continued at Montrose—at around thirty thousand tons per year—until 1982.57 Ironically, it was the strong dollar undermining its exports, rather than environmental legislation, led to the downfall of Montrose. DDT use was permitted from time to time for specific pests, such as the pea leaf weevil in the Northwestern United States in 1973, but, in contrast to Britain, general DDT use appears to have stopped.58

DDT in Britain How much DDT was produced or used in Britain is unclear, as the relevant statistics are unavailable. From our limited knowledge, it was used almost solely in agriculture, although advertisements for domestic DDT use did appear in trade journals such as Chemist and Druggist in the 1950s. I do not recall it being used in homes at all

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in the 1960s. It has been reported that 266 tons per year were used in agriculture/­horticulture in Britain in the early 1960s, 152 tons in 1969, about 120 tons per year in the early 1970s, and just over 100 tons per year in the mid-1970s.59 This level of use is tiny compared with the United States (even allowing for the different size of the two economies) and largely explains why DDT was never a major issue in the United Kingdom. British production is even harder to pin down. Geigy first produced DDT at its factory at Trafford Park, Manchester, in November 1943.60 Hickson & Welch evidently began producing DDT in 1944 in Castleford, Yorkshire, and became the major producer in the early 1950s.61 Ayrton Saunders, a well-known pharmaceutical manufacturer in Liverpool, seems to have produced DDT purely for anti-malaria use abroad, especially in India. James Cox & Co. were still operating in 1955 a very small “DDT Works” in the residential area of South Harrow, London (fig. 9.1).62 However, Hickson & Welch halted DDT production in 1957, and DDT manufacture in Britain had ceased altogether by 1969.63 One of the main reasons for the relative lack of interest in DDT was the British government’s promotion of the use of pyrethrins. Extracts of the daisy-like pyrethrum flower were also powerfully toxic to insects with a low mammalian toxicity (but harmful to fish). Its action was more rapid than that of DDT, and as a natural plant product, it was biodegradable, then considered disadvantageous. Its major disadvantage, however, was that it was a natural product, which had initially made it expensive. However, the British were developing plantations to grow the flowers and their associated processing plants in Kenya, then a British colony, to boost the local economy.64 In the medium term, this step made pyrethrum more competitive while giving the British a vested interest in using pyrethrum rather than synthetic insecticides. Even in the 1960s, British household sprays were usually pyrethrinbased in contrast to the synthetic insecticides used in the United States. This meant there was almost a complete lack of concern about DDT among the British public at large.65 The banning of DDT in Sweden in 1970 and the effective US ban in 1972 first brought the controversy to the attention of the British public, and only to a limited extent. For example, DDT was covered in the progressive British science magazine New Scientist until the early 1970s about four times a year, and even then, the discussion was often about the United States or other foreign countries.66 I do not remember DDT coming up as a topic of discussion at all in the 1960s and 1970s.

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Figure 9.1  Image of DDT-impregnated cardboard parrot to kill houseflies, made by James Cox & Co., South Harrow, London, early 1950s (courtesy of Wellcome Collections).

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The initial concerns in Britain were the safety of farmworkers being exposed to pesticides, and the risk posed to food.67 The Committee on Health, Welfare and Safety in Non-Industrial Employment recommended wearing protective clothing when poisonous sprays were used as early as 1949. Pesticides were considered by working parties of scientists headed by Solly Zuckerman. Prompted by the Nature Conservancy, the third Zuckerman working party considered the impact on wildlife in 1952 but found it difficult to obtain relevant information. From 1954 pesticides were kept under observation by the Advisory Committee on Poisonous Substances Used in Agriculture and Food Products (which became the Advisory Committee on Pesticides and Other Toxic Chemicals in June 1964) which arose out of the Zuckerman working party and was initially chaired by Zuckerman. In 1957, the committee introduced the Notification Scheme whereby manufacturers did not introduce any new pesticide until it was cleared by the committee. It was a voluntary scheme but it was never breached. This led to a ban on aldrin and dieldrin seed dressings in 1961 but did not directly affect DDT. A research committee was set up in 1962 to assist the advisory committee. The advisory committee looked at the organochlorine pesticides in 1964 and recommended a ban on dieldrin, aldrin, and heptachlor. Realizing this would probably lead to an increase in DDT use, it recommended a review of DDT (and lindane) in 1967. The publication of this review was postponed because of disagreements among scientists about the impact of DDT on raptors. The arguments were partly about the strength of the ecological evidence but also about the nature of the restrictions. Some scientists argued for a more or less complete ban, while others felt DDT should continue to be used under tightly regulated conditions. Eventually, the advisory committee called for a more or less complete voluntary suspension of DDT use in 1969. The manner in which DDT and the related organochlorine pesticides aldrin and heptachlor were controlled in Britain bore the hallmarks of the British approach to environmental pollution in general, namely a cautious approach based on firm scientific evidence, a desire for scientific consensus before restricting chemicals, and close collaboration between the government and industry, leading to voluntary rather than legally mandated regulation.68 DDT use halved between 1965–1969 and 1969–1974 but then leveled out, so its use in the late 1970s was not very different from the immediate post-ban period.69 In 1979, the Royal Commission on Environmental Pollution chaired by Sir Hans Kornberg produced its seventh report, on the issue

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of agriculture and pollution, which requested the ACPOTC review the use of organochlorine pesticides (including DDT) and that the control of pesticides be given a statutory basis.70 The wheels of government grind slowly and it was not until 1985 that the Food and Environment Protection Act brought in the statutory registration of pesticide in place of the three-decade old voluntary scheme. A year later, the Control of Pesticides Regulations effectively banned the agricultural use of DDT by withdrawing the remaining licenses. This British legislation appears to have been almost completely independent of pesticide control by the EEC. Indeed, in its first decade in the EEC, the British government firmly pushed back against the EEC’s attempts to create a common environmental policy.71 At the EEC level, DDT was partly banned under Council Directive 79/117/EEC in December 1978, which entered force in 1981.72 In the United Kingdom as a result of this regulation, the recommended use of DDT was restricted to cutworms. This was still a voluntary scheme, and DDT use in Scotland is said to have actually increased.73 DDT was completely banned for agricultural use under Council Directive 83/131/EEC in March 1983, but how this was applied in Britain is unclear, although it is often said DDT use in Britain was banned in 1984 and hence before the COPR was introduced in 1986.74 The manufacture and use of DDT is now also banned under the European Union’s REACH regulations, in addition to regulations arising from the Stockholm Convention on Persistent Organic Pollutants.75

Why the Difference between the United States and the United Kingdom?​ The way in which DDT was banned in the United Kingdom was clearly very different from the United States.76 DDT was restricted in the United States as a result of several legal hearings and growing unpopularity, making it impossible for the president to support its widespread use. By contrast, the British ban was the result of pressure from expert panels, which themselves were divided on DDT use, without any significant input from the public, which was largely indifferent to DDT. In my view, there are three reasons for this difference. First is how DDT was used. In the United States, it was used in the home and in the environment at large, for example, at Clear Lake. This broad use both brought it more to public attention and caused more damage to wildlife. People are more likely to protest DDT if it is being sprayed

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on the trees outside their homes or on their nearby lakes. This relative level of use was partly because insects are more prevalent in the United States and partly because pyrethrins were often used instead of DDT in Britain. In Britain, DDT was almost entirely restricted to agriculture. Furthermore, by the 1960s, Britain was a largely urban society, and, being an island, trips tended to be to the seaside rather than the country. Many people would have been unaware DDT was being used and even less aware of any impact on wildlife, which was minimal in any case. A major group who did roam the British countryside was foxhunters; concerned something else was killing their prey, they pressed the government to launch an investigation, which was carried out the Nature Conservatory and industry.77 As a result, the formulation of seed dressings was changed, but this did not involve DDT. A survey of articles on the negative impact of pesticides in The Times (London) from 1940 to 1975 using The Time Digital Archive reveals much about the British attitudes toward pesticides and DDT in particular.78 The first negative The Times article on pesticides appeared on 4 March 1963—just over two weeks after Silent Spring was reviewed (anonymously) in the newspaper—and was about the impact on wild birdlife, a continuing concern, as sixteen articles (19 percent of the total) were about wild birds (which accounted for nearly all the articles on wildlife in general), and only four mentioned DDT. Overall, only four articles mentioned DDT between 1963 and 1967 (14 percent of the total for that period), whereas twenty-nine (23 percent) mentioned DDT between 1968 and 1975. There are two possible reasons for this (apart from a lack of interest in DDT). Before the mid-1960s, it was very difficult to distinguish traces of DDT from other chlorinated hydrocarbons, so the more general term was often employed. Many of the articles on DDT stemmed from the Nature-Times News Service, which began publishing articles on pesticides in 1968, amounting to 65 percent of its articles on pesticides and 45 percent of all the articles on DDT between 1968 and 1975.79 Of the eleven articles (13 percent) about the control of pesticides in the United States, six mentioned DDT. Most of these articles appeared in 1963–1964 (four) and 1969–1972 (six), the DDT-related ones falling completely in the latter period. However, it is easy to overstate the significance of these articles about the developing US situation. Most were very brief, and there was no attempt to sustain a story; even the one announcing Ruckelshaus’s DDT ban in June 1972 was only 206 words. Significantly, none of these stories prompted a leader article. In fact, the only pesticide-

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related article that led to a leader (in August 1971) was about DDT residues in British food. Taking all the articles into account, there were two peaks, 1964–1965 (eight articles each year) and 1972 (twelve articles), with a trough of one to four articles a year from 1966 to 1968. Similarly, the number of articles on DDT declined after 1972, and even more tellingly, the articles in 1974 and 1975 (with one exception about a mass poisoning of geese in Yorkshire) were “News in Brief” about pesticide poisonings abroad or short “Science News” pieces by the new Science Correspondent Pearce Wright or the Nature-Times News Service. The second reason is the different political culture in the two countries.80 By the 1960s, Americans felt—and were encouraged to believe— they had the right to be consulted through votes or public hearings about most things; the British until recently did not. Hence, the public US hearings have no counterpart in Britain. The expert committees and even the Royal Commission on Environmental Pollution were not so much nonpolitical (although they were), they were effectively outside the mainstream of political debate altogether. The Green Party (founded in 1973) was still very much a fringe party in the 1980s, and its succeeding Green Party of England and Wales (founded in 1990) largely still is, despite having an MP for the first time in the 2010 elections. Furthermore, as Ronald Brickman, Sheila Jasanoff, and Thomas Ilgen have pointed out, the popularity of litigation to prevent or limit pesticide use had no UK counterpart.81 The third difference was the growing distrust of the chemical industry and science more generally in the United States, which was not reflected in Britain on the whole. The uneasy relationship between big business and the public in the United States is a complex subject that goes well beyond the scope of this chapter.82 A new factor in the late 1960s was the role of chemical companies manufacturing napalm and Agent Orange defoliant for the Vietnam War.83 There was doubtlessly a synergy between the growing Vietnam War protests and the campaign against DDT, although I have never come across a direct connection. Britain was not in the Vietnam War, and protests against the war (and other radical protests) were largely limited to university campuses at a time when only a small minority of British people went to university. Thanks to the high-profile campaigns of Campaign for Nuclear Disarmament, nuclear disarmament rather than the environment captured the interest of most left-wing idealists in this period.84 Most British people, up to the early 1970s at least, trusted the experts if not the politicians who were becoming increasingly discredited. Furthermore, the big-science-based

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issue in Britain in the late 1960s and early 1970s was the thalidomide scandal, which put the focus on safety of pharmaceutical drugs rather than pesticides.85 Despite the different routes to a ban and the different timescales involved, there does not seem to be much difference in the outcome. The United States was quicker to ban DDT, and its ban was more immediately effective. But DDT is now banned in both countries, and the environmental impact in Britain does not seem to be any greater despite the slower rate at which the ban took effect.86 This is doubtlessly the result of the much lower use of DDT in Britain. British DDT use per capita seems to have been roughly three one hundredths of that of the United States in the early 1960s (266 tons for a population of fifty-six million against 31,000 tons for a population of two hundred million). Furthermore, there was another possible route to a US ban. This parallel official track is rather overlooked by Dunlap, who prefers to focus on the activists he clearly admires. Two expert panels acting on behalf of President John F. Kennedy’s Office of Science and Technology had issued reports on pesticides in May 1963, in the immediate wake of the controversy of Silent Spring, and in November 1965. Following the General Accounting Office’s criticisms of the USDA’s pesticide policy, the Persistent Pesticides Committee of the National Research Council had made a report to the USDA in May 1969.87 And, as we have seen, there was the Mrak report of December 1969. In a nutshell, all these reports said more research and monitoring were needed, the impact on the environment should be reduced, and everything should be done to reduce the use of persistent pesticides. However, none of these reports, even Mrak, called for an immediate ban. Nonetheless, DDT use clearly would have been gradually reduced and as quickly as economically practicable even in the absence of legal action. This is shown by the USDA’s withdrawal of the registration of DDT for many domestic uses and use on various food crops between 1967 and 1970. So, the banning of DDT might have been slower, as in Britain, but it would have surely happened anyway. The fact remains: DDT was banned relatively quickly in the United States because of public opposition but eventually withdrawn in Britain on the recommendation of experts.

Why Did the Chemical Industry Defend DDT?​ One of the most remarkable aspects of the history of DDT is the ineptitude of the US chemical industry, specifically, the major pesticide

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producers. They attacked Rachel Carson vehemently and personally at a time when she was already suffering from cancer, an ad hominem attack that only increased public support for her views.88 The industry then failed to appreciate the danger posed by the Wisconsin hearings and initially failed to support the only participant defending the industry on his own initiative. The pesticide manufacturers regrouped in time to win the consolidated hearings but failed to gain Nixon’s political support, which turned the successful outcome of the hearings into a Pyrrhic victory. But even more puzzling than their lack of PR and political skills was the pesticide manufacturers’ eagerness to defend DDT. The problem of insect resistance to DDT was already becoming a major drawback even in the field of malaria eradication by the mid-1960s, which thus severely reduced its usefulness. As we have seen, US consumption fell from nearly thirty-six thousand tons in 1959 to under fourteen thousand tons in 1969. DDT users faced with legal action found it relatively easy to switch to alternative methods. DDT was cheap to make but had low profit margins. For manufacturers, there was surely a financial advantage in pushing second-generation pesticides. Such replacements already existed, notably organophosphates (e.g., malathion) and carbamates (e.g., Sevin). However, these replacements were generally much more expensive, and malathion had significant human toxicity. Furthermore, the manufacturers of DDT (and other organochlorine pesticides) tended not to be the producers of the second-generation pesticides. Montrose Chemical in particular had nowhere else to go. One would also assume damage to wildlife, however controversial in its details, was not desirable PR even in the 1960s. In terms of tactics, it is surprising manufacturers did not quickly concede a ban on use in the United States in return for being allowed to produce for export, which was a far more important market than domestic use by 1968. Brickman and colleagues attribute the aggressiveness of the US chemical industry to the country’s laissez-faire tradition.89 David Vogel says US executives blamed increased environmental regulation for “reducing productivity, increasing inflation and unemployment,” and much else. He also makes the good point that, US businesses, in contrast to their British counterparts, who enjoyed a relationship of close collaboration with their government, had to fight their own corner in the political arena and in Congress, which engendered a more aggressive approach.90 However, in the specific case of DDT, I would argue the key to understanding the manufacturers’ dogged support of DDT

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was the common perception on the part of the pesticide producers that DDT represented the first “domino” in the attack on pesticides, an emotive analogy borrowed from the Vietnam War.91 “Encouraged by (restrictions on DDT), the anti-pesticide groups now are going after Malathion and Dieldrin, thereby offering a living example of the domino theory.”92 This comment was somewhat wide of the mark, as anti-DDT campaigners such as the EDF actually advocated malathion use in place of DDT.

The Controversy Continues One might think that a pesticide that was introduced seventy years ago and was banned in most developed countries at least thirty years ago would now be a historical curiosity. In fact, one could argue that such an elderly broad-spectrum insecticide would have long fallen out of use even without such bans. If we are talking about the agricultural uses of DDT, that would doubtlessly be true. But DDT is really two different pesticides with the same name. Obviously, they share the same chemical formula, but DDT for malaria vector control has had a very different history from DDT for agricultural or residential use. Nearly all the slack in the US market for DDT in the early 1960s was taken up by the US Agency for International Development and the UN for vector control. All the early bans of DDT applied only to residential or agricultural uses. China, for example, banned DDT for agricultural use in 1983, and India in 1989.93 However, the agricultural use of DDT in China has continued despite this ban.94 The UN Environment Programme had issued a call in 1995 for a new assessment of persistent organic pollutants, chief among which were DDT and its chemical relatives aldrin, dieldrin, endrin, heptachlor, and chlordane.95 The International Programme on Chemical Safety laid the ground for a conference, blacklisting twelve chlorinated hydrocarbon pollutants including DDT. The conference was held in Stockholm in May 2001, echoing the famous UN Stockholm Conference in June 1972, and the Stockholm Convention entered force in 2004. China continued to produce DDT for malaria vector control for several years. In the early 2000s, China produced three to four thousand tons of DDT a year.96 The government indicated in 2004 that it intended to accede to the convention and three years later produced an implementation plan.97 However, this plan committed China only to begin phasing out

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DDT production by 2009, and production for “acceptable ­purposes”— unstated but presumably vector control as allowed under the Stockholm Convention—would continue, but all imports and exports would be banned. China apparently completely halted DDT production in 2008. India continues to produce DDT for vector control both at home and in Africa, about 4,500 tons per year.98 North Korea produces about 160 tons per year, mostly for agricultural use. According to the DDT register established under the Stockholm Convention, Ethiopia is still manufacturing about seven hundred tons of 75 percent DDT a year for vector control in a factory erected by a Chinese company.99 It is its use for malaria vector control that keeps it in the spotlight of controversy, even in countries that have completely banned it. DDT is remarkable for the amount of support it has received over the years, which far outstrips any other pesticide I am aware of, except perhaps Michael Fumento’s support for Alar, a far easier pesticide to defend.100 The author of the first defense of DDT, the journalist and medical toxicologist Rita Gray Beatty, had the assistance of the leading pesticide analyst Francis Gunther, an entomology professor at the University of California, Riverside.101 Faced with an almost complete lack of popular support, at least in the United States, advocacy for DDT use then largely dried up until around 2000, when Richard Tren, a South African economist, started to argue the pro-DDT case afresh. 102 The oft-cited example of malaria eradication thanks to DDT is Ceylon (now Sri Lanka). Incidences there fell from five million cases and eighty thousand deaths in a 1934–1935 epidemic to seventeen cases, all nonfatal, in 1963.103 However, the picture is more complicated than it first appears. Since 1966, malaria cases in Sri Lanka have shown several peaks and troughs, so it is not just a matter of cases soaring once DDT was banned. In fact, there was a resurgence of malaria cases in the late 1960s while DDT was still available, although its use had been suspended, as seemingly it had been successful. The initial setback to the vector elimination program was DDT resistance—which was found in local mosquitoes in 1969—rather than any ban on its use.104 Once DDT resistance is encountered, the program can switch to malathion, but the organophosphorus insecticide is much more dangerous to poorly trained and unprotected personnel. While the United States stopped exporting DDT for vector control, other countries stepped into the breach and indeed still do so. The World Health Organization continues to approve the indoor spraying of DDT for vector control.105 The Stockholm Convention specifically allows DDT use for vector control

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under tightly controlled conditions, essentially indoors.106 The WHO has presented this as a reversal of an earlier anti-DDT policy, but its support for indoor spraying seems to have been consistent.107

Conclusion Noted DDT expert Kenneth Mellanby speculated how we could have used DDT better.108 For example, had its use been restricted from the outset for public health and in agriculture for specific pests under carefully controlled conditions, its history may well have turned out to be very different. But to speculate in this way is to deal in counterfactual history. None of the US or British restrictions, although I have followed the general trend in calling them “bans,” prevented the use of DDT to prevent malaria. The support of the USAID program for the use of US DDT in vector control programs became controversial in the late 1970s.109 President Jimmy Carter banned the export of DDT just before he left office, but incoming President Ronald Reagan overturned the ban. The use of US DDT for malaria control ended when Montrose ceased production in 1982, rather than as a result of environmental protest. The enthusiastic use of DDT in the United States in the home, in agriculture, and for mosquito/gnat control led to both environmental problems and pesticide resistance. Persistence, eagerly sought by Müller and considered an advantage in the 1940s, had become a major environmental hazard by the early 1960s.110 No one seems have considered persistence as a desirable feature in insecticides before Müller, and DDT (along with other chlorohydrocarbon pesticides) was the first to create problems with its persistence in the environment (as Clear Lake demonstrated). DDT was also the first pesticide to produce pesticide resistance, in particular, in Californian houseflies as early in 1948.111 As this resistance spread to other species, it made DDT less attractive in the United States.112 This combination of increasing problems and decreasing effectiveness led to its abandonment, but only because of a legal campaign supported by donations from the public. By contrast, in Britain, where its use had always been much lower, DDT was quietly withdrawn step by step on the advice of experts without much public interest either way. The pressure to withdraw DDT completely came from the EEC seeking a common policy rather than from politicians or the public in the United Kingdom. The use of DDT for malaria control is likely to continue at a low level for some time, but—despite a cam-

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paign to rehabilitate DDT for vector control—its use is very unlikely to attain the levels of the 1960s ever again. Peter J. T. Morris was Keeper of Research Projects in the Research and Public History Department at the Science Museum in London and retired in 2015. He has written extensively on many aspects of recent chemistry. A chemist by training, he earned his D.Phil at the University of Oxford under Margaret Gowing on the history of synthetic rubber at IG Farben. He has since published books on the history of synthetic rubber and polymers, modern chemical instrumentation, and the work of Robert Burns Woodward. He was awarded the Sidney M. Edelstein Award for Outstanding Achievement in the History of Chemistry in 2006 and was editor of Ambix from 2001 to 2012. His most recent book is The Matter Factory (2015), a history of the chemical laboratory from 1600 to 2000. Notes 1. David Vogel (National Styles), carried out a similar exercise, but on a much wider scale and pesticides, perhaps surprisingly, are only considered comparatively briefly. 2. Zeidler, “Verbindungen,” 1180–81. Zeidler’s birth year is often given as 1859, which is clearly incorrect, as that would mean he earned his doctorate when he was about fourteen. Chemiker Zeitung announced his death as 17 June 1911, at sixty-one, which suggests he might have been born in 1850. “Vermischte Nachrichten,” Chemiker Zeitung 35 (1911): 718. His Wikipedia entry now gives a birth date of 29 August 1850. “Othmar Zeidler,” Wikipedia, last edited 30 October 2017, 22:32, https://en.wikipedia.org/wiki/Othmar_​ Zeidler. 3. Mulliken et al., “DDT,” 3. 4. Brand and Bausch, “Über Verbindungen,” 222. 5. Müller, “Dichloro-diphenyl-trichloroethane.” See also Mellanby, DDT Story, 5–9. 6. Wolfgang von Leuthold had patented compounds containing the -CCl3 group as insecticides in 1934 (DRP Nr 673246, 27 April 1934), but DDT was not one of the compounds given as examples. It is unclear if Müller was aware of this patent. 7. Chattaway and Muir, “Formation.” 8. “Kerr-Muir, Ronald John,” Who’s Who and Who Was Who, 1 December 2007, https://doi.org/10.1093/ww/9780199540884.013.U156348. 9. West and Campbell, DDT, chap. 4. 10. Fischer, “Award Ceremony Speech.”

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11. Ross and Amter, Polluters, 52. 12. “Trimz Schedules DDT-Paper Promotion,” Chemical Industries 60 (1947): 1040. 13. West and Campbell, DDT, 8; Russell, War and Nature, 127–29; Kinkela, DDT, 27–31. 14. Mellanby, DDT Story, 20–23. 15. “Paul Müller: Biographical,” Nobel Media, accessed 12 February 2019, https://www.nobelprize.org/prizes/medicine/1948/muller/biographical. 16. Mellanby, DDT Story, 59. 17. West and Campbell, DDT, 11. 18. Dunlap, DDT, 194–97; Mellanby, DDT Story, 66. 19. Russell, War and Nature, 147–49. 20. EPA, DDT, 149, table 3D. The figures have been converted from pounds. 21. USTC, Synthetic Organic Chemicals, 1963, 11, table 7A. 22. The Synthetic Organic Chemicals: United States Production and Sales reports can be downloaded from the US International Trade Commission website but are best accessed via a search engine using “US Tariff Commission Synthetic Organic Chemicals [year in question].” In 1958, for example, the list of DDT producers appears in USTC, Synthetic Organic Chemicals, 1958, 161, table 21B. 23. Irvin I. Rubin, interview by James G. Traynham in Brooklyn, NY, 26 February 2002, CHF Oral History Transcript #0235, 30. 24. Kehoe and Jacobson, “Environmental Decision Making,” 640–75. 25. “Ciba-Geigy Corporation (McIntosh Plant),” EPA, 23 October 2018, http:// www.epa.gov/region4/superfund/sites/npl/alabama/cibageicpal.html. 26. “The History of Lebanon Seaboard Corporation,” Lebanon Seaboard Corporation, accessed 12 February 2019, http://www.lebsea.com/OurHistory. 27. EPA, “DDT Regulatory History.” 28. Lear, Rachel Carson, 408, 416. 29. Ibid., 447–51. 30. Ibid., 480. 31. Dunlap, DDT, 144–46; Graham, Since “Silent Spring,” 252–55. 32. Sellers, Crabgrass Crucible, 133–35. 33. Dunlap, DDT, 45. See also his own account of his campaign, Wurster, DDT Wars. 34. Dunlap, DDT, 147–52; Graham, Since “Silent Spring,” 256–58. 35. Dunlap, “DDT on Trial,” 2–24; Dunlap, DDT, 155–96. See also Berry, Banning DDT. 36. Dunlap, DDT, 159. 37. Morris, “Parts per Trillion,” 259–84. 38. Gunther, “Advances,” 293. 39. Vogel, National Styles, 182. 40. Flippen, Nixon, 31; Dunlap, DDT, 200–203; Kinkela, DDT, 144–47. 41. Kinkela, “Question,” 170. See also Rodgers, “Persistent Problem.”

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42. Dunlap, DDT, 202. 43. IARC, Occupational Exposures. 44. EPA, “DDT Regulatory History.” 45. Hilton, “Report,” 43. 46. Dunlap, DDT, 212–34, Kinkela, “Question,” 171–75. 47. EPA, Consolidated DDT Hearing, 98 (“Section E: Examiner’s Opinion”). 48. Kinkela, DDT, 159–60. 49. Dunlap, DDT, 234. 50. Flippen, “Pests,” 444. 51. Abelson, “Geophysicist’s Watch,” 798. At this stage, Muskie seemed likely to be the Democratic candidate, but in the event, it was, of course, George McGovern. 52. Ruckelshaus, “Oral History Interview.” 53. Flippen, Nixon, 172. 54. Ibid., 142. For the post-ban history of DDT in the United States, see Davis, Banned, chap. 7. 55. Flippen, Nixon, 101. 56. Flippen, “Pests,” 453. 57. The figure of thirty thousand tons is based on US production for 1972, which is largely Montrose by this point. See EPA, DDT, 149; Kehoe and Jacobson, “Environmental Decision Making,” 669 (though the latter is not very informative about the level of production or sales). 58. EPA, “DDT Regulatory History”; EPA, DDT, 220–21. 59. Newton, “Uses,” 81, table 1. The 1969 figure is for imports (no DDT was made in Britain at the time). Amey, “DDT,” 3. 60. West and Campbell, DDT, 5. 61. For the starting date, see “Dichlor-diphenyl-trichlorethane (DDT): Manu­ facture by Hickson & Welch Ltd,” TNA document AVIA 22/2059; “Ernest Hickson—History,” Hickson & Welch, accessed 12 February 2019, http:// www.hicksonandwelch.co.uk/history.htm. 62. Advertisement for DDT flycards, Chemist and Druggist 163, no. 3921 (1955): 36. 63. “Hickson News Release,” The Economist, 18 April 1970, 111; “Tighter Controls on Pesticides to Be Recommended,” The Times (London), 5 November 1969, 1. 64. Swainson, Development, 176. 65. Wilson, “To What Extent”; Mellanby, DDT, 85. 66. As shown by a search of the New Scientist from 1960 to 1989 in Google Books, as all the issues are available in full view. 67. Mellanby, DDT, 83–85. For an overview of pesticide regulation in Britain, see Gillespie, “British” 202–24; Vogel, National Styles, 90–93. 68. Vogel, National Styles, esp. 90–93, 172, 184, 269–76. 69. Caufield, “Britain,” 147. 70. RCEP, Seventh Report, 217 (sec. 7), 218 (sec. 20). 71. Vogel, National Styles, 102–3, 185.

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72. 73. 74. 75. 76.

Caufield, “Britain.” Newton, “Uses,” 82. E.g., Lerner, “DDT.” EC, “Presence.” For another case of national difference in pesticide practice, see Palladino, “Ecological Theory.” 77. Vogel, National Styles, 91. 78. Gale hosts the Times Digital Archive on a subscription-only platform (accessed 21 November 2014). 79. Vogel (National Styles) did a similar exercise with The Times and noted the number of articles on environmental issues increased by 281 percent from 1965 to 1969. However, he did not realize this was largely a result of the articles produced by the Nature-Times News Service. 80. For a discussion of these differences, see ibid.; Jasanoff, Designs on Nature. 81. Brickman et al., Controlling Chemicals, 100. 82. See, e.g., Bud, “Antibiotics.” 83. Edmoundson, “Anatomy.” 84. Wilson, “To What Extent,” 21–22. 85. Sunday Times, Suffer the Children; Quirke, “Thalidomide,” 151–80. 86. Vogel (National Styles, 23, 146) also argues the British voluntary approach worked. 87. EPA, “DDT Regulatory History.” 88. Lear, Rachel Carson, 434–56; Smith, “Silence,” 733–52. 89. Brickman et al., Controlling Chemicals, 240. 90. Vogel, National Styles, 22, 172. 91. Ireton, “Domino Theory,” 2; MacIntyre, “Pesticides,” 573n17. 92. “AG Chem’s Tale,” Agricultural Chemicals 23 (1968): 72. 93. For China, see Wong, et al., “Review,” 742; for India, see Dash et al., “Resurrection,” 1. 94. Pitt, “Chinese Farmers.” 95. UNEP, “Decision 18/32.” 96. Wong, et al, “Review,” table 1. Production in 2004 was 3,945 (presumably metric) tons. 97. PRC, “National Implementation Plan.” 98. Berg, “Global Status,” table 1; Berg et al., “Global Trends,” fig. 1. 99. Mesfin, “DDT Registration Form.” 100. Fumento, “Anatomy.” 101. Beatty, DDT Myth. 102. Tren and Bate, Malaria; Roberts and Tren, Most Excellent Powder. 103. Konradsen et al., Malaria, 7, fig. 5. 104. Ibid., 32. 105. WHO, “Use of DDT.” 106. “Stockholm Convention Continues to Allow DDT Use for Disease Vector Control,” Stockholm Convention, accessed 12 February 2019, http://chm.

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107. 108. 109. 110. 111. 112.

pops.int/Implementation/DDT/DDTRelatedArticles/SCallows​DDT​useford​ iseasevectorcontrol/tabid/2998/Default.aspx. “WHO Backs DDT for Malaria Control,” BBC, last updated 15 September 2006, http://news.bbc.co.uk/2/hi/science/nature/5350068.stm. Mellanby, DDT, 92–93. Kinkela, DDT, 175–80. One of the earliest articles to examine DDT persistence in the environment was Welch and Spindler, “DDT Persistence,” 1285–92. March and Metcalf, “Laboratory and Field Studies,” 93–101. Russell, War and Nature, 197–98.

Bibliography Archives CHF (Chemical Heritage Foundation), Philadelphia, PA. TNA (The National Archives), Kew, London.

Publications Abelson, Philip Hauge. “A Geophysicist’s Watch on the Environment.” New Scientist 50, no. 756 (1971): 796–98. Amey, Leo. “DDT Being Phased Out.” The Times, 18 November 1969, 3. Beatty, Rita Gray. The DDT Myth: Triumph of the Amateurs. New York, 1973. Berg, Henk van den. “Global Status of DDT and its Alternatives for Use in Vector Control to Prevent Disease.” Environmental Health Perspectives 117, no. 11 (2009): 1656–63. Berg, Henk van den, Gamini Manuweera, and Flemming Konradsen. “Global Trends in the Production and Use of DDT for Control of Malaria and Other Vector-Borne Diseases.” Malaria Journal 16 (2017): art. 401. Berry, Bill. Banning DDT: How Citizen Activists in Wisconsin led the Way. Madison, WI, 2014. Brand, Kurt, and Walter Bausch. “Über Verbindungen der Tetraaryl-butanreihe 10: Über die Reduktion organischer Halogenverbindungen und über Verbin­ dungen der Tetraaryl-Butanreihe.” Journal für Praktische Chemie 127 (1930): 219–39. Brickman, Ronald, Sheila Jasanoff, and Thomas Ilgen. Controlling Chemicals: The Politics of Regulation in Europe and the United States. Ithaca, NY, 1985. Bud, Robert Franklin. “Antibiotics, Big Business, and Consumers: The Context of Government Investigations into the Postwar American Drug Industry.” Technology and Culture 46, no. 2 (2005): 329–49. Caufield, Catherine. “Britain Fails to Stem the Silent Spring.” New Scientist 92 (1981): 147.

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Chattaway, Frederick Daniel, and Ronald John Kerr Muir. “The Formation of Carbinols in the Condensation of Aldehydes with Hydrocarbons.” Journal of the Chemical Society (Resumed) 0 (1934): 701–3. Curtis, Adam, dir. “Goodbye Mrs Ant.” Pandora’s Box. season 1, episode 4. Aired 2 July 1992, on BBC. Dash, A. P., K. Raghavendra and M. K. K. Pillai. “Resurrection of DDT: A Critical Appraisal.” Indian Journal of Medical Research 126, no. 1 (2007): 1–3. Davis, Frederick Rowe. Banned: A History of Pesticides and the Science of Toxicology. New Haven, CT, 2014. Dunlap, Thomas R. “DDT on Trial: The Wisconsin Hearing, 1968–1969.” Wisconsin Magazine of History 62, no. 2 (1978): 2–24. _____. DDT: Scientists, Citizens and Public Policy. Princeton, NJ, 1981. EC (European Commission). “Presence of Persistent Chemicals in the Human Body Results of Commissioner Wallstrom’s Blood Test.” Press release, 6 November 2003. MEMO/03/219. http://europa.eu/rapid/press-release_​MEMO-03-219_​ en.htm?​locale=​en. Edmoundson, Brittany. “Anatomy of a Tragedy: Agent Orange during the Vietnam War.” BA thesis, Columbia University, 2012. EPA (Environmental Protection Agency). Consolidated DDT Hearing: Hearing Examiner’s Recommended Findings, Conclusions, and Orders. 40 CFR 164.32. Washington, DC, 1972. _____. DDT: A Review of Scientific and Economic Aspects of the Decision to Ban Its Use as a Pesticide. EPA-540/1-75-022. Washington, DC, 1975. _____. “DDT Regulatory History: A Brief Survey (to 1975).” Last updated 14 September 2016. https://archive.epa.gov/epa/aboutepa/ddt-regulatory-his tory-brief-survey-1975.html. Fischer, Gunnar. Award ceremony speech for the Nobel Prize in Physiology or Medicine 1948 to Paul Müller. Nobel Media, accessed 11 February 2019. https:// www.nobelprize.org/nobel_​prizes/medicine/laureates/1948/press.html. Flippen, John Brooks. Nixon and the Environment. Albuquerque, NM, 2000. _____. “Pests, Pollution, and Politics: The Nixon Administration’s Pesticide Policy.” Agricultural History 71, no. 4 (1997): 442–56. Fumento, Michael. “The Anatomy of a Public Scare.” Investor’s Business Daily, 16–23 July 1993. http://fumento.com/alar/ibdalar.html. Gillespie, Brendan. “British ‘Safety Policy’ and Pesticides.” In Directing Technology: Policies for Promotion and Control, edited by Ron Johnston and Philip Gummett, 202–24. London, 1979. Graham, Frank. Since “Silent Spring.” London, 1970. Gunther, Francis Alan. “Advances in Analytical Detection of Pesticides.” In Scientific Aspects of Pest Control, 276–302. Washington, DC, 1966. Hilton, James G., ed. “Report of the DDT Advisory Committee to William D. Ruckelshaus, Administrator, Environmental Protection Agency.” 9 September 1971. https://nepis.epa.gov/Exe/ZyPDF.cgi/91012N2Q.PDF?​Dockey=​​91012​ N​2Q.PDF.

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IARC (International Agency for Research on Cancer). Occupational Exposures in Insecticide Application, and Some Pesticides. Oxford, 1991. Ireton, Barbara. “Domino Theory.” Guest editorial. NAC News and Pesticide Review 27, no. 5 (1969): 2. Jasanoff, Sheila. Designs on Nature: Science and Democracy in Europe and the United States. Princeton, NJ, 2005. Kehoe, Terence, and Charles Jacobson. “Environmental Decision Making and DDT Production at Montrose Chemical Corporation of California.” Enterprise and Society 4, no. 4 (2003): 640–75. Kinkela, David. DDT and the American Century: Global Health, Environmental Politics, and the Pesticide That Changed the World. Chapel Hill, NC, 2011. _____. “The Question of Success and Environmental Ethics: Revisiting the DDT Controversy from a Transnational Perspective, 1967–72.” Ethics, Place and Environment: A Journal of Philosophy and Geography 8, no. 2 (2005): 159–79. Konradsen, Flemming, F. P. Amerasinghe, W. van der Hoek, and P. H. Amerasinghe. Malaria in Sri Lanka: Current Knowledge on Transmission and Control. Colombo, 2000. Lear, Linda. Rachel Carson: Witness for Nature. London, 1998. Lerner, Ivan. “DDT May Be Used to Prevent Malaria in Third World.” ECN, 8 February 2008. https://www.icis.com/explore/resources/news/2008/02/25/9099583/ddtmay-be-used-to-prevent-malaria-in-third-world. MacIntyre, Angus A. “Why Pesticides Received Extensive Use in America: A Political Economy of Agricultural Pest Management of 1970.” Natural Resources Journal 27, no. 3 (1987): 533–78. March, R. B., and R. L. Metcalf. “Laboratory and Field Studies of DDT-Resistant Flies in Southern California.” Bulletin of the California Department of Agriculture 38 (1949): 93–101. Mellanby, Kenneth. The DDT Story. Farnham, 1992. Mesfin, Dessalegne. “DDT Registration Form: Ethiopia.” Stockholm Convention, 12 September 2006. http://chm.pops.int/Implementation/Exemptions/Acceptable Purposes/AcceptablePurposesDDT/tabid/456/Default.aspx (click Ethiopia). Morris, Peter J. T. “‘Parts per Trillion Is a Fairy Tale’: The Development of the Electron Capture Detector and Its Impact on the Monitoring of DDT.” In From Classical to Modern Chemistry: The Instrumental Revolution, edited by Peter J. T. Morris, 259–84. Cambridge, 2002. Müller, Paul. “Dichloro-Diphenyl-Trichloroethane and Newer Insecticides.” Nobel Prize Lecture, 11 December 1948. https://www.nobelprize.org/nobel_​ prizes/medicine/laureates/1948/muller-lecture.html. Mulliken, David L., Jennifer D. Zambone, and Christine G. Rolph. “DDT: A Persistent Lifesaver.” Natural Resources and Environment 19, no. 4 (2005): 3–7. Newton, Ian. “Uses and Effects on Bird Populations of Organochlorine Pesticides.” In Agriculture and the Environment, edited by David Jenkins, 80–88. Cambridge, 1984.

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Palladino, Paolo. “Ecological Theory and Pest-Control Practice: A Study of the Institutional and Conceptual Dimensions of a Scientific Debate.” Social Studies of Science 20, no. 2 (1990): 255–81. Pitt, Adam. “Chinese Farmers Plant Seed for a Chemical-Free Future.” The Development Advocate 2 (28 January 2013): 4. http://www.undp.org/content/ undp / en / home / ourwork / ourstories / in - china - - farmers - plant - a - seed - for - a chemical-free-future.html. PRC (People’s Republic of China. “National Implementation Plan for the Stockholm Convention on Persistent Organic Pollutants.” Stockholm Convention, 18 April 2007. http://chm.pops.int/Implementation/NationalImplementation Plans/NIPTransmission/tabid/253/Default.aspx. Quirke, Viviane Marguerite. “Thalidomide, Drug Safety Regulation and the British Pharmaceutical Industry: The Case of Imperial Chemical Industries.” In Ways of Regulating Drugs in the 19th and 20th Centuries, edited by Jean-Paul Gaudillière and Volker Hess, 151–80. London, 2013. RCEP (Royal Commission on Environmental Pollution). Seventh Report: Agri­ culture and Pollution. Cmnd. 7644. London, 1979. Roberts, Donald, and Richard Tren. The Most Excellent Powder: DDT’s Political and Scientific History. Indianapolis, IN, 2010. Rodgers, William H., Jr. “The Persistent Problem of the Persistent Pesticides: A Lesson in Environmental Law.” Columbia Law Review 70, no. 4 (1970): 567–611. Ross, Benjamin, and Steven Amter. The Polluters: The Making of Our Chemically Altered Environment. New York, 2012. Ruckelshaus, William R. “Oral History Interview.” EPA 202-K-92-0003. January 1993. https : / / archive . epa . gov / epa / aboutepa / william - d - ruckelshaus - oral - his​tory interview.html. Russell, Edmund. War and Nature: Fighting Humans and Insects with Chemicals from World War I to Silent Spring. New York, 2001. Sellers, Christopher. Crabgrass Crucible: Suburban Nature and the Rise of Environ­ mentalism in Twentieth-Century America. Chapel Hill, NC, 2012. Smith, Michael B. “‘Silence, Miss Carson!’ Science, Gender, and the Reception of ‘Silent Spring.’” Feminist Studies 27, no. 3 (2001): 733–52. Sunday Times. Suffer the Children: The Story of Thalidomide. London, 1979. Swainson, Nicola. The Development of Corporate Capitalism in Kenya, 1918–1977. London, 1980. Tren, Richard, and Roger Bate. Malaria and the DDT Story. London, 2001. UNEP (United Nations Environment Programme). “Decision 18/32: Persistent Organic Pollutants.” 25 May 1995. http://chm.pops.int/Portals/0/docs/from_​ old_​website/documents/meetings/inc1/inf8.htm. USTC (United States Tariff Commission). Synthetic Organic Chemicals: United States Production and Sales, 1958. Report no. 205. Washington, DC, 1959. _____. Synthetic Organic Chemicals: United States Production and Sales, 1963. TC Publication 143. Washington, DC, 1964.

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Vogel, David. National Styles of Regulation: Environmental Policy in Great Britain and the United States. Ithaca, NY, 1986. Welch, E. B., and J. C. Spindler. “DDT Persistence and Its Effect on Aquatic Insects and Fish after an Aerial Application.” Journal of the Water Pollution Control Federation 36, no. 10 (1964): 1285–92. West, Trustham Frederick, and George Alexander Campbell. DDT: The Synthetic Insecticide. London, 1946. WHO (World Health Organization). “The Use of DDT in Malaria Vector Control.” WHO position statement, May 2011. Wilson, Mark. “To What Extent was the British Reaction to ‘Silent Spring’ Indicative of a Tradition of Top-Down Environmentalism?​” MSc thesis, University of St Andrews, 2010. Wong, M. H., A. O. W. Leung, J. K. Y. Chang, and M. P. K. Choi “A Review on the Usage of POP Pesticides in China, with Emphasis on DDT Loadings in Human Milk.” Chemosphere 60, no. 6 (2005): 740–52. Wurster, Charles F. DDT Wars: Rescuing Our National Bird, Preventing Cancer, and Creating the Environmental Defense Fund. New York, 2015. Zeidler, Othmar. “Verbindungen von Chloral mit Brom- und Chlorbenzol.” Berichte der deutschen chemischen Gesellschaft 7, no. 2 (1874): 1180–81.

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CHAPTER 10

War and Peace The Phenoxy Herbicides Amy M. Hay

A 1942 Science news update discussing a newly identified group

of chemicals known as plant hormones noted the need for further research. The question was whether this new category of chemicals, these growth regulators, would harm crops, or if their actions might promote growth and even be added to fertilizers. The news brief concluded: “The idea would be good, but the results might be disastrous.”1 These words might also be applied to a US military operation that took place twenty years later in South Vietnam. Here, phenoxy compounds were used to destroy the natural environment. Operation Ranch Hand sprayed more than twenty million gallons of various combinations of two phenoxy herbicides—2,4-dichlorophenoxyacetic acid (2,4-D) and the chemically related, synthetically produced 2,4,5-trichlorophenoxyacetic acid (2,4,5-T)—in the mountain highlands, around US bases, and in the Mekong Delta region. Part of an intensification of the war under John F. Kennedy’s administration, the spraying missions began in 1962 and fully ended in 1971. Designed to remove jungle foliage, especially along the numerous South Vietnamese roads and waterways, and to destroy crops, the herbicides provoked controversy, an ongoing theme of their existence from discovery to today.2

“Modern Harmless Substances”: The Origins of Phenoxy Herbicides Research on plant hormones, primarily on auxin-like compounds, began in the interwar period, although who discovered the herbicidal

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effects of the compounds appeared to be a contested point, at least at the immediate conclusion of World War II.3 Many saw the origins of plant growth regulators dating back as far as Charles Darwin, in his experiments with plant movement toward light. Work on plant growth regulators proceeded throughout the early twentieth century, with efforts intensifying in the 1930s.4 Researchers began identifying chemical compounds that mimicked the plant hormones that regulated plant growth. Before World War II, the research occurred simultaneously in Britain and the United States.5 The advent of the war intensified research but also ended publication of research results, as both governments classified the growth regulators as potentially important war work. The Chemical Warfare Service conducted experiments on plant growth regulators in Fort Detrick, Maryland. George Merck, of Merck & Co. and director of biological and chemical research during the war, claimed only the war’s end prevented the use of plant growth regulators against Axis enemies.6 This wartime designation also allowed a fertile cross-pollination between academic, industry, and military scientists. Major research in Britain was conducted at Rothamsted Research under the auspices of the Agricultural Research Council and the Imperial Chemical Industries Jealott’s Hill Research Station. US research teams came from the Boyce Thompson Institute in New York, the Hull Botanical Laboratory at the University of Chicago, Cornell University’s New York State Agricultural Experiment Station in Geneva, the USDA Beltsville Agricultural Research Center, and the US Department of Defense’s Fort Detrick.7 A key conceptual shift occurred during this intense time of experimentation when researchers began thinking of the chemicals in terms of killing plants rather than using them to promote growth, such as ripening fruits, promoting root growth, and developing seedless fruits.8

“Death to Weeds!” Weed Killers for Fields and Lawns The research done before and during World War II developing plant growth regulators proceeded in a roughly sequential manner. Initially, researchers focused on documenting the effects of different chemicals on plant growth, slowly narrowing down the most promising ones. They then tested to determine which chemicals were the most effective and then experimented with the best ways to apply them, measured

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results, and finally identified what the practical applications of these new chemical herbicides were. The substituted phenoxy compounds 2,4-D and 2,4,5-T emerged as two of the most effective chemicals in experiments in killing plants, partly because the chemicals affected plant parts beyond just the point of application. British researchers described another important advantage: “[2,4-D] is not readily leached from soil but yet possesses the advantage of ultimately losing its toxicity, thus it would be unlikely to poison the land.”9 Further experiments discovered which plants were the most sensitive, with the good news that common broadleaf weeds like bindweed, dandelions, marigold, buttercups, thistle, and sweet pea appeared to be particularly vulnerable. Even more important were the plants that appeared to be resistant to the chemicals: cereal and rice crops.10 The chemicals’ biological selectivity was considered especially opportune, making them especially suited for weed control. Phenoxy herbicides represented a major breakthrough in weed control, and coverage in popular media meant chemical companies could not wait to begin satisfying the new need.11 At the end of the war, there appeared to be some confusion as to who held the patent rights to the new synthetic plant hormones, specifically the phenoxy herbicides 2,4-D and 2,4,5-T. With at least three sites of military experiments and at least three civilian research teams investigating plant growth regulators, multiple claims of discovery could be made. It was eventually agreed that British researchers had first discovered phenoxyacetic acid compounds and their herbicidal properties, although Americans published their experimental results first.12 Media coverage in farming and popular magazines like Better Homes & Gardens and Reader’s Digest extolled the new herbicide discoveries, fueling farmers and homeowners’ desire to eradicate weeds.13 The patent dilemma in the United States was resolved by the decision of American Chemical Paint Co., the nominal patent holder, to license manufacturing rights to other companies such as Du Pont, Sherwin-Williams, and Dow Chemical.14 While chemical companies sorted through who held patent rights, 2,4-D was tested in the US in fields across the country at agricultural extension stations. The USDA demanded toxicity studies, which indicated no problems.15 American Chemical Paint Co. produced the first commercial weed killer as Weedone in 1945, with thirty other products soon following.16 The large number of products resulted in part from the different forms— esters, salts, and mixtures—in which the chemicals were combined with other herbicides.

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In subsequent decades, Dow Chemical, Monsanto, Hercules, Northwest Industries, Diamond Shamrock, and North American Phillips became the major US producers of herbicides. One measure of how quickly the industry responded can be seen when examining production numbers: “In 1945, the first year of public testing when only limited amounts of 2,4-D were available, total production climbed to 5,466,000 pounds—an increase of nearly 500 percent. By 1950 annual production exceeded 14,000,000 pounds.”17 Almost sixty million acres of agricultural fields had been treated by 1959. Chemical companies offered effective herbicides and, with DDT, pesticides that helped farmers modernize farm operations, and homeowners achieve perfect lawns.18 The case of US farmers provides the most extreme use of phenoxy herbicides as a means of modernizing agricultural operations but still represents the global process. The effectiveness of phenoxy herbicides, especially 2,4-D’s less potent action, and preferential plant eradication made them important contributions to the chemical weed control arsenal. Previously, farmers had used cultural practices to control weed growth. These practices included spring and fall plowing, and routine cultivation during the growing season, all time- and labor-intensive practices during peak work periods. Herbicides cost very little, about $10 a gallon in 1948 and approximately half that after 1950.19 Using herbicides made money in two ways: they cut expenses (fuel and labor) even as they increased crop production. Despite the herbicides’ significant positive effect on crop production, they were not without complications. Applying phenoxy herbicides produced two major problems that caused tensions among farmers and between farmers and public officials. The first issue, the drift of herbicide sprays onto other crops susceptible to the chemicals, such as grapes and cotton crops, resisted any kind of easy solution: “A three-mile-perhour breeze could carry a droplet eight miles when applied from ten feet above the field.”20 Farmers began complaining about crops killed by herbicide drift as early as 1948 to both state and federal agricultural officials. The other difficulty posed by herbicide use appeared in the early 1960s. In this predicament, farmers began seeing new, resistant weeds appear in their fields. This second problem was addressed by the development and use of more chemicals, but no easy solution was discovered for the inherent problem of herbicide drift.21 While county and state extension agents urged a mix of weed eradication practices, using cultural practices and chemical weed control, US farmers enthusiastically embraced chemical herbicides.

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Another group, homeowners, saw the benefits of herbicides in creating a manicured, symmetrical, uniform aesthetic of public space: the American lawn. Perfect lawns once symbolized the wealth and status of seventeenth- and eighteenth-century European aristocracy, but by the late twentieth century, immaculate lawns represented middle-class democracy. Lawn care became the other major market for phenoxy herbicides, as homeowners tried to achieve the perfect lawn—smooth, unblemished grass vistas duplicating previous generations’ propertied wealth. The post-1945 US housing boom resulted in an especially strong market for lawn-care herbicides.22 The historian Virginia Scott Jenkins has noted: “By 1960 the nearly thirty million home lawns in the United States were being added to at the rate of almost half a million a year . . . Thirty million lawns in 1960 added up to more than thirty-six hundred square miles of turf.”23 Similar to agricultural products, chemical lawn care helped reduce the time and labor needed for lawn maintenance. Combination products like Weed and Feed helped achieve these time savings: “The bundling of fertilizer and herbicide spelled bad news for dandelions . . . Meanwhile, the demand for Weed and Feed helped boost 2,4-D production from fourteen million pounds in 1950 to thirty-six million in 1960 to fifty-three million just four years later (1964).”24 Phenoxy herbicides proved invaluable to not just farmers but homeowners as well. The USDA also played an important role in domestic lawns, similar to the one it played in agriculture as it helped develop agricultural products to increase crop production, and a lawn aesthetic that required intensive attention in attaining the perfect lawn. Ecological imbalance, similar to the expansion of other kinds of weeds farmers saw in their fields, also resulted from the creation of a monoculture lawn.25 While 2,4-D worked well on dandelions, it allowed homeowners’ other bane, crab grass, to flourish.26 So, in the immediate post-1945 period, the United States led the world in its use of phenoxy herbicides for agricultural and domestic homeowner use. In the 1960s, the US government devised another application for 2,4-D and 2,4,5-T: as a means of uncovering enemy troops and saving American lives in a conflict halfway around the world. Using phenoxy herbicides in wartime ignited a worldwide controversy and highlighted concerns that persist today.

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“Only We Can Prevent Forests”: Herbicides and War in Southeast Asia Phenoxy herbicides were sprayed using modified C-123 cargo planes, and the chemicals offered an inexpensive and simple means of achieving jungle growth eradication. These herbicides became essential to the US government’s attempts to contain the Communist threat in Asia. The herbicides also worked in helping modernize South Vietnam as a part of the Strategic Hamlet Program and as a means of revealing enemy combatants and supply lines and enabling high-tech aerial warfare. Working with South Vietnamese President Ngo Dinh Diem, US President John F. Kennedy’s advisers sought military interventions that could be used to support the Diem regime. One of the first was designed to clearly identify national borders and map the South Vietnamese countryside, revealing North Vietnamese forces in the process. Chemical defoliation was tested and approved at the end of 1961, with formal spraying missions beginning in 1962. The missions were intended to be a joint venture with the South Vietnamese air force but quickly came under US supervision, to the point where no South Vietnamese military personnel were present on spraying missions.27 Operating under the slogan “Only You Can Prevent a Forest,” Operation Ranch Hand crewmembers (mis)appropriated a popular US Forest Service announcement that featured Smokey Bear. But the ironic editing captured the mission assigned to the US Air Force and South Vietnamese military forces. After the failure of, and public outcry against, napalm (jellied gasoline) in clearing South Vietnamese jungle growth, military advisers turned to different chemical compounds in their efforts to expose enemy troops and supply lines. These “rainbow” herbicides—Agents White, Purple, Pink, Green, and Orange—proved to be far more effective in destroying crops and eradicating jungle growth. All the rainbow herbicides contained either 2,4-D or 2,4,5-T alone or in mixture, except for one. The different combinations of 2,4-D and 2,4,5-T occurred in a roughly sequential order, with Agents Green, Purple, and Pink sprayed from 1962 to 1965 and Agent Orange primarily after 1965. Agent Blue, composed of cacodylic acid, an organic compound containing arsenic, was used primarily for crop destruction. Agent Orange, a fifty-fifty mixture of 2,4-D and 2,4,5-T gained its iconographic name from the orange stripes marking storage barrels. Pilots would leave at dawn when weather conditions were right—no

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rain, no wind, and before the heat of day. Their C-123s sprayed 430 gallons of herbicide a minute, applying three gallons to 240 acres, typically over ten minutes.28 The first plane shot down in Vietnam was flying a Ranch Hand mission. Early missions used Agent Orange and other herbicides to destroy food crops with the intent of denying food to enemy troops. It also served the purpose of accelerating the relocation of what were essentially environmental refugees from rural villages to US–South Vietnamese constructed “strategic hamlets,” barricaded village clusters designed to isolate peasant farmers and supplies from North Vietnamese troops.29 A summary of the amount of herbicide used and the land area sprayed helps explain subsequent scientific concerns over an ecocide of the South Vietnamese countryside. Over the approximate decade when defoliation activities took place in South Vietnam (1962–1971), almost twenty million gallons of the various herbicide mixtures were sprayed. The area sprayed with herbicides, more than 1.6 million acres, equaled the state of Massachusetts. A more inflammatory and rhetorical depiction of the land area sprayed appeared in a 1970 graph published in Broken Arrow, a “radical GI newspaper.” The graph calculated what the United States would look like if sustaining the same mathematical proportions of the Vietnamese population. The US map included categories like “Refugees,” “Killed,” and “Defoliated,” with this last category covering the Eastern Seaboard from Maine to the top of Florida and extending west to Indiana.30 Defoliation operations began slowly, with two hundred thousand gallons of herbicides sprayed between 1962 and 1964 and activities peaking in 1967. By 1965, four hundred thousand gallons had been ordered. Some spraying operations were intended to destroy crops, using cacodylic acid and picloram, Agents Blue and White. Picloram was developed from chlorinated product of picolinic acid and is considered a pyridine herbicide. Anticipated military demands of 5.6 million gallons in 1967 and 11.9 million gallons in 1968 strained the capacity of major chemical manufacturers like Dow, Monsanto, Hercules, and Diamond Shamrock to produce enough herbicides. Spraying for crop destruction drew immediate criticism, where destroying food in a part of the world where famine was common seemed especially horrific. Wartime conditions made it difficult if not impossible to assess how repeated herbicide applications were affecting the ecosystem.31 From 1968 to 1974, different bodies conducted research on the spraying of phenoxy herbicides and its effect on the South Vietnamese eco-

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system. As early as 1966, E. W. “Bert” Pfeiffer, a University of Montana wildlife biology professor, challenged the American Association for the Advancement of Science on the safety of the ongoing, large-scale herbicide spraying campaign. His request that the herbicides’ effects be studied followed a public 1966 petition signed by Harvard and other Boston-area scientists urging the cessation of the herbicide campaign. The issue heated up as more scientists began raising concerns about the herbicide campaign’s effects, including the Yale University plant physiologist Arthur Galston, the Harvard University molecular biologist, experienced science policy adviser, and critic of biological and chemical weapons Matthew Meselson, and the Washington University biologist and scientific activist Barry Commoner. Responding in part to such requests, the US Department of State asked for an assessment of defoliation activities, a task undertaken by the USDA Agricultural Research Service scientist Fred Tschirley in March and April of 1968.32 Tschirley reported his findings in February 1969 in Science. In the article, “Defoliation in Vietnam,” he admitted the difficulties of evaluating the long-term consequences of herbicide spraying. He acknowledged the ecosystem had been affected and that some of those effects might take an extended period to reverse. For example, a single application of herbicide was sufficient to kill mangrove trees, and restoration of a healthy mangrove forest could take twenty years. It took repeated spraying to affect other forest timber, with the primary negative effect being invasive bamboo growth. More troubling, even less information existed on how long it would take to restore these forests. Tschirley observed little harm to wildlife, although he admitted he knew “far less about animals than about plants.”33 He concluded his article by recommending herbicide-spraying effects be studied during and after the war. He specifically suggested spraying be done in a checkerboard or strip pattern to increase chances of regenerating the area. The report did little to resolve questions about the effect of phenoxy herbicides, although Tschirley’s experiences in a war zone brought home the difficulties a research trip might face. After Tschirley’s trip in the spring of 1968 and before his report in early 1969, the AAAS Board of Directors approved its own study of the long-term effects of defoliation.34 The concerns expressed by concerned scientists like Pfeiffer, Galston, and Commoner and the AAAS-sponsored study eventually appeared to have significant influence. The Herbicide Assessment Committee made a five-week site visit to South Vietnam in 1970 under Meselson’s leadership. The HAC reported its findings at the 1970 AAAS general

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meeting. In contrast to Tschirley’s more tentative and benign findings, the HAC said the phenoxy-herbicide-spraying campaign was causing severe harm to the South Vietnamese ecosystem. The report focused on one vulnerable biological species already identified by Tschirley: the mangrove forest. The HAC, however, identified much more serious conditions, including destruction of 20 to 50 percent of mangrove forests, extensive bamboo growth in forests that would prevent reforestation, and the destruction of civilian food supplies as opposed to those of enemy soldiers. The report ignited a firestorm, one not resolved by another 1974 study done by the National Academy of Sciences.35 It seemed to have influenced President Richard Nixon’s administration, as it announced plans to end the herbicide program in Vietnam. Additional pressure to end Agent Orange spraying would have been brought by a 1968 Bionetics Research Laboratory study, commissioned by the National Institutes of Health and released in 1969, which indicated a manufacturing contaminant of the 2,4,5-T form of the phenoxy herbicide, dioxin, might cause birth defects. The report was released in part because of the actions of Galston and a group of scientists who alerted Nixon Science Advisor Lee Alvin DuBridge about it.36 The increasing attention paid to the problem of herbicide use in Vietnam also exposed opposing views among the scientific community that existed on the safety of Agent Orange herbicides. An undated Army report from sometime in 1966 or thereafter, “The Use of Herbicides in Vietnam” by the Army scientist C. E. Minarik, examined press coverage to argue that herbicides allowed tree foliage to be removed, thus making defoliated areas safer from the risk of ambush.37 Industry and other “weed scientists” questioned the ability of biological scientists to properly evaluate herbicide effects, or worried politics had affected their science, although their own connections remained unexamined.38 A paper published in the 1973 Montana Weed Control Conference proceedings directly addressed this dilemma, noting the extensive scientific studies examining the herbicide operations in Vietnam. Farmers paid little attention at first but grew increasingly concerned about the negative coverage. “After all, it is the military and it is in a land on the other side of the world.”39 A letter from the Weed Science Society of America to DuBridge dated 22 December 1969 questioned a proposed Science article on the possible harmful effects of 2,4,5-T and ended by reasserting the reviewed paper did not support the compound’s classification as teratogenic when it was used “according to label instructions.”40 Even

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as concerned scientists had won the battle in protesting the use of Agent Orange in warfare, the battle was shifting to a domestic fight over its use as an herbicide at home. For much of the 1970s, the chemical industry would face increasing concerns over the safety of chemical pesticides, including 2,4-D and 2,4,5-T.41

“The Ecological Turn”: Americans Question Chemical Safety In Silent Spring, Rachel Carson focused primarily on the perils of persistent agrochemicals like DDT, but she also included concerns about the overuse of 2,4-D and 2,4,5-T. She devoted an entire chapter to examining chemical herbicides, singling out the West and the fight against sage or other unwanted brush as examples. Here, Carson emphasized that while herbicides like 2,4-D and 2,4,5-T might not cause as much direct harm as DDT, they still profoundly affect the ecosystem. Herbicides eradicated more than sagebrush. Willows, wildflowers, and bees disappeared along with sagebrush, as did the aquatic ecosystems that depended on them.42 Carson provided the number of acres sprayed across the country; more than 125 million acres of western rangelands had been sprayed to promote grass, to control mesquite brush, for rights-of-way, and an unknown but substantial number of timberlands. These totals did not include the fifty-three million acres of farmland routinely treated with phenoxy herbicides to control weeds. She also exposed the allure weeds sprayed with 2,4-D held for livestock, which resulted in dead cattle after the animals ate weeds sprayed with the herbicide. Carson decried the changed vegetative landscape where the eradication of broadleaf plants only led to the emergence of new kinds of weeds. She also proposed alternatives to the chemical weed control achieved through compounds like phenoxy herbicides, advocating selective spraying for brush management and biological controls for other kinds of weed control.43 By the late 1960s, environmentalists had begun to convince the American public that action needed to be taken in response to the warning sounded by Silent Spring. Responding to the perceived ­political threat the environmental movement posed, Nixon helped pass and create several laws and agencies to oversee environmental issues and concerns, most prominently passing the Clean Air Act of 1970 and Clean Water Act in 1972 and establishing the Environmental Protection Agency in 1970. Building on the successful public hearings

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in Wisconsin, the Environmental Defense Fund sued to end DDT use, and the EPA held a series of hearings in 1971 and 1972. DDT use was banned in the United States in 1972. Chemical manufacturers thought their industry was under attack and spent much of the rest of the decade defending their chemical products. Their case was not helped by the testimony of a prominent chemical firm executive officer at congressional hearings held to evaluate the safety of 2,4,5-T.44 The “Effects of 2,4,5-T and Related Herbicides on Man and the Environment” congressional hearings were held in April and June of 1970. Chaired by Senator Philip Hart, a Democratic senator from Michigan, they sought to determine if the herbicide and related compounds posed a public health threat and had been prompted in part by the 1968 Bionetics study that suggested 2,4,5-T and its dioxin contaminant might cause birth defects. This fear was confirmed in 1976 after the plant explosion in Seveso, Italy. Residents were exposed to a cloud containing at least two grams of the highly toxic dioxin. Some women had abortions proactively, and some women had children with birth abnormalities.45 The most stunning testimony came when Dow Chemical Vice President Julius E. Johnson admitted the company had detected a dioxin contaminant as early as 1964. This meant supplies provided for Operation Ranch Hand contained a higher than normal quantity of dioxin and that defoliation spraying deposited the toxic chemical on Vietnamese citizens, countryside, and soldiers—both Vietnamese and American. Johnson followed his public testimony in 1970 with a 1971 BioScience article in which he discussed the safety of 2,4-D and 2,4,5-T specifically, reassuring readers the herbicides themselves were safe and it was the dioxin contaminant had caused any problems. Moreover, the contaminant quantities could be minimized through proper manufacturing controls. His reassurances were not enough.46 Grassroots domestic activism opposing phenoxy herbicides appeared in 1969, as citizens began protesting aerial sprayings. Aroused both by Carson’s work and the increased scrutiny of the herbicides brought by the Vietnam War and subsequent congressional investigations, the activities of two communities represent public response in the decades following the war. Billee Shoecraft led the community of Globe, Arizona, in protesting a USFS spraying campaign designed to increase the watershed that started in 1965. The 1969 sprayings provoked a community response as community members complained of dead plants, deformed animals, and ill health. Residents in the surrounding canyons joined her in protesting the herbicide drift and eventually suing Dow

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Chemical. Two scientific investigations failed to find any evidence of problems. Finally, a 1970 scientific panel sponsored by the NIH Office of Science Education attempted to definitively resolve residents’ concerns, although February was not the best time for data collection or analysis. The panel concluded that herbicides had not caused vegetative or human harm, and no evidence of dioxin was found in soil samples taken.47 Unhappy with the report, residents sued Dow Chemical. The lawsuit was settled in 1981 for an undisclosed sum, four years after Shoecraft died of cancer. The other example of domestic protests against phenoxy herbicides came from the timberlands of central Oregon, as the actions of residents in two communities achieved mixed results but ultimately resulted in the banning of 2,4,5-T in 1985. In this, the US ban occurred approximately more or less than a decade after 2,4,5-T was banned in other countries; Hungary banned it in 1971, Norway in 1973, and Sweden in 1977. Other nations took action around at the same time as the United States, most prominently Thailand (1983), India (1984), Switzerland (1987), and Germany (1988). In 1975, families in Five Rivers, Oregon, became concerned when a local paper published an article written by the local forestry professor Michael Newton that extolled the virtues of phenoxy herbicides, noting their safety for animals and humans. Newton had been a member of the 1974 NAS study evaluating herbicides in South Vietnam. Carol and Steven van Strum, who had just moved to Five Rivers in 1974, challenged Newton’s safety proclamations. Their four children had been inadvertently sprayed with the herbicides earlier in the year and had been ill afterward. The Van Strums contacted various agencies and researched the safety of the herbicides. They had dropped the matter but were angered by Newton’s casual claims of safety to write a letter to the editor. Their actions mobilized the community.48 Official indifference led residents to eventually pursue legal remedies. Residents met and shared accounts of dead plants, deformed and dead animals, and family illnesses. They tried to get the attention of USFS officials but to no avail, prompting concerned residents to form Citizens Against Toxic Sprays, which focused on the USFS Environmental Impact Statement evaluating the herbicide-spraying campaign’s potential harm. They noted the report had omitted significant studies questioning the safety of phenoxy herbicides, especially 2,4,5-T and its dioxin contaminant. Given these omissions, CATS used the incomplete EIS to sue the USFS and hoped to stop the spraying program. While the group failed to discontinue the

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program, it succeeded in postponing spraying. Events in nearby Alsea, Oregon, intensified the debates over herbicide safety. Alerted by CATS’ challenges to herbicide safety, eight women in Alsea sent a letter to the EPA that linked their miscarriages to the USFS herbicide-spraying program. Led by Bonnie Hill, a local teacher, the women charted their miscarriages against spraying, which showed a correlation between spring spraying and miscarriages. The letter and chart provided enough information to draw the attention of the EPA, which conducted a health study of local women. Although heavily criticized, the findings still resulted in an emergency ban issued by the EPA in 1979 based on a “no safe level” policy. This policy was retracted once the EPA realized the extent of individuals, activities, and industries that would be affected (e.g., Vietnam veterans, plastics production, paper pulp mills, pharmaceuticals, wood preservatives, gasoline). Out of the public eye, the EPA negotiated with Dow Chemical, and propelled by leaked toxicology data, the temporary 1979 suspension of 2,4,5-T was made permanent in 1985.49 Happening at almost the same time, the next challenge to phenoxy herbicides came from another community mobilized through media coverage and government indifference: Vietnam veterans.

Fighting the “Deadly Fog”: Vietnam Veterans Protest Agent Orange Agent Orange: Vietnam’s Deadly Fog first appeared on 3 February and 27 February 1978, on a CBS television station in Chicago. An investigative piece by the local reporter Bill Kurtis, the documentary focused on the use of Agent Orange as a defoliant in the Vietnam War. Veterans had begun complaining about a variety of illnesses, many of them different kinds of cancer, that they suspected were caused by Agent Orange exposure in their wartime service. Maude DeVictor, a benefits counselor at the regional Veterans Administration office in Chicago, had investigated a series of the complaints, began compiling information about the veterans’ illnesses and exposure, and published studies on the toxic effects of dioxin exposure, a contaminant present in the herbicide. DeVictor spoke to an Army specialist, Alvin Young, and documented her findings in a 1977 memo. She also appeared in Kurtis’s documentary, itself prompted by stories of her continued work to link veterans’ illnesses to Agent Orange exposure. DeVictor and Kurtis

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served as critical catalysts in uncovering veterans’ previously unrecognized suspicions about a possible link between wartime exposure to Agent Orange and their seemingly inexplicable illnesses. In the process of publicizing DeVictor’s popular epidemiology, the documentary also alerted the nation to a perceived threat to an entire generation of soldiers and, perhaps even more shocking, their children.50 Vietnam veterans and their fears of toxic contamination became a national concern. In reporting and producing Agent Orange, Kurtis successfully publicized DeVictor’s work and veterans’ fears that they had been exposed to a life-threatening toxin on a national level.51 The documentary and the alarm it sounded reverberated throughout the media, with important consequences. Checking wire news sources, Agent Orange appeared in headlines or lead paragraphs only once between 1 January 1974 and 22 March 1978, in a story on disposal of excess herbicide. From 23 March 1978 to 31 December 1980, Agent Orange was the main topic of more than 150 stories, most dealing with Agent Orange and veterans’ claims of harm.52 The major New York Times three-piece series “Agent Orange: A Legacy of Suspicion” documented ordinary citizens’ as well as veterans’ fears of damaged health in the spring of 1979.53 As early as 11 October 1978, news sources reported approximately five hundred veterans had filed Agent Orange exposure disability suits with the VA. A little short of two years after Agent Orange aired, more than five thousand veterans had submitted claims. One of the most significant actions taken, however, demanded redress from the legal arena rather than the VA. In the spring of 1978, the Vietnam veteran Paul Reutershan appeared on NBC’s Today show and declared he had died during his service in Vietnam, even if he “didn’t even know it.”54 The documentary and subsequent activism also prompted differing responses from various groups. The VA and official government position seemed to be one of denial. When the local Chicago VA office was inundated with veterans calling after Agent Orange aired, the national VA official Paul Haber emphasized that scientific literature thus far supported the relative mildness of any toxic reactions.55 Responding in the fall of 1978 to the increasing number of veteran disability claims, Major General Garth Dettinger, the USAF deputy surgeon general, admitted that while extensive amounts of the herbicide had been used in Vietnam, “our best evidence right now is that we do not have a problem.”56 Within the broader medical community, a more mixed reaction appeared, with views on both sides of the issue expressed. A

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brief article detailed the controversy over herbicide exposure in the spring of 1979, while the physician Gilbert Bolger alerted physicians to some of the symptoms they might see in treating Vietnam veterans in a letter to the editor dated 30 November 1979.57 In a much more scathing example, the physician and academic Ronald Gots described a much more negative understanding of Agent Orange exposure cases. Commenting on the medical records of two children whose stories had appeared in television documentaries, he noted: “I personally reviewed the medical records of two children, alleged victims of Agent Orange, who had deformities of their upper extremities . . . These defects had existed for generations . . . [and] were longstanding inherited disorders, clearly unrelated to the father’s Vietnam experience.”58 Such scientific pronouncements failed to deter veterans from seeking redress for the ill health they attributed to Agent Orange exposure. Reutershan achieved two things before his death in December 1978. His decision to sue the Agent Orange manufacturers launched a class action that eventually represented 2.5 million veterans, their spouses, and their children; the lawsuit requested damages between $4 billion and $40 billion. Supported by his family, the local Veterans of Foreign Wars post, and the Vietnam veteran Frank McCarthy, Reutershan created Agent Orange Victims International, a group dedicated to informing veterans about Agent Orange and seeking financial and political redress. The group played a major role in enlisting veterans across the country to participate in the lawsuit.59 It took more than five years to bring the case to trial, and in a controversial decision, it was settled out of court for $180 million ($189 million with accumulated interest) awarded to veterans. This meant an exposed veteran would receive $12,000 broken into multiple payments. A surviving widow might receive $3,700 if it could be proved her spouse died of Agent Orange exposure. Veterans’ children would receive no monetary payments.60 Australian military troops provided support to the United States and South Vietnam during the war. In contrast to official US government and VA policy, Australian Vietnam veterans won recognition of their disease conditions in the actions of DeVictor, Kurtis, Reutershan, and the millions of veterans they inspired to take action, eventually leading to a multitude of studies on the health of Vietnam veterans, the insurance coverage of some conditions, and the $180 million ­settlement designed to ensure continuing care of Vietnam veterans and their health care needs. While Agent Orange had been put on trial, the out-of-court settlement prevented a public decision on the safety of

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phenoxy herbicides and the responsibility of chemical manufacturers. Despite growing concerns about phenoxy herbicides, they continued to be used around the world.61

Agent Orange Herbicides and the Global Community As noted earlier, English researchers actually discovered phenoxy compounds before World War II before their American counterparts did, even as US chemical companies raced to mass produce chemical herbicides. In a talk before a European Congress of Crop Protection in 1958, Chairman of the British Weed Control Council E. Holmes noted the significant contributions of British research teams. He also acknowledged the work done by French researchers but admitted he had focused on the work done in Britain in developing 2,4-D and a different phenoxyacetic acid herbicide, 2-methyl-4-chlorophenoxyacetic acid (MCPA). In his conclusion, Holmes noted he focused mostly on Britain not because of his own bias as a British scientist but rather because “until recently more work and, as it happens, more rewarding work has been done in Britain.”62 When asked how many people were working full-time on weed-killer research, he answered: in Britain, fifty industry graduates, with fewer at official research stations, approximately 250 workers in all; he estimated the numbers for Continental Europe at two to three times those he gave for Britain. He singled out the work being done by Bayer and BASF, both of Germany. Other European manufacturers included Italy, Sweden, Denmark, and New Zealand. While not all production increases could be attributed solely to herbicide use, much of the gains could. Like their US counterparts, European farmers began to see significant gains in crop production by the late 1960s, as well as some of the same health and safety questions. The clear success of using phenoxy herbicides made it difficult to stop. Wheat production in England increased from 1,500 pounds per acre in 1900 to 3,000 in 1970 after the advent of chemical herbicides. Similarly, corn yield went from approximately twenty bushels an acre in 1940 to eighty-four in 1969. Japanese rice production increased by almost half, and labor time was cut by more than half.63 Due to its significant timber industry, Sweden became a major user of phenoxy herbicides for brush control. The initial quantity used when the herbicides were introduced in 1947 came to 1 metric ton, a figure that increased to 600 by 1960 and 1,700 by 1970. 2,4-D and 2,4,5-T

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represented the major herbicides used in Swedish forestry by 1976. In 1968, 120 metric tons were used to treat 635 hectares of Swedish forests. By 1970, 180 hectares of land were treated with 180 metric tons of mostly 2,4,5-T. In the 1970s, several cases of harm to animal populations including reindeer, elk, and fish and human beings raised questions about the safety of phenoxy herbicides. Several children with birth defects whose mothers thought they might have been exposed to phenoxy herbicides, coupled with information about similar problems in Vietnam, caused grave concern. After forest industry workers and berry pickers both appeared to be afflicted with unknown conditions, Swedish researchers were charged with studying the herbicides. Suspicion grew on the presence of dioxin in the herbicide mixtures. In 1971, the expert commission initially recommended all uses of 2,4-D and 2,4,5-T be banned, but this was later relaxed to allow spraying under specific conditions in timber brush control. Complicating the picture, the subject drew significant media attention. Use fell to nine metric tons, but increased to sixty-one by 1976, when the forest industry began testing alternative herbicides.64 Swedish agriculture represented the other major use of phenoxy herbicides, although to a lesser degree than the forest industry. Approximately sixty metric tons of various salts and combinations of 2,4-D and 2,4,5-T were used in agriculture in 1975, although MCPA remains the most applied herbicide at 1,100 metric tons. One significant difference between the application of phenoxy herbicides in Sweden and the United States appears to be restriction that only pressurized field sprayers can be used to apply the herbicides on agricultural lands.65 Phenoxy herbicide use in other parts of the world has seen some of the same patterns and problems (increased crop yields; harmful effects to other crops, plants, animals, and humans) and some effects distinct to the regions and economic status of the countries. One infamous case of herbicide harm occurred in Tala Valley in Natal, South Africa. 2,4-D and 2,4,5-T were used to kill broadleaf weeds in sugarcane fields before 1986. Herbicide drift had become an increasing problem for local farmers growing fresh produce for market, with herbicide sprays traveling as much as five kilometers. A voluntary ban was agreed on in 1986, although two sugarcane growers and timber farmers refused to participate. Herbicides destroyed farmers’ vegetable crops and cost them a great deal of money. The Natal Fresh Produce Growers’ Association sued but lost their case because the judge ruled that phenoxy herbicide manufacturers could not be held responsible for manufacturing, adver-

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tising, and selling the herbicides to consumers. The farmers should have sued the herbicide users, not the manufacturers.66 Another case of involuntary exposure occurred in Guayaibi, Paraguay, where a large landowner arranged for seven thousand hectares of rangeland to be aerially sprayed with 2,4-D. The problem arose when the contractor negligently sprayed another two hundred hectares of land owned by small farmers, with 334 families affected. Crops like manioc, cotton, potatoes, maize, and vegetables were destroyed, but people living on the land became ill as well. When no Paraguay Ministry of Agriculture official investigated, the families marched to the capital to protest, demanding a cash settlement. In 1990, Paraguay imported almost $65,000 worth of 2,4-D from Argentina and the United States. Dating back to the 1970s, large landowners spray to protect their commercial crops of cotton and soy, and small landowners constantly experience involuntary exposure.67 New challenges include upgrading the quality and production standards of the former Eastern Bloc countries and new applications (literally) for phenoxy herbicides in Asia. In Poland, manufacturing of 2,4-D commenced in 1960 at the Rokita chemical plant with a planned annual production of five hundred tons. Modifications of the manufacturing process in the 1960s proved ineffective and expensive. In 1968, an ambitious manufacturing installation capable of producing three thousand tons of 2,4-D was assembled. The 1976 discovery and use of a liquid form of the chemical intermediates in making 2,4-D allowed for much more successful production and a better final product. Sources on the Polish production of 2,4-D note the challenge of handling the waste products, which totaled fifteen tons per one ton of manufactured 2,4-D, including various forms of dioxin.68 Phenoxy herbicides have been used to perfect the high-maintenance golf courses that have appeared throughout Asia in countries like the Philippines, Malaysia, Thailand, Indonesia, and, ironically, Vietnam. Japan ranked second after the United States in 2005 with 2,300 golf courses. Because of their limited landscape, the Japanese promoted the development of golf courses throughout Asia, because it was easier to fly somewhere else than to build them at home. Even as new applications have been found for phenoxy herbicides, questions concerning their safety have continued to mount.

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Conclusion Significant uncertainty on the safety of phenoxy herbicides plays a major role in the controversial “life” of phenoxy herbicides. In a postwar world determined to modernize and promise “better living through chemicals,” phenoxy herbicides represented exemplars of the productive and aesthetic contributions chemicals could make to human society. Not until scientists questioned their use in destroying an ecosystem and US soldiers sought answers to unexplained illnesses was the possibility of harm taken seriously. Clear evidence shows that 2,4,5-T’s dioxin contaminant made it unsafe for use, although the chemical was still sold overseas. Growing evidence suggests 2,4-D may not be safe either. A 1986 study published in the Journal of the American Medical Association linked 2,4-D use among farmers and an increased appearance of non-Hodgkin lymphoma. A 1996 health study suggested 2,4-D might cause birth defects. In 2004, more than thirty environmental groups signed a letter protesting the EPA’s “human health risk assessment for 2,4-D.” Among the concerns raised were increased incidence of non-Hodgkin lymphoma and its action as an endocrine disrupter.69 Activists continue to contest a 2005 New Zealand Department of Labor report finding no dioxin contamination from 2,4,5-T production between 1948 and 1987 at the Dow AgroSciences plant in New Plymouth, New Zealand.70 Vietnam veterans in 1991 finally achieved medical coverage for all those who served in Vietnam, coverage for certain conditions for veterans’ children in 2003, and disability benefits in 2005.71 Internationally, efforts intensified after 2000, but dating back to the war itself, Vietnamese citizens have sought acknowledgment of, and reparations for, the toxic contamination of their country. The heavy use of phenoxy herbicides left dioxin “hot spots” throughout South Vietnam, and generations of children have suffered severe deformities and disabilities. US veterans have taken up their cause as Vietnamese activists seek reparations for the massive harm done to the Vietnamese environment and health. As recently as 2004, Vietnamese activists sued the US government, seeking war reparations for damages caused by phenoxy herbicides; the case was dismissed in 2005.72 From their wartime discovery to the present day, 2,4-D and 2,4,5-T have remained elusive, controversial figures in the chemical world. Given current debates on whether DDT should have been banned, the

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questions about the safety of phenoxy herbicides appear even more difficult to answer. Their use in the Vietnam War aroused scientific concern, which both reflected the newly emerging environmental consciousness and required a new name: ecocide. These weapons of war seemed to be the inheritors of previous chemical generations’ legacy, as they promised both benefits and potential hazards. Agent Orange’s toxic legacy continues to be debated. Of the $35 billion spent on pesticides worldwide in 2007, herbicides including plant growth regulators comprised 40 percent, or $15.5 billion, of sales.73 But, as noted by Rachel Carson and others, the human desire to control nature, to achieve “chemical weed control,” betrays a fundamental misunderstanding of nature—both the environmental and human kind.74 Amy M. Hay studies twentieth-century US history, focusing on public health and environmental activism. She is Associate Professor of History at the University of Texas Rio Grande Valley. Her book examining the use of phenoxy herbicides and domestic and international protests against aerial spraying of these chemicals is forthcoming from the University of Pittsburgh Press. She was a 2012 Carson Fellow at the Rachel Carson Center for Environment and Society. Recent publications include “Everyone’s Backyard: The Love Canal Chemical Disaster” (History Now, 2014) and “Dispelling the ‘Bitter Fog’: Fighting Chemical Defoliation in the American West” (Endeavor, 2012). Her current research looks at the health, well-being, and environment of the Rio Grande Valley of South Texas. Notes   1. “Science News,” Science 95, no. 2479 (1942): 10–12 (11).  2. Much scholarship on hazardous substances has appeared in recent years. Exemplars of such work are Erker, “Hazardous Substances”; Mart, Pesticides.   3. The three key articles claiming British discovery all appeared in a 1945 issue of Nature: Blackman, “Plant-Growth Substances”; Nutman et al., “Plant-Growth Substances”; Slade et al., “Plant-Growth Substances.”  4. Peterson, “Discovery,” 243; Holmes, “Role,” 245; Thompson et al., “New Growth-Regulating,” 476.   5. “Science News,” 11; Hamner and Tukey “Herbicidal Action”; Beal, “Further Observations,” 165; Marth and Mitchell, “2,4-Dichlorophenoxyacetic,” 224.   6. “Science and Life in the World,” Science 103, no. 2683 (1946): 662–66 (662–63); “Plant Growth Regulators,” Science 103, no. 2677 (1946): 469.

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 7. Russell, History of Agricultural Science, 441–43.   8. Hamner and Tukey, “Herbicidal Action”; Quastel, “2,4-Dichlorophenoxyacetic”; Rasmussen, “Plant Hormones,” 299.   9. Nutman et al., “Plant-Growth Substances,” 488, 499. 10. Hamner and Tukey, “Herbicidal Action”; Beal, “Further Observations,” 167–77; Marth, “2,4-Dichlorophenoxyacetic”; Blackman, “Plant-Growth Substances”; Crafts, “Selectivity.” 11. For chemicals and the world market, see Kinkela, DDT. 12. Slade et al., “Plant-Growth Substances,” 497; Nutman et al., “Plant-Growth Substances”; Blackman, “Plant-Growth Substances,” 500; Crafts, “Selectivity,” 355; “Science News,” 11; Beal, “Further Observations,” 165. 13. Rasmussen, “Plant Hormones,” 309–10. 14. Ibid., 308–9; Peterson, “Discovery,” 243–50. 15. Peterson, “Discovery,” 251. 16. Doyle, Trespass, 55. 17. Peterson, “Discovery,” 252. 18. Doyle, Trespass, 55. 19. Anderson, “War on Weeds,” 733. 20. Daniel, Toxic Drift, 51. 21. Ibid., 50–52; Anderson, “War on Weeds,” 730–31. 22. For the postwar US housing boom, see Jackson, Crab Grass Frontier; Rome, Bulldozer; Steinberg, “Lawn and Landscape,” 62–64. 23. Jenkins, Lawn, 99. 24. Steinberg, American Green, 46. 25. Ibid., 24; Jenkins, Lawn, 99–102; Robbins, Lawn People, 36, 38, 45. 26. Steinberg, American Green, 51. 27. Phuong-Lan, “When the Forest,” 11–16. 28. Scott, Vietnam Veterans, 78. 29. Ibid., 76–78; Milne, America’s Rasputin, 103–7; Phuong-Lan, “When the Forest,” 85–92. Several historians have studied the use and scientific uncertainty surrounding Agent Orange. See Martini, Agent Orange; Sills, Toxic War. 30. Zierler, Invention of Ecocide, 16, 94. 31. For more on the development and uses of picloram, see Fredrickson, “From Ecocide.” 32. For an extended discussion of the scientists involved in protesting Agent Orange herbicides, see Zierler, Invention of Ecocide. 33. Tschirley, “Defoliation,” 786. 34. Ibid., 779–86; Zierler, Invention of Ecocide, 100–110. 35. Hay, “Kind of Mylai,” 69–82. 36. Zierler, Invention of Ecocide, 16, 94; Scott, Vietnam Veterans, 82; Doyle Trepass, 57–59. 37. C. E. Minark, “The Use of Herbicides in Vietnam,” undated, Young Collection, Item ID 256, Box 18.

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38. Behrens, “WSSA”; Rodgers, “Weed Science Today,” 466. 39. “The Orange Controversy and Its Implications to Weed Control Programs,” Montana Weed Control Association, State Weed Conference, 15–16 November 1973, Miles City, MT, Young Collection, Item ID 3814, Box 133. 40. Letter from Weed Science Society of America to Lee Alvin DuBridge, 22 December 1969, Young Collection, Item ID 1503, Box 56. 41. Scott, Vietnam Veterans, 82–83. 42. Carson, Silent Spring, 63–69. 43. Ibid., 70–83. 44. Dunlap, “DDT on Trial,” 24; Dunlap, DDT, 197–230; Gottlieb, Forcing the Spring, 148–59. 45. The Seveso disaster was widely studied. For further reading, see Böschen, this volume. 46. Johnson, “Statement”; Johnson, “Public Health Implications,” 904–5. 47. W. Binns, “Investigation of Spray Project Near Globe, Arizona,” Investigation conducted February 1970, typewritten manuscript, Young Collection, Item no. 2908, Box 106, Collection Series “Animal Studies.” 48. Van Strum, Bitter Fog, 80–82. 49. Van Strum, “Back to the Future.” 50. Scott, Vietnam Veterans, 88–90. On the long quest for compensation of veterans exposed to mustard gas, see Smith, Toxic Exposures. 51. Scott, “Competing Paradigms,” 149. Scott details the efforts Kurtis took to attract attention to the documentary, which included sending copies to local and state elected officials. 52. This crude survey of Agent Orange stories was done by searching LexisNexis Academic News Wire sources for the dates listed (accessed 15 November 2006). 53. Severo, “Two Crippled Lives”; Severo, “U.S., Despite Claims”; Severo, “Herbicides Pose.” Scott, Vietnam Veterans, 90. 54. Quoted in Wilcox, Waiting, xi. 55. News Wire, Associated Press, 24 March 1978, PM cycle, LexisNexis Academic. 56. M. Shanahan, News Wire, Associated Press, 11 October 1978, AM cycle, LexisNexis Academic. 57. Gunby, “Dispute”; “Letter from Gilbert Boger, M.D., to the Editor of the Journal of the American Medical Association, 30 November 1979,” Journal of the American Medical Association 242, no. 22 (1979), cited in Wilcox, Waiting, 195, appendix. 58. Gots, Toxic Risks, 172. 59. Schuck, Agent Orange, 40–48. 60. Wilcox, Waiting, xvii. 61. Scott, Vietnam Veterans, 90–96, 101–14; Martini, Agent Orange, 179–96. 62. Holmes, “Role of Industrial Research,” 249. 63. Ennis, “Benefits.” 64. Bäckström, “Phenoxy Acid”; Bärring, “Use of Phenoxy Herbicides.”

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65. Granstöm, “Use of Phenoxy Acid.” 66. Dinham, Pesticide Hazard, 154; “Natal Fresh Produce Growers’ Association and Others v. Agroserve (Pty) Ltd and Others,” in Compendium of Judicial Decisions in Matters Related to Environmental: National Decisions, vol. 1, ed. UN Environmental Programme and UN Development Programme, 387–93 (Nairobi, 1998). 67. Dinham, Pesticide Hazard, 118–22. 68. Moszczyński and Białek, “Ecological Production,” 354–55; Steinberg, “Lawn and Landscape,” 65–66. 69. “RE: 2,4-D Risk Assessment,” letter to EPA, 23 August 2004, https://www. beyondpesticides.org/assets/media/documents/watchdog/comments/24D_​ 0804.pdf. 70. OHS, Risk Evaluation; Bramhall, “NZ’s Dioxin Legacy.” 71. Palmer, “Case of Agent Orange,” 174. 72. Ibid., 172; Cline, “Agent Orange,” 1. 73. Grube et al., Pesticides Industry, 4. 74. Zierler, Inventing Ecocide, 14–32. For more on reparations, see Mauch et al., “Legacy.”

Bibliography Archives The Alvin L. Young Collection on Agent Orange consists of materials collected by Alvin L. Young (1942– ), a PhD in agronomy and an Army colonel charged with researching the herbicides used in defoliation missions in the Vietnam War. Young accumulated his materials when he researched Agent Orange. The collection dates back to the 1800s, but the bulk of the 120 linear feet of materials comes from the 1960s to 1980s. The collection includes government reports, letters, journal articles, newspaper clippings, congressional and trial testimonies, pamphlets, and maps. The collection is housed at the National Agricultural Library in Beltsville, Maryland.

Publications Anderson, J. L. “War on Weeds: Iowa Farmers and Growth-Regulator Herbicides.” Technology and Culture 46, no. 4 (2005): 719–44. Bäckström, J. “The Phenoxy Acid Problem in Sweden.” Ecological Bulletins 27 (1978): 109–15. Bärring, U. S. M. “The Use of Phenoxy Herbicides in Swedish Forestry: Amounts, Types, and Modes of Application.” Ecological Bulletins 27 (1978): 222–29. Beal, J. M. “Further Observations on the Telemorphic Effects of Certain GrowthRegulating Substances.” Botanical Gazette 106, no. 2 (1944): 165–77.

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Behrens, Richard. “WSSA: Progress and Challenges.” Weed Science 16, no. 4 (1968): 412. Blackman, G. E. “Plant-Growth Substances as Selective Weed-Killers: A Comparison of Certain Plant-Growth Substances with other Selective Herbicides.” Nature 155, no. 3939 (1945): 500–501. Bramhall, Stuart. “NZ’s Dioxin Legacy: Lies and Cover-Up.” The Most Revolutionary Act. 14 February 2014. https://stuartbramhall.wordpress.com/2014/02/14/ nzs-dioxin-legacy-lies-and-cover-up. Carson, Rachel. Silent Spring. New York, 1962. Cline, David. “Agent Orange: A Continuing Legacy of the War.” The Veteran 36, no. 2 (2006): 1–2. Crafts, A. S. “Selectivity of Herbicides.” Plant Physiology 21, no. 3 (1946): 346–55. Daniel, Pete. Toxic Drift: Pesticides and Health in the Post–World War II South. Baton Rouge, LA, 2005. Dinham, Barbara. The Pesticide Hazard: A Global Health and Environmental Audit. London, 1993. Doyle, Jack. Trepass against Us: Dow Chemical and the Toxic Century. Monroe, ME, 2004. Dunlap, Thomas R. “DDT on Trial: The Wisconsin Hearing, 1968–1969.” Wisconsin Magazine of History 62, no. 1 (1978): 2–24. _____. DDT: Scientists, Citizens, and Public Policy. Princeton, NJ, 1981. Ennis, W. B. “Benefits of Agricultural Chemicals.” Weed Science 19, no. 6 (1971): 631–35. Erker, Paul, ed. “Hazardous Substances: Perceptions, Regulations, Consequences.” Special issue, Global Environment 7, no. 1 (2014). Fredrickson, Leif. “From Ecocide to Eco-ally: Picloram, Herbicidal Warfare, and Ivasive Species, 1963–2005.” Global Environment 7, no. 1 (2014): 172–217. Gots, Ronald E. Toxic Risks: Science, Regulation, and Perception. Boca Roca, FL, 1993. Gottlieb, Robert. Forcing the Spring: The Transformation of the American Environ­ mental Movement. New York, 2005. Granstöm, B. “The Use of Phenoxy Acid Herbicides in Swedish Agriculture.” Ecological Bulletins 27 (1978): 231–33. Grube, Arthur, David Donaldson, Timothy Kiely, and La Wu. Pesticides Industry, Sales and Usage, 2006 and 2007 Market Estimates. Washington, DC, 2011. Gunby, P. “Dispute over Some Herbicides Rages in Wake of Agent Orange.” Journal of the American Medical Association 241, no. 14 (1979): 1443–44. Hamner, Charles L., and H. B. Tukey. “The Herbicidal Action of 2,4 Dichloro­ phenoxyacetic and 2,4,5 Trichlorophenoxyacetic Acid on Bindweed.” Science 100, no. 2590 (1944): 154–55. Hay, Amy M. “‘A Kind of Mylai . . . Against the Indochinese Countryside’: American Scientists, Herbicides, and South Vietnamese Mangrove Forests.” In Environmental Change and Agricultural Sustainability in the Mekong Delta, edited by Mart A. Stewart and Peter Coclanis, 69–82. New York, 2011.

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Holmes, E. “The Role of Industrial Research and Development in Weed Control in Europe.” Weeds 6, no. 3 (1958): 245–50. Jackson, Kenneth. Crab Grass Frontier: The Suburbanization of the United States. New York, 1987. Jenkins, Virginia Scott. The Lawn: The History of an American Obsession. Washington, DC, 1994. Johnson, Julius E. “The Public Health Implications of Widespread Use of the Phenoxy Herbicides and Picloram.” BioScience 21, no. 17 (1971): 899–905. _____. “Statement.” In Hearings Before the Subcommittee on Energy, Natural Resources, and the Environment of the Committee on Commerce, United States Senate, Ninety-First Congress, Second Session on Effects of 2,4,5-T on Man and the Environment, 7 and 15 April 1970, 360–404.Washington, DC, 1970. Kinkela, David. DDT and the American Century: Global Health, Environmental Politics, and the Pesticide That Changed the World. Chapel Hill, NC, 2011. Mart, Michelle. Pesticides, A Love Story: America’s Enduring Embrace of Dangerous Chemicals. Lawrence, KS, 2015. Marth, Paul C., and John W. Mitchell. “2,4-Dichlorophenoxyacetic Acid as a Differential Herbicide.” Botanical Gazette 106, no. 2 (1944): 224–31. Martini, Edwin A. Agent Orange: History, Science, and the Politics of Uncertainty. Amherst, MA, 2012. Mauch, Christof, Nga Le, Christian Lahnstein, and Amy Hay. “The Legacy of Agent Orange: A Conversation about Risk and Responsibility.” Global Environment 7, no. 1 (2014): 218–36. Milne, David. America’s Rasputin: Walt Rostow and the Vietnam War. New York, 2009. Moszczyński, Wiesław, and Arkadiusz Białek. “Ecological Production Technology of Phenoxyacetic Herbicides MCPA and 2,4-D in the Highest World Standard.” In Herbicides: Properties, Synthesis and Control of Weeds, edited by Mohammed Naguib Hasaneen, 347–62. London, 2012. Nutman, P. S., H. G. Thornton, and J. H. Quastel. “Plant-Growth Substances as Selective Weed-Killers: Inhibition of Plant Growth by 2:4-Dichlorophenoxyacetic Acid and other Plant-Growth Substances.” Nature 155, no. 3939 (1945): 498–500. OHS (Occupational Safety and Health). Risk Evaluation of Dioxin Exposure to Workers at Dow AgroSciences. New Plymouth, NZ 2007. Palmer, Michael G. “The Case of Agent Orange.” Contemporary Southeast Asia 29, no. 1 (2007): 172–95. Peterson, Gale E. “The Discovery and Development of 2,4-D.” Agricultural History 41, no. 3 (1967): 243–51. Phuong-Lan, Bui Thi. “When the Forest Became the Enemy and the Legacy American Herbicidal Warfare in Vietnam.” PhD diss., Harvard University, 2003. Quastel, J. H. “2,4-Dichlorophenoxyacetic Acid (2,4-D) as a Selective Herbicide.” Agricultural Control Chemicals, Collected Papers from the Symposia on Economic Poisons, 244–46. Washington, DC, 1950.

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Rasmussen, Nicholas. “Plant Hormones in War and Peace: Science, Industry, and Government in the Development of Herbicides in 1940s America.” Isis 92, no. 2 (2001): 291–319. Robbins, Paul. Lawn People: How Grasses, Weeds, and Chemicals Make Us Who We Are. Philadelphia, 2007. Rodgers, E. G. “Weed Science Today.” Weed Science 22, no. 5 (1974): 464–68. Rome, Adam. The Bulldozer in the Countryside: Suburban Sprawl and the Rise of American Environmentalism. New York, 2001. Russell, E. John. A History of Agricultural Science in Great Britain: 1620–1954. London, 1966. Schuck, Peter H. Agent Orange on Trial: Mass Toxic Disasters in the Courts. Cambridge, MA, 1987. Scott, Wilbur J. “Competing Paradigms in the Assessment of Latent Disorders: The Case of Agent Orange.” Social Problems 35 (1988): 145–61. _____. Vietnam Veterans since the War: The Politics of PTSD, Agent Orange, and the National Memory. Norman, OK, [1993] 2004. Severo, Richard. “Herbicides Pose a Bitter Mystery in U.S. Decades after Discovery.” New York Time, 29 May 1979. _____. “Two Crippled Lives Mirror Disputes on Herbicides.” New York Times, 27 May 1979. _____. “U.S., Despite Claims of Veterans Says None Are Herbicide Victims.” New York Times, 28 May 1979. Sills, Peter. Toxic War: The Story of Agent Orange. Nashville, TN, 2014. Slade, R. E., W. G. Templeman, and W. A. Sexton. “Plant-Growth Substances as Selective Weed-Killers: Differential Effect of Plant-Growth Substances on Plant Species.” Nature 155, no. 3939 (1945): 497–98. Smith, Susan L. Toxic Exposures: Mustard Gas and the Health Consequences of World War II in the United States. New Brunswick, NJ, 2017. Steinberg, Ted. American Green: The Obsessive Quest for the Perfect Lawn. New York, 2006. _____. “Lawn and Landscape in World Context, 1945–2000.” OAH Magazine of History 19, no. 6 (2005): 62–68. Thompson, H. E., Carl P. Swanson, and A. G. Norman. “New Growth-Regulating Compounds.” Botanical Gazette 107 (1946): 476–507. Tschirley, Fred H. “Defoliation in Vietnam.” Science 163, no. 3869 (1969): 779–86. Van Strum, Carol. “Back to the Future: EPA Reinvents the Wheel on Reproductive Effects of Dioxin.” Synthesis/Regeneration 7–8 (1995). http://www.greens.org/ s-r/078/07-25.html _____. A Bitter Fog: Herbicides and Human Rights. San Francisco, 1983. Wilcox, Fred A. Waiting for an Army to Die: The Tragedy of Agent Orange. Santa Ana, CA, 1989. Zierler, David. The Invention of Ecocide: Agent Orange, Vietnam, and the Scientists Who Changed the Way We Think About the Environment. Athens, GA, 2011.

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CHAPTER 11

Raising a Stink The Short, Happy Life of MTBE John K. Smith

The rapid rise and meteoric fall of methyl tert-butyl ether as a gasoline

component in the United States from 1980 to 2007 is an example of environmental regulation with constantly shifting priorities combined with interest group politics and widespread chemophobia.1 MTBE was added to gasoline and later removed for environmental reasons, primarily because of fears about its toxicity. By contrast, in Europe, where MTBE was not determined to be a significant risk to the environment or public health, its use continued. The outcome was different because the Europeans maintained a consistent priority, and MTBE did not become tangled up in larger public, industrial, and political controversies. Perhaps oversimplifying the issue, technocratic experts in Europe made environmental policy, whereas, in the United States, issues were hashed out in public and political arenas. Democratic societies, in general, continually confront the dilemma of balancing ­technocratic—versus political—decision-making, especially when the issues are technical. The impacts of every aspect of technological change must be assessed in contrast to the present situation and future alternatives. The complexity of technological and environmental systems makes this endeavor a difficult one to say the least. Predicting the effects of changes in dynamic systems always contains a considerable degree of uncertainty. Assessing the risks and benefits of technological change should highlight factors that are uncertain. In the case of MTBE, its use in gasoline in small quantities to increase octane levels was an environmental and health improvement over its precursor tetraethyl lead (TEL). The later decision to increase MTBE levels significantly to improve air quality was an

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unproven benefit that introduced an uncertain risk of environmental and health effects. In the case of MTBE, the Environmental Protection Agency, in the name of cleaner air, created an environmental controversy that ended in a purely political resolution with undetermined environmental consequences. Automobile exhaust has long been a recognized and major source of air pollution that causes adverse health effects, especially in cities. After World War II, scientists discovered incomplete gasoline combustion led to emitted hydrocarbons that contributed to the formation of what became known as smog. In the 1960s, research revealed the increasing contamination of the environment—and human beings—with lead from the combustion of gasoline containing TEL, which had been added to improve the performance of internal combustion engines.2 Since the mid-1920s, TEL had been added in very small quantities to gasoline because it was a cheap and effective way to increase its octane rating. In the United States, where car ownership was becoming widespread, TEL promoted increased automobility by increasing fuel efficiency by 45 percent.3 Burning it in gasoline added lead to automobile exhaust, but those few physicians who cared about lead poisoning initially focused their attention on lead-based paints. Before World War II, TEL was the solution to the octane problem.4 During and immediately after the war, new oil-refining techniques were developed to rearrange petroleum molecules to increase octane ratings. Refining innovations such as catalytic cracking and platforming not only increased the total yield of gasoline from a barrel of oil but also created a higher-octane product. Platforming, developed in the late 1940s, increased the octane rating by dramatically increasing the concentration of aromatic organic compounds, including benzene.5 The toxicity of benzene had been long recognized, and it is now classified as a human carcinogen.6 By 1970, aromatics represented about onequarter of gasoline’s content. One industry expert predicted aromatics would have had to increase to one-third if the TEL was removed.7 In the 1950s and 1960s, low-mpg American cars were running on gasoline that spewed lead, carbon monoxide, and other toxic, even carcinogenic, hydrocarbons into the atmosphere. It is hardly surprising the emerging environmental movement in the United States would identify this as an area of concern. In many US cities, but especially Los Angeles, smog had become both an aesthetic and public health issue. To address this problem, in the 1970s, the automobile industry, especially General Motors, decided to use a catalytic converter to combust unburned hydrocarbons

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in car exhaust. Coincidentally, the use of catalytic converters required removing TEL because lead poisoned the catalyst. Ironically, removing the lead was only a collateral environmental benefit.8 With the gradual removal of TEL, the oil industry needed to find other ways to increase gasoline octane ratings. MTBE soon emerged as a prime candidate.9 It could be made rather easily from isobutylene and methanol, both of which were available at oil refineries and from natural gas. These chemicals could be made from inevitable byproducts of the catalytic cracking of petroleum, thus upgrading their value and minimizing the temptation to flare or dump them. According to an industry expert, the MTBE-forming chemical reaction occurs at “fairly modest conditions, the equipment needed is simple and relatively inexpensive, (and) produces very high yields with essentially no side reactions or losses.”10 From the raw material and production side, MTBE appeared to be a sound environmental choice. In terms of conserving oil, one barrel of MTBE was equivalent to 2.2 barrels of gasoline because of its 120-octane rating and because it reduced the need to obtain higher octane gasoline by severely refining crude oil fractions that resulted in losses of up to 30 percent of the oil in low value byproducts.11 The chemical properties of MTBE made it compatible with gasoline—and, significantly, with internal combustion engines—and adding only a small percent would raise the octane rating significantly. European countries had begun to restrict TEL in early the 1970s; both Germany and Italy already were adding MTBE to gasoline.12 In the United States, the EPA approved of the use of MTBE in gasoline in February 1979 because MTBE had proved to be no more toxic than gasoline in inhalation, ingestion, and skin absorption tests.13 At that time, annual world production equaled roughly one million barrels, which was only about 0.01 percent of the world’s gasoline consumption. After EPA approval, US oil companies announced plans to increase total production six fold in the next year. By 1984, annual US production reached seven million barrels. By 1986, there were thirty MTBE plants, and another twenty were in the planning stage. Consumption was increasing at 40 percent per year.14 To entirely replace the octane lost by removing TEL from gasoline would require one hundred million to two hundred million barrels per year of MTBE to be consumed in the United States alone. By 1990, US production had reached forty million barrels per year; gasoline now contained about 1 percent MTBE.15 Continuing concern about air quality in some cities led to the addition of much larger quantities of MTBE to gasoline. Although catalytic

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converters improved the air quality in most US cities, some of them continued to experience pollution caused by carbon monoxide and ozone. In 1987, Colorado began an oxygenated fuel program, which meant incorporating oxygen-containing ingredients into gasoline to promote fuller combustion.16 Soon, the EPA began to consider adding extra oxygen to gasoline in the winter to forty areas, mostly Northern cities, to reduce carbon monoxide emissions. Oxygenated fuel typically had a 2.7 percent oxygen content, which required 15 percent by volume MTBE. In addition, the ten areas with the worst air pollution were to shift to what was called reformulated gasoline containing even higher levels of oxygen to promote more complete combustion of hydrocarbons. To explore these options, the EPA conducted a “regulatory negotiation” process that included the auto and oil industries, environmental groups, state and federal agencies, and agricultural interests. The resulting Clean Air Amendments of 1990 stipulated that RFG contain a minimum of 2 percent oxygen. This requirement could be met by gasoline containing 11 percent by volume MTBE and increasing production by several hundred percent, but refiners could add capacity rather cheaply.17 At this point, however, another option emerged: ethanol. The RFG requirement could also be met by gasoline containing 5.7 percent ethanol.18 Ethanol from corn fermentation was also being produced on an industrial scale in modest-sized plants throughout the Corn Belt of the Midwestern United States. During the 1979 oil crisis, Congress had encouraged the production of ethanol for gasoline by providing substantial tax subsidies.19 This exemption made ethanol economically competitive with gasoline, but whether there was any renewable energy in ethanol was hotly debated. The major proponent of “gasohol” was William Scheller, a University of Nebraska chemical engineering professor. In the mid-1970s, Scheller had calculated energy balances that supported his contention that corn ethanol contained more energy than it took to produce it.20 Other analysts, using different sets of assumptions, came to the opposite conclusion.21 Regardless of corn ethanol’s renewability, politicians had been hesitant to remove ethanol’s tax exemption because several Corn Belt states are critical swing states in presidential elections. To meet the 1990 amendments’ oxygenate requirement with ethanol would require increasing its production by at least a factor of three, meaning many more plants would have to be built.22 In the early 1990s, MTBE was the oil industry’s preferred oxygenate because it could be transported by pipeline and easily mixed with gasoline,

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whereas, ethanol, because of its affinity for water, had to be shipped by truck to blending stations. In the early 1990s, MTBE consumption in the United States still was increasing at about 25 percent per year.23

Growing Concerns Soon after oxygenated gasoline with higher levels of MTBE was introduced in the United States, consumer complaints began. In Fairbanks, Alaska, in 1992, people complained of “headaches, dizziness, irritated eyes, and nausea.”24 MTBE has a pronounced odor that has been compared to paint thinner or turpentine. In the fall of 1993, people in New Jersey were making similar complaints. This is rather curious, because citizens are not allowed to pump their own gas in that state.25 Responding to these concerns over the possible adverse health effects of MTBE, Chemical & Engineering News, published by the American Chemical Society, reported that in 1987 the Oxygenated Fuels Association, an MTBE-related petrochemical industry trade group, had begun a long-term $3.5 million study on animals to determine MTBE’s potential chronic health effects.26 This study was initiated to meet the requirements of the Toxic Substances Control Act in 1976, which allowed the EPA to require testing of new chemicals. The law was passed in the wake of discovering the toxic effects of vinyl chloride, PCBs, and other compounds in the early 1970s.27 The intent of the law was to determine the potential hazards of new chemicals before they were manufactured and used. To test MTBE, two lifetime studies of rats were done at high levels of exposure, which led to an “increased incidence of benign tumors in the livers of female rats and an increase in renal tubular cell tumors.”28 In response to the public complaints about MTBE, the EPA in early 1993 started planning an additional extensive test program and called a conference of interested parties to discuss the issue. C&EN noted that “Many experts—in and out of industry—believe that the scientific data presented went a long way toward restoring MTBE’s tarnished reputation.”29 To further address these health concerns, the White House’s Office of Science and Technology Policy prepared a study that concluded “MTBE does not pose a substantial human health risk” but called for more definitive data. At the EPA’s request, a National Research Council panel critiqued this study and concluded more studies were needed to provide a more definitive assessment.30 Doubts about the toxicity of

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MTBE created an opportunity for ethanol. The ethanol lobby, which included the influential Democratic Senator Thomas Daschle of South Dakota, was ready to take advantage of potential problems with MTBE. Under pressure from President Bill Clinton’s administration in July 1994, the EPA announced that 30 percent of the oxygen in reformulated fuel must come from “renewable sources,” that is, ethanol, by 1996.31 This seemed to be an overtly political move by the EPA, and one that had little to do with its mandate to protect the environment. The courts agreed when they ruled that the EPA had indeed overstepped its authority.32 In 1995, after the EPA mandated introduction of RFG in certain locations, other problems surfaced for MTBE, when more consumers complained about health effects and the higher cost of oxygenated gasoline. Interestingly, an expert at the Natural Resources Defense Council, an environmental lobbying organization, defended MTBE by attributing these complaints to the “overall climate of anti-Washington, anti-big government.”33 In this same federalist spirit, thirty-eight counties in Maine, New York, and Pennsylvania asked to opt out of the RFG program, and a bill was introduced in California to ban the use of MTBE in gasoline. At that time, California, with its severe urban air pollution problems, was consuming 10 percent of the world’s production, more than the entire Asia-Pacific. The rather widespread local opposition to MTBE began to worry the industry. The East-West Center, a US institute established to promote cooperation with Asia, studied the MTBE controversy and presciently predicted, “These concerns regarding the safety of MTBE, whether scientifically supported or not, have led to a short term reduction in demand for MTBE, which could develop into a long term death spiral for this gasoline blending component.”34 These fears soon would be amplified when MTBE was discovered in groundwater. The source was most likely leaks from underground gasoline storage tanks. Because of its solubility in water, MTBE tended to diffuse farther than other gasoline components. In April 1995, the US Geological Survey reported MTBE had been found in shallow groundwater in eight urban areas. None of this water was used for drinking, and only 3 percent of the samples were above EPA advisory limits. The average concentration was 0.6 parts per billion, while the advisory limits were twenty to two hundred parts per billion.35 But in some specific locations, the problems could be worse; Santa Monica, California, found MTBE in wells supplying 70 percent of its water supply.36 A 1996 assessment by independent risk science consultants published in

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Risk Analysis concluded 5 percent of the US population was exposed to potentially significant amounts of MTBE and, based on the data available at the time, that there were “virtually no health risks associated with chronic or sub-chronic human exposures to MTBE in tap water.”37 An added layer of protection against ingestion of contaminated water was that the low odor and taste thresholds of MTBE meant people would be warned of the presence of MTBE at levels well below any toxic threshold. Just how toxic MTBE is and how much clean air benefit resulted from its use became major scientific and political issues in the United States. The expected improvement in air quality from oxygenated and reformulated gasoline had been based on laboratory experiments rather than real-world testing. Toxicology studies using rodents exposed to varying amounts of MTBE produced many data, but experts argued about the relevance of this data to actual exposures of human beings. Rather defensively, the EPA argued MTBE was at least less of a threat than other chemicals in gasoline, such as benzene, which it was replacing.38 The uncertainty inherent in toxicology studies became apparent in 1999 when several organizations attempted to decide whether MTBE was a human carcinogen. The government National Toxicology Program voted 6–5, and the California toxicology authority voted 3–3.39 The International Agency for Research on Cancer determined MTBE was “not classifiable as to its carcinogenicity in humans,” while a panel of scientists at the University of California, Berkeley, concluded it did pose a human cancer risk. The situation became more complicated in 1997 when the California Air Resources Board implemented stricter air pollution standards that required year-round use of cleaner burning fuels.40 To accomplish this goal by 1999, California was consuming one-quarter of the world’s output of MTBE.41 At the same time, California law restricted the use of chemicals known to be carcinogens or reproductive toxins.42 To address the MTBE controversy at the national level, EPA Administrator Carol Browner in 1998 appointed a thirteen-member panel that included state, industry, and environmental groups and was headed by Daniel S. Greenbaum, the president of the Health Effects Institute in Massachusetts. At the press conference announcing his report, Greenbaum said: “The problem of MTBE in the water supply is not a health and safety issue, but an environmental one. Although five to ten percent of drinking water supplies in areas where high oxygenate gasoline is being used have detectable amounts of MTBE the majority

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are well below levels of public health concern.”43 In some contaminated areas, communities had stopped using their water supplies because of problems of taste and odor. Based on the findings of another government advisory panel, the EPA asked for a reduction of MTBE use as quickly as possible in 1999, but without sacrificing air quality. The NRC had studied the impact of oxygenated gasoline on air quality, “looked at the environmental performance of the compound and concluded that its use on the reduction of ozone has been slight” and that “much more air pollution was prevented by gasolines that have lower vapor pressure and lower sulfur content.”44 With the benefits of MTBE on air quality unproven, the Oil & Gas Journal reported that “some petroleum companies have taken the position that, even though MTBE does not pose any clear health risks, if consumers are concerned that such health risks might exist, refiners would prefer to supply some other fuel,” noting also, “because the public is uncertain about the effects of low concentrations of MTBE in drinking water, regulators are under pressure to ban the material.”45 To address the problem, the petroleum refiners asked the 2 percent oxygen requirement be repealed because cleaner burning gasoline could be produced by other means. MTBE levels would then be lowered significantly, back down to the small percent necessary for octane enhancement. An unusual political coalition of the American Petroleum Institute, the Northeast States for Coordinated Air Use Management, the American Lung Association, and the Natural Resources Defense Council combined efforts to ask the EPA to remove the 2 percent mandate—as did California.46 The Corn Belt ethanol interests, however, wanted to keep the requirement, hoping ethanol would replace MTBE. One industry expert estimated California would need to put an additional two hundred tank trucks on the road each day to transport this ethanol. In a pessimistic assessment, Chemical & Engineering News noted: “MTBE is likely to be gone . . . in the next few years, once again by government fiat, leaving the industry with a lot of useless capacity. As a result, more demands will be put on refiners to reformulate gasoline, and EPA will set new regulations to improve air quality. I hope they have better luck this time.”47 In response to growing publicity about MTBE in groundwater, in March 1999, California Governor Gray Davis issued an executive order banning MTBE by the end of 2002.48 By that date, at least sixteen states planned to restrict or ban MTBE use.49 One year later, in 2000, the Clinton administration decided MTBE should be removed from gasoline:

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Citing concerns about the environment, low farm commodity prices, and U.S. dependence on imported oil . . . Clinton Administration officials unveiled plans to phase out use of MTBE and simultaneously boost sales of ethanol . . . (EPA head Carol) Browner says the best way to address MTBE is for Congress to amend the Clean Air Act. But as a “backstop measure” EPA has begun a regulatory action under the Toxic Substances Control Act to ban the use of MTBE in gasoline, a process that may take up to three years, she said. That process has been used successfully on seven or eight times in the 23 years since the statute was enacted.50

MTBE’s fate had been decided at the highest levels of government, and the EPA was assigned the task of finding a way to ban MTBE quickly. Oil & Gas asserted the Clinton administration “has played the ethanol card to win Vice-President Al Gore a promotion next November.”51 Gore was the Democratic presidential candidate that year. The Clinton administration’s decision to remove MTBE from gasoline did not derive from any conclusive scientific or technical assessment of MTBE’s overall environmental benefits and hazards and health risks compared to those of ethanol. Concerning the latter, a 2001 review of MTBE’s toxicological studies by a member of the Department of Radiation Oncology at East Carolina University’s medical school concluded, “The totality of evidence shows that, for the majority of non-occupationally exposed human population, MTBE is unlikely to produce lasting adverse health effects, and may in some cases improve health by reducing the composition of emitted harmful [volatile organic compounds] and other substances.”52 In Europe, where MTBE was being used in low concentrations as an octane enhancer, a more formalized scientific procedure for risk assessment had been established. In accordance with this policy, the European Union in late 2001 published an MTBE risk assessment report, which had been written by the chemicals division of the Finnish Environment Institute. The report made two major conclusions: “MTBE is not considered to cause adverse health or ecotoxic effects at (its) taste and odour threshold level,” but “even a relatively small amount of MTBE may render large reserves of groundwater useless.” Because of the latter problem, the report concluded “a need for limiting the risk.” However, the report said measures were already being undertaken to prevent groundwater contamination.53 Based on this study, the European Commission found no “compelling reasons” to limit MTBE use.54

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If MTBE pollution in the United States was primarily an environmental issue, not a public health one, then it was necessary to evaluate the extent of the problem and the feasibility of remediation. One such evaluation was published in Environmental Engineering Science in 2003. The six authors—two academic engineering professors and representatives from the EPA, the California State Water Resources Control Board, and a public health school—concluded, “MTBE’s occurrence in drinking water sources over time in three states showed that the frequency of MTBE detection since 1999 appears to be stabilizing in groundwater and slightly decreasing over time in surface water.” The major sources of contamination were leaks in pipelines and underground storage tanks. The EPA had required an underground storage tank upgrade in 1988, and by 1998, two-thirds of the 180,000 gasoline stations in the United States had upgraded their tanks. When this program was completed in 2000, leaks were expected to be significantly reduced.55 According to an environmental assessment of remediation: “Recent studies have demonstrated the effectiveness of conventional treatment technologies and promise of emerging technologies for MTBE removal from contaminated media. However, the removal of tertiary butyl alcohol an impurity in MTBE-blended fuels and an MTBE breakdown product can be problematic using some conventional technologies such as air stripping and granular activated carbon.”56 Improved remediation technologies could result from additional research. There do not seem to be any estimates of the total cost of remediation. Because of the increasingly unfavorable political environment, MTBE production and usage in the United States peaked in 2001. MTBE production accounted for 3.7 percent of US gasoline—a volume larger than the gasoline consumption of all but nine countries. The country was importing about 30 percent of its MTBE, mostly from the Middle East and Canada. At that time, Europe was using one-third as much as the United States, producing what it consumed. Asia used 20 percent of US consumption and again produced its own supplies.57 In most countries, MTBE was used in low concentrations, 1 to 4 percent, as an octane enhancer. The United States was probably the only country that used MTBE in high concentrations (10–15 percent) for smog and ozone reduction. To replace MTBE with ethanol would require tripling the industry’s output. Ethanol cost twice as much to produce as gasoline and contains only two-thirds as much energy per gallon.58 Ethanol’s use in gasoline resulted from an exemption from the dating back to legislation enacted

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during the 1979 oil crisis.59 At that time, ethanol was touted as a renewable domestic source of gasoline.60 By 2002, sixteen new ethanol plants were under construction, and fifty-nine others were under development. Hydrocarbon Processing noted, “With such an aggressive capacity expansion, does the ethanol industry know something that the (the petroleum industry) is missing?​”61 By this point, the API had given up on MTBE. It joined with the Renewable Fuels Association, an ethanol lobbying organization, to support a Senate bill to replace MTBE with ethanol and remove the 2 percent oxygen requirement in reformulated gasoline, but it also included a mandate to use increasing amounts of ethanol in gasoline.62 The API seemed to have decided not to fight this deal. To make it acceptable to the oil industry, the bill also would have provided $250 million to help MTBE producers convert plants to other uses. In the big picture, MTBE was a relatively small investment for the petroleum giants. On the other hand, the National Petrochemical & Refiners Association opposed the bill, most likely because of the difficulties in transporting ethanol and blending it with gasoline. Oil & Gas argued: “This [bill] isn’t energy policy. Its agricultural welfare bought by the notoriously generous political contributions of Archer Daniels Midland Co., the dominant ethanol producer.”63 The energy bill enacted in 2004, a presidential election year, did not deal directly with the oxygenate issue but included a mandate to blend 7.5 billion gallons of ethanol into gasoline by 2012. At this point, the environmental aspects of gasoline seemed to have become subsumed under the desire for a domestically produced and potentially renewable fuel.64 As Oil & Gas noted in 2006: “Congress has made a political investment. There’s no turning back. The ethanol mandate will grow.”65 Whether corn-based ethanol is actually renewable was debatable, and the environmental and economic impacts of increased production had not been ascertained.66 After 2001, ethanol use increased dramatically and had passed MTBE consumption by 2004; by 2007, MTBE had virtually disappeared from US gasoline.67 After two decades of rapid growth, MTBE use declined on an even steeper trajectory, falling from its peak to near zero in just six years. In Europe and the rest of the world, MTBE consumption continued to increase. The EU, in an attempt to decrease carbon dioxide emissions and promote “renewable fuels,” began to subsidize fermentation ethanol production. After 2003, the EU required a biofuel content in gasoline.68 A major reason for this action was to decrease carbon dioxide emissions implicated in global warming, though whether grain

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alcohol actually lowers greenhouse gas emissions is uncertain.69 This requirement was met by using ethanol in gasoline directly or converting the ethanol to ethyl tert-butyl ether, a compound with properties nearly identical to MTBE. In 2008, 75 percent of European ethanol was converted to ETBE, probably because it is easier to transport and blends better with gasoline.70 At that point, ETBE production equaled that of MTBE.71 Since then, ETBE production has continued to expand at the expense of MTBE, because the EU has supported increasing biofuel production. In Europe, though, ETBE is considered a biofuel.72 Regarding groundwater contamination in Europe, a comprehensive 2012 study, admittedly by an oil industry association, found no significant problems.73 Given the pronounced odor of these ethers, if water supplies were being contaminated, one would expect Europeans to also be raising a stink.

Conclusion: Hazard, Risk, and Change In the United States, the Clinton administration determined MTBE was a hazard, acting on the fears of the American public of chemicals generally and chemicals in water specifically, and because of the importance of the Corn Belt states in presidential elections. At that point, the actual health threat of MTBE was uncertain, the extent of the problem was unknown, and the cost of prevention and remediation had not been calculated. Scientific and technical assessments take time, but modern media-driven fears and domestic politics demanded quick action. In the United States, the corn ethanol interests that had been well organized for two decades saw the opportunity surrounding the uncertainties concerning MTBE to push for the substitution of ethanol, not only for octane enhancement but also for air quality improvement, even though oxygenated gasoline had not been shown to improve air quality. Under the banner of renewable energy, the ethanol lobby pushed for everincreasing amounts of ethanol in gasoline. Most gasoline in the United States today contains 10 percent ethanol despite its lowering the energy content of gasoline by 3 percent and causing some problems in engine performance. The overall technological, economic, social, and environmental hazards and risks associated with intensive ethanol production for use in gasoline have not been assessed. To ward off critics, ethanol interests have argued that corn ethanol is only a transitional technology until cheaper cellulosic feedstock can be used, a technology that for

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two decades has been deemed to be nearing commercial viability.74 In Europe, where MTBE was used only for octane enhancement, EU technical studies determined MTBE was not a health hazard and that water contamination, though potentially a problem, was not a serious enough risk to ban it.75 In the case of MTBE, the outcomes were different in the United States and Europe because of the differences in the relative mix of politics and expertise in environmental decision-making. In Silent Spring, Rachel Carson’s most compelling argument was that the politically unaccountable technocrats (in the US Department of Agriculture) were determining the hazards and risks—and desired benefits—of widespread aerial spraying of DDT.76 Her book caused a furor largely because she took her argument to the public instead of keeping it within the community of experts to which she belonged. Carson brought environmental issues into democratic politics. In the 1970s, exposés on toxic chemicals in the environment became routine in the US media leading to widespread public chemophobia. As a petroleum trade journal editor observed during the MTBE controversy: Does the public fear chemicals?​Yes. In general, the public harbors great anxiety over possible harmful effects from chemicals, even chemicals that are used daily such as gasoline. So it is very easy to get the populace whipped into a frenzy through new announcements . . . Now, MTBE has been detected in drinking water. The media certainly inflamed that issue. It is detected at very low levels, yet MTBE is present. The public’s perception of MTBE has deteriorated to such an extent, many doubt it is repairable.77

The case of MTBE illustrates the complexities of environmentally oriented innovation and regulation in the late twentieth and early twentyfirst centuries. The addition of MTBE to gasoline was the result of initiatives to reduce photochemical smog produced by volatile organic compounds in automobile exhaust. The environment had become a major domestic political concern in the United States, and there was political pressure in the 1970s to move quickly, thus reinforcing the decision to use available technology in the form of catalytic converters. With a mandate to remove TEL from gasoline immediately, the oil refiners sought a feasible substitute and soon settled on MTBE. Cheap, easy to make, and certainly an environmental improvement over TEL, MTBE seemed an ideal solution.

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At the time, no one seemed to worry about groundwater contamination with MTBE, even though anyone versed in basic organic chemistry could have pointed out its affinity for water, especially when compared to other compounds in gasoline. One 1978 article did refer to the solubility of MTBE in water but only to point out that is was much less than that of toxic methanol, another candidate for octane enhancement.78 This particular problem remained unanticipated until groundwater contamination was discovered in the mid-1990s. At this point, a major debate occurred about the extent of the contamination and whether it posed a significant public health risk. In the United States, the EPA contested with states over who had jurisdiction to regulate MTBE use. The issue became even more politicized when the Corn Belt seized the opportunity to push alcohol made from corn as an alternative to MTBE, and as fuel itself. The EPA was subjected to intense political pressure, to which it ultimately succumbed. An analysis of the MTBE case by members of the Energy and Resources Group at the University of California, Berkeley, concluded that the failure to anticipate the groundwater problem was because of the EPA’s lack of a holistic approach to the environment and a failure to do enough toxicological testing of MTBE before permitting its use.79 Overall, their solution appears to be a call for more intensive evaluation; however, given the complexity of modern technological systems and their myriad interactions with the environment, it is not at all certain that future MTBE-like surprises can be avoided by simply insisting on being more diligent. This approach also assumes the environment can be addressed as a system, independent of economic, social, and political factors.80 The larger techno-environmental frame in which to analyze MTBE is within the automobile system. Of course, the environmental ramifications and public health costs of automobiles are profound, but because of the perceived centrality of the automobile to modern society, we do not demand an accounting of all these hazards and risks. If automobile exhaust is considered a problem, we have chosen to fix the exhaust rather than seek other forms of transportation. The automobile system has depended on petroleum, a nonrenewable natural resource.81 There should also be a commitment to use this resource wisely. With the powerful tools available to process petroleum, gasoline of extremely high quality can be produced, but that quality comes with an economic cost. It is technically feasible to make high-octane, clean-burning gasoline without using MTBE or ethanol.82 However, in the United States, where the price of gasoline is a political issue, most gasoline sold is the

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minimum quality that will function adequately in the engine. Overall, making cars more fuel efficient is probably the best approach to solving these problems. MTBE was introduced to make air cleaner, but the issue was ultimately complicated by international oil politics, the push for renewable fuels, and the fear of climate change. Environmental concerns must be weighed against these other factors. A fundamental precept of environmentalism is that ecological systems are interconnected webs that respond to changes in complex ways. Even a vigilant environmentalism may not be able to predict these outcomes a priori and make choices based on narrow considerations. Much of what has been said about the environment also applies to public health, which is a broad subject that goes far beyond the effects of exposure to toxic substances. For example, is it better to use MTBE, some of which will get into water supplies, or corn ethanol, which increases food prices and puts thousands or more trucks on the road?​Less affluent people might care more about cheap food than smelly water. Environmental problems have a major political component and “solutions” can be arrived at through political means, as in the US case of MTBE. However, framing issues within a narrowly defined environmental context, especially by playing on public fear of toxic chemicals, will not lead to satisfactory incomes. In the case of better, cleaner-burning gasoline, there are many ways to achieve it, but a careful analysis of environmental and other factors will be necessary. In the United States, the sudden switch from MTBE to ethanol was not the result of careful consideration, unlike in Europe, where MTBE and its analog, ETBE, continued to be used mainly to increase the octane rating of gasoline. John Kenly Smith is Associate Professor of History at Lehigh University. He teaches on the history of technology from American and world perspectives. He specializes in R&D and chemical technologies. He wrote, with David A. Hounshell, Science and Corporate Strategy: Du Pont R&D, 1902–1980 (1988), which won the Newcomen Prize in Business History in 1992. He has published many articles on technological innovation and the chemical industry.

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Notes   1. MTBE is made by reacting methanol and tertiary butylene, both of which can be made from the byproducts of gasoline manufacture.   2. Octane is an experimentally determined parameter connected to the tendency of internal engines to knock. Higher-octane gasoline allows for more powerful and efficient engine performance. Generally, highly branched and aromatic molecules have high octane ratings, whereas straight chain molecules have low octane ratings.   3. Edgar, “More Miles,” 204.   4. See Warren, this volume.  5. Spitz, Petrochemicals, 176–91.   6. Sellers, “From Poison”; TASA Group, “Overview.”   7. Struth, “Impact,” 96.   8. Lester, “Development.”   9. Other alternatives at the time were aromatics or the organometallic MMT, which contained manganese. Although the toxic effects of MMT were not seen as serious, it apparently interfered with the operation of catalytic converters. “Which Antiknock Will It Be—Aromatics or MMT?​” CHEMTECH 8, no. 8 (1978): 484–87. 10. Miller, “MTBE,” 53. An alternative use of butylene was to create high-octane gasoline fractions by a process called alkylation, which used highly concentrated sulfuric acid as a catalyst and created environmental and health/safety issues. Romanow, “Not So Silent,” 19. 11. Holusha, “Technology.” 12. “MTBE Being Evaluated,” Automotive Engineering 86, no. 8 (1978): 64–67 (64–65). 13. Taniguchi and Johnson, “MTBE,” 505. 14. Anderson, “MTBE.” 15. Ainsworth, “Booming MTBE Demand,” 13. 16. Knudson, “Antipollution Plan.” 17. Ainsworth, “Booming MTBE Demand,” 13. 18. Franklin et al., “Clearing the Air,” 3857–58. The amendments required the removal of aromatics by 1995, which would increase the need for more octane enhancement. 19. Weiss, “Ethanol Lobby.” 20. Scheller and Mohr, “Gasoline.” 21. Farrell et al., “Ethanol.” 22. This number was calculated from ethanol production statistics in Weiss, “Ethanol Lobby.” There are limits to scaling up fermentation plants, and the corn must be trucked to the plant. 23. Ainsworth, “Booming MTBE Demands.” 24. Williams, “MTBE,” 20. A University of Alaska study later concluded the smell of Alaska gasoline was related more to the sources of crude oil than to MTBE.

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25. “Toxicity, Emissions Test Results for RFG,” Oil & Gas Journal 94, no. 2 (1996): 35. An independent study of garage workers in north and south New Jersey indicated no difference in complaints even though MTBE was not used in the south. 26. Anderson, “Health Studies,” 10. 27. Vogel and Roberts, “Why.” 28. The major producer of MTBE’s manager of toxics and regulatory affairs said these tumors “seem to occur by mechanisms that aren’t relevant to humans” and that, overall, “these tests show that MTBE is not very toxic.” Anderson, “Health Studies,” 9. On the situation in New Jersey, see Cavaluzzi, “Debate.” 29. Anderson, “Health Studies,” 9–10. 30. Crow, “NRC,” 25. 31. “Oil Industry Objects to Oxygenates Ruling,” Chemistry & Industry (8 July 1994): 540. 32. Hogue, “Getting.” 33. Salpukas, “New Gas.” 34. “Shifting U.S. Gasoline Programs Cloud MTBE Future,” Oil & Gas Journal 93, no. 20 (1995): 20–23 (23). The East-West Center promotes better relations and understanding among the people and nations of the United States, Asia, and the Pacific through cooperative study, research, and dialogue. Established by Congress in 1960, the EWC serves as a resource for information and analysis on critical issues of common concern, bringing people together to exchange views, build expertise, and develop policy options. It is an independent, public, nonprofit organization with federal funding and additional support provided by private agencies, individuals, foundations, corporations, and governments in the region. EWC, “About EWC.” 35. “USGS Reports MTBE in Groundwater,” Oil & Gas Journal 93, no. 1 (1995): 21–22. 36. Chang and Last, “Clean Air,” 911. 37. Stern and Tardiff, “Risk,” 727. 38. “Perceived Merits, Demerits of MTBE Still Argued,” Oil & Gas Journal 93, no. 16 (1995): 22–23. 39. “US Scientists Vote against Fuel Additive Ban,” Chemistry & Industry 63, no. 1 (4 January 1999): 4. The NTP is an interagency program run by the US Department of Health and Human Services to coordinate, evaluate, and report on toxicology within public agencies. NTP, “About NTP.” 40. Wilson, “Scientists.” 41. Hanson, “MTBE.” 42. “US Scientists Vote.” 43. Grisham, “Cutting Back.” The panel also recommended the 2 percent oxygen requirement be removed, allowing refiners to meet air quality standards by other means. Supporters of ethanol as an alternative oxygenator wanted to keep the 2 percent standard and the renewable component. Miller, “MTBE,” 55. 44. Hanson, “MTBE.”

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45. Vautrain, “California Refiners,” 18. 46. Crow, “MTBE Debate.” 47. Hanson, “MTBE.” 48. Chiang, “Controversy.” 49. “API, NPRA, and Ethanol,” Oil & Gas Journal 101, no. 16 (2003): 17. 50. Hogue, “Getting.” Thirty percent of MTBE came from foreign sources. Romanow, “Monsters.” 51. “An MTBE Political Squeeze,” Oil & Gas Journal 98, no. 913 (2000): 25. 52. Ahmed, “Review,” 89. 53. EC, “European Union Risk,” 247. 54. “Study: MTBE Poses Limited Threat to Health and the Environment,” EHS Today, 20 December 2011, https://www.ehstoday.com/news/ehs_​imp_​35032. 55. Chiang, “Controversy,” 34–35. 56. Deeb et al., “MTBE,” 434. 57. Romanow, “Monsters.” 58. Romanow, “Not So Silent,” 19. 59. Congress finally ended the ethanol subsidy in 2012, after providing the industry with $45 billion over the past three decades. This money would have gone to the Highway Trust Fund. Watson, “How.” 60. Mohr, “Carter.” 61. Romanow, “Not So Silent,” 19. 62. Wald, “Bipartisan Bill.” 63. “API, NPRA.” 64. Snow, “Energy Bill,” 28–29. In 2007, Congress mandated the US consume fifteen billion gallons of alternative fuels per year, and thirty-six billion gallons by 2015. Watson, “How.” The energy balance calculations on ethanol usually show a relatively small renewable component per unit of corn, meaning that, to make a significant contribution to energy supplies, a very large amount of corn would have to be grown. 65. “The Ethanol Craze,” Oil & Gas Journal 104, no. 38 (2006): 19. 66. For a recent a recent analysis of ethanol renewability, see USDA, “2015 Energy Balance.” 67. EIA, “U.S. Oxygenate.” 68. FAS, “EU Strategy for Biofuels.” 69. Snow, “Fresh Questions.” 70. Mirabella, “Fuel Bio Ethers.” 71. EFOA, “Fuel Ethers’ Markets.” 72. For a recent report on European ethanol, see FAS, “EU-28.” 73. CONCAWE, Gasoline Ether. 74. DiPardo, “Outlook.” “There is no commercial production of (cellulosic ethanol), although reports of technical progress appear frequently. Even if cellulosic ethanol crosses the commercial threshold soon, the ability of the industry to expand production fast enough to satisfy future mandates remains in doubt.” “Lessons from Biofuels,” Oil & Gas Journal 107, no. 19 (2009): 16.

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75. “Study: MTBE.” 76. Carson, Silent Spring, 127. 77. Romanow, “Perception,” 78. “MTBE Being Evaluated,” 67. 79. Franklin et al., “Clearing the Air.” 80. A tempting yet simplistic narrative is to attribute environmental problems to the actions of greedy, shortsighted actors who just need to be policed into doing the right thing. Certainly, there are cases in which this is true, but they do not get at the core of the problem of assessing hazards associated with alternate technologies. 81. What is interesting about enthusiasm about electric cars is the lack of concern about the environmental consequences of electric generation, especially from coal. 82. Petroleum is not mostly gasoline; to get more gasoline requires processing the other chemical fractions to turn them into gasoline. Of course, this additional processing comes at a cost of lost petroleum, though much of the energy content of that petroleum can be captured and used.

Bibliography Ahmed, Farid E. “Review: Toxicology and Human Health Effects Following Exposure to Oxygenated or Reformulated Gasoline.” Toxicology Letters 123, nos. 2–3 (2001): 89–113. Anderson, Earl V. “Health Studies Indicate MTBE Is Safe Gasoline Additive.” Chemical & Engineering News 71, no. 38 (1993): 9–12. _____. “MTBE Strengthens Hold on Octane Booster Market,” Chemical & Engineer­ing News 64, no. 41 (1986): 8. Ainsworth, Susan J. “Booming MTBE Demand Draws Increasing Number of Producers.” Chemical & Engineering News 69, no. 23 (June 10) (1991): 13–16. Carson, Rachel. Silent Spring. New York, 1962. Cavaluzzi, Joe. “A Debate Arise.” New York Times, 28 November 1993, 10. Chang, Daniel P. Y., and Jerold A. Last. “Clean Air, Dirty Water?​The MTBE Story.” Journal of Environmental Engineering 124, no. 10 (1998): 910–12. Chiang, Thi. “Controversy Over MTBE in Gasoline Rages On.” Oil & Gas Journal 97, no. 51 (1999): 34–35. CONCAWE (Conservation of Clean Air and Water in Europe). Gasoline Ether Occurrence in Europe, and a Review of Their Fate and Transport Characteristics in the Environment. Report no. 4/12. Brussels, 2012. Crow, Patrick. “MTBE Debate.” Oil & Gas Journal 98, no. 7 (2000): 25. _____. “NRC: More Studies Required on MTBE.” Oil & Gas Journal 94, no. 25 (1996): 25. Deeb, Rula A., Kung-Hui Chu, Tom Shih, Steven Linder, Irwin Suffet, Michael C. kavanaugh, and Lisa Alvarez-Cohen. “MTBE and Other Oxygenates:

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Environmental Sources, Analysis, Occurrence, and Treatment.” Environmental Engineering Science 20, no. 5 (2003): 433–47. DiPardo, Joseph. “Outlook for Biomass Ethanol Production and Demand.” Environment Informtion Administration, January 2000. EC (European Commission). “European Union Risk Assessment Report: Tert-Butyl Methyl Ether.” CAS No. 1634-04-4. EINECS No. 216-653-1. Luxembourg, 2002. _____. “An EU Strategy for Biofuels.” COM (2006) 34 final. Brussels, 8 February 2006. EWC (East-West Center). “About EWC: Mission and Organization Overview.” Accessed on 8 April 2019. https://www.eastwestcenter.org/about-ewc/mis sion-and-organization. Edgar, Graham. “More Miles per Gallon.” Scientific American 162, no. 4 (1940): 204–6. EFOA (European Fuel Oxygenates Association). “Fuel Ethers’ Markets.” Accessed on 12 February 2019. http://www.efoa.eu/en/markets.aspx. EIA (US Energy Information Administration). “U.S. Oxygenate Plant Production of MTBE.” Last updated 31 January 2019. https://www.eia.gov/dnav/pet/hist/ LeafHandler.ashx?​n=​PET&s=​M_​EPOOXT_​YOP_​NUS_​1&f=​M. FAS (USDA Foreign Agricultural Service). “EU-28: Biofuels Annual.” Global Agricultural Information Network Report no. NL7015, 21 June 2017. Farrell, Alexander E., Richard J. Plevin, Brian T. Turner, Andrew D. Jones, Michael O’Hare, and Daniel M. Kammen. “Ethanol Can Contribute to Energy and Environmental Goals.” Science 311, no. 5760 (2006): 506–8. Franklin, Pamela M., Catherine P. Koshland, Donald Lucas, and Robert F. Sawyer. “Clearing the Air: Using Scientific Information to Regulate Reformulated Fuels.” Environmental Science and Technology 34, no. (2000): 3857–63. Grisham, Julie. “Cutting Back MTBE.” Chemical & Engineering News 77, no. 31 (1999): 5. Hanson, David. “MTBE Villain or Victim.” Chemical & Engineering News 77, no. 2 (1999): 49. Hogue, Cheryl. “Getting the MTBE Out.” Chemical & Engineering News 78, no. 13 (2000): 6. Holusha, Joshua. “Technology: Giving Gasoline a Lift.” New York Times, 21 June 1979, D2. Knudson, Thomas J. “Antipollution Plan Stirs Ire of Colorado Motorists.” New York Times, 27 July 1987, A8. Lester, George R. “The Development of Automotive Exhaust Catalysts.” In Heterogeneous Catalysis: Selected American Histories, edited by Burton H. Davis and William P. Hettinger, 415–34. Washington, DC, 1983. Miller, K. Dexter. “MTBE Faces an Uncertain Future.” Oil & Gas Journal 98, no. 28 (2000): 52–56. Mirabella, Walter R. “Fuel Bio Ethers: A Prime Avenue to Channel Bio Ethanol into EU Market.” Paper presented at the Third Annual BioFuels Meeting, Berlin, 30 October 2008.

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Mohr, Charles. “Carter to Announce Gasohol Plan Soon.” New York Times, 7 January 1980, D3. NTP (National Toxicology Program). “About NTP: Organization.” Accessed on 8 April 2019. https://ntp.niehs.nih.gov/about/org/index.html. Romanow, Stephany. “Monsters Everywhere.” Hydrocarbon Processing 80, no. 11 (2001): 13. _____. “A Not So Silent Spring for MTBE.” Hydrocarbon Processing 81, no. 4 (2002): 19–20. _____. “Perception Becomes Reality.” Hydrocarbon Processing 78, no. 11 (1999): 13. Salpukas, Agis. “New Gas Arouses Grass Roots Ire.” New York Times, 18 February 1995, 37. Scheller, William A., and Brian J. Mohr. “Gasoline Does, Too, Mix with Alcohol.” CHEMTECH 7, no. 10 (1977): 616–23. Sellers, Christopher. “From Poison to Carcinogen: Towards a Global History of Concerns about Benzene.” Global Environment 7, no. 1 (2014): 38–71. Snow, Nick. “Energy Bill Effects Begin as Refiner Exits MTBE Business.” Oil & Gas Journal 103, no. 30 (2005): 28–29. _____. “Fresh Questions about Biofuels.” Oil & Gas Journal 106, no. 7 (2009): 31. Spitz, Peter H. Petrochemicals: The Rise of an Industry. New York, 1988. Stern, Bonnie R., and Robert G. Tardiff. “Risk Characterization of Methyl Tertiary Butyl Ether (MTBE) in Tap Water.” Risk Analysis 17, no. 6 (1997): 727–43. Struth, Bert W. “The Impact on the CPI of Removing Lead from Gasoline.” CHEMTECH 2, no. 2 (1972): 96–97. Taniguchi, Brian, and Richard T. Johnson. “MTBE for Octane Improvement.” CHEMTECH 9, no. 8 (1979): 502–10. TASA Group. “Overview of Benszene Toxicity.” TASA ID 1351. Accessed on 12 February 2019. https://www.tasanet.com/knowledge-center/articles/artmid/ 477/articleid/1251368/overview-of-benzene-toxicity. USDA (US Department of Agriculture). “2015 Energy Balance for the Corn Ethanol Industry.” February 2016. Vautrain, John H. “California Refiners Anticipate Broad Effects of Possible State MTBE Ban.” Oil & Gas Journal 97, no. 3 (1999): 18–22. Vogel, Sarah A., and Jody A. Roberts. “Why the Toxic Substances Control Act Needs an Overhaul, and How to Strengthen Oversight of Chemicals in the Interim.” Health Affairs 30, no. 5 (1999): 898–905. Wald, Matthew L. “Bipartisan Bill Seeks Change in Formula for Gasoline.” New York Times, 5 May 2000, A20. Watson, Bruce. “How the (Finally Ended) Corn Ethanol Subsidy Made Us Fatter.” DailyFinance, 4 January 2012. https://www.aol.com/2012/01/04/how-thefinally-ended-corn-ethanol-subsidy-made-us-fatter. Weiss, Michael J. “Ethanol Lobby.” New York Times, 1 April 1990, SMA 19.

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Williams, Bob. “MTBE, Ethanol Advocates’ Squabble May Complicate RFG Implementation.” Oil & Gas Journal 93, no. 17 (1995): 17–22. Wilson, Elizabeth. “Scientists Wrangle over MTBE Controversy.” Chemical & Engineering News 75, no. 18 (1997): 54–56.

/ Conclusion Ernst Homburg and Elisabeth Vaupel

The “substance biographies” sketched by the chapters of this volume

transcend simple generalization. Some hazards were discovered only after thousands of tons of a substance had been produced and employed: think of the pesticide DDT (Morris) or the gasoline highoctane component MTBE (Smith). In other cases, the toxic properties of substances, or the unhealthy nature of production processes, were apparent almost from the start. Examples are organophosphates (Davis), the extreme toxicity of which had already been discovered during the research phase, or the occupational disease of chloracne that became known very soon after chlor-alkali electrolysis was introduced in Germany (Böschen). In yet other instances, specific material qualities, not just quantities, played a crucial role. A striking example is Schweinfurt green (Mertens), a pigment that contained arsenic, the poisonous character of which had been known for a long time. However, the brilliance of the green color was such that, within a few years, the substance found its way in different areas of application, causing negative health effects almost everywhere. As a result, the authors in this book have highlighted different aspects of their materials in the substance biographies they have written. In this conclusion, we will evaluate some major findings of the preceding chapters against the background of the existing historiography, mainly on periodization but also by homing in on recent developments and discussing some critical perspectives on these developments.

Conclusion  377

Hazardous Chemicals and Their Regulation over Time Previous authors on industrial and chemical hazards and their regulation had different viewpoints on the periodization of these developments. Some looked primarily to phases in the industrial development itself, while others focused mainly on changes in regulatory systems or on scientific developments in toxicology. In his study of industrial pollution in France, Thomas Le Roux investigated in detail how the growing social and political role of industrialists and chemists during the Industrial Revolution led to an adaptation of the regulatory system to the needs of industry. Building on this analysis, François Jarrige and Thomas Le Roux called that period (1770–1830) the years of the “liberation of the environment,” in which the strict rules of the ancien régime by which factories could be forbidden and products banned were replaced by regulatory procedures in which industrialists could continue to produce toxic products, as long as they tried to reduce the dangers for their workers and neighbors by technical means. These policies continued during the next phase, so Jarrige and Le Roux characterized that period (1830–1914) as the years in which a “normalization” and “naturalization of pollution” took place. Industrial hazards and environmental pollution became an unpleasant fact of life. Scientists, industrials, and civil servants were confident problems could be solved by “technical fixes.”1 Christopher Sellers followed a similar approach to periodization, with industry as the prime mover, in his studies of industrial hazards. Focusing on the unequal distribution of hazards across the globe, Sellers is well aware the transition from one “industrial hazards regime” to the next does not happen at the same time in different regions. Regarding Europe and the United States, the character of the periods he distinguishes corresponds reasonably well with those defined by Jarrige and Le Roux, although Sellers sets the turning points at slightly different dates. In his view, the first “industrial hazard regime” emerged between 1790 and 1870, during the wake of industrialization, when the risk-laden industry was born. During the late nineteenth and the early twentieth centuries, this regime spread to developing regions in other parts of the world. A second “industrial hazards regime” emerged in the Western world between 1870 and 1914 in response to controversies over established production, via a widening recognition of its impact. Better laws to protect workers were enacted in Europe and the United

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States during those years. After the middle years of the twentieth century, that regime—called “the toxic century” (1914–1973) by Jarrige and Le Roux, characterized by unlimited growth and pollution—spread to other parts of the globe. In his characterization of the years since 1980, Sellers reflects on Ulrich Beck’s concept of “risk society” but at the same time emphasizes that the industrial and political treatment of hazards uses double standards, with different rules in the West compared to other parts of the globe. According to Jarrige and Le Roux, that period since 1973 can even be called “the road to the abyss.”2 Although they were fully aware of the dynamics produced by the globalization of chemical markets, Soraya Boudia and Nathalie Jas presented a more refined periodization for the post–World War II period based on a closer analysis of the regulatory mechanisms. They argued regulation should be interpreted broadly. It should, for instance, include environmental and factory regulations, labeling and specific protection measures, levels of impurity authorized, lists of substances that meet specific criteria, classifications of the most dangerous substances, and research to arrive at limit values to guarantee health. With this in mind, they differentiate between three, partly overlapping, regulatory periods: (a) regulation through thresholds, from before 1940 to around 1970; (b) regulation via risk assessment, from around 1960 to 1985; and (c) regulation via adaptation, since around 1980. Claas Kirchhelle also emphasizes the uncertainties and ambiguities that characterize the past few decades. He calls it a period of “fragmentation,” with a fragmented public and expert understanding of toxic substances, in which toxicity is unequally distributed over different social groups, and societies have had to adapt to a permanent toxic exposure.3 As well as paying attention to the roles played by industrial dynamics and regulatory governance, the present volume also applied a perspective from the history of science, especially in the introduction, where we investigated the conceptual history of poisons and the development of toxicology. In common with publications by Le Roux, this volume shows the decades around 1800 indeed were a turning point, because of not only the factory act of 1810 and transport regulations since around 1830 but also fundamental changes in terms of scientific ideas on poisons. But whereas Le Roux appears to have a highly romantic and positive image of regulation under the Ancien Regime, and a strongly negative view of industry, this volume shows much continuity. The French Factory Act of 1810 incorporated several older regulations, and in other countries under French control during the Napoleonic wars,

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where the factory act was introduced as well, it was not a marked break with the past either.4 In keeping with this, in his chapter on Schweinfurt green, Joost Mertens shows how several of the relevant rules and regulations were rooted in ordinances of the ancien régime. Furthermore, the stabilization of a new concept of poison took several decades within the scientific community, and several more among the public at large. The innovations emerging around 1800 reached their full potential only after 1870. Part I of this volume therefore covers a period in which industry, the regulation of hazards, and relevant scientific ideas were still changing considerably. What unites the three chapters of this part is that they are all on known hazards, although the distinction between acute and chronic poisoning was being crystalized. Most regulations in the nineteenth century were based on economic criteria and arguments, but the three chapters show that health issues also played a prominent role. At the same time, as Mertens and Lestel show, the measures chosen in France were industry friendly: information of health aspects was distributed, but the manufacture of Schweinfurt green and white lead was never prohibited, owing to lack of continuity between the successive political regimes. In Germany, by contrast, the Sanitätspolizei more actively monitored production of hazardous chemicals. Therefore, it seems Le Roux’ analysis of the French situation cannot be generalized easily to other countries.5 The chapters on white lead (Lestel; Warren) also clearly demonstrate the “parts” distinguished in this volume are not clearly demarcated periods. The phases discussed in the literature and in this book are “cumulative.” Several problems and features characteristic of a certain phase continue to play a role during the next one that witnesses the rise of new “characteristic” features. The hazards of lead compounds, already regulated around 1900, had a long historical tail. Even in recent decades, new cases of childhood lead poisoning were discovered in France and the United States. As argued in the introduction, the decades around 1900 formed a new turning point. After the conceptual distinction between toxicology and fields such as bacteriology were made, industrial toxicology with its threshold values started to dominate the regulation of toxic substances, as also argued by Boudia and Jas. Moreover, these decades witnessed several improvements of regulation: for factory workers, the safety of international transport, foodstuffs, and pesticides. These developments fit very well with Sellers’s second “industrial hazards regime,” in which governments had recognized

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impacts of industrial production, and laws and conventions had been introduced to reduce the industry’s negative impact on human health. Against this background, the chapters of part II focus on the discovery of new health effects that had not yet been recognized or adequately regulated: new types of health effects of carcinogens (Travis and Stoff) and mutagens (Schwerin), the unknown effects of cadmium (Kaji), and the unforeseen high toxicity and widespread occurrence of dioxins (Böschen). Although the first industrial carcinogen had already been discovered in the 1890s, Travis and Stoff show consensus on the list of substances that should be forbidden or regulated was not reached until the 1950s. Only in the case of carcinogens in foodstuffs regulation was implemented relatively quickly, particularly in Germany. By the 1960s, the discovery of these new health effects and, especially, some scientists’ assumption that there was no safe minimum dose for carcinogenic and mutagenic substances had the effect of undermining regulation by thresholds as it had been practiced in the 1940s and 1950s. But there was no agreement on that issue, and as a result, the notion of (scientific) “uncertainty” entered the political arena, which gave the years from 1960 to 1985 a character different from the previous period. Furthermore, the discovery of “environmental poisons” introduced a new perspective in toxicology that at first glance might be called nonanthropocentric, but at a deeper level, worries that humans would be affected via the food chain certainly played a role. Because of these two fundamental developments, the 1960s can be considered the third watershed within the two centuries covered by this volume, after the decades around 1800 and 1900. Both in Europe and the United States, numerous new laws and regulations on the environment, factory work, transport, pharmaceuticals, foodstuffs, and pesticides were drawn up, as documented extensively in our introduction. Moreover, international harmonization of regulation gained increasing momentum. But there were great differences as well. In the United States, risk assessment and economic cost-benefit analysis started to dominate regulation. But in Europe, that was much less the case. Boudia and Jas’s proposal to call this the period of risk assessment is therefore appropriate perhaps for the United States but not unconditionally for Europe.6 Although formal risk assessment played a less prominent role in Europe, Schwerin demonstrates convincingly, in his chapter on the (possible) mutagenic properties of cyclamates, how scientific uncertainties began to dominate the political debates on both sides of the Atlantic. Under these conditions, Schwerin argues, the

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risk assessment approach even had subversive effects on the regulatory system, because the “enduring uncertainty about low-dose effects was in striking contrast to the promises of risk assessment” to produce a unique solution and unambiguous policy advice. In his chapter on dioxins, Böschen arrives at a similar conclusion when he says that the way in which “risk analysis and risk policy addressed dioxins can be seen as a paradigmatic example of blurring boundaries between (scientifically defined) risks and (public) risk perception.” Against this background on growing uncertainties, and growing divergences between different social groups, the chapters of part III focus mainly on the discovery and handling of the environmental effects of hazardous chemicals. They all illustrate that decision-makers had to cope with numerous uncertainties not only about the type of effect (cancer, for instance) or the current state of medical science but also now in relation to the broader geographical, biological, and, later, climatological aspects. Should the highly toxic organophosphates be preferred over the less toxic but more persistent chlorinated hydrocarbons like DDT (Davis)?​Satisfactory answers to these questions were difficult to achieve. In practice, public opinion and chemical industry interests tipped the balance. Introducing new chemicals into society and the environment without a careful screening during the research phase, inevitably, as Morris shows, leads to a story of moving targets: persistence, considered an advantage in the 1940s, had become a major environmental problem by the early 1960s. In the past five decades, new uncertainties kept coming up all the time, as the use of MTBE illustrates. When pressure groups succeeded in banning its use from gasoline, “the actual health threat of MTBE was uncertain,” Smith concludes, “the extent of the problem was unknown, and the cost of prevention and remediation had not been calculated.” Because of these and other uncertainties, different political viewpoints and conflicts started to dominate the debates on the substances discussed, as shown by most of the chapters in parts II and III. The uncertainties produced by scientifically more complex ecological and toxicological systems, as well as by new developments in analytical techniques that could measure virtually “anything,” started playing a growing role in a society in which scientific and political authority declined because of general cultural and sociopolitical developments. In response to public unrest, or even anxieties, of the 1960s and 1970s, and to the great scientific uncertainties in relation to new chemical products entering the market every year, Western countries began to legislate on

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chemicals in general, from the late 1970s onward.7 As a result, as indicated in our introduction, several strands of regulation came together after around 1980.

From the Regulation of Hazardous Substances to the Regulation of Chemicals?​ In the introduction, we argued the classification of hazards within the “Orange Book” (Transport of Dangerous Goods) and the Globally Harmonized System of Classification and Labeling of Chemicals increasingly took place in chemical terms, especially since around 1980. This was the combined result of changes in the public perception of chemistry and the chemical industry, and of the growing influence of a technical logic embraced by regulators. Slogans promoted by chemists and the chemical industry (“man in a chemical world,” “better living through chemistry,” “chemistry is everywhere”) rebounded on the industry after the publication of Silent Spring. With the growth of the environmental movement in the 1960s and 1970s, the public increasingly opposed synthetic chemicals to natural products, which were considered healthier. Chemists and the industry argued there was no difference between the synthetic and natural variants of the same chemical substance, but this did not help very much to change the public image that all chemicals were suspect. The low-dose debate added new credibility to that view. Every chemical now became a potential danger in the eyes of large parts of the public—the more so because the industry itself stressed that “all things are poison,” depending on the dose (following Paracelsus). As a result, chemicals, even if they were not poisonous, were now often called “toxic chemicals,” and the dangers of “chemical waste” and of “chemical substances” in the workplace were widely discussed.8 The shift in regulatory attention from specific categories, such as poisons and explosives, to chemicals in general was also promoted by the increasing role played by chemists and other experts in monitoring and evaluating the dangers associated with specific substances. In line with the dominant reductionist logic of industrial toxicology, the potential risks of certain substances were interpreted increasingly in terms of quantitative molecular and macroscopic properties of these chemicals. When scientists and regulators felt the need to have a more comprehensive picture of the dangers of a given chemical in the 1960s and 1970s, not only its LD50 and MAC value but also its boiling point,

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flash point, acidity, and solubility in water, as well as several other parameters, were important. After the publication of the “Yellow Book” in 1962, many other handbooks with relevant data followed within a remarkable short period. Examples include the Hazardous Chemicals Data, published by the US National Fire Protection Association in 1969; the Registry of Toxic Effects of Chemical Substances, by the NIOSH in 1975 and 1976; the Handbook of Existing Chemical Substances, by the Japanese Ministry of International Trade and Industry chemical products safety division in 1977; the commercially published British Handbook of Reactive Chemical Hazards, which has gone through many editions since 1975; and the US Hazardous Chemicals Data Book of 1980. At the international level, the UN Environmental Programme, created in 1972, initiated the International Register of Potentially Toxic Chemicals. The UNEP, the ILO, and the WHO together launched the International Programme on Chemical Safety in 1980 (Morris). Although these initiatives and data collections were mostly far from perfect (and because many important data were, and still are, missing), their existence and use reinforced the association between chemicals and hazards made in the minds of administrators and the public at large.9 In the 1970s, the data sets mentioned not only played a role in the implementation of environmental and labor laws but also became relevant for new approaches to the regulation—and, especially, ­registration—of chemicals, based on what since the late-1980s would be called the “precautionary principle.” This principle emerged in the context of the protection of marine environments and rose to prominence in debates on climate change since the Montreal Protocol of 1987. The focus on the prevention of irreversible damage implied by this principle was first introduced, unsuccessfully, in the US Federal Food, Drug, and Cosmetic Act (1938) and took shape when, in the 1960s, the admission and registration procedures for pharmaceuticals and pesticides were implemented.10 The next step of introducing legal requirements for the registration of (industrial) chemicals in general was first set in the United States. In 1971, the Nixon administration submitted the Toxic Substances Control Act to Congress, but it was not passed until 1976 (see also Smith). In the following decade, the act was not a great success. It put a heavy burden on the shoulders of the EPA, which had to develop a program for reviewing new chemicals, as well as specifying the rules for the registration or rejection of existing chemicals. This was an enormous

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task, not least because several companies initiated lawsuits against the EPA’s decisions. By 1991, the US Court of Appeals for the Fifth Circuit decided the EPA had not met its statutory obligations, and the act became toothless. In the meantime, to bypass the stalemate, but also because of the neoliberal policies of the Reagan administration and its successors, the US government increasingly collaborated with industry on environmental issues. The Pollution Prevention Act of 1990 symbolized this turn.11 In Europe, similar attempts were made to develop registration procedures for new industrial chemicals and to regulate chemicals that were already on the market. In Germany, the Chemical Substances Act (Chemikaliengesetz) entered force on 1 January 1982 and included procedures for the registration and screening of all new chemical substances introduced to the market. Three years later, in December 1985, a similar act was passed in the Netherlands (Wet Milieugevaarlijke Stoffen). Because of the poor quality of the data relating to hazards of chemicals, the Netherlands National Institute of Public Health and the Environment carried out a research program from 1988 to 1996 on the criteria and methods for the risk assessment of new chemical substances, and similar activities took place in other countries. Furthermore, the chemical industry in Europe closely monitored these “chemicals policies,” which were partly implemented in collaboration with the industry.12 In 1997, these activities were raised to the level of the European Union, after several EU countries had argued a new chemicals policy was needed that would be more in line with the precautionary principle the organization had adopted in 1992. By 1997, there were still many uncertainties about the potential hazards of thousands of chemicals regarding health aspects (toxicity, carcinogenicity) and their persistence, bioaccumulation, and mobility in the environment. At the end of the 1990s, the dangers of substances such as phthalates and bromine flame retardants were also intensively discussed during what was called the “toxic ignorance” debates in the United States. These problems were central to the EU’s REACH initiative on the Registration, Evaluation and Authorisation of Chemicals that began in 1997, leading in 2001 to a white paper on the screening, evaluation, and admission of new and existing chemicals, with the long-term goal of abandoning the distinction between these two classes of substances. This major novelty, according to Martin Scheringer, Stefan Böschen, and Konrad Hungerbühler, could become in principle the start of “a third generation of chemicals policy,” after the paradigm of industrial toxicology of the first part of

Conclusion  385

the twentieth century, and the risk-oriented policies focusing on the evaluation of new chemicals of the 1970s and 1980s.13 The REACH regulations were passed by the European Parliament in December 2006 and entered force on 1 June 2007. Key elements were (a) the obligation that all chemicals produced in greater amounts than one ton per year be registered, and (b) the passing of an authorization procedure coordinated by the European Chemicals Agency, a newly created institution in Helsinki, based on (c) extensive information provided by the industry on health-related and environmentally relevant aspects of the chemicals involved. During the entire process of the drafting of the regulation and during its subsequent implementation and execution, the chemical industry was heavily involved, mainly through what is now called the European Chemical Industry Council. Although that form of publicprivate cooperation was not new, it underlined the reality that most of the sensitive data on health and environmental aspects of chemicals were in private hands. It was partly a compromise between a comprehensive regulation of hazardous chemicals on one hand and corporate control of the entire process on the other. It was also a deliberate attempt to put a larger share of the responsibility on the shoulders of the producers and others directly involved in the chemical economy. The legislation distinguished between the environmentally dangerous PBT (persistent, bioaccumulative, and toxic) chemicals and the CMR (carcinogenic, mutagenic, and toxic to reproduction) chemicals that are hazardous for human health. Implementation took place in three stages from June 2007 to June 2018.14 REACH is closely linked to the Classification, Labeling and Packaging Regulation of chemicals (see the Introduction) and to the UN Strategic Approach to International Chemicals Management. Because of these regulatory activities during the past ten to fifteen years, a well-­connected legal framework for the authorization, labeling, and transport of hazardous chemicals has emerged within the EU. The Orange Book rules on the transport of dangerous goods are currently not yet fully integrated into the REACH-CLP framework. Hazardous radioactive substances, for instance, which are covered by the Orange Book rules, do not fall under the REACH regulations. They already had their own stringent regulations and were excluded from the regulations of chemical substances introduced since the 1960s.15 The European regulation of chemicals is partly connected to larger transnational frameworks, mostly by means of rules set by the UN. Nevertheless, many less-developed countries are not part of this framework, and in the United States, for instance, at least until recently, the responsibility of the GHS was divided

386  Ernst Homburg and Elisabeth Vaupel

among no less than four authorities: the Department of Transport, the Occupational Health and Safety Administration, the Consumer Product Safety Commission, and the EPA.16

Living with Uncertainty?​ If we look back to the history of poisons, hazardous substances, and chemicals presented here, we see a multifaceted history in which conceptual changes and changing political and regulatory regimes interacted in various ways. Especially in the past four decades, the regulatory activities have become more intense. Disasters (e.g., the Seveso release of TCDD (dioxins), the Bhopal disaster, the Sandoz warehouse fire in Basle that polluted the Rhine) played a great role in that respect, as did the recognition of chlorofluorocarbons as threat to the ozone layer. Nonetheless, the regulation of chemical hazards is far from perfect. In many less-developed countries, working conditions and environmental protection are in a poor state. Even in highly developed economies, new uncertainties about hazards are debated almost every day: the ongoing discussions on glyphosate and neonicotinoids are good examples of this, as are similar controversies about phthalates, bisphenol A, and other endocrine disruptors, as well as recent scandals concerning chromium6-paints and C8 (perfluorooctanoic acid) in the blood of workers at Du Pont’s spin-off Chemours Company.17 Although the REACH regulations included the concept of precaution as its guiding principle, the implementation of that precautionary principle still largely follows the tradition technical-scientific paradigm with its strong emphasis on finding comprehensive empirical evidence. Giving priority to scientific data, even in cases where important normative issues are involved, makes the regulatory agencies vulnerable to interventions by the “merchants of doubt”—experts paid by interested parties who deliberately exaggerate scientific uncertainties with the aim of sabotaging decision-making.18 The result of this state of affairs is that the lack of knowledge that exists in many cases has not been taken seriously enough by the REACH regulators, or by many other parties involved in the low-dose debates. For more sustainable ways of coping with hazardous chemicals, not only a deeper reflection on the limitations of scientific knowledge but also more democratic and comprehensive practices of regulation are needed, taking more stakeholders on board than is the present case, thereby including the Global South.19

Conclusion  387

Ernst Homburg is Professor Emeritus of History of Science and Technology at Maastricht University. He studied chemistry in Amsterdam and was connected to the universities of Groningen, Nijmegen, Eindhoven, and Maastricht. From 1989 to 2003, he coedited two book series on the history of technology in the Netherlands in the nineteenth and twentieth centuries. He has published widely on the history of the chemical profession, technical education, the chemical industry, textile printing, and the environment. He was president of the Dutch Society for the History of Medicine, Mathematics, Science, and Technology (1995–1998) and of the European Working Party on the History of Chemistry (2003–2009). In 2014, he received the American Chemical Society HIST Award. His most recent books are, with Nicolas Coupain and Kenneth Bertrams, Solvay: History of a Multinational Family Firm (2012), and, with Ineke Pey, Een kabinet vol kleur: De collectie schildersmaterialen van de Amsterdamse verfhandelaar Michiel Hafkenscheid (1772–1846) (2018). Elisabeth Vaupel is a historian of chemistry at the Forschungsinstitut of the Deutsches Museum. She focuses on the history of chemistry in the nineteenth and twentieth centuries. Recent publications include “Ersatzgewürze (1916–1948): Der Chemie-Nobelpreisträger Hermann Staudinger und der Kunstpfeffer” (Technikgeschichte, 2011), “Edelsteine aus der Fabrik: Produktion und Nutzung synthetischer Rubine und Saphire im Deutschen Reich (1906–1925)” (Technikgeschichte, 2015), and “Kinder, sammelt Knochen! Lehr- und Propagandamittel zur Behandlung des Themas Knochenverwertung an deutschen Schulen im ‘Dritten Reich’” (NTM, 2018). She coedited, with Stefan L. Wolff, Das Deutsche Museum in der Zeit des Nationalsozialismus: Eine Bestandsaufnahme (2010).

Notes   1. Le Roux, Laboratoire; Le Roux, “Governing”; Fressoz and Le Roux, “Protecting Industry”; Jorland, “Review”; Jarrige and Le Roux, Contamination, 27–207; cf. Kirchhelle, “Toxic Tales,” 214–16.   2. Sellers and Melling, Dangerous Trade, 1–13, 195–206; Sellers, “Conclusion”; Jarrige and Le Roux, Contamination, 208–325, 326–66.   3. Boudia and Jas, “Introduction”; Boudia and Jas, “Gouverner”; Jas, “Gouverner”; Kirchhelle, “Toxic Tales,” 217–18.   4. Homburg, “Schrikbeelden,” 440–45; Klein, “Risques industriels.”

388  Ernst Homburg and Elisabeth Vaupel

  5. Next to highlighting similarities, Le Roux himself also addresses some differences between France and Great Britain. Le Roux, “Governing.”   6. Brickman et al., Controlling Chemicals, 28–53, 301–17.   7. Ibid., 187–217.  8. Morrison, Man; Bunte, Leven; Boogert, Chemie; Schummer et al., Public Image; Homburg, “Schrikbeelden,” 439–40, 466; Lönngren, International Approaches, 21; Alston, “International Regulation.”   9. Based on literature search in library catalogs. See also Carson and Mumford, Hazardous Chemicals, xi–xii; Alston, “International Regulation,” 400, 418–22; Lönngren, International Approaches, 25, 29. 10. O’Riordan and Cameron, Interpreting. 11. Ibid.; EEA, Late Lessons; Bodansky, “Precautionary Principle”; Cameron and Abouchar, “Precautionary Principle”; Brosnan, “Law and Environment,” 539; Roberts, “Unruly Technologies,” 257–58. 12. Engelhardt and Lange, Chemikaliengesetz, 18–19, 22–23; Gelbke and Fleig, “Entwicklung,” 342; Jans, “Legal Problems”; Alston, “International Regu­lation,” 400–408; Schot et al., Geven; Fischer and Schot, Environmental Strategies; Schot et al., Greening of Industry; VNCI, Jaarverslag, 22–23; Scheringer et al., “Will We Know,” 700–702. 13. Brosnan, “Law and Environment,” 539; Führ, “REACH,” 109, 132–34; Scheringer et al., “Will We Know.” 14. Fischer, “REACH”; Vogelezang-Stoute, “Regulering”; Lefèvre, “Cinq ans”; Führ, “REACH,” 111–12. 15. CSP, “Differences.” 16. EC, Chemicals at Work; Kessler, “GHS.” 17. Lönngren, International Approaches, 29; Langston, “Precaution”; Beintema, “Pesticiden”; “Hexavalent Chromium,” Wikipedia, last edited 1 February 2019, 15:19, https://en.wikipedia.org/wiki/Hexavalent_​chromium; Schreuder, “We durven geen.” 18. Markowitz and Rosner, Deceit and Denial; Oreskes and Conway, Merchants of Doubt; Ross and Amter, Polluters; Jas, “Chemicals”; Demortain, “Expertise”; Kirchhelle, “Toxic Tales,” 217–26. 19. Scheringer et al., “Will We Know”; Reinhardt, “Regulierungswissen.”

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Conclusion  389

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Lönngren, Rune. International Approaches to Chemicals Control: A Historical Overview. Stockholm, 1992. Markowitz, Gerald, and David Rosner. Deceit and Denial: The Deadly Politics of Industrial Pollution. Berkeley, CA, 2002. Morrison, A. Cressy. Man in a Chemical World: The Service of the Chemical Industry. New York, 1937. Oreskes, Naomi, and Erik M. Conway. Merchants of Doubt: How a Handful of Scientists Obscured the Truth on Issues from Tobacco Smoke to Global Warming. New York, 2010. O’Riordan, Timothy, and James Cameron, eds. Interpreting the Precautionary Principle. London, 1994. Reinhardt, Carsten. “Regulierungswissen und Regulierungskonzepte.” Berichte zur Wissenschaftsgeschichte 33, no. 4 (2010): 351–64. Roberts, Jody A. “Unruly Technologies and Fractured Oversight: Towards a Model for Chemical Control for the Twenty-First Century.” In Boudia and Jas, Powerless Science?​ 254–68. Ross, Benjamin, and Steven Amter. The Polluters: The Making of Our Chemically Altered Environment. New York, 2010. Scheringer, Martin, Stefan Böschen, and Konrad Hungerbühler. “Will We Know More or Less about Chemical Risks under REACH?​” Chimia 60, no. 10 (2006): 699–706. Schot, Johan, Ellis Brand, and Kurt Fischer. The Greening of Industry for a Sustainable Future: Building an International Research Agenda. Rijswijk, 1997. Schot, Johan W., Bas de Laat, and Ronald van der Meijden. Geven om de omgeving: milieugedrag van ondernemingen in de chemische industrie. The Hague, 1990. Schreuder, Arjen. “We durven geen kraanwater te drinken.” NRC Handelsblad, 4 May 2017, 8. Schummer, Joachim, Bernadette Bensaude-Vincent, and Brigitte Van Tiggelen, eds. The Public Image of Chemistry. Singapore, 2007. Sellers, Christopher. “Conclusion: À l’aube du risque moderne: Comment les régimes du risque sont devenus industriels.” In Le Roux, Risques industriels, 305–43. Sellers, Christopher, and Joseph Melling, eds. Dangerous Trade: Histories of Industrial Hazard across a Globalizing World. Philadelphia, 2012. Vogelezang-Stoute, E. M. “De regulering van chemische stoffen: Na 40 jaar een nieuw begin met REACH.” SEW: Tijdschrift voor Europees en economisch recht 56, no. 3 (2008): 89–100. VNCI (Vereniging van de Nederlandse Chemische Industrie). Jaarverslag VNCI 1991. Leidschendam, 1992.

/ Index A Abbott Laboratories, 182, 192, 194–97 Abel, Frederick, 30 Abelson, Philip, 307 absorption (of toxic substances by organisms), 35, 120–22, 125–26 through the skin, 76, 116, 141, 239, 256n23, 271, 356 Academy of Sciences (France), 73, 102n25. See also National Academy of Sciences; Royal Swedish Academy acceptable daily intake (ADI), 19, 156, 184, 202n27 accidents (disasters, environmental/ occupational), 13, 29, 31, 38, 67, 72, 116–17, 119–20, 147, 240, 250–252, 271, 273, 386. See also Bhopal; Boehringer; insurance; Sandoz; Seveso activism, 14, 108, 112–13, 126–27, 129n50, 184, 186, 188–89, 198, 201, 220, 284, 301–02, 314, 335, 338, 341, 346–47, 357, 360 adulteration, 16, 18, 111–12, 149 aflatoxin, 187–88 Agent Orange, 27, 38, 40, 42n10, 163, 237, 242, 257nn31–32, 313, 333–34, 336–37, 340–43, 347, 348n32, 349n52 Agfa, 139, 143 agnotology, 249, 251–52, 254 Agricultural Chemicals Control Law (Japan), 26 Agricultural Research Council, 329 agriculture, 3, 10, 19, 24–25, 27, 39, 138, 214, 216–17, 219, 223, 225, 229nn24–25, 229nn27–28, 230n44,

236, 240, 247, 268, 272, 276, 287–89, 295, 297, 307–08, 310–12, 316–18, 329–32, 344–45, 357, 364 air force, 333 air pollution, 6, 9–13, 21–22, 27, 69, 125–26, 214, 228n18, 246, 302, 307, 337, 354–57, 359–63, 365, 368, 369n18, 370n43 air transport, 31–32 American Association for the Advancement of Science (AAAS), 335 American Cancer Society, 164 American Chemical Paint Co., 330 American Chemical Society, 358 American Cyanamid Company, 141, 270, 273, 276–77, 281 Ames, Bruce N., 14, 189, 204n67 Ames test, 14, 189–90, 195, 200, 244 analytical chemistry. See chemical analysis Ancien régime, 65, 377–79 Andral, Gabriel, 65–67, 74 Anglo-American Oil Company, 117 aniline, 1–2, 21, 137–44, 146–47, 152, 156–59, 164–65, 170n76 cancer, 2, 138, 141, 145–46 (see also cancer, occupational) See also dyes animal experiments (tests; models), 7, 11–12, 14, 19, 26, 120, 137–38, 141, 144, 146, 153, 157, 160, 163, 165, 183–85, 189–90, 192–97, 199, 239, 243, 257n33, 268–69, 271–72, 274–75, 277, 282, 285–87, 303–04, 306, 339, 358 Ansart, Florentin-Joseph, 75–78

394 Index aromatic amines, 3, 37, 137–39, 141–47, 156, 158, 160–65, 168n25, 168n31. See also aniline; betanaphthylamine; benzidine arsenic (arsenic trioxide, white arsenic), 20–21, 29, 35–36, 63–64, 66, 71, 75–76, 139, 145 compounds, 3, 20–21, 25–26, 29, 35–36, 63–78, 80–81, 82n25, 333, 376 (see also Schweinfurt green) Association of British Chemical Manufacturers (ABCM), 158–60 Auerbach, Charlotte, 194 automobiles (cars), 87, 109, 117, 119, 121, 125–26, 253, 355, 357, 366–68, 372n82. See also gasoline; octane; TEL Avicenna, 5 B Baden, 20, 68–69 Baillou, Guillaume de, 6 Baltimore, 115, 123–24 banning of (specific) chemicals, 11–12, 18–19, 22–23, 27, 29, 68–70, 73–74, 87, 94, 97, 99–100, 114, 116, 150, 180, 183–86, 188–89, 191–92, 195, 197–99, 204n67, 236, 247, 267–68, 285–87, 289, 301–02, 304–08, 310–12, 314–18, 338–40, 344, 346, 359, 361–62, 366, 377, 381. See also legislation Barruel, Claude-François, 66–67, 74 BASF Company, 139, 144–45, 147–48, 151, 157, 159–60, 238, 240, 251–52, 343 Bauer, Karl Heinrich, 152, 154 Bayer Company, 139, 143–44, 151, 157–59, 239, 268–69, 271, 343 Beijerinck, Martinus Willem, 10 Belgium, 22, 97, 99, 103n51, 214 benzidine, 139–40, 142–45, 147, 157–59, 161–65 Berenblum, Isaac, 145–46 Berne Convention (1890), 30–31 beta-naphthylamine, 139–40, 142, 144–47, 156–59, 162–65, 170n76

Bettmann, Siegfried, 238 Bezançon, Louis Pierre, 91–94, 102n19 Bhopal, 386 bioaccumulation, 281, 285–86, 289, 384–85 biocides. See pesticides biologists, 39, 97, 190, 281, 298, 300–02, 335 birth defects, 13, 242, 244–45, 254, 257n33, 336, 338, 344, 346 Blandet, Dr., 69–70, 72, 74 Boehringer Ingelheim (accident, Hamburg), 240, 248, 256n27, 258n71 Boehringer, Ernst, 240 Bonser, Georgiana M., 146 Bookchin, Murray, 13 Boyland, Eric, 138, 161 Braconnot, Henri, 64, 75 breast milk, 245, 248, 281, 304 Breton, Jules-Louis, 95, 97, 103n41 Britain. See United Kingdom (UK) British Petroleum (BP), 117–18 Butenandt, Adolf, 150–52, 154–55 butter yellow, 19, 37, 137, 139, 147–48, 150–53, 155–57, 165 byproduct, 25, 107, 109, 126, 143, 226, 235–36, 240–41, 243, 356, 369n1 C Cadet de Gassicourt, Charles-Louis, 66 cadmium, 3, 13, 37, 211, 214–19, 221–23, 225–27, 228n8, 229n32, 231, 61, 380 cadmium yellow, 226 Canada, 79, 199, 363 cancer, 1, 2, 10, 14, 19, 24, 36, 39, 148–51, 154, 156–57, 160, 183, 194, 236, 239, 244–45, 249, 251, 256n27, 300, 315, 339 occupational, 1, 2, 23, 37, 137–139, 141–48, 157, 159, 161–163, 165, 168n25, 204n79, 252, 258n71, 285, 340 (see also aniline cancer) prophylaxis, 155 (see also EUROTOX) research, 14, 145–46, 149, 188, 200, 257n33, 360

Index  395

risk(s), 189–90, 194–97, 200, 304, 381 theory, 152–53, 155–56, 160 (see also carcinogenicity) carcinogenicity (and carcinogenesis), 1, 14, 17, 19, 23–24, 27, 35–38, 137–39, 144–48, 150–51, 153–55, 157–65, 168n31, 170n76, 179, 180, 183–200, 204n79, 205n100, 250, 285, 304, 306, 355, 360, 380, 384–85. (see also cyclamates) Carson, Rachel, 13–14, 26, 39, 129n50, 163, 236, 267, 281–86, 289, 300, 315, 337–38, 347, 366. See also Silent Spring Carter, Jimmy, 318 Case, Robert A.M., 159–62 catalysts and catalytic converters, 40, 126, 151, 355–57, 366, 369nn9–10 Celsus, 5 chemical analysis (analytical chemistry), 7–8, 11, 13, 24, 26, 39, 64, 66, 75–76, 104n56, 141, 217, 246, 250, 271, 273–74, 279, 303, 360, 363, 366. See also Marsh test chemical industry, 4, 9–10, 12, 22, 28, 38, 41, 76, 117, 138–39, 145, 150, 159, 237, 240, 242, 244–46, 248, 251, 284–85, 289, 313–14, 337, 358, 381–82, 384–85 chemical substances carcinogenic (see carcinogenicity) corrosive (see corrosive substances) explosives (see explosive substances) hazardous (see hazardous substances) inflammable (see inflammable substances) irritating (see irritating substances) mutagenic (see mutagens) noxious (see noxious substances) oxidizing (see oxidizing substances) persistent (see persistence) radioactive (see radioactive substances) teratogenic (see teratogenicity) toxic (see poisons, toxic substances) Chemical Warfare Service, 329. See also Fort Detrick

chemical weapons (and chemical warfare), 12, 24–25, 27, 241–43, 245, 252, 257n33, 268–69, 335 Chemische Fabrik Griesheim, 141–42, 238 chemists, 7–8, 22, 25, 30, 32, 45n55, 69, 71, 74, 76, 88–89, 91–92, 95, 101n8, 121, 140, 143, 148, 150–51, 155–56, 217, 240, 268, 278, 295, 301, 303, 377, 382 Chester Beatty Research Institute, 158–59 Chevallier, J.B. Alphonse, 66–67, 70, 72–74, 76, 78, 80, 92–93, 97, 102n24 children’s health, 9, 13, 18, 36, 72–73, 87, 100, 107, 112, 114–16, 121–24, 127, 187, 236, 242–43, 257n40, 283, 287–88, 297, 338–39, 341–42, 344, 346, 379 China, 108, 127, 214–15, 316–17 chloracne, 238–41, 243, 245, 249–50, 256n12, 256n23, 376 chlorinated hydrocarbon. See organochlorine compounds chlorine, 2, 238–39, 246, 296, 299, 376 chlor-alkali electrolysis. See chlorine cholinesterase, 270, 276–79, 281–83, 287 Christison, Robert, 9 CIBA (and Ciba-Geigy), 142, 279 citizens, 3, 10, 16, 39, 150, 223, 231n58, 302, 338–39, 341, 346, 358 Citizens Against Toxic Sprays (CATS), 339–40 Citizens Natural Resources Association (Wisconsin), 302 Classification, Labeling, and Packaging (CLP), 29, 34, 382, 385 Clayton Aniline Company Ltd. (Manchester), 138, 158–59 Clean Air Act, 307, 337, 357, 362 Clear Lake, 298, 300, 311, 318 Clemenceau, Georges, 95, 103n35 Clément-Desormes, Nicolas, 91, 102n18 Clichy, 88–90, 92–93, 101n8 Clovis, Hughes, 95–96 CMR chemicals (carcinogenic, mutagenic or toxic for reproduction), 179, 385 coal tar, 25, 145, 150, 238–39

396 Index Cohn, Ferdinand, 10 Colborn, Theo, 286 colors. See pigments colorants, 37, 139–40, 148–52, 154–56, 164. See also butter yellow; dyes; food-additives combustion, 107, 120, 235, 253, 259nn74–75, 355–57 Commoner, Barry, 13, 335 confectionary, 18, 65–68, 72–74, 78–80 contact insecticides, 26, 271, 275, 295–96 Conseil de salubrité (Council of Public Sanitation), 65–66, 74, 78, 80, 102n24 contamination (and contaminants), 27, 38, 87, 121, 125, 138–40, 149, 156, 187, 223, 226, 336, 338–40, 247–48, 253, 274–75, 341, 346, 355, 360–63, 365–67 copper, 25, 63, 90, 211, 229n25 compounds, 18, 63–77, 80 (see also Schweinfurt green) Corn Belt, 357, 361, 365, 367 corrosive substances, 5, 7, 28, 32–33 cosmetics, 17, 72, 88–89, 183, 287, 303, 383 Coulston, Frederick, 186–87 cracking, 355–56. See also gasoline cumulative effects, 14, 35–36, 152, 154, 198, 246, 270, 272, 274, 287, 385 Curschmann, Fritz, 143 cyclamates, 3, 19, 37–38, 40, 179–92, 194–99, 204n67, 380 cyclohexylamine, 179, 187–88, 203n62 D danger. See hazard; risk Dangerous Substances Directive (DSD), 33–34 DDT (dichlorodiphenyltrichloroethane), 3, 13, 26–27, 39, 184, 187, 198, 236, 267–70, 272–75, 279, 281–82, 284–86, 289, 294–318, 331, 337–38, 346, 366, 376, 381 defoliation, 27, 243, 313, 328, 333–35, 338, 340, 350

degradability, 27, 308. See also persistence Delaney clause, 19, 39, 183–85, 192–94, 199–200, 303–04 Dessauer, Friedrich, 153 detection method, 75–76, 104n56, 190, 196, 217, 244, 250, 258, 303, 360. See also Ames test; chemical analysis, Marsh test Deutsche Forschungsgemeinschaft (DFG), 154, 189 Deutsches Krebsforschungszentrum, 187 developing regions (countries), 126–27, 288, 377 DeVictor, Maude, 340–42 diabetes, 182–83, 185–87, 197, 216 Diamond Shamrock, 331, 334 dieldrin, 273, 281, 285, 302, 310, 316 dioxins, 3, 13, 27, 38, 39, 235–37, 239–50, 252–54, 255n2, 255n6, 259n74, 259n75, 336, 338–40, 344–46, 380–81, 386. See also Seveso dirty dozen, 236 Dölz, Johann Christian, 7 dose, 6–7, 11–15, 19, 24, 27, 34, 36, 38, 43n17, 151–53, 155–56, 160, 163, 183, 191, 193–94, 198, 200, 241–42, 252, 257n34, 270, 272, 275, 280, 282, 380–82, 386. See also lethal dose, low level effect; threshold; Paracelsus dose-time relationship, 151, 153, 155–56 Doull, John, 270, 276 Dow Chemical Company, 241, 253, 330–31, 334, 338–40, 346 drift, 331, 338, 344 Druckrey, Hermann, 148, 152–56 drugs. See pharmaceuticals DuBois, Kenneth, 269–71, 273–78, 280–81, 283, 286–87 DuBridge, Lee Alvin, 336 Duchesne, Édouard-Adolphe, 74, 78 Duisberg, Carl, 12 Du Pont Company, 116, 144, 146–47, 157, 163, 168n32, 182, 280, 298–99, 330, 386

Index  397

dust, 21, 68–69, 73, 76, 90, 119, 123, 219, 225, 243. See also workplace dyes, 2, 13, 19, 21, 25, 37, 138–39, 141, 143–44. See also colorants; magenta E ecocide, 334, 347 ecological, 26, 300, 310, 337 ecology, 39, 164 ecosystem, 12, 26, 235, 289, 302, 306, 332, 334–37, 346, 368, 381 ecotoxicology, 10, 13, 26, 39. See also toxicology Eichholtz, Fritz, 152 emissions, 22, 89, 126, 231n61, 246, 252, 357, 364–65. See also dust; vapor endocrine disruptor, 286, 386 endocrine system, 27, 245, 286, 346, 386 Engel, Hans, 144–47, 158 England. See United Kingdom (UK) environment, 2–3, 13–14, 23, 25–27, 35–36, 94, 107, 120–21, 123, 241, 243–44, 246, 249–50, 253, 289, 298, 300–01, 305–07, 311, 314, 328, 334, 355, 362, 366–67, 377, 380–81 environmental consciousness, 9, 225, 347 environmental groups (see activism) environmental protection, 231n57, 235, 237, 246, 248, 311, 383, 386 (see also Environmental Protection Agency) environmental pollution (see pollution) environmental toxicology (see ecotoxicology) Environmental Defense Fund (EDF), 284, 301–03, 305–06, 316, 338 Environmental Mutagen Society (EMS), 14, 188–90, 193 Environmental Protection Agency (EPA), 26–27, 139, 163–64, 267, 284–89, 305–06, 337–38, 340, 346, 355–63, 367, 383–84, 386 epidemiology, 2, 95, 115, 123–25, 138, 159–63, 165, 189, 195, 217, 221–22, 244, 250–52, 341. See also statistics

ethanol, 40, 357–59, 361–65, 367–68, 370n43, 371n59, 371n64 Ethyl Corporation, 116–17, 119. See also TEL Eulenberg, Hermann, 10, 43n22 Europe, 1, 4–5, 9–10, 19, 23–26, 28–29, 31, 33, 40, 64, 87, 109, 113–17, 119, 123–25, 140, 144, 146, 148, 151, 155–56, 159, 168n25, 179, 188–89, 191, 197, 228n11, 230n38, 236, 268, 294, 297, 311, 332, 343, 354, 356, 362–66, 368, 377, 380, 384–85 European Environmental Mutagen Society (EEMS), 188 European Union (EU), 197, 294, 311, 362, 384 EUROTOX, 155 Evans, A.E.J., 165 Expert-Bezançon, Charles-Frédéric, 91, 94–95, 102n19 explosions, 28–29, 33, 338 explosive substances, 5, 28, 30–33, 143, 382 Explosives Act, 30 F factory, 10, 21–22, 37, 72, 76–78, 89–90, 93–94, 102n27, 113, 119, 137, 142–44, 157, 159, 162, 220, 298–99, 308, 317, 380. See also workers; workplace inspector, 10, 22, 76, 92, 113, 223 regulation, 10, 22–23, 28, 156, 378–79 physician, 37, 141–45 Fahlberg, Constantin, 180 fashion, 70, 73, 78 Federal Food, Drug, and Cosmetic Act (FFDCA). See US Federal Food, Drug and Cosmetic Act financial compensation, 23, 97, 99, 113–14, 145–46, 156, 161, 165, 215, 217, 220, 229n27, 242 fire, 28–29, 33, 75, 253, 259n74, 383, 386 flash point, 30, 32–34, 383 Flury, Ferdinand, 12 Follin, Eugène, 72 Fonblanque, John, 9 Fontana, Fellice, 7

398 Index food, 13, 16, 18–20, 25, 28, 35, 65–66, 121, 124, 149, 154, 182–84, 187, 197–9, 245, 247–48, 273–75, 288–89, 300, 304, 306, 310, 314, 334, 336, 368, 379–80. See also milk; nutrition; rice food additives, 18–19, 37, 150–51, 154–55, 179–80, 183, 185, 191–92, 195, 198, 303 (see also butter yellow; Schweinfurt green) food contamination, 13, 18–19, 37, 112, 121, 149–51, 275, 279–81, 313 food chain, 14, 26–27, 380 food industry, 155, 181, 183, 195, 197 food safety, 3, 19–20, 65–66, 73, 150 Food and Drug Administration (FDA). See US Food and Drug Administration Food Quality Protection Act (FQPA), 19, 287 forensic medicine (chemistry; toxicology), 7–8, 11, 14, 65, 76, 119 Fort Detrick, 241, 329 Fracastoro, Girolamo, 6 France, 3, 18, 20, 22–23, 30, 35–36, 64, 67–68, 74–75, 78, 80, 87–91, 94–95, 97–101, 112, 119, 124, 186, 191, 377, 379 Franklin, Benjamin, 111–12 Friberg, Lars, 225 fuel, 40, 117, 119–20, 259n75, 331, 355, 357–61, 361, 363–5, 367–68. See also gasoline fungicides, 240, 247, 287, 305 G Galen, 5, 16, 20 Galston, Arthur, 335–36 gases, 10, 12–13, 21–22, 28, 31–32, 34, 69, 94, 116, 143, 219, 239, 243, 282, 356, 358, 365. See also air pollution; chemical weapons gasoline, 5, 20, 36, 40, 87, 116–7, 119–20, 122, 124–26, 133, 333, 340, 354–68, 369n1, 372n82, 376, 381 Gaultier-Claubry, Henri-François, 67 Gautier, Armand, 92–93, 102n25, 102n27

Geber, 5 Gehrmann, George, 146, 157 Geigy, 142, 279, 295–99, 308. See also CIBA genetics, 14–15, 37, 148, 152, 187–95, 198–99 General Motors, 116, 355 German Federal Ministry of Health (BMG), 185, 187, 189, 199 German Food Law, 18, 185, 199 Germany, 3, 13, 17–20, 22–23, 25–26, 31, 35, 37, 40, 64, 67–69, 80, 95, 97, 99, 103n51, 112, 115, 117, 119, 126, 137, 139, 141–43, 145, 147–51, 155–56, 165–66, 167n17, 180, 182–83, 185, 187, 191, 197–98, 200, 214, 238, 241, 247, 251–52, 268–69, 275, 296, 339, 343, 356, 376, 379–80, 384 Gilfillan, Colum, 121 Globally Harmonized System of Classification and Labeling of Chemicals (GHS), 34, 382, 385 Gmelin, Johann Friedrich, 14 Gmelin, Leopold, 68–69, 74 Godesberger decrees on food additives, 155–56 Grandhomme, Wilhelm, 141–42 GRAS (generally recognized as safe), 19, 183–84, 205n119 growth disorder, 245 H Haber, Fritz, 12 Haberland, Ulrich, 151 Hahnemann, Samuel, 76 Hamilton, Alice, 12, 113, 145, 168n25 Havender, William, 192, 194 hazard, 2–4, 15, 23, 28–29, 31–35, 38, 40, 68, 71–72, 81, 91, 117, 138, 142–44, 161, 189, 198, 236, 254, 274, 284–85, 305, 318, 362, 365–67, 372n80, 376–79, 382, 384, 386. See also risk hazardous substances, 2, 3–5, 15–16, 21, 25, 28–34, 38–39, 65, 71–72, 76, 199, 237, 246, 254, 347n2, 377, 379, 381–83, 385–86

Index  399

health, 13–14, 16, 18, 21–22, 27–28, 36, 65, 121. See also public health health food, 20, 183 health inspection, 113, 122 (see also hygiene) health problems, 1, 13, 36, 70, 78, 124, 127, 236, 247 (see also cancer; itai-itai) Heidelberg, 69, 148, 152, 187, 238 Heisenberg, Werner, 154 Henry, S. A., 145 herbicides, 3, 27, 38, 40, 69, 187, 240–43, 247, 257n32, 257n33, 287, 328–47 Hercules Company, 298, 331, 334 Hergt, Wilhelm, 145, 157–58 Hermbstädt, Sigismund Friedrich, 68 Herxheimer, Karl, 238 Heubner, Wolfgang, 12 Hinds, William, 74–75 Hippocrates, 6, 109 Hirt, Ludwig, 9 Hoechst, 1, 139, 140–44 Hofmann, August Wilhelm, 140, 148 Hollaender, Alexander, 188 Holland. See Netherlands Holmes, E., 343 hormones, 155, 196, 245, 250, 328–330. See also endocrine disruptor; endocrine system hospital, 36, 91–93, 111–13, 123, 128n11, 141–144, 160, 162, 221, 230n52, 238, 244, household, 183, 247, 282, 288, 308 Howard, Frank, 116 Hueper, Wilhelm C., 146 Hugues, Clovis, 95–96 humoral pathology, 7 hygiene, 65, 73, 95, 113. See also health; public hygiene occupational hygiene, 113, 116, 121, 141 hygienists, 141–144 I IG Farben, 25, 147, 150 Imperial Chemical Industries (ICI), 145, 158, 162, 164–65, 329 immune system, 27, 245, 250

induction time, 159. See also latency period industrialization, 109, 149, 156, 218, 248, 253, 377 industrial disease. See occupational disease industrial hygiene, 10–13, 25, 80, 113, 138–39, 141, 143–46, 161 industrial liberty, 73–75, 78, 80–81 infectious substance, 6, 10–11, 32, 123, 245. See also miasma inflammable substances, 5, 28, 30, 32–34 inhalation, 141, 239, 256 insecticides, 25–26, 236, 240, 267–77, 279–89, 295–98, 305, 308, 316–18. See also contact insecticides; systemic insecticides insurance, 15, 29, 30–31, 145, 147, 161, 252, 342 intermediates, 137–42, 146–47, 159, 164, 179, 187–88, 243, 295, 345 International Agency for Research on Cancer (IARC), 189–91, 195–96, 205n100, 304, 360 International Labor Conference (ILC), 98–100 International Labor Organization (ILO), 22, 32–33, 87, 95, 98, 100, 104n53, 114–116, 383 International Maritime Organization (IMO), 31 International Programme on Chemical Safety, 316, 383 irritating substances, 10, 28, 31, 33 itai-itai disease, 37–38, 211, 215–19, 221–23, 225–26, 229n27, 229n32, 230n38, 230n41, 230n42, 230n52 Italy, 27 Ivanovski, Dimitri, 10 J Japan, 3, 13, 26, 34, 37–38, 40, 88, 120, 148, 160, 186, 211–12, 214–16, 219–22, 224–27, 228n11, 241, 297, 343, 345, 383 Jinzū River, 37, 211–19, 221, 226, 230n44, 231n61

400 Index Johnson, Julius E., 338 Joint FAO/WHO Expert Committee on Food Additives (JECFA), 19, 26, 155, 184, 197 K Kalle & Co. (Biebrich/Rhine), 139 Kamioka mine, 211, 213–26, 288n11, 231n59, 231n61 Kehoe, Robert, 35–36, 117, 119–21, 157 Kennaway, Ernst, 145, 158 Kennedy, John F., 284, 314, 328, 333 kerosene, 30. See also petroleum Kettering Laboratory of Applied Physiology (University of Cincinnati), 117, 120 Kinosita, Riojun, 148 Kletschke, Gustav, 20, 29, 71–72 Kobayashi, Jun, 217, 221, 229n28 Koch, Robert, 10 Koelsch, Franz, 143 Kollath, Werner, 149 Kuhn, Richard, 148 Küpfmüller, Karl, 153 Kurtis, Bill, 340–42, 349n51 L labeling, 18, 29–30, 32–35, 71–72, 79, 184–85, 192, 199, 257n32, 336, 378, 382, 385 labor union, 11, 24, 95, 100 Lafarge, Marie, 76 latency period, 1, 137–38, 142, 144, 146, 157, 160, 165 Lavoisier, Antoine, 7, 88 laws. See legislation lawsuit, 38, 40, 215, 220–23, 226, 242, 251–52, 339, 342, 384 lawn care, 287, 329, 331–32 lead, 25, 88, 108–09, 111, 116, 211 blood lead levels, 114, 125–26 lead compounds, 3, 18, 20, 35–36, 65, 86–88, 107, 111, 120, 379 (see also white lead) lead poisoning, 91–93, 98–99, 107, 112, 114–16, 120–22 (see also children’s health)

Leclaire, Edme-Jean, 97 Lefebvre, Theodore, 90–91, 93, 102n11 Legator, Marvin, 187–88 legislation (laws), 4, 14–23, 26–32, 34–35, 38–40, 65, 67, 72, 74, 76, 80, 87, 94–97, 100, 113–15, 139, 149–50, 154–56, 162, 165, 180, 184–86, 192, 199, 205n116, 221, 252, 294, 307, 311, 358, 360, 363, 377, 380, 383, 385. See also banning Lehman, Arnold, 271–75, 281 Lemery, Nicolas, 6 Lenzner, Curt, 149, 152 Le Roux, Thomas, 377–79 lethal dose, 11, 27, 34, 270, 272, 280, 282, 382 Leuenberger, S. G., 142 Liebig, Justus, 64, 68, 75 Liek, Erwin, 149, 152 life reform, 149–50, 152 Lille, 89–91, 93, 95, 102n11, 102n19 lithopone, 22, 97–98, 103n51 low level effect, 34, 36, 38, 121–125, 127, 287, 300, 304, 318, 366. See also chronic poisoning Los Alamos, 241 lymphoma, 242, 346 M magenta, 1, 21, 142, 161 malaria, 26, 280, 297–99, 301, 308, 315–18 malathion, 26, 276–78, 280–83, 286, 289, 315–17 malformation. See birth defects Marsh test, 75–76 Matsunami, Jun-ichi, 220, 222, 230n42, 230n48 maximal allowable concentration (MAC), 11–12, 23–24, 382 medical police, 8, 20, 80, 82n8 medicine (medical), 5–9, 11–12, 16–17, 36, 39, 65–69, 72, 74, 80, 99, 102n25, 107, 111, 113–14, 119, 122, 138, 141, 143, 145–46, 148, 150, 157–58, 161–62, 185–86, 215–18, 221–22, 230n52, 237, 251–52, 255n9,

Index  401

256n23, 271, 273, 285, 341, 346, 362, 381 Merck, 298, 329 mercury, 13, 20, 25, 63, 188, 220 Meselson, Matthew, 335 miasma, 6, 10 migration, 122 military, 3, 25, 143, 151, 211, 214, 237, 241–42, 268–69, 297–98, 328–30, 333–34, 336, 342 milk, 158, 248, 272, 274, 278. See also breast milk Minamata disease, 215, 220–21. See also mercury mining, 21, 112, 214–19, 221–22, 224–25, 227, 239. See also Kamioka mine miscarriage, 245, 257, 340 Mitsui Group, 37–38, 211–12, 214–15, 218–24, 226, 228n6, 228n11, 230n42 monoculture, 25, 332 Monsanto, 240–41, 251, 256n23, 301, 331, 334 Montrose Chemical Corporation, 299, 305, 307, 315, 318, 321n57 mortality rate, 2, 112, 126–27, 245, 279–80, 286 MTBE, 3, 35, 40, 354–68, 369n1, 369n24, 370n25, 370n28, 376, 381 Müller, Paul, 295–97, 318, 319n6 mutagens, 14, 17, 27, 35, 37–38, 139, 164–65, 179–80, 187–91, 193–95, 198–200, 380, 385 mutagenicity, 27–28, 164, 188–91, 195, 200, 204n67, 205n100, 250 mutation, 153–54, 190–91, 193–94, 198 N napalm, 313, 333 Nassauer, Fritz, 143 National Academy of Sciences (NAS, USA), 195, 242, 336 National Audubon Society, 300, 306 National Cancer Institute (NCI), 164, 168n32, 192, 304 National Institute for Occupational Safety and Health (NIOSH), 164, 383

National Institute of Environmental Health Sciences, 26, 164 National Research Council (NRC), 184, 195–97, 314, 358, 361 national socialism, 137, 148–49, 151 navy, 76–77, 94–95, 103n33 neonicotinoids, 27, 386 Netherlands, 20–22, 29, 88–89, 99, 101n11, 191, 384 nineteenth century, 8–13, 18, 23, 25, 28, 36, 65, 75, 80–81, 87–89, 94, 99, 112, 138–39, 149, 377, 379 nitroglycerine, 29–30 Nitze, Maximilian, 142 Nixon, Richard, 27, 184, 257n33, 304–07, 315, 336–37, 383 non-knowledge. See agnotology Nonox S (antioxidant), 160, 162, 164 North American Phillips, 331 Northwest Industries, 331 noxious gases. See air pollution noxious substances, 6, 9–10, 13, 21–22, 29, 33–34, 77 nuisance, 13, 21, 28–29, 43n22, 126, 301 nutrition, 35, 149, 151, 154–55, 165, 216, 218–19 O obesity, 182–83, 185 occupational disease, 1, 8, 21, 23, 73, 90, 95, 99–100, 145, 147, 376 occupational health, 3, 70, 113, 120, 165 occupational hygiene, 113, 116, 121 occupational medicine, 9, 12, 161, 237, 251–52, 255n9, 256n23 occupational safety, 23, 163, 241 Occupational Safety and Health Act (1970), 23, 163 octane (and octane rating), 40, 117, 119, 354–56, 361–63, 365–68, 369n2, 369n10, 369n18, 376 Operation Ranch Hand, 328, 333–34, 338 Oppenheimer, Robert, 144 Orange Book, 29, 32, 382, 385. See also transport of dangerous goods Orfila, Mathieu, 7, 76

402 Index organochlorine compounds, 24, 26–27, 236, 239, 247, 250, 255n2, 267, 272–76, 281–83, 285–86, 288–89, 290n13, 310–12, 315–16, 381. See also DDT; dioxins; PCB; PCN; PCP organophosphates, 3, 19, 25, 27, 39, 267–89, 290n23, 315, 317, 376, 381 O’Shaughnessy, William Brooke, 67–68, 74 oxidizing substances, 32–33 ozone, 40, 357, 361, 363, 386 P paint, 68, 70, 72–73, 88, 94–95, 97, 107–09, 112, 114–15, 122–23, 125, 160, 296, 355, 358, 386 painters (and painting), 22, 36, 63, 65, 76–77, 87–89, 92–100, 107, 112, 114, 116 Paracelsus, 4, 6, 8, 21, 43n17, 382 Parathion, 270–79, 282–83, 288 Paris (France), 65–67, 70, 72–74, 78–80, 89, 91–92, 95, 97, 102n19, 112, 123–24 Parkes, Guy, 161–62, 165 Pasteur, Louis, 10 Patterson, Clair, 121, 125, 127 PBT chemicals, 385 PCB, 13, 236, 286, 358 Peeters, Léon, 9 pentachlorophenol (PCP), 240, 247 persistence, 27, 112, 236, 246, 285, 289, 295, 297–98, 300, 302, 304, 311, 314, 316, 318, 337, 381, 384–85 pesticides, 6, 10, 12–13, 18–19, 24–28, 34, 39, 180, 247, 250, 253, 267–68, 272–73, 278–79, 281, 283–89, 298, 300, 302–06, 310–18, 331, 337, 347, 376, 379–80, 383. See also fungicides; herbicides; insecticides petroleum, 29–30, 117, 355–56, 361, 364, 366–67, 372n82 Petroleum Act (UK), 30 Pfeiffer, E.W., 335 pharmaceuticals, 5–6, 11, 13, 15–17, 20, 28, 138, 151–52, 155, 183–88,

197–99, 270, 280, 294, 296, 308, 314, 340, 380, 383 pharmacist, 8–9, 66, 74, 91, 295 pharmacologist, 11–12, 148, 152, 155, 279 pharmacology, 11, 152–53, 271–73, 275, 279, 305 Pharmacy Act (UK), 16 phosphorous, 22–23 physiology, 7, 11, 117, 120, 215, 269, 297 picloram, 42n10, 334, 348n31 pictogram, 29, 33–34, 71 Pietra Santa, Prosper de, 73–74, 76 pigments, 3, 18, 22, 25, 35, 63–74, 76, 78, 88, 97–98, 104n56, 112, 214, 376. See also cadmium yellow; Schweinfurt green; white lead; zinc white plant hormone, 328–30 platforming, 355 Pliny, 11 plumbism, 107, 112, 121, 126. See also children’s health; lead poisoning poisons (poisonous substances), 3–4, 28–29, 32–36, 38, 67, 71–72, 74, 78, 108, 146, 149, 155, 236–37, 243, 246, 253–54, 271, 282–83, 310, 376, 378, 382, 386. See also toxic substances concept of, 4–15, 379 environmental poisons, 12–13, 15, 302, 380 regulation of, 15–28 trade, 20–21 poison gas. See chemical weapons poisoning, 36, 71, 75–76, 78 , 90–93, 96–100, 107–09, 111–17, 121–24, 126, 128n23, 129n39, 139, 152, 154, 156, 215, 217–18, 220, 225–27, 228n8, 236–39, 286, 313, 330, 355, 379. See also toxicity acute, 8–9, 11, 26, 34–38, 43n21, 141, 160, 165, 220, 239, 242, 271, 275, 287, 341, 379 (see also chloracne; toxicity, acute) chronic, 8–9, 36–38, 43n21, 115, 121, 138, 239, 275, 379 (see also toxicity, chronic

Index  403

Poland, 99, 120, 345 police, 8, 18, 20, 63, 65–68, 71, 74, 78, 80, 92 pollution, 3, 11–13, 21, 124–25, 198, 214–27, 229n27, 248, 310–11, 313, 355, 357, 359–61, 363, 377–78, 384. See also air pollution; mining; water pollution polychlorinated naphthalene (PCN), 239, 256n22 precautionary principle, 17, 24, 27, 39, 127, 186–87, 193–94, 199–200, 218–19, 383–84, 386. See also Delaney Clause Prestwich, John, 14 prevention, 4, 70, 73, 78, 107, 115, 122–23, 125, 140, 150, 158, 217–18, 223–24, 365, 381, 383–84 Proctor, Robert, 149, 249 production methods, 2, 70–72, 74, 78, 88–89, 91, 94, 99–100, 112–13, 142, 149 protective measures, 21–23, 71, 78, 80, 90, 115, 125, 141, 143, 310, 360, 378, 383 protest, 9–10, 21, 300, 311, 313, 318, 337–40, 345–46 Prussia, 18, 20–22, 71–72, 74–75 public debate/opinion, 4, 9–11, 13–16, 24, 26, 36, 95, 117, 120, 122, 150–52, 155–56, 161, 165, 180, 184, 186–87, 198–200, 215–16, 225, 227, 235, 237, 241–43, 246, 248, 254, 267, 281, 284, 289, 307, 333, 335, 337–38, 358, 365–66, 368, 379, 381–82 public health, 10, 65–66, 69–70, 72, 74–75, 78–81, 92, 116, 119–22, 124, 218, 267, 272–73, 285–86, 296–97, 302, 306, 318, 338, 354, 355, 361, 363, 367–68 public hygiene, 10, 66, 218 Pure Food and Drug Act, 16, 18 Purple Book, 29, 34 pyrethrin, 308, 312 pyrethroid, 288 pyrethrum, 268, 295, 297, 308

R radiation, 14, 37, 188, 191, 193, 198, 362 radioactive substances, 28, 32, 33, 42n12, 385 railways, 21, 29–32, 120. See also transport Railway Clauses Consolidation Act, 30 rainbow herbicides, 257n32, 333–34. See also Agent Orange Ramazzini, Bernardino, 8, 21, 111 REACH (Registration, Evaluation and Authorisation of Chemicals), 40, 311, 384–86 Reagan, Ronald, 318, 384 recycling, 247 regulation, 3–4, 10–11, 14–25, 28–32, 34–35, 37, 65, 68, 71–72, 87, 80, 87, 94–95, 99–100, 109, 112, 116, 126, 137, 139, 144–45, 147, 151–52, 156, 160, 162, 165–66, 179–80, 183–86, 190–91, 193–96, 198–200, 235–37, 245, 267, 271, 284, 287–88, 294, 304, 310–11, 315, 354, 361, 366, 377–80, 382–83, 385–86. See also banning; legislation Rehn, Eduard, 154 Rehn, Ludwig, 1, 141–142, 145, 152, 154 Reiter, Hans, 149–50 Remer, Wilhelm Hermann Georg, 66–67 residue, 13, 18–19, 26, 90, 273–75, 279, 281–82, 300, 303, 313 resistance, 26, 155, 222, 298, 315, 317–18, 330–31 Reutershan, Paul, 341–42 Rhine, 20–21, 29, 386 rice, 211, 214–15, 226–27, 241–42, 330, 343 Ringaud, Henri, 65, 77–78 Rio de Janeiro Earth Summit (1992), 34 risk (risk assessment), 2–4, 11, 15, 17, 27, 34–35, 38–39, 88–90, 109, 112, 117, 119–25, 142–43, 151–52, 156, 160–61, 163–64, 166, 180, 183, 185–86, 189–91, 193–96, 198–200, 235, 237, 239–41, 243–46, 248, 252, 254, 267, 271–75, 281–87, 289, 301, 304, 306, 310, 336, 346, 354–55, 358–62, 365–67, 377–78, 380–82, 384–85

404 Index Roard, Jean-Louis, 88, 90, 92, 191n8 Rome, 111, 121, 297 Rothamsted Research Station, 329 Roussin, Zacharie, 75–78 Roux, Wilhelm, 10 Royal Academy of Medicine (France), 65, 67, 102n25 Royal Swedish Academy of Sciences, 63 rubber, 138, 141, 160–63, 165, 299 Rubber Manufacturing Employers’ Association (Birmingham), 161–62 Ruckelshaus, William, 267, 284–85, 306–07, 312 Russia. See Soviet Union S saccharin, 180–83, 185, 190–91, 195, 199, 205n100 safety measures, 3, 15–17, 19, 21, 24, 29–30, 32, 39, 75, 80, 119, 157, 165, 180, 183–84, 192, 194, 240–41, 243–44, 272, 274, 284, 310, 314, 335–40, 342–47, 359–60, 379, 383 Sandermann, Wilhelm, 240 Sandoz (accident at), 386 Sattler, Wilhelm, 64, 73 Scheele, Carl Wilhelm, 63 Scheele’s green, 63–64, 67, 76 Scheller, William, 357 Schlatter, Jim, 180 Schoental, Regina, 138 Schrader, Gerhard, 25, 268–71 Schrötter, Anton, 22 Schweinfurt green, 18, 22, 25, 35, 63–81, 376, 379 Scott, T. S., 138, 158–61 selectivity, 330 Sertürner, Friedrich, 7 Seveso, 27, 38, 236–37, 240–41, 243–46, 250, 255n2, 257n40, 338, 349n45, 386 Sherwin-Williams, 79, 330 Shimabayashi, Tatsuru, 220–21, 230n42 shipping, 20, 29, 30–32, 71. See also Rhine, transport Shoecraft, Billee, 338–39 side effect, 11, 17, 38, 235, 242–43, 248

Silent Spring, 13, 26, 39, 163, 236, 267, 281, 283–84, 286, 289, 300, 303, 312, 314, 337, 366, 382 skin (acne, damage, irritation, ulcers), 33, 70, 73, 75–77, 89, 238–40, 256n12, 271, 356. See also absorption; chloracne slum, 100, 122, 124 smoke, 13–14, 21, 29, 225 smog, 125, 355, 363, 366 Souci, Walter, 151 Soviet Union, 12, 30, 119–20, 125, 159, 275 Standard Oil, 116–17 statistics, 2, 91–92, 97–100, 113–115, 142, 147, 149, 162, 250–51, 258n73, 307 stench, 21, 29 Stockholm Convention, 236, 311, 316–17 Stoeckhardt, Julius Adolf, 72 storage, 3, 15–16, 20–21, 28–31, 71, 111, 272, 333, 359, 363 Störck, Anton, 7 Strobel, Käte, 155, 186–87 substitutes (alternative products; ersatz), 3, 22, 68–70, 78, 81, 87, 89, 94, 98–99, 159, 179, 268, 285, 300, 330, 337, 344, 354, 366–67, 369n9, 370n43, 371n64 sulfur dioxide, 10, 126, 219 Sweden, 27, 99, 191, 307–08, 339, 343–44 sweeteners, 19–20, 37, 40, 111, 179–87, 197–99, 204n79. See also cyclamates Switzerland, 23, 119, 142–43, 147, 159, 192, 248, 296–97, 339 Sydenham, Thomas, 6, 43n21 Sylvius, 6 systemic insecticides, 271, 274–76. See also contact insecticides T Tanquerel des Planches, Louis, 91, 99, 112–13 Taylor, Alfred S., 9, 36 TCDD (tetrachlorodibenzodioxin). See dioxins

Index  405

TEL (tetraethyl lead), 336, 40, 107, 116–17, 119–120, 125–27, 354–56, 366 Teleky, Ludwig, 239 teratogenicity, 14, 17, 27, 35, 38, 187–88, 193, 336 test, 8, 17, 19, 26, 30, 76, 97, 147, 164, 179, 181, 183–84, 187, 189–91, 193, 195–97, 199, 270, 278–80, 295, 329–30, 333, 344, 356, 358, 360, 367. See also animal test; chemical analysis thalidomide, 13, 17, 187, 198, 314 The Hague Convention, 25 Thomas, Albert, 95 threshold limit value (TLV), 11–14, 19, 23–24, 30, 33–35, 37, 120–21, 124, 126, 163, 191, 277, 360, 362, 378–80 toxicity, 11, 15, 17, 25–27, 87–90, 94, 139, 198, 242, 244, 250, 253–54, 255n6, 270–81, 283, 285–86, 296–97, 308, 315, 330, 355, 358, 376, 378, 380, 384. See also ecotoxicity; poisoning acute, 8, 9, 11, 23, 26, 36, 38, 141, 239, 241–42, 270–75, 277, 280–83, 285–86, 289, 296, 379 chronic, 8, 9, 23, 36, 38, 121, 191, 193, 198, 217, 225, 139, 241–42, 250, 256n23, 271, 274–75, 281 cumulative, 14, 36, 152, 154, 246, 270, 272, 274, 287, 385 toxicology (and toxicologists), 6–14, 26, 34, 36–39, 76, 138–39, 187–91, 194, 198–99, 252, 271–72, 269–70, 276, 280, 282, 284, 289, 303, 317, 340, 360, 377–80, 382, 384. See also ecotoxicology toxic substances (toxicants), 2–3, 8, 10–11, 13–15, 17, 23–25, 28, 33–34, 38, 43n22, 66, 73–74, 78, 80, 100, 123, 126, 139, 141, 143, 147–49, 153, 158, 165, 168n31, 179, 191, 235, 239–40, 242–43, 248, 255n6, 267–73, 276–83, 285–86, 288–89, 302, 308, 338, 340–41, 346–47,

355–56, 358, 360, 366–69, 369n9, 370n28, 376–79, 381–82, 385. See also poisons Toxic Substances Control Act (US, 1976), 23, 163, 358, 362, 383 toys. See children’s health transport, 3–4, 20–21, 26, 28, 117, 120, 141, 357, 361, 364–65, 367, 378–80, 386. See also railways; shipping of dangerous goods, 29–32, 42n12, 382, 385 Treilhard, Achille Libéral, 65, 67 Trevan, John William, 11 trichlorophenol (TCP), 240–41, 243, 251 Tschirley, Fred, 335–36 tumors, 1, 137–138, 142–49, 151, 153, 157–61, 164–65, 183, 188, 190, 195–96, 304, 358 Turner, William, 63 2, 4–D, 27, 257n32, 328, 330–33, 337–38, 343–46 2, 4, 5–T, 27 240, 242, 328, 330, 332–33, 336–40, 343–44, 346 Tyndall, John, 10 typhus, 6, 297 U ubiquity, 13, 109, 122, 187, 235, 237, 246, 248, 253, 255n9, 259n74 uncertainty, 3–4, 12, 15, 34, 37–38, 164, 191, 200, 275, 346, 354, 360, 380–81, 386 United Kingdom (UK), 3, 18, 20–23, 27, 30, 32, 39–40, 63–64, 67, 69, 74–75, 88, 90, 95, 97, 99–100, 101n9, 103n51, 111–12, 117, 139, 147–48, 157, 160, 163–65, 191, 214, 294, 296, 307–08, 310–14, 318, 321n59, 321n67, 329, 343 United Nations (UN), 32–35, 254, 316, 383, 385 United States (US), 1, 3, 17–19, 23–27, 30, 35–37, 39, 40, 42n12, 99, 103n51, 104n51, 107–09, 113–15, 117, 119, 121–23, 125–26, 139–40, 144, 146–47, 159, 163–65, 179,

406 Index United States (US) (cont.) 182–83, 185–87, 193, 198–99, 214, 236, 267–71, 275, 282, 286–87, 289, 296–99, 302, 304, 306–08, 311–15, 317–18, 329–330, 332, 334, 338–39, 342, 344–45, 354–57, 360, 363, 365–68, 377, 379–80, 383–85 US Department of Agriculture (USDA), 27, 273–74, 284, 303–06, 314, 329–330, 332, 335, 366 US Federal Food, Drug and Cosmetic Act (1938), 17, 183, 287, 303, 383 US Food and Drug Administration (FDA), 17, 180–82, 184–85, 187–88, 192–95, 197–99, 271, 273, 275–76, 278–81, 283–85 US Forest Service (USFS), 338–340 US Public Health Service, 122, 184, 303 V vapor, 6, 9, 29, 77, 119, 142, 361 vector control, 288, 306, 316–19 ventilation, 70, 90, 141, 231n62 verdigris, 64 veterans, 27, 40, 243, 340–42, 346 Veuve Jules Perus et Cie., 90, 102n12 Vietnam War, 3, 27, 38, 40, 237, 241–45, 252, 257n32, 307, 313, 316, 328, 333–36, 338–42, 344–47. See also Agent Orange vinyl chloride, 24, 358 volatile organic compound (VOC), 362, 366 W wallpaper, 65, 68–70, 72–75, 77–78, 80, 82n27, 296–97 war. See Chemical Warfare Service; Vietnam War; World War I; World War II Washington (DC), 99, 188, 195, 198, 302, 305, 335, 359 waste, 9, 12, 21, 38, 77, 139, 214–16, 219–21, 226–27, 236, 245–46, 248–50, 253, 345, 382

water pollution, 6, 11–12, 14, 21, 27, 91, 109, 112, 121, 124, 139–40, 149, 158, 214, 216–19, 253, 274, 282–83, 300, 302, 328, 337–38, 358–63, 365–68, 383 weed killers. See herbicides Weimar Republic, 149 white lead, 8, 12, 21–23, 36, 87–100, 101n5, 101n8, 102n19, 102n21, 102n24, 103n37, 103n51, 107, 112, 114–16, 379. See also cosmetics White Lead Convention (ILO), 98, 114–16 Williams, Michael H.C., 158, 160 Wisconsin hearings, 302–04, 315, 337–38 wood preservatives, 247, 252, 340 women, 99, 143, 149–50, 155, 162, 202n18, 215–16, 271, 300, 338, 340 workers, 1–2, 8, 11–12, 21–24, 36–37, 69–70, 72–73, 75–78, 89–93, 95–96, 99–100, 109, 112–14, 116–17, 122, 127, 137, 140–47, 156–59, 162–64, 180, 214, 236–38, 251–52, 258n71, 267, 269, 280, 283, 286–87, 310, 343–44, 377, 379. See also painters workplace (and working conditions), 9, 21–24, 28–29, 32–33, 35, 95, 107, 112–13, 141, 146–47, 156, 159, 161, 163, 165, 237–38, 255n9, 382, 386 World Health Organization (WHO), 26, 34, 199, 288, 317–18, 383 World Summit on Sustainable Development (Johannesburg), 34 World War I, 12, 25, 97, 113, 144–45, 214, 228n11, 239, 299 World War II, 19, 22–23, 26, 32, 37, 107, 119, 156, 214–15, 219, 229, 241, 256n22, 267–69, 281–82, 296, 329, 343, 355, 378 wrapping paper, 67–68, 72–74, 78, 80 WT Henley (Telegraph Works) Company (North Woolwich), 162–63 Wyandotte Chemical Corporation, 299

Index  407

Y Yellow Book, 29, 33, 383 Yoshida, Tomizo, 148

Z Zentrallaboratorium für Mutagenitätsprüfung, 189 zinc, 37, 68, 211–12, 214, 216–17, 225–26, 228n11 zinc white, 22, 94–95, 97–98, 100, 103n42, 103–04n51, 104n56