Air pollution: Sources, prevention and health effects 9781624177460, 1624177468

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AIR, WATER AND SOIL POLLUTION SCIENCE AND TECHNOLOGY

AIR POLLUTION SOURCES, PREVENTION AND HEALTH EFFECTS

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AIR, WATER AND SOIL POLLUTION SCIENCE AND TECHNOLOGY

AIR POLLUTION SOURCES, PREVENTION AND HEALTH EFFECTS

RAJAT SETHI EDITOR

New York

Copyright © 2013 by Nova Science Publishers, Inc. All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS. Additional color graphics may be available in the e-book version of this book.

Library of Congress Cataloging-in-Publication Data Air pollution : sources, prevention, and health effects / editor, Rajat Sethi (Texas A&M Health Science Center (TAMHSC), Kingsville, Texas). pages cm Includes bibliographical references and index. ISBN:  (eBook)

1. Air--Pollution--Health aspects. I. Sethi, Rajat, editor of compilation. RA576.A535 2013 363.739'2--dc23 2012049992

Published by Nova Science Publishers, Inc. † New York

Dedicated to my beloved parents, loving wife and kids, respected mentors, honored professionals, and esteemed colleagues for their love and support

CONTENTS Preface and Letter to Mother Earth Chapter 1

Linking Molecular Mechanisms to Biomarkers in Cardiac Disease Resulting from Prolonged Chronic Inhalation of Ozone: A Gaseous Component of Air Pollution Rajat Sethi, Shubham Manchanda, Magdalena Ramirez and Vishal Sethi

Chapter 2

Air Pollution and Cancer: The Cycle of Insult to Injury Deborah K. Arnold

Chapter 3

Vulnerability to Ozone Air Pollution in Different Landforms of Europe Svetlana Bičárová, Hana Pavlendová and Peter Fleischer

Chapter 4

Chapter 5

Chapter 6

Chapter 7

Chapter 8

Genotoxicity of Airborne Particulate Matter as a Tool to Prevent the Effects of Environmental Pollution on Health Vera Maria Ferrão Vargas and Andréia Torres Lemos

ix

1

15

25

65

Is Air Pollution Contributing to the Obesity Epidemic? New Connections for Further Review Alison F. Pittman

85

Respiratory Epithelium Response to Air Pollutants, and the Preventive Role of Antioxidants M. Rojas-Lemus and T. I. Fortoul

95

Is Air Pollution the New Risk Factor in the Diabetes Epidemic? Ayesha Akhtar de la Fuente

119

Applying Computational Fluid Dynamics (CFD) to Model Localized Atmospheric Pollution A. A. Karim and P. F. Nolan

131

viii

Contents

Chapter 9

Tobacco Smoke Pollution and Oral Health Darren M. Roesch

Chapter 10

Integrated Environmental Management System and Pollution Prevention Framework for Control of Mercury Emissions Using H2O2 Enhanced Oxidation and Wet Scrubbing Prajay A. Gor, Alexander J. Murillo and Alvaro I. Martinez

171

Air Quality Modelling through Evolutionary Computing: A Review J. C. M. Pires and F. G. Martins

185

Chapter 11

Chapter 12

Pollution and Climate Impact on Respiratory Hospitalizations for Elderly People in São Paulo, Brazil Airlane Pereira Alencar, Thelma Sáfadi and Francisco Marcelo Monteiro da Rocha

165

197

Chapter 13

Occupational Exposure to Polycyclic Aromatic Hydrocarbons Klara Slezakova, Marta Oliveira, Cristina Delerue-Matos, Simone Morais, and Maria do Carmo Pereira

209

Chapter 14

Air Remediation Using Non-Thermal Plasmas Koichi Takaki

251

Chapter 15

Trends of PM2.5 Pollution and Its Mutagenic Properties in Turin: A 7-Year Study D. Traversi, L. Alessandria, R. Bono and G. Gilli

Chapter 16

Chapter 17

Index

The CO2 Hypothesis - The Stress of Global Warming on Human Health: pH Homeostasis, the Linkage between Breathing and Feeding via CO2 Economy Donatella Zappulla Air Quality Study in Belgrade: Particulate Matter and Volatile Organic Compounds as Threats to Human Health M. Tomašević, Z. Mijić, M. Aničić, A. Stojić, M. Perišić, M. Kuzmanoski, M. Todorović and S. Rajšić

279

293

315

347

PREFACE AND LETTER TO MOTHER EARTH Dear Mother Earth, All I need is the air that I breathe and to love you…. While that phrase is most remembered as the title of a hit single by the Hollies in early 1974, 21st century air is not-so-lovable. Since World War II, post-industrial children have and are doing quite a number on the troposphere. The air quality of urban America is being adulterated by activities aimed at “the good life” through the ability to travel via car and/or truck fast and often. Another convenience of this life of convenience is the mass production of goods. While the up-side is we are now privy to a disposable lifestyle and “more-thanenough stuff”; the down side is an “over-the-top” energy demand necessary to make “all this stuff.” Production energy in the form of fossil fuel, on which this economic lifestyle is built, is the main culprit behind the excessive industrial pollution, particularly, and the dirtiest of all, coal. It is therefore not surprising that industrial pollution is the largest fountain of air offenses in most of the developed world. Statistics from the U.S. Environmental Agency confirm that more than half of the nation’s total pollution is courtesy of industry. What’s more, six out of every ten people in the United States live in urban areas and are currently inhaling the bi-products of “the good life.” Unfortunately, however, 2.4 million of them will draw the short straw and die from causes directly connected with air pollution. So what about the other four out of the ten? Where are they? They are living the clean life in rural America. They too, however, have their dirty little secrets. While the advantages of fertilizers and pesticides have allowed for increase in crop production, major disadvantages include significant insult to the ecosystem and the health and well-being of all inhabitants. It is estimated that around 98% of sprayed insecticides and 95% of herbicides reach a destination other than their target species, which means that they can easily become a major source of environmental pollution. Extensive use of pesticide is not only detrimental ecologically, but unhealthy as well. Statistics issued by The World Health Organization suggest 3 million workers in agriculture in the developing world experience severe poisoning from pesticides, 18,000 of whom are expected to die. The consequence of air misuse is glaring: Approximately four percent of all deaths in the United States are attributed to air pollution. "Air Pollution: Sources, Prevention, and Health Effects" exposes what the spoiled children of Mother Earth have done to their air and ultimately their health. While this book aptly titled highlights sources and effects, it also puts

x

Rajat Sethi

forth solutions. Successful pollution prevention is the essential to our future well-being. Quintessential is prevention through education – the goal of this publication. Two closing comments: The first in thanks and the second in warning. Special thanks are extended to Ms. Lisa Benavides and to Ms. Makenna Lange for their diligent editing and proof-reading. Appreciation is also tendered to Mr. Vishal Sethi and to Mr. Shubham Manchanda for their organizational savvy, offered while in the throes of medical school, as well as to all of the contributing writers. Now the warning: Nature always bats last. Sincerely, Rajat Sethi Your son and breathing member of Planet Earth

In: Air Pollution: Sources, Prevention and Health Effects ISBN: 978-1-62417-735-4 Editor: Rajat Sethi © 2013 Nova Science Publishers, Inc.

Chapter 1

LINKING MOLECULAR MECHANISMS TO BIOMARKERS IN CARDIAC DISEASE RESULTING FROM PROLONGED CHRONIC INHALATION OF OZONE: A GASEOUS COMPONENT OF AIR POLLUTION Rajat Sethi, Shubham Manchanda, Magdalena Ramirez and Vishal Sethi Texas A&M University System Health Science Center, College of Nursing, Bryan, TX, US

ABSTRACT Studies from our and other laboratories confirm myocardial dysfunction subsequent to chronic ozone (O3 ) exposure in animals and humans is associated with a decrease in antioxidant reserve and with an increased activity of inflammatory mediators. This chapter discusses the involvement of caveolin-1 and caveolin-3 levels in O3- induced cardiac toxicity when Sprague Dawley (SD) rats were exposed 8 hrs/day for 28 and 56 days to filtered air or 0.8 ppm O3. In-vivo cardiac function was assessed by measuring left ventricular developed pressure (LVDP), 24 hrs after termination of the O 3 exposure. Compared to rats exposed to filtered air, LVDP values were significantly decreased in all O3 exposed animals. This attenuation of cardiac function was associated with increased myocardial TNF- levels and decreased myocardial activities of superoxidase dismutase (SOD). Progressive increases in the expression of myocardial TNF- in 28 days and 56 days O3 exposed animals were followed by decreases in cardiac caveolin-1 levels. On the other hand, differential changes in the expression of caveolin-3 in hearts from 28 days and 56 days O3 exposed animals were independent of intra-cardiac TNF-levels. These



Corresponding author: Dr. Rajat Sethi. Assistant Dean for Research and Evidence Based Practice. TAMHSCCollege of Nursing. Health Professions Education Building. 8447 State Highway 47, Suite 3010. Bryan, Texas 77808-3260. E-mail: www.tamhsc.edu.

2

Rajat Sethi, Shubham Manchanda, Magdalena Ramirez et al. novel findings suggest the interesting possibility that a balance between caveolin-1 and caveolin-3 may be involved in O3- mediated cardiac toxicity.

INTRODUCTION Cardiovascular disease (CVD) is the major cause of death in North America. Approximately 1 million people per year die of CVD in the United States (US) which accounts for over 40% of all deaths in the US. Numerous advances have been made in the field of health sciences, which have resulted in reduced deaths due to CVD. Recent statistical data suggests that CVD induced mortalities are on the rise again, and due to significant increases in the incidence of diabetes and obesity, the total burden of CVD in the future may be even greater. Numerous risk factors such as age, race, and lifestyle play an important role in the development of CVD. However, many patients with cardiac diseases show no obvious established risk. Furthermore, it has been shown that when genetically similar populations migrate to a new environment, the CVD risks are altered, suggesting that environmental factors may play an important role in the development of heart disease. Out of 350,000 sudden cardiac deaths each year in the US, 60,000 deaths could be related to air (environmental) pollution. Ample evidence for links between environmental exposure and CVD has been accumulated over the years, the importance of these exposures as risk factors for the induction and development of CVD has only recently been seriously considered [1-4]. Funding agencies such as the National Institute of Health (NIH), American Heart Association (AHA), and Health Effects Institute (HEI) have recognized the detrimental role played by air pollution in cardiac diseases and have accordingly increased the priority of research funding in an effort to understand the role of environmental pollutants in CVD. The United States Environmental Protection Agency (USEPA) is required to set National Ambient Air Quality Standards (NAAQS), under the Clean Air Act and Ozone (O3) is one of the six pollutants under consideration. Understanding the relationship between O3 exposure, disease, and mortality can significantly affect decisions related to the stringency of air pollution controls, and thus has important implications for the impact of these controls on human health. The concern is that while considering the benefits of air pollution standards, the mortality risks associated with O3 exposure were excluded from the USEPA analyses. Health risks in human populations are increasingly being assessed by the use of empirical data from epidemiological studies. Although epidemiologic evidence for air pollution as an important and modifiable determinant of cardiovascular diseases is very strong, epidemiologic data have limitations of imprecise measurements. Air pollution epidemiologic research is challenged by the complexity of human exposure to environmental agents, and by the difficulty of accurately measuring exposure. Residents are usually ubiquitously exposed to air pollution. In order to detect small effects of air pollution, both high statistical power and sophisticated study design are required. In addition, the characteristics of air pollutants vary and their concentrations change both spatially and temporally. Although everyone is susceptible to high concentration of pollution, its concentrations are not evenly distributed across populations. In addition, epidemiologic studies are limited by joint exposure to multiple pollutants, and a lack of clinical experimental models makes it difficult to systematically study the effects of individual pollutants, and to demonstrate the individual risk [5]. Due to such complexities, there are still many research questions to be addressed by

Linking Molecular Mechanisms to Biomarkers in Cardiac Disease …

3

future air pollution epidemiological studies. We believe that use of new tools such as geographic information systems, personal monitoring devices, and better measures of the full toxic air pollution mix may provide more refined estimates of the adverse health effects (diseases) that can be related to specific components of air pollution. Epidemiological studies show statistical associations between health outcomes and exposure; they cannot establish a definite cause-effect relationship. Although the utility of animal studies is to establish this relationship, in some cases the evidence from animal experiments is of uncertain relevance for human populations. The interspecies dose extrapolations used to adjust for differences between humans and laboratory animals, and the extrapolations using statistical bioassay models for the high doses used in animal experiments to the much lower doses to which humans are likely to be environmentally exposed, are the two major extrapolations required when animal data are used to estimate risks of human exposure [5]. In order to evade the drawbacks with involvement of confounding factors in human studies, we established a systematic approach to researching the dose-dependent effects of single pollutant exposure in animals using a controlled environment. Our current observations in normal adult rats are made from precise ozone measurements in the absence of other confounding factors, such as particle matter (PM) or pre-existing diseased states such as diabetes. Using a controlled single pollutant rat exposure model, we reported chronic O3 inhalation for prolonged duration can cause cardiac dysfunction in otherwise normal adult rats [6, 7]. In another set of rat experiments we showed exposure to chronic levels of O3 enhanced the sensitivity to myocardial ischemic-reperfusion injury (I/R) [8]. These studies confirmed that O3-induced cardiac toxicity is associated with decreased and increased levels of myocardial antioxidant reserve (SOD levels), and inflammation (TNF-α levels) respectively. Interestingly, other laboratories report beneficial effects of acute O3 exposure in the injured myocardium [9, 10]. Collectively, the studies described herein suggest that acute and chronic exposure to O3 may have different effects on myocardial function. We hypothesize that the O3-induced cardiac injury as demonstrated in our studies may be associated with the chronic effects of O3 on organs (“Toxic rain”- due to prolonged exposure) [4]. On the contrary, in studies from other labs, when isolated hearts are exposed to O3, the progressive toxicity of O3 exposure would be absent [9,10] and the O3 associated effects in that case may be acute in nature. Laboratories have shown involvement of lipid raft proteins; caveolin-1 and caveolin-3 on the generation of death and survival signaling in ischemic heart injury through their differential interactions with p38MAPKs [11]. Similarly, in the O3 model of lung injury, an inverse correlation between the caveolin-1 and TNF-content exists [12]. Collectively the results suggest a regulatory role of lipid rafts in inflammation mediated cell injury. Although chronic O3–mediated myocardial dysfunction pre- and post- I/R was shown to be directly dependent on cardiac inflammation with regards to increased TNF-α levels [6-8], involvement of lipid raft proteins in O3–induced and TNF-α mediated cardiac toxicity was never studied. The published results from our laboratory on the regulatory involvement of caveolin-1 and caveolin-3 in the pathogenesis of O3–induced cardiac toxicity are being discussed in this chapter with prior permission from ref 7. For this study the experimental and animal procedures were in compliance with the principles of the American Physiological Society and with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85-23, revised 1996).

4

Rajat Sethi, Shubham Manchanda, Magdalena Ramirez et al.

Figure 1. Chamber used for exposure to filtered air and O3 in a controlled environment.

The work conformed to the IACUC–TAMUK guidelines concerning the care and use of experimental animals. Male SD adult rats were used. Rats were housed in a room maintained at 22 +/- 1 0 C, with a 12:12 hour light: dark cycle, and fed Purina rat chow and tap water ad libitum. The rats in Control Groups-1 and 2 were placed in an environmental chamber and exposed to filtered air (0.0 ppm O3) for 8hr/day for 28 days or 56 days. The Experimental Groups-1 and 2 were placed in the chamber and exposed to 0.8 ppm O3 mixed with air for 8hrs/day for 28 or 56 days. Rats were kept within a common PlexiglasTM environmental chamber supplied with a constant air flow, and subjected to O3 as described previously [6-8] and seen in Figure 1. In summary, rats were habituated by placing them in the environmental chamber for 5 days prior to O3 exposure. O3 was generated by passing filtered air across an ultraviolet light. The concentration of O3 was regulated by adjusting the inlet flow of air to an ozonator, thus controlling the quantity of O3 produced. The O3 concentration was continuously measured using a calibrated UV photometric O3 monitor connected to the outlet line of the chamber. For control exposures, rats were simultaneously kept in a same-sized chamber provided with filtered room air at the same flow rate. During all experimental procedures, animals were monitored closely to insure there was no unusual distress, discomfort, or pain. In order to minimize the involvement of ammonia produced by rat urine and feces, sodium-based ZeolitesTM were used and the rat cages were cleaned on a daily basis. Humidity and temperature values similar to the room conditions were maintained in the chamber for the duration of the experimental protocol. It is possible that animals acclimate to the effects of chronic O3, which could play a role in the outcome. Therefore, the length of time after exposure may have an impact on the results. If the hearts are studied immediately after O3 exposure, then the acute effects of O3 cannot be excluded. Examining the hearts 12-24 hrs after the final O3 exposure would provide a more accurate assessment of the chronic effects. Therefore, in this study, the O3 effects on cardiac function were evaluated after 24 hrs of the final exposure. Thus twenty-four hours after the completion

Linking Molecular Mechanisms to Biomarkers in Cardiac Disease …

5

of O3 exposure, i.e. on the 29th and 57th day of the experiment, cardiac function were assessed in intact rats, and hearts were then extracted for biochemical estimations. The concentration of O3 used was substantially lower than levels used in several previous studies (e.g., 1.0–2.5 ppm), and still higher than both USEPA’s NAAQS (0.075 ppm) and Occupational Health and Safety Administration (OSHA) permissible exposure limit (0.1 ppm) regulatory levels. Rodents are routinely recognized as less susceptible to O3 insult (five to six times) than humans due to obligatory nose breathing and other intrinsic factors. National averages remain around 0.1-0.15 ppm, and even in the highest urban areas readings remain under 0.5ppm. Thus, the employed exposure paradigm represented an approach useful for delineating potential pathobiological sequelae in humans. After the completion of the exposure protocol as described above, the rats were anesthetized with an intraperitoneal injection of a mixture of ketamine (90 mg/kg) and xylazine (10 mg/kg). The animals were assessed hemodynamically with a micro-tipped pressure transducer (model SPR-249, Millar Instruments, Houston, TX). LVDP was calculated as LVSP – LVEDP. After obtaining these parameters hearts were extracted for the biochemical studies. Superoxide dismutase activity in left ventricles from heart tissue was determined from a standard curve of percent inhibition of pyrogallol auto-oxidation using a commercially available SOD with known activity. SOD specific activity was expressed as units/mg protein, where 1 unit of SOD is defined as the amount that shows 50% inhibition of pyrogallol auto-oxidation at room temperature and pH 7.8. For the detection of myocardial TNF- α, caveolin-1, and, caveolin-3 levels rat hearts were washed with PBS. Left ventricular tissue was flash frozen in liquid nitrogen. Frozen tissue (0.5–1.0 g) was homogenized and membrane and cytosolic fractions were collected. Membrane-bound fractions of TNF-α was analyzed by ELISA using a commercially available kit (R and D Systems, Minneapolis, MN). Membrane bound fractions of caveolin-1 and caveolin-3 were analyzed by western blot technique using antibodies to caveolin-1 and caveolin-3 and β-actin. Protein bands were visualized by enhanced chemiluminescence according to the manufacturer's instructions, and band intensities were quantified using a Chemidoc Molecular Imaging from Bio-Rad. Relative levels of protein expression were normalized to β-actin. The difference between control and experimental groups was evaluated statistically using one-way ANOVA, followed by the Newman-Keuls test. Differences were considered significant at P < 0.05. LVDP was significantly decreased in rats exposed to 0.8 ppm O3 for 28 or 56 days compared to rats exposed to filtered air (Figure 2). The 56 day LVDP values in the O3exposed group were significantly less than the LVDP values for the rats exposed to filtered air and the 28 day O3-exposed group. Since LVDP values for 28 and 56 day air exposed groups were not significantly different, only the 56 day air exposure data are shown. As shown previously in hearts from O3 -exposed rats, the decreases in LVDP were associated with previously observed increases in left ventricular end diastolic pressure (LVEDP) and decrease in rate of pressure development (+dP/dt) and rate of pressure decay (-dP/dt) [6]. Myocardial antioxidant reserve was also significantly decreased, as indicated by decreased levels of the antioxidant enzyme SOD in rats which were exposed to 0.8 ppm O3 for 28 or 56 days (Figure 3).

6

Rajat Sethi, Shubham Manchanda, Magdalena Ramirez et al.

From reference 7, with permission. Figure 2. Left ventricular developed pressure (LVDP) in 28 and 56 days of air and O 3 - exposed rats. Since the LVDP values for both the 28 and 56 day air exposed group were not significantly different from each other, only the 56 day air exposed data are shown. Values represent the mean  SEM of 6 animals in each group. LVDP was the difference between LV systolic pressure and LVEDP. Values represent mean  SE from 6 animals in each group as described under materials and methods. Values marked by an asterisk are significantly different from corresponding air exposed group at *P120 below (L) and over (H) target value of 25 days indicate considerably larger O3 burden in highlands than lowlands. Number of daily max 8h>120 exceedances were calculated for each O3 monitoring station individually. Averaged annual and decadal values sorted in increasing order (Figure 7) also show relevant majority of H sites in group of stations with max 8h>120 frequency above level of target value.

Svetlana Bičárová, Hana Pavlendová and Peter Fleischer

44

Table 4. Frequency of exceedance of air quality standards according to Directive 2008/50/EC L H 1 nD max 8h >120 nD max 8h >120 5 6 5 IT AT IT 2 2 total avg mean total avg mean 619 19 181 2 1412 44 145 2000 2001 493 15 124 2 1484 46 122 4 2002 611 19 18 39 1 1324 41 41 44 4 2003 1046 33 22 385 10 2500 78 714 55 4 2004 449 14 22 31 0 1130 35 136 52 4 2005 551 17 21 86 2 1459 46 99 53 4 2006 797 25 19 202 3 1556 49 253 43 4 2007 424 13 18 64 0 1337 42 76 45 4 2008 365 11 17 11 0 931 29 0 40 4 2009 319 10 12 23 0 982 31 2 34 2000-2009 5674 1588 18 1146 20 14115 44 1 nD - number of days with maximal daily 8-hour mean higher than 120 μg m-3 (total – summed all sites, avg – averaged over all sites). 2 averaged over three years. 3 exceeded target value (425 days). for the protection of human health. 5,6 Number of exceedances. 5 IT information threshold 1-hour average O3 concentration >180 μg m-3. 6 AT alert threshold 1-hour average O3 concentration >240 μg m-3. O3 [μg m-3]

1

6

AT

0 0 0 2 0 0 0 0 0 0 2 entire

AOT40 Air Quality Index for Protection of Forest and Vegetation AOT40 index for protection of forest shows relatively high inter-annual variability during study period 2000 - 2009 (Table 5). Main differences are linked to unusual O3 events influenced by extraordinary heat wave weather in 2003, and partially in 2006. Annual AOT40 values for individual monitoring stations varied from 1530 to 48954 ppb h, in ten-year average from 4653 to 36888 ppb h. Increase of AOT40 in relation to type of landform is illustrated in Figure 8. Obtained results also indicate altitudinal growth and latitudinal decrease of AOT40 (Figure 9). Although it should be taken into account that highaltitude monitoring stations are usually located in the region of Central Europe, and the latitudinal dependence is partially covered by the altitudinal dependence. Similar results have been reported in previous studies [100, 101]. The critical level of 5000 ppb h was exceeded in 89 ±7% of assessed values (standard deviation is based on annual mean exceedance). Number of stations that exceeded the critical level during whole study period was 42 of 64 (66%). The exceedance in individual years varied from 80 % (2000, 2007, 2009) to 98 % (2003), and maximum 100% was achieved in 2006. Lower frequency of exceedance was observed in the North Atlantic and Scandinavia region as well as in lowlands of Central Europe in comparison with highland sites. Monitoring stations situated above 500 m a.s.l. recorded exceedance more than 99%. AOT40 for vegetation varied from 477 to 27883 ppb h for individual sites, in ten-year average from 2215 to 21682 ppb h. Inter-annual variability shows substantive differences in years 2003 and 2006 (Table 6).

Vulnerability to Ozone Air Pollution in Different Landforms of Europe

45

Figure 7. Target value for the protection of human health and occurrence of O3 concentrations over maximal daily 8-hour mean higher than 120 g m-3 for L and H sites.

Table 5. Mean annual values of index AOT40 for forest protection ppb h

2000

2001

2002

2003

2004

2005

2006

2007

2008

2009

L H1 H2 H3 H4

11494 15993 24815 37064 39606

10634 16750 27666 35816 38224

12823 15878 23444 32692 35817

17145 25600 36179 41682 46028

10173 14207 23312 25843 31927

10710 15788 25718 27502 35920

14389 18716 28130 35476 37116

9018 14654 22123 31340 35481

9480 13788 20200 26118 28094

8516 12796 20873 29617 30562

2000 2009 11438 16417 25246 32315 35878

Table 6. Mean annual values of index AOT40 for vegetation protection ppb h

2000

2001

2002

2003

2004

2005

2006

2007

2008

2009

L H1 H2 H3 H4

7152 9276 14292 20179 21382

6808 10521 17868 20912 23422

6970 9894 15040 20087 20777

9390 13562 19532 22146 24849

5230 7766 13535 14522 18363

6496 9988 16820 17513 21512

10384 13573 20324 24291 24539

5311 8202 12167 18322 19876

6602 9075 13316 16175 17421

4269 6353 10719 15396 16370

2000 2009 6861 9821 15361 18954 20851

Similarly to AOT40 for forest, also AOT40 for vegetation increased with altitude and decreased with latitude (Figures 10 and 11). The critical level (CL) of AOT40 for protection of vegetation is set to 9000 ppb h expressed as 5-year average (or less in case of insufficient data). The long-term objective (LTO) is set to 3000 ppb h for actual year [90]. When assessing the exceedance in individual years, the value 9000 ppb h was exceeded in 49±11% of assessed values (standard deviation is based on annual mean exceedance). During whole study period, 17 of 64 (27%) monitoring stations exceeded CL and 16 stations did not exceeded CL at all.

46

Svetlana Bičárová, Hana Pavlendová and Peter Fleischer

Figure 8. Changes of decadal (2000-2009) mean of AOT40 for forest protection in relation to landform classes.

Figure 9. Altitudinal and latitudinal dependence of AOT40 for forest protection from selected EMEP monitoring stations.

Table 7. Values of index AOT40 for vegetation protection expressed as 5-year average 2000 2009 L 7152 6980 6976 7580 7110 6979 7694 7362 6805 6612 7125 H1 9276 9899 9897 10813 10204 10346 10957 10618 9721 9438 10117 H2 14292 16080 15733 16683 16053 16559 17050 16476 15232 14669 15883 H3 20179 20546 20393 20831 19569 19036 19712 19359 18165 18339 19613 H4 21382 22402 21860 22607 21759 21785 22008 21828 20342 19944 21592 * values from years 2000 – 2003 are expressed as 1, 2, 3, respectively 4-year average. ppb h

2000* 2001* 2002* 2003*

2004

2005

2006

2007

2008

2009

The inter-annual variability of CL exceedance was high: 31% in 2009, 61% in 2003 and 72% in 2006. However, when assessing the exceedance for a 5-year average (Table 7), the CL was exceeded in 50±2% of all cases. 41 % of monitoring stations exceeded the CL during whole study period; the same number of stations did not exceed the CL in any case.

Vulnerability to Ozone Air Pollution in Different Landforms of Europe

47

Figure 10. Changes of decadal (2000-2009) mean of AOT40 for vegetation protection in relation to landform classes.

Figure 11. Altitudinal and latitudinal dependence of AOT40 for vegetation protection from selected EMEP monitoring stations.

Figure 12. Meteorological and air quality monitoring station in Stará Lesná.

The inter-annual variability of exceedance was lower, the exceedance varied from 47% in 2009 to 53% in 2006 and 2007. Similarly to AOT40 for forest protection, the lowlands and North European monitoring stations reached lower values of AOT40 for vegetation protection than highland and South European monitoring stations.

48

Svetlana Bičárová, Hana Pavlendová and Peter Fleischer

The lowland landform class was the only class with no exceedance of CL during the whole study period. Stations from this type of landform class and some selected stations from H1 landform class (Scandinavian and North Atlantic monitoring stations) have potential to meet the LTO set for vegetation protection [102].

3. ESTIMATION OF PHYTOTOXIC OZONE DOSE (POD) FOR FORESTED AREA OF THE HIGH TATRA MTS., SLOVAKIA Study Area and Measurement The study area Stará Lesná (49 9´N, 20 17´E, elevation 808 m asl.) is situated in the foothills of the High Tatra Mts. near the Slovak-Polish border (Figure 12). It is the background area without industrial sources, surrounded mostly by forests and pastures. The moderately cool climate is characterised by annual means of basic climatic parameters: air temperature 5.9 °C, air humidity 77.5 % and precipitation 736 mm. Dominant soil units is Planosols developed from Fluvi-Glacial sediments. The prevailing texture class of topsoil is sandy-loam. Norway spruce (Picea abies (L.) Karst) is dominant tree species in this area; other prevalent tree species are European larch (Larix decidua Mill.), Scots pine (Pinus sylvestris L.) and Grey alder (Alnus incana (L.) Moench) near streams. After a windstorm in November 2004, almost all mature spruce stands in the vicinity of the study site were destroyed. The subsequent young stands mostly consist of spruce and pioneer species, mainly Silver birch (Betula pendula Roth) and Goat willow (Salix caprea L.); anyway, target species composition is spruce with admixture of larch, pine and aspen. The air quality monitoring station of EMEP is also located in Stará Lesná. Measurement of O3 concentration is provided by Slovak Hydrometeorological Institute (SHMI) that is national participating institute in EMEP project. Continuously operating air monitoring station measures O3 concentration by analyzer Horiba APOA360 and mean hourly O3 are registered in EMEP database under code SK04 (www.emep.int). The experimental workplace of the Geophysical Institute of the Slovak Academy of Sciences (GPI SAS) in Stará Lesná has carried out meteorological observations since 1988. Meteorological parameters such as air temperature (°C), relative humidity of air (%), wind speed (m s-1), wind direction (°), air pressure (Pa), global radiation (W m-2) and precipitation (mm) useful for O3 deposition modelling are available in central measurement data system ESM 200.

Phytotoxic Ozone Dose (POD) PODY is the accumulated value of hourly mean stomatal O3 fluxes exceeding the threshold Y nmol m-2 s-1, during vegetation season. The recent Y value for forest trees is proposed to 1 nmol m-2 s-1. Model DO3SE has been developed to estimate total and stomatal O3 flux on a site-specific basis, according to local meteorological and O3 concentration data. Application version of DO3SE was processed in the Stockholm Environment Institute (SEI) in accordance with UNECE LRTAP methodologies for effects-based risk assessment. The

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model calculation of stomatal flux is based on the assumption that the concentration of O3 at the top of the canopy (cz1 [nmol m-3]) measured in tree height (z1) represents a reasonable estimate of the concentration at upper surface of the laminar layer. Stomatal O3 flux (Fst [nmol m-2 PLA s-1]) is given by [103]: Fst = c(z1) * gsto * (rc / (rb + rc))

(1)

where c(z1) is O3 concentration (nmol m-3) at canopy level at height z1 (m), rb and rc are quasi-laminar resistance and leaf surface resistance (s m-1), gsto is stomatal conductance for O3 (m s-1): gsto = gmax * fphen * flight * max {fmin, (ftemp * fVPD * fSVP)}

(2)

where gmax is the species-specific maximum stomatal conductance (mmol O3 m-2 PLA s-1), PLA is projected leaf area, f(phen, light, min, temp, VPD, SVP) are parameters determined the effect of environment and phenophase on stomatal conductance. PODY is calculated according to equation (3) with accumulation of hourly stomatal O3 flux during whole vegetation season (defined for tree species and year of the assessment). PODY = Σ(1;n) [Fsti - Y] for Fsti >= Y

(3)

where Fsti is hourly mean stomatal O3 flux (nmol m-2 s-1) n is count of hours within accumulation period. The critical level of PODY is proposed to 8 mmol m-2 PLA for spruce (evergreen coniferous) with expected biomass increment reduction 2 %. Version 2.0 of the model DO3SE was used for the calculation of stomatal O3 flux to the spruce forest. The model includes parameterisation for different biomes, agricultural and tree species in different regions of Europe. A subset of site and species parameters can be saved and applied in any project in the future. Since it is a pilot study, local parameterisation has not been done yet. “Real” species parameterisation of Norway spruce for Continental Central Europe has been used as described in Mapping Manual of ICP Modelling and Mapping [104]. In addition, the model calculation of stomatal O3 flux allows calculation of the total O3 deposition to vegetation. As the forest ecosystem is an important sink for gaseous pollutants in general, in this way we are able to quantify the ability of forest to remove O3 from the atmosphere. Detailed description of algorithm and derivation of physical relationships for the final calculation is given in the manual for modelling and mapping of critical level exceedance [104].

PODY in the High Tatras The new concept of critical levels has been recently adopted by LRTAP Convention 2010 as an alternative to exposure indices that take into account effects of environmental parameters on the stomatal uptake of O3 by vegetation. The following paragraphs present parameterisation of DO3SE model and results of PODY estimation for forested area of the High Tatras represented by site Stará Lesná covering decadal period 2000-2009.

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Meteorological Parameters As shown in Figure 13, seasonal courses of main meteorological parameters did not perform substantive interannual differences during years of the study period. Annual mean air temperature reached values from 5.4 to 6.9 °C; average value 6.2 °C for period (2000-2009) slightly exceeded long-term (1988 – 2007) 5.9 °C average. Air temperature during vegetation period (April – September) reached mean values from 11.4 to 13.2 °C with an average value 12.5 °C. Annual precipitation totals varied from 562 to 903 mm with an average value 791 mm. Precipitation totals during vegetation season varied from 409 to 702 mm, 539 mm in average. Years 2003 and 2006 were hot and dry. Annual amount of global solar radiation energy varied from 1066 to 1234 kWh m-2, with average value 1147 kWh m-2. Ozone Concentration Typical seasonal O3 pattern with simple or double maximum during spring and summer was observed for whole study period (Figure 14).

Figure 13. Seasonal courses of selected meteorological parameters. Monthly mean, minimum and maximum of air temperature (°C), monthly sum of hourly values of global solar radiation (kWh m-2), monthly sum of precipitation (mm).

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Figure 14. Monthly mean, minimum and maximum of O 3 concentration.

Mean O3 concentration for vegetation period (36.6 ppb) moderately overcame mean O3 value (32.3 ppb) covering all months of year. Yearly O3 concentrations varied from 27.5 to 37.2 ppb and during vegetation period from 32.2 to 40.9 ppb. High abundance of O3 occurred in 2003 and period of 2005-2008. The diurnal pattern of O3 concentration was similar to typical O3 daily course in lowlands and valley areas of Central Europe [105]. The night and morning minimum was followed by daylight increase to afternoon maximum and decrease from the mid afternoon till late evening. Annual and seasonal (April – September) mean diurnal patterns are shown in Figure 15. While night and morning minimum O3 concentrations were comparable, considerable differences occurred throughout daily hours.

Total and Stomatal Ozone Fluxes The total O3 flux showed typical seasonal variation within study period (Figure 16). The lower winter values were followed by a rapid increase forced mainly by stomatal uptake at the beginning of vegetation period. Maximal O3 fluxes occurred in the first half of vegetation period slowly decreased to minimal level in autumn and winter. Similar seasonal variations were reported in the previous studies [78, 106]. Stomatal O3 fluxes were calculated using the DO3SE model (based on latitude function) only for daylight hours and the accumulation period. The highest values of stomatal O3 flux occurred at the first half of the vegetation period, and then O3 fluxes slowly decreased till the end of vegetation period. Variations in this course were associated with unfavourable climatic conditions, especially by drought. Many authors agreed that though stomatal uptake during night is low, it could have considerable contribution to the total stomatal uptake of O3 [107, 108, 109]. Furthermore, the physiological activity of conifers during winter is more influenced by temperature than phonological stage. Mikkelsen et al. [110] estimated the winter stomatal uptake (November – February) in range 4 – 9% of the total O3 deposition. According the flux model parameterisation of the Mapping Manual of ICP [104], the function of phenology fphen for Central European Norway spruce (evergreen coniferous) should be substituted by the function of temperature ftemp.

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Figure 15. Mean diurnal pattern of O3 concentration covering whole year and vegetation period (April – September).

Figure 16. Average seasonal courses for total downward O3 flux (mmol m-2 day-1) and sunlit leaves stomatal O3 flux (mmol m-2 PLA day-1) during period 2000-2009 (based on daily sum of O3 flux).

The mean diurnal patterns of O3 concentration, leaf stomatal O3 conductance, total and stomatal O3 fluxes, and deposition velocity during accumulation period are presented in Figure 17. Stomatal O3 flux was forced mainly by stomatal conductance with rapid increase in the early morning during O3 minimum. The stomatal conductance decreased during afternoon hours, limited by high values of VPD resulted in decrease of stomatal O3 uptake. Average daily maximum of downward O3 flux reached value -15 nmol m-2 s-1 with peak values about -30 nmol m-2 s-1. During dormancy period, the daily pattern of total O3 flux was not so distinct. These calculated patterns are similar to data presented by [78, 79, 108, 111] and other authors. According to DO3SE model results, the total annual O3 flux into the mature spruce stand in Stará Lesná reached average value 7.58 ±0.56 g m-2. These results are in coincidence with reports of other authors. For example Fares et al. [78] reported value 6.7 g m-2 and Kurpius et al. [112] 6.1 g m-2 (127 mmol m-2) as total annual O3 flux into the Pinus ponderosa forest stand. Mikkelsen et al. [110] quantified annual deposition of 12.6 g m-2 (126 kg ha-1) into the Norway spruce stand in Denmark. On the other hand, the total annual O3 flux into the sub

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alpine forest reported by Zeller et al. [113] was only 2.9 g m-2. As we mentioned, stomatal O3 flux only for upper canopy sun-lit leaves cannot quantify the proportion of stomatal uptake to the total O3 deposition. The stomatal O3 uptake can contribute to the total O3 deposition from 21% [110] to more than 50 % [78, 113].

Phytotoxic Ozone Dose Over a Threshold of 1 Nmol M-2 PLA S-1 - POD1 Model estimations suggest that POD1 for mature spruce forest in Stará Lesná varied around 21.09 ±2.19 mmol m-2 PLA during ten consecutive years 2000-2009.

Figure 17. Diurnal patterns of O3 concentration, O3 fluxes, deposition velocity and stomatal conductance during accumulation period (2000-2009). Vertical bars indicate standard deviation.

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Figure 18. POD1 and AOT40 for mature spruce forest in Stará Lesná, CL- critical levels.

Calculated values partially reflected the values of O3 concentration during vegetation period, except year 2003 when high temperatures and drought during July and August resulted in reduced stomatal O3 fluxes and lower value of POD1. On the other hand, the highest value of POD1 was reached in 2006, in the year with similar climatic conditions during vegetation period. However, the temperature in 2006 was slightly lower than in 2003 and precipitations were evenly distributed. POD1 were compared with values of AOT40 calculated by DO3SE. The resulted AOT40 values slightly differ from those presented in previous part of this chapter because the DO3SE model defines daily hours by level of global solar radiation and vegetation period is derived on base latitude model instead of fixed period April- September. Obtained results show that both POD1 and AOT40 substantially exceeded their CLs during all years of study period (Figure 18); CL of POD1 is 8 mmol.m-2 PLA for protection of Norway spruce and CL of AOT40 is 5 ppm h for protection of forest trees, It was proved [79, 108, 114] that accumulated O3 flux (POD0 or POD1) fitted better to O3 effect on forest trees than the exposure indices such AOT40. Current critical level of POD1 for spruce is based on experiments with young trees up to 15 years. The age criteria is very important and there is strong need for dose-effect research aimed at mature forest trees for the future revision of critical levels [91].

CONCLUSION Ozone air pollution affects human health and the environment. There is evidences that exposure to ambient O3 concentrations causes’ adverse health effects ranged from minor sensory irritation to premature death. In addition, O3 in the ambient air seriously damages a variety of ecosystems including crops, forests and grasslands. These ecosystem impacts have important implications for productivity, biodiversity, and food security. Enhanced ozone formation in the lower atmosphere during the second half of the 20th century was serious motivation for development of new strategy to achieve effective control of emissions produced from road transport and industry. We have found a slight decline in the course of mean annual O3 concentrations observed at different landform areas in Europe during last

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decade period (2000-2009) that suggests partial accomplishment of strategy to reduce primary emission sources. Despite decreasing of anthropogenic emissions of O3 precursors (especially NOx and VOC) within EU since 1990, daily O3 concentrations during spring and summer still remain high. Results presented in this chapter indicate that target value for protection of human health was exceeded predominantly in highland areas situated in a large distance from main emissions sources. Furthermore, SOMO35 and AOT40 indices also suggest that highlands in Europe are more vulnerable to health and environmental risk associated with the long-term O3 exposure. Current emission policies are probably insufficient to substantially reduce O3 levels in Europe because O3 variability in the lower atmosphere is strongly influenced also by climate, meteorology and baseline O3 concentration. Changes of O3 abundance in dependence of type of landforms noticed in this study accent the role of environmental factors. A new type of research enabling integration of experimentation and high-resolution modelling should better resolve local topography, fine variation in land cover and use, and O3-VOC-NOx chemical nonlinearties, which all have effect on the strength of surface O3 responses to emission changes. This chapter includes results of the pilot study assessing O3 critical levels for forests based on new methodical approach. Investigation of total and stomatal O3 fluxes using deposition model DO3SE, showed potentially harmful effect of O3 exposure on forest stands in the High Tatra Mts. in Slovakia.

ACKNOWLEDGMENTS This research was supported by the Grant Agency of the Slovak Republic under the project VEGA No. 2/0097/11 and by the Slovak Research and Development Agency under the contract No. APVV-0608-10. The authors are grateful to the Slovak Hydrometeorological Institute and Ms. Anne Hjellbrekke from EMEP for providing data.

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In: Air Pollution: Sources, Prevention and Health Effects ISBN: 978-1-62417-735-4 Editor: Rajat Sethi © 2013 Nova Science Publishers, Inc.

Chapter 4

GENOTOXICITY OF AIRBORNE PARTICULATE MATTER AS A TOOL TO PREVENT THE EFFECTS OF ENVIRONMENTAL POLLUTION ON HEALTH Vera Maria Ferrão Vargas1,2,* and Andréia Torres Lemos1,2 1

Programa de Pesquisas Ambientais, Fundação Estadual de Proteção Ambiental Henrique Luís Roessler, (FEPAM), Porto Alegre, Rio Grande do Sul, Brazil 2 Programa de Pós-graduação em Ecologia, Universidade Federal do Rio Grande do Sul (UFRGS), Rio Grande do Sul, Brazil

ABSTRACT Release of hazardous compounds into the environment has a significant effect on the integrity of ecosystems and on the quality of life of the population. After these substances are released, they are distributed and interact according to their own characteristics and those of the receiving environment. Concerning chemical dispersion, the atmospheric compartment allows modifying ecosystems all the way back to the original sources and increases the risk of population exposure. Thus, the atmospheric compartment receives different chemicals many of which, or their mixtures, are known genotoxic agents. The atmospheric particulate matter contains many different compounds, and human beings are constantly exposed to mutagenic agents in the air. Epidemiological studies have clearly associated related health problems, especially acute or chronic respiratory and cardiovascular diseases, to exposure to air pollution. This particulate matter can be deposited in different parts of the respiratory tract, depending on its aerodynamic size. The total suspended particles (TSP), with an equivalent aerodynamic diameter of up to 25-50µm, can be filtered in the nose and in the nasopharynx, although part of this material is inhalable. On the other hand, the PM10 particles, of up to 10µm, may reach the upper respiratory tract, while those that are smaller than 2.5µm (PM2.5) may reach the alveolar regions. In this review, comparative data will be presented on the genotoxic *

[email protected].

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Vera Maria Ferrão Vargas and Andréia Torres Lemos effects of these different fractions of atmospheric particulates in an urban-industrial area in the state of Rio Grande do Sul, Brazil, using the Salmonella/ microsome assay. This assay is a short duration bacterial test which has proved efficient to investigate the mutagenic potential and identify the presence of hazardous compounds in atmospheric compartments. The responses obtained indicated a genotoxic effect in all fractions analyzed, and the mutagenic potential tended to be greater in smaller-diameter particles, raising the risk for human exposure. In this study, mutagenesis was detected even in particulates that were below the quality parameters according to Brazilian Law or WHO recommendation, showing the importance of this biomarker in early protection of human health. This assay is widely studied, standardized and internationally applied; therefore it is recommended as a legal environmental parameter.

1. INTRODUCTION Modern society, in its constant quest for economic development and improved quality of life, has caused growing environmental degradation. Human and industrial activities release into the environment a variety of chemicals that are harmful to the ecosystem. It is estimated that, daily, about 100,000 chemicals are used. The production, distribution, use and final disposal of these chemical compounds lead to their almost inevitable presence in the environment. After release, these substances may undergo changes, be transported or remain stable for long periods of time, and are difficult to degrade. Hence, most of these compounds may persist in the environment and/or suffer bioaccumulation, interfering in the flow of energy and nutrients of the biological chain (Holtz, 2000; Tagliari et al., 2004). Anthropogenic impacts on ecosystems were classified by Grantz et al. (2003) as four main groups, namely: 1- physical restructuring, such as changes resulting from land use; 2introduction of exotic species; 3- Excessive use of natural resources; and 4- introduction of toxic substances. If these impacts are not removed or mitigated, they diminish the ecosystem capacity to adapt and also change their structure and normal function. This degradation process may diminish biodiversity, reduce primary and secondary production and diminish the ecosystem’s capacity to recover and return to its original state. Furthermore, there may be more diseases, nutrient cycling may be reduced and the number of exotic and opportunistic species may increase (Rapport and Whitford, 1999). Disturbances caused by the release of toxic substances into the air, soil and water, may have acute and chronic effects (Grantz et al., 2003).

2. ENVIRONMENTAL CONTAMINANTS AND GENOTOXICITY Some of the contaminants present in the environment may impair the structure or function of the DNA molecule, and they are called genotoxic. The lesions produced are corrected by the repair mechanism of the cells themselves; however, unrepaired or erroneously repaired alterations give rise to point and/or chromosomal mutations (Pfeiffer et al., 1996). These substances are generally in the environment at concentrations below the level needed to cause acute effects. However, even at small concentrations, when an organism is exposed to these conditions it may become incapable of maintaining its ecological function (Scott and Sloman, 2004). It is possible that chemical substances that induce mutations affect

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somatic and germ cells, giving them the potential to cause fertility problems and induce cancer (Mortelmans and Zeiger, 2000). Non-specific mutations may accumulate in the genome and potentially persist in the population, sometimes resulting in reduced adaptability and population size (Belfiore and Anderson, 2001). Hence, it is necessary to investigate these genotoxic substances to ensure the integrity of the populations exposed and their biological function in the ecosystem. Among the environmental contaminants that call attention due to their genotoxic potential, are organic and inorganic substances. Outstanding among them are the polycyclic aromatic hydrocarbons belonging to the first group. Despite the known effect of these substances alone, it should be emphasized that the combined action of these chemicals can alter their initial characteristics, resulting in complex mixtures whose effect is often unknown. Polycyclic aromatic hydrocarbons (PAHs) are a group of chemicals composed exclusively of carbon and hydrogen, containing two or more condensed aromatic rings (Barra et al., 2007; Pereira Netto et al., 2000) PAHs are contaminants widely distributed in the environment, and they are emitted when organic matter from natural and from anthropogenic sources burns. The sources of anthropic emissions are burning fossil fuels, oil spills and their byproducts, incineration of wastes and cigarette smoke. The natural sources include burning biomass in forests and volcanic eruptions (Lopes and Andrade, 1996; Manahan, 2003). These substances are found at different levels of concentration in all environmental compartments and in the biota. Their nitrated and oxygenated derivates also occur widely, but generally in environmental concentrations about 100 to 1000 times lower than those of PAHs (Lopes and Andrade, 1996; Pereira-Netto et al., 2000). They are a global problem, because they are transported long distances through the atmosphere and present mutagenic and carcinogenic characteristics (Barra et al., 2007; Meire et al., 2007). When they are present in the atmosphere, PAHs can be in a gaseous phase or associated with particulate matter. The concentration of PAHs in each phase will depend on the volatility and affinity for the surfaces of the atmospheric particles of each compound. The volatility of these compounds depends on their molecular weight, diminishing as weight increases (Pereira Netto et al., 2000). PAHs are considered prioritary pollutants by the United States Environmental Protection Agency (USEPA), and 16 of them are particularly important for environmental monitoring. These compounds present 2 to 6 aromatic rings fused to each other, with a molecular weight varying between 128 and 278g/mol (Meire et al., 2007). Some PAHs are classified by the IARC (International Agency for Research on Cancer) as possible (Group 2B), probable (Group 2A) or carcinogenic (Group 1) to humans. Among the 16 species of PAHs listed as a priority according to USEPA, eight are classified in one of the groups cited above: Acenaphthene, acenaphthylene, anthracene, benzo(a)anthracene (2B), benzo(a)pyrene (1), benzo(b)fluoranthene (2B), benzo(ghi)perylene, benzo(k)fluoranthene (2B), chrysene (2B), dibenzo(a,h)anthracene (2A), phenanthrene, fluoranthene, fluorene, indeno(1,2,3-cd)pyrene (2B), naphthalene (2B) and pyrene.

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3. BIOMONITORING Environmental monitoring of the impacted areas is generally conducted using physicalchemical measures that, due to the complex nature of these samples may not be sufficient to ensure biological safety (Claxton et al., 1998; Fernandez et al., 2005). It is not possible to perform a risk analysis on the effects of each substance that is really in use. Besides, individuals are rarely exposed to a single contaminant, but to a mixture of them, which present toxic properties different from the original constituents. On the other hand, bioassays are a useful tool to detect the effects of a wide variety of chemicals and their interactions, even when there is no detailed information about their identity or physical-chemical properties (Ohe et al., 2004). Biomarkers are biological responses corresponding to the exposure, effect or susceptibility of individuals to the chemicals and/or environmental stressors (Van der Oost et al., 2003). These markers generate functional, physiological or biochemical responses at cellular level or molecular interactions. When measured, they allow detecting whether the environmental contamination is at a sufficient level to cause physiological effects. Biomarkers are considered excellent early indicators of contamination, and are important tools for the adoption of preventive measures against damage caused by environmental pollution. This occurs because effects at higher levels of biological organization are preceded by changes in the biological processes, so that biomarkers can be used as an early warning of late effects (Bayne et al., 1985; Van der Oost et al., 2003). The use of genotoxicity biomarkers is appropriate for environmental risk analysis and several studies relate DNA damages to subsequent molecular, cellular and tissue alterations in organisms (Ohe et al., 2004).

4. SALMONELLA/MICROSOME ASSAY A widely used biomonitoring assay is the Salmonella/microsome Test (Ames Test), which allows identifying both pure substances and complex mixtures that cause genetic damage. This test was specifically developed to detect chemically induced mutagenesis, and became widely used as an initial screening method for the genotoxic potential of new drugs and biocides. It is acknowledged by the scientific community and control agencies (Mortelmans and Zeiger, 2000). It has already been established that there is a high correlation between mutagenic responses measured in the Salmonella assay and carcinogenesis evaluated in rodents, varying from 77% to 90%, depending mainly on the chemical group to which the substance studied belongs (McCann et al., 1975; Mortelmans and Zeiger, 2000; Zeiger, 1998). This assay is based on strains of Salmonella typhimurium containing a specific mutation in the histidine operon that makes them unable to synthetize this amino acid (his -) and grow in its absence in the culture medium. New mutations at these sites may restore the function of the genes, allowing the cells to synthetize histidine. In this way, when sown in a culture medium that does not contain this amino acid, only the cells that revert spontaneously (his +) will form colonies. The values of spontaneous mutations are relatively constant for each strain, but if a mutagenic substance is added to the culture medium, the mutation values may increase significantly (Claxton et al., 1987; Umbuzeiro and Vargas, 2003).

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On the contrary of what occurs in mammals and other vertebrates, bacteria are unable to metabolize substances via cytochrome P450. The primary function of the liver metabolization system is to protect the cell, degrading and detoxifying substances that are strange to the organism. However, some mutagenic compounds (pro-mutagens) are inactive unless they are metabolized to active forms. Therefore, an exogenous system for metabolic activation of mammals is included in the assays. This system, known as S9 mix, is prepared from SpragueDawley rat liver cells that were previously treated with an enzymatic inducer (Aroclor 1254). In this way, it is possible to mimic the metabolism of mammals and analyze the genotoxicity of the metabolites resulting from the compounds tested. The metabolic activation of samples with these enzymes increases the correlation between the mutagenesis observed in this assay and carcinogenesis in mammals (Claxton et al., 1987; Maron and Ames, 1983; Umbuzeiro and Vargas, 2003). This bioassay has proved appropriate for the quick evaluation of availability and action of contaminants from complex environmental matrices. It has been useful to prevent and investigate environmental problems. According to Claxton et al. (2010), the Salmonella assay was essential for the recognition of mutagenic agents in environmental samples, allowing researchers to discover that there are agents with mutagenic activity in a large part of our environment. Currently, this is the most used methodology to evaluate the mutagenicity of complex environmental matrices, and is present in approximately 37% of the total number of studies in soils (White and Claxton, 2004), 41% in sediments (Chen and White, 2004), 37% in air (Claxton and Woodall, 2007) and 50% in water (Ohe et al., 2004). In a recent review, Claxton et al. (2010) analyzed the number of papers published per year using the Ames Test on various types of environmental samples. The authors observed that studies on natural products, water and air comprise most of the current publications, while relatively few articles refer to soil and sediment samples. White and Claxton (2004) ascribed the extensive use of the Salmonella assay in samples of atmospheric particulate matter to characteristics of the methodology, such as (a) the possibility of using small amounts of sample, (b) performing a diagnosis by using different strains and protocols, (c) simplicity and dissemination in many laboratories, (d) speed and low cost compared to other analytic methods.

5. ATMOSPHERIC PARTICULATE MATTER Pollution of the atmospheric compartment has aroused growing interest, since the number of papers reporting its association with adverse effects on the environment and on human health is increasing (Grantz et al., 2003; Vargas, 2003). Air pollutants can be divided into primary ones, which are discharged directly by the sources of emission and secondary, which are formed later by chemical reactions between the primary pollutants and natural atmospheric components. As to the sources of emission, they can be classified as fixed or stationary, producing point loads of pollutants, or mobile, resulting in diffuse loads of pollution (CETESB, 2011; Vieira, 2009). The concentration of pollutants in air is a function of emissions, transport, dispersion and deposition of pollutants, and also of the way in which they react with each other, besides the prevailing meteorological conditions. Some of the important meteorological parameters are:

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temperature, which influences the photochemical reactions that generate secondary pollutants in the atmosphere; precipitation, which acts by removing pollutants from the air; and the direction and velocity of winds which are related to dispersion mechanisms (Vieira, 2009). Severe episodes of pollution have already been related to meteorological conditions unfavorable to pollutant dispersion (Lippmann, 2009). Local topography is another factor that influences this dispersion. Greater dispersion occurs at sites close to the coast, while in areas surrounded by mountains, hills or in urban centers they are more concentrated. Another major factor is the proximity to specific sources of emission, since the levels of atmospheric pollutants can be higher in places such as highways and industrial plants, making it necessary to take special measures of protection for the population that live around these emissions (WHO, 2005). The World Health Organization considers good air quality a basic requirement for the health and well-being of humans (WHO, 2006). Air quality is generally determined by monitoring a restricted group of pollutants, selected due to their greater occurrence, their adverse effects and to the resources available to measure them. The pollutants adopted universally as air quality indicators are: sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), nitrogen oxides (NOx) and particulate matter (PM) (CETESB, 2011; FEPAM, 2011; WHO, 2006). A very complex pollutant, among those listed, is particulate matter (PM). This consists of a mixture of wide variety of organic and inorganic substances, in solid or liquid state, that are in suspension in the atmosphere (WHO, 2005). These particles differ as to size (from 0.001 µm to 100 µm), origin, formation mechanism, chemical composition and behavior in the atmosphere. The main form of classification of these particles refers to their aerodynamic diameter (particle size), which determines the transport patterns, residence in air and effects associated with human health (Englert, 2004; WHO, 2006). Particulate matter is emitted both in natural and in anthropogenic events. The natural sources consist of emissions of volcanic ash, forest fires, resuspension of dust, marine salts and biological materials (e.g. pollens and bacteria), while the anthropogenic ones are characterized by industrial activities, burning fossil fuels, thermoelectric generation, vehicular traffic and burning biomass (Vieira, 2009). The total suspended particles (TSP) include all diameters of particles suspended in the atmosphere, but particles larger than 30-70 µm remain suspended for a short time (Englert, 2004). Thus, there are actually few particles in the atmosphere measuring over 20 μm in diameter except for areas very close to the sources of emissions. For practical purposes, TSP are defined by the Brazilian Association of Technical Standards (Associação Brasileira de Normas Técnicas - ABNT, 1997) as the suspended particulates measuring up to 50 µm collected in samplers that take in large volumes of air. The particulate matter with a diameter of less than 10 µm is the inhalable air fraction, and it is subdivided into: coarse inhalable particles (PM10), with a 2.5 – 10 µm diameter; fine inhalable particles (PM2.5) with a size less than 2.5 µm; and ultrafine particles (UF), less than 0.1 µm. The smaller fractions of particulates are contained in the larger one (Englert, 2004). Sedimentation and precipitation processes remove the larger particles from the atmosphere a few hours after emission, but particles smaller than 2.5 µm may remain in suspension for days, or even a few weeks. Consequently, these particles can be transported long distances, while the coarse suspended particulates are closer to the sources of emission (WHO, 2005).

Genotoxicity of Airborne Particulate Matter as a Tool …

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TSP and PM10 are composed mainly of elements of the earth’s crust, marine salts and biological elements, and are formed especially by mechanical erosion and resuspension processes. On the other hand, the fine (PM2.5) and ultrafine (UF) inhalable particles are constituted primarily of metals and hydrocarbons. Combustion processes and secondary reactions in the atmosphere are the predominant mechanisms forming these particles (De Kok et al., 2006; Squadrito et al., 2001). The inhalable fraction of the atmospheric particulate matter poses a potential risk to human health, due to its capacity to penetrate and deposit in the respiratory airways. Its levels in the environment have been related to the occurrence of acute respiratory infections, chronic pulmonary and cardiovascular diseases, cancer in respiratory system, and rise of population mortality rates (Vargas, 2003). The depth of penetration of the particles in the respiratory system is a function of their aerodynamic size. Particles larger than 10 µm (TSP) are filtered or deposited in the extrathoracic region of the respiratory tract, constituted by nasal and oral tracts, pharynx and larynx. Particle retention in the extrathoracic region is considered the first form of defense against deeper penetration of the PM, but it also makes this region more susceptible to infections, toxic responses and respiratory diseases. Only the particles smaller than 10 µm penetrate the intrathoracic region of the respiratory system, which is divided into the tracheobronchial region and alveolar regions. The PM10 particles are deposited mainly in the tracheobronchial region, while particles