Reviews of Environmental Contamination and Toxicology Volume 190

Reviews of Environmental Contamination and Toxicology VOLUME 190 Reviews of Environmental Contamination and Toxicolog...

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Reviews of Environmental Contamination and Toxicology VOLUME 190

Reviews of Environmental Contamination and Toxicology Continuation of Residue Reviews

Editor

George W. Ware

Associate Editor

David M. Whitacre

Editorial Board Lilia A. Albert, Xalapa, Veracruz, Mexico Pim de Voogt, Amsterdam, The Netherlands · Charles P. Gerba, Tucson, Arizona, USA O. Hutzinger, Bayreuth, Germany · James B. Knaak, Getzville, New York, USA Foster L. Mayer, Las Cruces, New Mexico, USA · D.P. Morgan, Cedar Rapids, Iowa, USA Douglas L. Park, Cabot, Arkansas, USA · Ronald S. Tjeerdema, Davis, California, USA Raymond S.H. Yang, Fort Collins, Colorado, USA Founding Editor Francis A. Gunther

VOLUME 190

Coordinating Board of Editors Dr. George W. Ware, Editor Reviews of Environmental Contamination and Toxicology 5794 E. Camino del Celador Tucson, Arizona 85750, USA (520) 299-3735 (phone and FAX) Dr. Herbert N. Nigg, Editor Bulletin of Environmental Contamination and Toxicology University of Florida 700 Experiment Station Road Lake Alfred, Florida 33850, USA (863) 956-1151; FAX (941) 956-4631 Dr. Daniel R. Doerge, Editor Archives of Environmental Contamination and Toxicology 7719 12th Street Paron, Arkansas 72122, USA (501) 821-1147; FAX (501) 821-1146

Springer New York: 233 Spring Street, New York, NY 10013, USA Heidelberg: Postfach 10 52 80, 69042 Heidelberg, Germany Library of Congress Catalog Card Number 62-18595 ISSN 0179-5953 Printed on acid-free paper. © 2007 Springer Science+Business Media, LLC. All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring St., New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identiﬁed as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. ISBN-10: 0-387-36900-7 ISBN-13: 978-0387-36900-6 springer.com

e-ISBN-10: 0-387-36903-1 e-ISBN-13: 978-0387-36903-7

Foreword

International concern in scientiﬁc, industrial, and governmental communities over traces of xenobiotics in foods and in both abiotic and biotic environments has justiﬁed the present triumvirate of specialized publications in this ﬁeld: comprehensive reviews, rapidly published research papers and progress reports, and archival documentations. These three international publications are integrated and scheduled to provide the coherency essential for nonduplicative and current progress in a ﬁeld as dynamic and complex as environmental contamination and toxicology. This series is reserved exclusively for the diversiﬁed literature on “toxic” chemicals in our food, our feeds, our homes, recreational and working surroundings, our domestic animals, our wildlife and ourselves. Tremendous efforts worldwide have been mobilized to evaluate the nature, presence, magnitude, fate, and toxicology of the chemicals loosed upon the earth. Among the sequelae of this broad new emphasis is an undeniable need for an articulated set of authoritative publications, where one can ﬁnd the latest important world literature produced by these emerging areas of science together with documentation of pertinent ancillary legislation. Research directors and legislative or administrative advisers do not have the time to scan the escalating number of technical publications that may contain articles important to current responsibility. Rather, these individuals need the background provided by detailed reviews and the assurance that the latest information is made available to them, all with minimal literature searching. Similarly, the scientist assigned or attracted to a new problem is required to glean all literature pertinent to the task, to publish new developments or important new experimental details quickly, to inform others of ﬁndings that might alter their own efforts, and eventually to publish all his/her supporting data and conclusions for archival purposes. In the ﬁelds of environmental contamination and toxicology, the sum of these concerns and responsibilities is decisively addressed by the uniform, encompassing, and timely publication format of the Springer triumvirate: Reviews of Environmental Contamination and Toxicology [Vol. 1 through 97 (1962–1986) as Residue Reviews] for detailed review articles concerned with any aspects of chemical contaminants, including pesticides, in the total environment with toxicological considerations and consequences. Bulletin of Environmental Contamination and Toxicology (Vol. 1 in 1966) for rapid publication of short reports of signiﬁcant advances and v

vi

Foreword

discoveries in the ﬁelds of air, soil, water, and food contamination and pollution as well as methodology and other disciplines concerned with the introduction, presence, and effects of toxicants in the total environment. Archives of Environmental Contamination and Toxicology (Vol. 1 in 1973) for important complete articles emphasizing and describing original experimental or theoretical research work pertaining to the scientiﬁc aspects of chemical contaminants in the environment. Manuscripts for Reviews and the Archives are in identical formats and are peer reviewed by scientists in the ﬁeld for adequacy and value; manuscripts for the Bulletin are also reviewed, but are published by photo-offset from camera-ready copy to provide the latest results with minimum delay. The individual editors of these three publications comprise the joint Coordinating Board of Editors with referral within the Board of manuscripts submitted to one publication but deemed by major emphasis or length more suitable for one of the others. Coordinating Board of Editors

Preface

The role of Reviews is to publish detailed scientiﬁc review articles on all aspects of environmental contamination and associated toxicological consequences. Such articles facilitate the often-complex task of accessing and interpreting cogent scientiﬁc data within the conﬁnes of one or more closely related research ﬁelds. In the nearly 50 years since Reviews of Environmental Contamination and Toxicology (formerly Residue Reviews) was ﬁrst published, the number, scope and complexity of environmental pollution incidents have grown unabated. During this entire period, the emphasis has been on publishing articles that address the presence and toxicity of environmental contaminants. New research is published each year on a myriad of environmental pollution issues facing peoples worldwide. This fact, and the routine discovery and reporting of new environmental contamination cases, creates an increasingly important function for Reviews. The staggering volume of scientiﬁc literature demands remedy by which data can be synthesized and made available to readers in an abridged form. Reviews addresses this need and provides detailed reviews worldwide to key scientists and science or policy administrators, whether employed by government, universities or the private sector. There is a panoply of environmental issues and concerns on which many scientists have focused their research in past years. The scope of this list is quite broad, encompassing environmental events globally that affect marine and terrestrial ecosystems; biotic and abiotic environments; impacts on plants, humans and wildlife; and pollutants, both chemical and radioactive; as well as the ravages of environmental disease in virtually all environmental media (soil, water, air). New or enhanced safety and environmental concerns have emerged in the last decade to be added to incidents covered by the media, studied by scientists, and addressed by governmental and private institutions. Among these are events so striking that they are creating a paradigm shift. Two in particular are at the center of ever-increasing media as well as scientiﬁc attention: bioterrorism and global warming. Unfortunately, these very worrisome issues are now super-imposed on the already extensive list of ongoing environmental challenges. The ultimate role of publishing scientiﬁc research is to enhance understanding of the environment in ways that allow the public to be better informed, The term “informed public” as used by Thomas Jefferson in the vii

viii

Preface

age of enlightenment conveyed the thought of soundness and good judgment. In the modern sense, being “well informed” has the narrower meaning of having access to sufﬁcient information. Because the public still gets most of its information on science and technology from TV news and reports, the role for scientists as interpreters and brokers of scientiﬁc information to the public will grow rather than diminish. Environmentalism is the newest global political force, resulting in the emergence of multi-national consortia to control pollution and the evolution of the environmental ethic. Will the new politics of the 21st century involve a consortium of technologists and environmentalists, or a progressive confrontation? These matters are of genuine concern to governmental agencies and legislative bodies around the world. For those who make the decisions about how our planet is managed, there is an ongoing need for continual surveillance and intelligent controls, to avoid endangering the environment, public health, and wildlife. Ensuring safety-in-use of the many chemicals involved in our highly industrialized culture is a dynamic challenge, for the old, established materials are continually being displaced by newly developed molecules more acceptable to federal and state regulatory agencies, public health ofﬁcials, and environmentalists. Reviews publishes synoptic articles designed to treat the presence, fate, and, if possible, the safety of xenobiotics in any segment of the environment. These reviews can either be general or speciﬁc, but properly lie in the domains of analytical chemistry and its methodology, biochemistry, human and animal medicine, legislation, pharmacology, physiology, toxicology and regulation. Certain affairs in food technology concerned speciﬁcally with pesticide and other food-additive problems may also be appropriate. Because manuscripts are published in the order in which they are received in ﬁnal form, it may seem that some important aspects have been neglected at times. However, these apparent omissions are recognized, and pertinent manuscripts are likely in preparation or planned. The ﬁeld is so very large and the interests in it are so varied that the Editor and the Editorial Board earnestly solicit authors and suggestions of underrepresented topics to make this international book series yet more useful and worthwhile. Justiﬁcation for the preparation of any review for this book series is that it deals with some aspect of the many real problems arising from the presence of foreign chemicals in our surroundings. Thus, manuscripts may encompass case studies from any country. Food additives, including pesticides, or their metabolites that may persist into human food and animal feeds are within this scope. Additionally, chemical contamination in any manner of air, water, soil, or plant or animal life is within these objectives and their purview.

Preface

ix

Manuscripts are often contributed by invitation. However, nominations for new topics or topics in areas that are rapidly advancing are welcome. Preliminary communication with the Editor is recommended before volunteered review manuscripts are submitted. Tucson, Arizona

G.W.W.

Table of Contents

Foreword ..................................................................................................... Preface .........................................................................................................

v vii

Dioxin Formation from Waste Incineration............................................ Takayuki Shibamoto, Akio Yasuhara, and Takeo Katami

1

Coca and Poppy Eradication in Colombia: Environmental and Human Health Assessment of Aerially Applied Glyphosate ............... Keith R. Solomon, Arturo Anadón, Gabriel Carrasquilla, Antonio L. Cerdeira, Jon Marshall, and Luz-Helena Sanin

43

Index ............................................................................................................. 127

xi

Rev Environ Contam Toxicol 190:1–41

© Springer 2007

Dioxin Formation from Waste Incineration Takayuki Shibamoto, Akio Yasuhara, and Takeo Katami

Contents I. Introduction .......................................................................................................... II. Sample Incineration to Investigate Dioxin Formation ................................... A. Incinerator Description .................................................................................. B. Temperature, O2, CO, CO2 and HCl Measurement in Exhaust .............. III. Exhaust Gas Collection ..................................................................................... IV. Dioxin Analysis in Exhaust .............................................................................. V. Dioxins Found in Exhaust ................................................................................ A. Newspaper Impregnated with NaCl, KCl, or CaCl2 ................................ B. Newspaper Impregnated with NaCl, FeCl3, MnCl2, and Other Salts ................................................................................................................ C. Plastics Alone and with NaCl ..................................................................... D. Polyvinyl Chloride Alone and with Other Plastics and Newspaper ...... E. Wood and Leaves ......................................................................................... F. Wood Impregnated with Seawater and Various Chlorides .................... G. Miscellaneous Materials .............................................................................. VI. Toxicity Equivalence Quantity in Exhaust from Incinerated Samples ...... VII. Dioxin Formation Mechanisms During Incineration ................................... Summary .............................................................................................................. References ...........................................................................................................

1 3 3 4 12 13 15 15 19 21 22 24 26 27 29 31 34 36

I. Introduction Adverse effects of dioxins—polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and coplanar polychlorinated biphenyls (PCBs)—on human health have been known for many years. In particular, PCDDs and PCDFs have received much attention recently, not only from environmental scientists but also by the public because they are

Communicated by Ronald S. Tjeerdema. T. Shibamoto ( ) Department of Environmental Toxicology, University of California, Davis, CA 95616, U.S.A. A. Yasuhara Environmental Preservation Center, Tokyo University of Science, 12-1 Funagawara-machi, Ichigaya, Shinjuku, Tokyo 162-0826, Japan T. Katami Gifu Prefectural Institute of Health and Environmental Science, 1-1 Naka-Fudogaoka, Kagamigahara, Gifu, 504-0838, Japan

1

2

T. Shibamoto et al.

formed during the incineration of industrial wastes (Coulston and Pocchiari 1983). Consequently, there is a pressing need to ﬁnd the formation mechanisms or reaction pathways of these chlorinated chemicals to reduce their environmental contamination. However, the formation mechanisms of these chlorinated chemicals are not yet completely understood because their reaction mechanisms are extremely complex (Huang and Buekens 1995; Fängmark et al. 1994). One of the major factors inﬂuencing dioxin formation from an incinerator is the presence of chlorides in combustion materials. There are numerous reports on formation of dioxins from chloride-containing materials, such as polyvinyl chloride, on combustion (Giugliano et al. 1989; Carroll 2001; Yasuhara et al. 2001; Katami et al. 2002). Also, dioxin formation has been reported from ﬂammable materials mixed with inorganic chlorides, such as NaCl, on incineration (Yasuhara et al. 2001, 2002, 2003; Luthe et al. 1998; Katami et al. 2000). According to a study using a ﬂuidized-bed furnace, there was a signiﬁcant correlation between the chloride content of combustion materials containing inorganic chlorides or organic chlorides and dioxin formation (Hatanaka et al. 2000). However, trace amounts of dioxin formation were observed from the combustion of nonchloride plastics (Katami et al. 2002). Formation of dioxins from combustion of ﬂammable materials is inevitable because trace amounts of NaCl particles are present in the atmosphere. For example, dioxin formation was observed from a nonchloride plastic, polystyrene, on combustion (Yasuhara et al. 2002). Combustion temperature plays an important role in dioxins formation in an incinerator (Addink and Olie 1995; Stanmore 2004). Appropriate management of combustion conditions, including temperature, is an important factor to reduce dioxin formation during incineration of domestic garbage. According to an experiment done using an experimental-scale furnace, dioxins were formed under 800°C from materials containing inorganic or organic chlorides (Kawabata et al. 2002). However, dioxins were reportedly degraded by 99.9999% at 1,000°C when burned with 1-sec residence time (Nagata 1992). Consequently, the combustion temperatures of an incinerator for domestic garbage have been set above 850°C to prevent the formation of dioxins (PCDDs, PCDFs, and coplanar PCBs) in Germany, France, England, and Japan (Fukunaga 1998). In this review, therefore, the amounts of dioxins formed from various materials with either inorganic chloride or organic chloride combusted under different temperatures in an incinerator are discussed. There have been many reports on investigations of dioxin formation from waste materials combusted in a small-scale electric furnace equipped with quartz tubing. However, this type of incinerator is not consistent with actual furnaces used to incinerate domestic wastes, and, consequently, the results obtained using this small-scale electric furnace are not always comparable to those obtained from an actual incinerator. It is difﬁcult to use a large-scale incinerator for experiments because even preparing combustion

Dioxin Formation

3

samples and changing the ﬁrebricks of the inside walls for each combustion are almost impossible. The small-scale incinerator used for the experiments in the core references of this review did not require tedious sample preparation for combustion experiments. Also, the ﬁrebricks were easily changed on the inside walls of this incinerator for each experiment. Therefore, the data obtained from this incinerator are comparable to those obtained from an actual incinerator.

II. Sample Incineration to Investigate Dioxin Formation There are many reports on dioxin formation from various materials, including newspaper (Katami et al. 2000; Yasuhara et al. 2001), plastics (Katami et al. 2002; Yasuhara et al. 2002, 2005a,b, 2006), wood (Yasuhara et al. 2003; Katami et al. 2004a), and domestic garbage (Katami et al. 2004b), incinerated a under-controlled conditions. A. Incinerator Description A typical incinerator designed to combust various samples reported in the core articles of this review is shown in Fig. 1 (Katami et al. 2002). The combustion chamber was made of ﬁrebrick with a volume of 0.22 m3. The area of the grate was 0.19 m2. The inlet for combustion samples was 0.35 m

Exhaust gases sampling port

Chimney

Inlet for combustion samples Exhaust gases processing device (cyclone)

Fire bricks

Subsidiary burners

Fan

Ash outlet

Air pipe

Fire bricks

Fig. 1. Typical incinerator used to combust various samples reported in core articles of this review.

4

T. Shibamoto et al.

(height) × 0.40 m (width). The incinerator was equipped with two subsidiary combustion burners (Kato Burner, Gifu, Japan), with a heat supply of 30,000 kcal/hr to completely combust samples. Firebricks of the inside walls were changed for each experiment to avoid contamination from previous experiments. Combustion gases were exhausted through a chimney after dust was removed by a cyclone (960 m3/hr) equipped at the outlet of the combustion chamber. Combustion temperatures were measured at the center of the chamber and at the grate. Subsidiary burners were turned on 2 hr before combustion of samples to maintain a constant temperature. Air was supplied through inlets located at the four corners of the chamber. Air ﬂow rate was adjusted with a ﬂow rate control valve. B. Temperature, O2, CO, CO2, and HCl Measurement in Exhaust The combustion chamber and ﬂame temperatures were measured by a LK1,200 thermocouple conductor interfaced to a CT-1310 digital thermometer (Custom, Tokyo, Japan). Pretreatment for water removal from exhaust gas was conducted by a PS-200SCR Scrubber (Horiba, Kyoto, Japan). Continuous measurement of CO, CO2, and O2 in exhaust gas was performed by a Horiba PG-230 Gas Analyzer (Horiba, Kyoto, Japan). HCL concentration was measured by a Yokogawa IC-7000S ion chromatograph (Yokogawa Analytical Systems, Tokyo, Japan) after exhaust gases were purged into water. The chloride content in the combustion samples was measured by a TOX-100 total organic halogen analyzer (Dia Instruments, Chigasaki, Japan). Tables 1–7 show typical combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ions in the exhaust gases from various samples incinerated, along with the Cl content of each sample. These tables present the results reported in 10 articles (refer to each table), in which samples were incinerated in the same equipment (see Fig. 1). Chamber conditions were kept constant and showed no signiﬁcant variations among the 10 experiments. Temperatures ranged from 456° to 919°C and grate temperatures ranged from 539° to 1,076°C. Generally, experiments were conducted at a chamber temperature below 800°C because sufﬁcient dioxin formation could be expected for the investigation (Yasuhara et al. 2003). Chamber and grate temperatures may be inﬂuenced by the nature of the combusting samples. The range of exhaust gas temperatures (408°–667°C) was smaller than temperatures of the chamber and grate. Average O2 concentrations in the exhaust gases were maintained above 10% through all experiments, indicating that the samples were well incinerated. Average CO2 concentrations in the exhaust gases were generally consistent among the samples, ranging from 2.4% to 7.1%, also suggesting that incineration was complete. Average CO concentrations varied signiﬁcantly. The overall proﬁle of CO in the exhaust gases is the higher the temperature the lower the concentration. It is difﬁcult to explain CO formation

Table 1. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incinerated NaCl, KCl, or CaCl2 Impregnated Newspapers. Combustion sample

Chlorine Avg cont chamber (wt%) temp (°C)

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

0.0064

653

—

526

918

17.2

2.4

1,000

ND

3.1

510

—

415

995

16.7

3.4

1,022

23

0.99

578

594

461

225

15.0

4.5

251

44

NaCl-I NP C

1.88

747

698

596

241

7.7

9.9

140

55

NaCl-I NP D

4.08

751

721

612

245

9.2

8.9

25

88

NaCl-I NP E

4.08

791

917

623

230

12.5

6.0

>2.0

83

KCl-I NP

1.25

689

595

455

225

15.3

4.3

271

79

CaCl2-I NP

0.79

653

664

475

232

15.3

4.4

129

65

Yasuhara et al. 2001 Yasuhara et al. 2001 Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2002

Dioxin Formation

Newspaper (NP) alone NaCl-impregnated (I) NP A NaCl-I NP B

References

Conc, concentration; avg, average; temp, temperature; —, not reported; ND, not detected.

5

6 Table 2. Combustion Chamber Conditions and Concentrations Of O2, CO, CO2, and Cl Ion in the Exhaust Gases from Incinerated Newspapers Impregnated with NaCl and Various Inorganic Metal Chlorides. Combustion sample

Chlorine Avg cont chamber (wt%) temp (°C)

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

0.99

578

594

461

225

15.0

4.5

251

44

NaCl/CuCl2-I NP

1.13

662

675

473

240

14.7

4.9

350

200

NaCl/MgCl2-I NP

1.34

689

595

456

222

15.9

4.0

400

120

NaCl/MnCl2-I NP

1.06

710

664

515

217

15.6

4.2

300

240

NaCl/FeCl2-I NP

1.14

659

660

481

206

14.6

5.0

310

170

NaCl/NiCl2-I NP

1.14

705

645

517

218

15.6

4.2

400

250

NaCl/CoCl2-I NP

1.07

664

673

476

226

15.2

4.4

350

120

NaCl-I NP + ﬂy ash

1.36

512

535

—

227

16.3

3.2

550

176

Yasuhara et al. 2002 Yasuhara et al. 2005b Yasuhara et al. 2005b Yasuhara et al. 2005b Yasuhara et al. 2005b Yasuhara et al. 2005b Yasuhara et al. 2005b Yasuhara et al. 2005c

T. Shibamoto et al.

NaCl-I NP B

References

Table 3. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incinerated Plastics and Plastics + NaCl. Chlorine Avg cont chamber (wt%) temp (°C)

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Polyethylene (PE)

<0.0005

656

799

533

Polystyrene (PS)

<0.0005

738

749

PS foam

0.025

668

Polyethylene tetraphthalate (PET) PE + NaCl

ND

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

231

14.5

4.6

77

4

514

263

13.9

5.5

130

2

951

513

274

15.2

4.0

30.9

656

769

550

240

13.7

5.2

14

5

3.14

759

722

502

279

14.2

4.8

118

41

PS + NaCl

2.38

803

810

570

265

13.3

6.0

150

60

PET + NaCl

2.80

672

932

589

232

13.3

5.5

NaCl-I NP + PE

—

473

—

434

1,020

17.2

3.2

3.0 990

—

38 59

References Katami et al. 2002 Katami et al. 2002 Yasuhara et al. 2005a Katami et al. 2002

Dioxin Formation

Combustion sample

Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2002 Yasuhara et al. 2001

7

8 Table 4. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incinerated PVC and PVC with Other Plastics (PE, PS, and PET) and Newspaper. Avg chamber temp (°C)

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

PE + polyvinylchloride (PVC) PS + PVC

4.58

747

771

576

255

12.7

5.8

41

420

4.58

677

731

570

242

14.2

4.7

40

170

PET + PVC

4.63

689

891

600

230

13.4

5.5

2

92

Avg O2 Avg CO2 conc (%) conc (%)

Avg CO conc (ppm)

Cl ion conc (mg/m3 N)

PVC in low CO conc

51.3

633

900

542

298

13.6

5.2

42

1,600

PVC in in high CO conc PVC-I NP

51.3

531

742

448

267

16.5

3.2

880

1,800

699

637

—

220

14.5

4.2

280

470

NP + PVC

35.7

456

—

416

967

17.4

3.0

1,500

640

4.38

NaHCO3-I NP

0.02

741

638

—

231

13.3

5.5

49

NaHCO3/PVC-I NP

4.51

726

619

—

220

15.2

5.3

310

3.5 560

References Katami et al. 2002 Katami et al. 2002 Katami et al. 2002 Katami et al. 2002 Katami et al. 2002 Yasuhara et al. 2005c Yasuhara et al. 2001 Yasuhara et al. 2005c Yasuhara et al. 2005c

T. Shibamoto et al.

Chlorine cont (wt%)

Combustion sample

Table 5. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incineration of Various Kinds of Wood and Leaves. Combustion sample

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

—

456

—

435

907

16.5

3.7

1,090

ND

<0.01

702

647

525

204

15.5

4.4

77

1.2

<0.01

563

597

472

228

15.7

4.0

310

3.2

Japanese cedar wood (CW) Beech wood

0.02

537

544

444

240

15.9

3.9

730

6.5

<0.01

917

969

667

242

10.9

7.1

<5.0

2.9

Leaves from cherry tree Leaves from konara oak tree

0.0074

746

705

408

219

15.4

4.2

240

15

0.023

692

635

513

237

16.0

5.5

270

15

References Yasuhara et al. 2001 Yasuhara et al. 2002 Yasuhara et al. 2003 Yasuhara et al. 2003 Yasuhara et al. 2003 Katami et al. 2004a Katami et al. 2004a

Dioxin Formation

London plane tree branches Bleached kraft pulp (BKP) Pine wood (PW)

Chlorine Avg cont chamber (wt%) temp (°C)

9

10 Table 6. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incineration of Various Kinds of Wood Impregnated with Seawater, Chlordane, or Pentachlorophenol. Combustion sample

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

4.25

684

594

504

209

16.2

3.8

159

46

Sea water (SW)-I PW 1.8

536

514

491

218

15.9

3.7

670

120

SW-I CW with bark

1.3

575

558

469

249

16.0

3.8

560

92

SW-I CW without bark Chlordane-I waste wood Pentachlorophenol-I waste wood

0.73

567

576

477

220

16.0

3.7

330

34

0.02

805

866

615

237

12.7

6.0

5.6

4.0

0.34

842

901

614

226

12.2

6.4

5.0

20

References Yasuhara et al. 2002 Yasuhara et al. 2003 Yasuhara et al. 2003 Yasuhara et al. 2003 Yasuhara et al. 2003 Yasuhara et al. 2003

T. Shibamoto et al.

NaCl-I BKP

Chlorine Avg cont chamber (wt%) temp (°C)

Table 7. Combustion Chamber Conditions and Concentrations of O2, CO, CO2, and Cl Ion in Exhaust Gases from Incineration of Miscellaneous Samples. Combustion sample

Avg grate temp (°C)

Avg exhaust gas temp (°C)

Avg amount dry exhaust gas (m3/hr)

Avg O2 conc (%)

Avg CO2 conc (%)

Avg CO Cl ion conc conc (ppm) (mg/m3 N)

0.036

857

1,076

617

231

10.8

7.1

7.4

0.027

760

754

—

223

13.0

5.9

<5

0.3

0.01

682

721

—

227

14.8

4.5

140

8.0

0.0064

709

726

504

265

13.5

5.9

4.59

674

697

570

241

15.4

4.4

103

1,400

Food sample A

0.99

652

753

478

247

14.1

5.5

18

65

Food sample B

1.22

696

756

527

245

13.9

5.2

22

65

PVC-coated electric wire PVC-removed electric wire

10.6

787

1,029

646

214

12.2

5.9

12

480

17.1

763

1,010

639

223

12.6

5.8

13

490

15.2

—

75

References Yasuhara et al. 2005a Yasuhara et al. 2005c Yasuhara et al. 2005c Yasuhara et al. 2006 Yasuhara et al. 2006 Katami et al. 2004b Katami et al. 2004b Yasuhara et al. 2005b Yasuhara et al. 2005b

Dioxin Formation

Plastic cover for air conditioner Cardboard for packaging Lightweight coated papers No printing (NP)-NP NP-NP + PVC

Chlorine Avg cont chamber (wt%) temp (°C)

11

12

T. Shibamoto et al.

according to the combustion conditions because it may depend signiﬁcantly on the nature of the samples. However, it is possible to adjust CO concentrations with chamber and grate temperatures so long as the same materials are incinerated. For example, the CO concentration of PVC samples was adjusted to a high level (880 ppm) and a low level (42 ppm) to investigate the formation difference of dioxins (Katami et al. 2002). Cl ion concentrations were somewhat proportional to the chloride content of the samples. When polyethylene (PE, chloride content = <0.0005%) was incinerated, Cl ion concentration in the exhaust gas was 4 mg/m3N, in contrast to 41 mg/m3N in the exhaust gas from the combustion of PE + NaCl (chloride content = 3.14%) (Katami et al. 2002). It should be noted that the Cl ion concentration tends to vary over the quantity samples incinerated/hr. Therefore, the factor inﬂuencing Cl ion concentration in an exhaust gas is not only the chloride content in the samples.

III. Exhaust Gas Collection Exhaust gases were collected at the sampling port located between the combustion chamber and the cyclone (see Fig. 1). The apparatus used for the collection of exhaust gases from the incinerator is shown in Fig. 2. Dust in the exhaust gas was removed with an in-line silica-ﬁber thimble ﬁlter. Exhaust gases were next drawn into two 1-L impingers, each containing 150 mL water (washed with hexane before use) and an empty impinger connected in series. The empty impinger was further connected to a column packed with 40 g XAD-2 resin that was interfaced to a 1-L impinger containing 250 mL diethylene glycol and an empty impinger connected in series. The impingers were kept at 5°C during sample collections in an ice-cooled water bath. Exhaust gas was drawn using a diaphragm vacuum pump with a ﬂow rate of 21–23 L/min, which was the same as that of exhaust gas in the duct. Dioxin standards (0.5 ng each),13C12-1,2,3,4-T4CDD, 13C12-1,2,3,4,7,8H6CDF, and 1,2,3,4,7,8,9-H7CDF, were added here to the ﬁrst impinger for sampling-spike recovery tests before sampling. XAD-resin

Silica-fiber thimble filter

Diaphragm Vacuum pump

Exhaust gas from incinerator

Ice-cooled water

Diethylene glycole

Hexane-washed water

Fig. 2. Apparatus used for collection of incinerator exhaust gases.

Dioxin Formation

13

After sampling, the dioxin standards, 13C12-2,3,7,8-T4-CDD, 1,2,3,7,8P5CDD, 1,2,3,6,7,8-H6CDD, 1,2,3,4,6,7,8-H7CDD, 1,2,3,4,6,7,8,9-O8CDD, 13 C12-2,3,7,8-T4CDF, 1,2,3,7,8-P5CDF, 1,2,3,4,7,8-H6CDF, 1,2,3,4,6,7,8H7CDF, 1,2,3,4,6,7,8,9-O8CDF, 13C12-3,3′,3,4′-T4CB, 3,4,4′,5T4CB, 3,3′,4,4′,5P5CB, 2′,3,4,4′,5-P5CB, 3,3′,4,4′,5,5′-H6CB, 2,3′,4,4′,5,5′-H6CB, and 2,3,3′, 4,4′,5,5′-H7CB, were spiked (0.5 ng each) at this point in the dust in the silica-ﬁber thimble ﬁlter and the diethylene glycol solution in the impinger for extraction and cleanup recovery tests. The dust trapped in the silica-ﬁber thimble ﬁlter (∼1 g) was washed with 20 mL HCL solution (2 mol/L) and combined with the XAD-2 resin after drying. The resin was then extracted with 200 mL toluene using a Soxhlet extractor for 16 hr. The HCL solution from the dust was triple extracted with 10-mL portions of dichloromethane. The water and diethylene glycol (250 mL) in the impingers, as well as the water trapped (trace) in the empty impingers, were combined and triple extracted with dichloromethane (1/10 volume of aqueous solution). After all extracts were combined, the extract was condensed by distillation using a rotary ﬂash evaporator, and the combined samples were cleaned with multilayer silicagel chromatography (JMHW 1997). The sample was further cleaned with a 120-mL hexane/dichloromethane (1/1) solution using alumina column chromatography. After an extract from each sample was condensed using a rotary ﬂash evaporator, 0.5 ng each of internal dioxin standard (13C12-1,3,6,8-T4CDD and 1,2,3,7,8,9-H6CDD) was added for quantitative analysis of dioxins by GC/MS. The volume of the sample was adjusted to exactly 50 mL with n-nonane. The samples were subsequently analyzed by GC/MS for dioxins.

IV. Dioxin Analysis in Exhaust A typical and representative method for dioxin analysis was previously reported (Katami et al. 2004b). An Agilent model 5,890 gas chromatograph (GC) interfaced to a Micromass double focus MS (Auto Spec; ULTIMA, Manchester, England) was used for determination of PCDDs, PCDFs, and coplanar PCBs. Gas chromatographic columns were a 60 m × 0.32 mm i.d. (df = 0.2 µm) SP-2331 bonded-phase fused-silica capillary column (Supelco, Bellefonte, PA, USA) for Cl1–Cl6-PCDDs and Cl1–Cl6–PCDFs; a 30 m × 0.25 mm i.d. (df = 0.25 µm) DB-5 bonded-phase fused-silica capillary column (J & W Scientiﬁc, Folsom, CA, USA) for Cl7,8-PCDDs and Cl7,8–PCDFs; or a 60 m × 0.32 mm i.d. (df = 0.25 µm) DB-5 bonded-phase fused-silica capillary column (J & W Scientiﬁc) for coplanar PCBs. Gas chromatographic oven temperatures were programmed from 130° to 190°C at 20°C/min and then to 250°C at 2°C/min for the SP-2331 column; programmed from 130° to 280°C at 10°C/min for the 30 m-DB-5 column; and programmed from 150°C (held for 1 min) to 185°C at 20°C/min and then programmed at 2° to 245°C (held for 3 min), and at 6° to 290°C (held for 10 min) for a 60 m-DB-5 column. The linear velocity of the helium carrier gas was 30 cm/sec. The

14

Table 8. Recovery Efﬁciencies of Standard Dioxins. Cleanup-spike Dioxins

Recovery (%)

Dioxins

Recovery (%)

81 ± 12.8 89 ± 12.4 87 ± 10.8 85 ± 10.8 79 ± 5.3 80 ± 12.0 89 ± 10.9 88 ± 8.5 79 ± 8.5 77 ± 4.5 79 ± 16.8 80 ± 16.2 79 ± 12.7 82 ± 5.3 89 ± 13.5 82 ± 6.1 93 ± 9.5

13 C -1, 2, 3, 4-T4CDD 13 12 C -1, 2, 3, 4, 7, 8-H6CDD 13 12 C12-1, 2, 3, 4, 6, 7, 8-H7CDF

88 ± 13.2 87 ± 8.3 94 ± 13.1

T. Shibamoto et al.

13 C -2, 3, 7, 8-T4CDD 13 12 C12-1, 2, 3, 7, 8-P5CDD 13 C -1, 2, 3, 6, 7, 8-H6CDD 13 12 C -1, 2, 3, 4, 6, 7, 8-H7CDD 13 12 C -1, 2, 3, 4, 6, 7, 8, 9-O8CDD 13 12 C -2, 3, 7, 8-T4CDF 13 12 C -1, 2, 3, 7, 8-P5CDF 13 12 C12-1, 2, 3, 4, 7, 8-H6CDF 13 C -1, 2, 3, 4, 7, 8, 9-H7CDF 13 12 C -1, 2, 3, 4, 6, 7, 8, 9-O8CDF 13 12 C -3, 3′4, 4′-T4CB 13 12 C12-3, 4, 4′, 5-T4CB 13 C -3, 3′, 4, 4′, 5-P5CB 13 12 C -2′, 3, 4, 4′, 5-P5CB 13 12 C -3, 3′, 4, 4′, 5, 5′-H6CB 13 12 C -2, 3′, 4, 4′, 5, 5′-H6CB 13 12 C12-2, 3, 3′, 4, 4′, 5, 5′-H7CB

Sampling-spike

Dioxin Formation

15

injector temperatures were 250°C for the SP-2331 column and 280°C for the DB-5 columns. MS ion source temperatures were 250°C for the SP-2331 column and 289°C for the DB-5 column. MS ionization voltage was 35 eV. A 60-m SP-2331 bonded-phase column has been used most widely to analyze speciﬁc dioxin isomers in various samples, such as papermill wastewater (Tiernan et al. 1989), soft-shell clam (Brown et al. 1994), sediments (Tong et al. 1990), exhaust gases from car (Bingham et al. 1989), and exhaust gases from an incinerator (Oehme and Kirschmer 1984; Katami et al. 2004b). A 30-m DB-5 bonded-phase column is also commonly used for determination of total dioxins and/or separation of PCDDs and PCDFs (Marquis et al. 1995; Wiliams and Giesy 1995; Kleopfer et al. 1989). For example, a 30-m DB-5 was used for the primary analysis of ﬁsh samples, and then a 60-m SP2331 was used to verify results (Marquis et al. 1994). One of the most widely used GC/MS quantitation methods for dioxins in different kinds of samples is the use of labeled internal standards, 13C12PCDDs/Fs and 13C12-coplanar PCBs. For example, in the case of 2,3,7,8T4CDD, its concentration is determined by comparing the ratio of the m/z at 322 from unlabeled 2,3,7,8-T4CDD and m/z 334 from labeled 2,3,7,8T4CDD to the calibration curve, which is established using the standard solutions (Rappe and Buser 1980). Typical recovery efﬁciencies of typical standard 13C12-dioxins with sampling spike and cleanup spike are shown in Table 8. Values are mean ± standard deviation (n = 11). The recoveries in both the sampling spike and the cleanup spike were satisfactory values greater than 77% (Yasuhara et al. 2002).

V. Dioxins Found in Exhaust The term dioxins is commonly used to describe a class of chlorinated aromatic hydrocarbons, including PCDDs, PCDFs, and coplanar PCBs. The general structures of the 75 PCDDs, 135 PCDFs, and 209 PCBs are shown in Fig. 3. Table 9 shows the dioxins measured in exhaust gases from an incinerator. They are mono- (M1CDD), di- (D2CDD), tri- (T3CDD), tetra- (T4CDD), penta- (P5CDD), hexa- (H6CDD), hepta- (H7CDD), and octa-chlorodibenzo-p-dioxin (O8CDD); mono- (M1CDF), di- (D2CDF), tri- (T3CDF), tetra- (T4CDF), penta- (P5CDF), hexa- (H6CDF), hepta(H7CDF), and octa-chlorodibenzofuran (O8CDF); and tetra- (T4CB), penta(P5CB), hexa- (H6CB), and hepta-chloro-coplanar biphenyl (H7CB). The most biologically active PCB congeners are 3,4,4′,5-tetra-, 3,3′,4,4′-tetra-, 3,3′,4,4′,5-penta-, and 3,3′,4,4′,5,5′-hexachlorobiphenyl, and their toxicities have been widely reported (Safe et al. 1985). A. Newspaper Impregnated with NaCl, KCl, or CaCl2 Old newspapers comprise the largest part of domestic wastes. They have been collected separately from other domestic garbage together with other

16

T. Shibamoto et al. O A

Clx

Cly O X = 0~4, Y = 0~4, X + Y >1

B

Clx

Cly O X = 0~4, Y = 0~4, X + Y >1

C

Clx

Cly X = 0~5, Y = 0~5, X + Y >1

Fig. 3. General structures of (A) 75 polychlorinated dibenzo-p-dioxins (PCDDs), (B) 135 polychlorinated dibenzo furans (PCDFs), and (C) 209 polychlorinated biphenyls (PCBs).

sorts of paper for the purpose of recycling. However, they are eventually burned in an incinerator. The chlorine content of the newspapers combusted in the experiments was 0.0064%. Metal contents in the newspapers used in the present study were 0.33 µg/g Cr, 2.7 µg/g Mn, 33 µg/g Fe, 0.23 µg/g Ni, 8.6 µg/g Cu, 2.3 µg/g Zn, 0.01 µg/g Cd, and 0.75 µg/g Pd; As (arsenic) was not detected. The calculated amounts of Cu and Fe present in the incinerator during combustion of 50 kg newspapers were 0.43 g and 1.65 g, respectively, suggesting that the low concentrations of these metals did not signiﬁcantly contribute to dioxin formation. Figure 4 shows the results of dioxin analysis in the exhaust gases from the combustion of newspapers impregnated with NaCl, KCl, or CaCl2 in an incinerator. The ﬁgure was constructed with the results from two articles (Yasuhara et al. 2001, 2002). The notation “×10” indicates that the actual values are 10 times the values shown in the ﬁgure. Table 1 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases along with chlorine content of the samples shown in Fig. 4. When NaCl-I NP with different chlorine contents—B (0.99%), C (1.88%), and D (4.08%)—were combusted under similar chamber and grate temperatures, the higher the chlorine content, the higher the amounts of dioxins that were formed. The decreasing order of total dioxins formed from these samples was D (174 ng/g) > C (121 ng/g) > B (49 ng/g). NaCl-I NP E contained exactly the same amount of as NaCl-I NP D, but it was combusted at a higher temperature (791°C) than NaCl-I NP (751°C).

Dioxin Formation

17

Table 9. Dioxin Congeners Determined in Exhaust Gases from Incineration of Various Samples. M1CDD 21D2CDD 1, 32, 32, 72, 81, 41, 71, 81, 61, 21, 9T3CDD 1, 3, 71, 3, 81, 3, 61, 2, 41, 3, 91, 2, 31, 7.81, 2, 71, 2, 81, 4, 61, 2, 92, 3, 71, 4, 7T4CDD 1, 3, 6, 81, 3, 7, 91, 3, 7, 81, 3, 6, 91, 2, 4, 81, 2, 6, 81, 4, 7, 82, 3, 7, 81, 2, 3, 71, 2, 3, 41, 2, 4, 91, 2, 4, 61, 2, 3, 81, 2, 3, 61, 2, 7, 91, 4, 6, 91, 2, 7, 81, 2, 3, 91, 2, 6, 91, 2, 6, 7-

1, 2, 8, 91, 2, 8, 9P5CDD 1, 2, 4, 6, 81, 2, 4, 7, 91, 2, 3, 6, 81, 2, 4, 7, 81, 2, 3, 7, 91, 2, 4, 6, 91, 2, 3, 4, 71, 2, 3, 7, 81, 2, 3, 6, 91, 2, 4, 6, 71, 2, 4, 8, 91, 2, 3, 4, 61, 2, 3, 6, 71, 2, 3, 8, 9H6CDD 1, 2, 3, 4, 6, 81, 2, 4, 6, 7, 91, 2, 4, 6, 8, 91, 2, 3, 6, 7, 91, 2, 3, 6, 8, 91, 2, 3, 4, 7, 81, 2, 3, 6, 7, 81, 2, 3, 4, 6, 91, 2, 3, 7, 8, 91, 2, 3, 4, 6, 7H7CDD 1, 2, 3, 4, 6, 7, 91, 2, 3, 4, 6, 7, 8O8CDD 1, 2, 3, 4, 6, 7, 8, 9-

M1CDF 1234D2CDF 1, 31, 71, 41, 81, 61, 2-

2, 43, 72, 72, 33, 62, 82, 61, 93, 44, 6T3CDF 1, 3, 71, 3, 81, 3, 61, 3, 41, 6, 81, 2, 41, 4, 71, 6, 71, 7, 81, 4, 81, 2, 31, 4, 61, 2, 72, 4, 71, 2, 81, 2, 62, 4, 82, 4, 62, 3, 71, 4, 92, 3, 42, 3, 83, 4, 72, 6, 71, 2, 93.4, 6T4CDF 1, 3, 6, 81, 3, 7, 81, 3, 7, 91, 3, 4, 71, 4, 6, 81, 2, 4, 71, 3, 6, 71, 3, 4, 81, 3, 4, 61, 2, 4, 81, 2, 4, 61, 2, 6, 8-

1, 4, 7, 81, 3, 6, 91, 2, 3, 71, 6, 7, 81, 2, 3, 42, 4, 6, 81, 2, 3, 81, 4, 6, 71, 2, 3, 61, 3, 4, 91, 2, 7, 81, 2, 6, 71, 2, 7, 91, 4, 6, 91, 2, 4, 92, 3, 6, 82, 4, 6, 71, 2, 3, 92, 3, 4, 71, 2, 6, 92, 3, 7, 82, 3, 4, 82, 3, 4, 62, 3, 6, 73, 4, 6, 71, 2, 8, 9P5CDF 1, 3, 4, 6, 81, 2, 4, 6, 81, 3, 6, 7, 81, 3, 4, 7, 91, 2, 3, 6, 81, 3, 4, 7, 81, 2, 4, 7, 81, 2, 4, 7, 91, 3, 4, 6, 71, 2, 4, 6, 71, 4, 6, 7, 81, 2, 3, 4, 71, 3, 4, 6, 91, 2, 3, 4, 81, 2, 3, 7, 81, 2, 3, 4, 61, 2, 3, 7, 91, 2, 3, 6, 71, 2, 4, 6, 91, 2, 6, 7, 81, 2, 6, 7, 91, 2, 3, 6, 92, 3, 4, 6, 81, 2, 3, 4, 9-

1, 2, 4, 8, 92, 3, 4, 7, 81, 2, 3, 8, 92, 3, 4, 6, 7H6CDF 1, 2, 3, 4, 6, 81, 3, 4, 6, 7, 81, 3, 4, 6, 7, 91, 2, 4, 6, 7, 81, 2, 4, 6, 7, 91, 2, 3, 4, 7, 81, 2, 3, 4, 7, 91, 2, 3, 6, 7, 81, 2, 4, 6, 8, 91, 2, 3, 4, 6, 71, 2, 3, 6, 7, 91, 2, 3, 4, 6, 91, 2, 3, 6, 8, 91, 2, 3, 7, 8, 91, 2, 3, 4, 8, 92, 3, 4, 6, 7, 8H7CDF 1, 2, 3, 4, 6, 7, 81, 2, 3, 4, 6, 7, 91, 2, 3, 4, 6, 8, 91, 2, 3, 4, 7, 8, 9O8CDF 1, 2, 3, 4, 6, 7, 8, 9-

T4CB 3, 4, 4′, 53, 3′, 4, 4′P5CB 3, 3′, 4, 4′, 52′, 3, 4, 4′, 52, 3′, 4, 4′, 52, 3, 3′, 4, 4′2, 3, 4, 4′, 5H6CB 3, 3′, 4, 2, 3′, 4, 2, 3, 3′, 2, 3, 3′,

4′, 5, 4′, 5, 4, 4′, 4, 4′,

5′5′55′-

H7CB 2, 3, 3′, 4, 4′, 5, 5′

18

T. Shibamoto et al.

Newspaper (NP) alone 8

NaCl-impregnated (I) NP A

7

PCDDs

NaCl-I NP B

6

NaCl-I NP C

PCDFs Coplanar PCBs

X 10

5

X 10

NaCl-I NP D 4

NaCl-I NP E

3

CaCl2-I NP 2

KCl-I NP 1

0

10

20

30

40

50

60

70

80

Amount of dioxins formed (ng/g)

Fig. 4. Dioxin analysis of exhaust gases from combustion of newspapers impregnated with NaCl, KCl, or CaCl2.

Consequently, NaCl-I NP E produced much less dioxins (2.68 ng/g) than NaCl-I NP D did (174 ng/g), suggesting that dioxin formation could be minimized by appropriate combustion conditions, even when the samples have a high chlorine content. NaCl-I NP A (chlorine content = 3.1%) was combusted in a different experiment from the other three samples (B, C, and D). Therefore, it is difﬁcult to compare its results to those of others, but the total amount of dioxins formed was within the comparable range (103 ng/g). The other research group also reported dioxin formation from NP alone (21.6 pg/g) and NaCl-I NP (51.9 pg/g) upon combustion (Katsumata et al. 2003). Dioxin formation from alkaline metal chlorides-I NP, in which chlorine contents were similar to each other, was 18.6 ng/g from CaCl2-I NP, 28.6 ng/g from KCl, and 49.0 ng/g from NaCl. These formation differences may be due to the bond energy differences between the metal and the Cl atom (455 kj/mol for CaCl2, 422 kj/mol for KCl, and 407 kj/mol for NaCl). The lesser the bond energy, the easier it is to release the Cl ion, and consequently more dioxins are produced. Formation of total PCDFs was much higher than that of PCDDs in all eight samples. The total PCDFs composed 78%–92% of the total dioxin formed. Coplanar PCBs were found at the lowest level among the dioxins formed. Their formation levels ranged from 0 (NP alone) to 3.32 ng/g (NaCl-I NP B).

Dioxin Formation

19

B. Newspaper Impregnated with NaCl, FeCl3, MnCl2, and Other Salts Dioxin formation in the presence of metals, such as Cu and Fe, at low temperatures (200°–500°C) has been reported (Tuppurainen et al. 1998). For example, it was hypothesized that the de novo synthesis at 300°C from particulate carbon proceeds through a direct ligand transfer of the halide, in which metal ions (Cu, Fe) are involved (Stieglitz et al. 2003). However, there are only a few reports on dioxin formation in a combustion chamber of incinerators in the presence of metals at high temperatures (>500°C), and knowledge of the formation mechanisms of dioxins in high-temperature processes is still considerably limited. More experiments and theoretical studies to elucidate the details of dioxin formation during combustion are a pressing need. Figure 5 shows the results of dioxin analysis of the exhaust gases from the combustion of newspapers impregnated with NaCl and various inorganic metal chlorides in an incinerator. This ﬁgure was constructed with the results from one article (Yasuhara et al. 2005b). The “×10” indicates that the actual values are 10 times the values shown in the ﬁgure. Table 2 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content, of the samples shown in Fig. 5. Newspaper (approximately 5 g) was soaked in a solution containing NaCl and each different metal chloride for 20 min and then dried in an oven at 110°C (Yasuhara et al. 2005b).

NaCl-impregnated (I) NP B

X 10 7

X 10

FeCl3/NaCl-I NP 6

PCDDs

X 10

MnCl2 /NaCl -I NP

PCDFs Coplanar PCBs

5

X 10

MgCl2 /NaCl -I NP 4

X 10

CuCl2 /NaCl -I NP

3

NiCl2 /NaCl -I NP CoCl2 /NaCl -I NP

X 10 2

X 10

1

X 10

NaCl-I NP + fly ash

X 10

0

1

2

3

4

5

6

7

8

9

10

11

Amount of dioxins formed (ng/g)

Fig. 5. Dioxin analysis of exhaust gases from combustion of newspapers impregnated with NaCl and various inorganic metal chlorides.

20

T. Shibamoto et al.

When newspaper alone was combusted, the total amount of dioxins (total of PCDDs, PCDFs, and coplanar PCBs) reached only trace level (0.18 ng/g). This value is quite low compared with those of the samples with chloride. NaCl-impregnated (I) newspaper (NP) alone yielded the greatest amount of total dioxins (103 ng/g) among the samples shown in this ﬁgure. The highest level of PCDDs (8.79 ng/g) was also formed from NaCl-I NP alone, whereas the highest level of PCDFs (59.0 ng/g) was obtained from CuCl2/NaCl-impregnated newspaper. PCDFs comprised more than 80% of the total dioxins formed from these samples. The results show that the addition of metal chlorides decreased the formation of dioxins from NaCl-I NP upon combustion. The decreasing order of total dioxins formed from NaCl-I NP with other metal chlorides is CuCl2 (67.0 ng/g) > MgCl2 (47.2 ng/g) > MnCl2 (39.7 ng/g) > FeCl3 (38.7 ng/g) > NiCl2 (37.8 ng/g) > CoCl2 (34.2 ng/g). The dioxin formation from NaCl-I NP upon combustion seemed to be reduced by the additional impregnation of other metals. Addition of ﬂy ash to NaCl-I NP produced 139 ng/g total dioxins upon combustion under similar conditions (Yasuhara et al. 2005c). Inorganic elements in the ﬂy ash comprised (wt%) Ca (49.0), Cl (28.0), K (8.5), Si (3.3), S (3.1), Al (2.2), Zn (1.9), Fe (1.0), Ti (0.97), Na (0.88), Pb (0.39), Cd (0.23), and Cu (0.15). Ca comprised nearly 50% of the ﬂy ash. Only trace amounts of heavy metals, which are known to catalyze dioxin formation, were present in the ﬂy ash. Experiments in a laboratory-scale ﬂuidized-bed reactor using a synthetic fuel that simulated municipal solid waste showed that small ﬂy ash particles (<2.2 µm) had a signiﬁcant inﬂuence on the formation of chlorinated aromatic compounds (Fängmark et al. 1994). Also, addition of dioxin-free ﬂy ash to NP, PE, and PVC increased dioxin formation signiﬁcantly (Takasugi et al. 2000). Dioxin formation from heated chlorophenols was increased by metals, such as Cu and Fe, and by metal oxides, such as CuO, NiO, and Fe2O3 (Gullett et al. 1990, 1992). When unburned carbonaceous particles, such as soot, were burned with various metal chlorides, the increasing order of metal activity toward dioxin formation was KCl < CaCl2 < FeCl3 < < CuCl2 (Kuzuhara et al. 2003). Copper seems to have higher activity than other metals tested; it acted not only as a catalyst but also as a transmitter of heterogeneous chlorine. Excess copper present as CuCl2 in municipal solid waste chlorinated activated carbon through to chlorinated benzenes and PCDD/F at 300°C (Jay and Stieglitz 1991). A correlation has been reported between chlorine content and dioxin formation if the level of chlorine content is higher than 1% (Wikström et al. 1996). When newspapers containing 0.99%, 1.88%, and 4.08% of chlorine were burned, 49.0, 121, and 174 ng/g of total dioxins were formed, respectively, indicating that there is an obvious relationship between chlorine content and dioxin formation (Yasuhara et al. 2002). The mechanisms of dioxin formation and degradation under the presence of metals are still not completely understood. Copper compounds,

Dioxin Formation

21

including CuO, have been known to catalyze dioxin formation, but then also catalyze the decomposition of dioxins, depending on their concentration (Luijk et al. 1994). In addition to copper, various metals are also known to play a role in dioxin formation (Addink and Olie 1995). Some metals also catalyze oxidative degradation of organic compounds, and their decreasing order of activity is Cu > Co > Fe > Ni > Pt (Inui et al. 1982). Therefore, it is hypothesized that the metals added to the combustion materials acted as catalysts for the oxidative degradation of organic compounds during combustion and consequently reduced dioxin formation in the exhaust gases. The foregoing reports indicate that some activities of alkaline metals toward dioxin formation remain incompletely understood. More intensive study on the role of metals in dioxin formation from incinerators used for burning domestic and industrial wastes is in order. C. Plastics Alone and with NaCl Polyethylene (PE), polystyrene (PS), and polyethylene terephthalate (PET) have been used to produce plastic sheets and bags, which are widely used at grocery stores and individual homes. Eventually, these plastic materials are combusted as domestic wastes in an incinerator in the presence of chlorines. Figure 6 shows the results of dioxin analysis in the exhaust gases from the combustion of plastics and plastics + NaCl in an incinerator. This ﬁgure

Polyethylene (PE)

PCDDs

X 10

PCDFs Coplanar PCBs

Polystyrene (PS) Polyethylene terephthalate (PET)

X 10

PS foam PE + NaCl PS + NaCl

X 10

PET + NaCl

X 10 X 10 X 10

NaCl-I NP + PE 0

1

2

3

4

5

6

7

8

9

Amount of dioxins formed (ng/g)

Fig. 6. Dioxin analysis of exhaust gases from combustion of plastics and plastics + NaCl.

22

T. Shibamoto et al.

was constructed from the results of three articles (Yasuhara et al. 2002, 2005a; Katami et al. 2002). The “×10” indicates that the actual values are 10 times the values shown in the ﬁgure. Table 3 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content of the samples shown in Fig. 6. The samples shown in this ﬁgure are nonchloride plastics. PE, PS, or PET + NaCl meant a mixture of plastic sheet and NaCl, not a NaCl-impregnated plastic sheet. NaCl was used because it is the most abundant metal chloride in the environment. Nonchloride plastics (PE, PS, and PET) produced dioxins even though their chlorine contents were negligible (<0.0005 from PE and PS sheet, 0.025 from PS foam, and 0.00 from PET). PET produced the greatest amount of dioxins (25.6 ng/g) among the nonchloride plastics combusted, followed by PE (11.8 ng/g). PS sheet gave only a trace amount (1.36 ng/g) of dioxins, whereas the PS form yielded an appreciable amount of dioxins (5.19 ng/g); this may be due to the amount of chlorine contamination. The foam form of plastics may absorb more contamination, and, consequently, produce more dioxins, than plastic sheet upon combustion. Addition of NaCl to PE reduced the total dioxin formation from 11.8 to 6.7 ng/g, mainly because of the reduction of PCDFs formation from 10.7 to 4.78 ng/g. On the other hand, a signiﬁcant increase of total dioxin formation (from 1.36 to 17.7 ng/g) was observed in the case of PS. In the case of PET, only a slight increase of the total dioxin formation (from 25.6 to 28.9 ng/g) was recognized. However, PCDD formation increased considerably, from 0.566 to 7.242 ng/g. When PE was burned with NaCl-NP, relatively high level of dioxins were formed (102 ng/g), compared with PE combusted with solid NaCl (6.07). An impregnated form of NaCl may release chlorine ions more readily than the solid form of NaCl. However, the results indicate that NaCl increases dioxin formation from plastics on combustion. It is reported that chloride sources in municipal wastes are 50% from NaCl and 45% from PVC (Kanters et al. 1996). Therefore, a role of PVC in dioxin formation from various materials was also investigated. D. Polyvinyl Chloride Alone and with Other Plastics and Newspaper PVC, with a chlorine content ranging from 35% to 55%, is one of the most widely used plastics. It is used in a wide range of consumer products, including packaging, cling ﬁlm, bottles, credit cards, audio records, imitation leather, window frames, cables, pipes, wallpaper, and window blinds. PVC is difﬁcult to recycle and consequently is combusted as a waste or ends up in landﬁlls. Formation of dioxins from PVC on thermal degradation has been reported (Sinkkonen et al. 1995; Kanters et al. 1996; Wikström and Marklund 2000; Wagner and Green 1993). Also, cocombustion of PVC together with common plastics, including PE, PS, polyurethane, and epoxy-

Dioxin Formation

23

and phenol/formaldehyde resin, produced dioxins in the high ng/g range (Wirts et al. 1998). Figure 7 shows the results of dioxin analysis in the exhaust gases from the combustion of PVC and PVC with other plastics (PE, PS, and PET) and newspaper in an incinerator. The “×10” and “×100” indicate that the actual values are 10 and 100 times the values shown in the ﬁgure, respectively. The ﬁgure was constructed from the results of three articles (Yasuhara et al. 2001, 2005c; Katami et al. 2002). Table 4 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content of the samples shown in Fig. 7. PVC was washed with hexane and ethanol to remove the phthalates used as a plasticizer. After removal of the phthalates, the chlorine content in the PVC was 51.3%. High levels of dioxin formation were expected from combustion of PVC because of its high chlorine content. The chamber and grate temperatures were adjusted to obtain low (42 ppm) and high (880 ppm) CO concentrations in the exhaust gases. The average chamber temperatures were 633°C for low CO concentration and 531°C for high CO concentration. The average grate temperatures were 900°C for low CO concentration and 742°C for high CO concentration. Generally, the lower the combustion temperature, the higher the CO concentration obtained. The results from the low CO concentration should be more comparable to the results from the rest of the samples than those from the high CO concentration because its combustion temperature is similar to those of others.

X 10

PVC

X 100

(incinerated in high CO concentration)

Polyvinyl chloride (PVC)

X 10

(incinerated in low CO concentration)

PVC + PE

X 10

PVC + PS

X 10

PCDDs PVC + PET

X 10

PVC + newspaper (NP)

PCDFs Coplanar PCBs

X 10

X 10

PVC-impregnated (I) NP NaHCO3-I NP

X 10

PVC/NaHCO3-I NP 0

10

20

30

40

50

60

70

80

90

Amount of dioxins formed (ng/g)

Fig. 7. Dioxin analysis of exhaust gases from combustion of PVC alone and PVC with other plastics and newspaper.

24

T. Shibamoto et al.

A mixed sheet of PVC with PE, PS, or PET (PVC + PE, PVC + PS, and PC + PET) was prepared from one PVC sheet sandwiched with two PE, PS, or PET sheets [PVC/PE, PS, or PET ≅ 1/10 (w/w)]. PVC-impregnated NP was prepared by soaking NP in a tetrahydrofuran solution of PVC and then allowing it to dry naturally at room temperature. NaHCO3impregnated NP was also soaked in a tetrahydrofuran solution of PVC and then dried naturally at room temperature to prepare PVC/NaHCO3impregnated NP. Among a mixture of PVC and plastics or NP, PE produced the greatest amount of total dioxins (463 ng/g) when it was combusted with PVC, followed by PVC + PS (142 ng/g), PVC + PET (128 ng/g), and PVC + NP (103 ng/g). Even though the chlorine content of the PVC samples was approximately twice of those of the NaCl samples, these nonchloride plastic sheets produced dioxins much more with PVC (organic chloride source) than with NaCl (inorganic chloride source). It is interesting that NP produced more dioxins with impregnated PVC (220 ng/g) than with mixed PVC (103 ng/g). Impregnating NaHCO3 apparently increased the dioxin formation from the PVC-I sample (288 ng/g). PVC itself is difﬁcult to burn, but when it is combusted with other waste materials under poorly controlled conditions, such as low temperature and high CO concentration, dioxins will probably form in signiﬁcant levels. These results indicate that both organic and inorganic chloride were a source of chloride for dioxin formation. There are many reports on dioxin formation from the combustion of various waste materials with organic chloride, such as PVC (Christmann et al. 1989). E. Wood and Leaves There have been many reports on the formation of dioxins during the combustion of various woods in various systems: a ﬁreplace in a home (Vikelsoe et al. 1994), a wood-chips boiler (Schatowitz et al. 1994; Samaras et al. 2001; Luthe et al. 1998; Pandompatam et al. 1997), an incinerator (Kolenda et al. 1994; Ikeguchi and Tanaka 2001; Salthammer et al. 1995), and an accidental ﬁre (Carroll 2001). Also, tremendous amounts of fallen leaves have been burned after they are raked up in various areas, including public parks, streets, forests, and homeowners’ yards. The smoke from burning leaves reportedly contained dioxins (Yasuhara et al. 2001). In particular, uncontrolled combustion, such as occurs during so-called “backyard burning” of domestic waste, produces dioxins due to inefﬁcient combustion (Gullett et al. 2001). Figure 8 shows the results of dioxin analysis in exhaust gases formed from various woods and leaves upon combustion. This ﬁgure was constructed from the results of four studies (Yasuhara et al. 2001, 2002, 2003; Katami et al. 2004a). The “×10” indicates that the actual values are 10 times the values shown in the ﬁgure. Table 5 shows the combustion chamber

Dioxin Formation

25

Siebold’s beech X 10

Japanese cedar X 10

Japanese red pine London plane tree branches X 10

Soft wood bleached kraft pulp Cherry tree fallen leaves

X 10

X 10

Konara oak tree fallen leaves 0.0

PCDDs PCDFs Coplanar PCBs

0.5

1.0

1.5

2.0

2.5

Amount of dioxins formed (ng/g)

Fig. 8. Dioxin analysis of exhaust gases formed from combustion of wood and leaves.

conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content of the samples shown in Fig. 8. These wood samples were prepared as follows: a log with bark (16 cm diameter) was cut into wood chips (5 cm3) using an automatic circular saw. Among ﬁve different kinds of wood, a log of Japanese cedar produced the greatest amount of total dioxins (22.3 ng/g) upon combustion, followed by Japanese red pine (18.0 ng/g). The formation of dioxins is inﬂuenced by chlorine content as well as by combustion conditions (see Table 1). Various forms of wood, such as logs with/without bark, wood chips, and various kinds of bark and leaves, have been incinerated in both public and private facilities. Therefore, there are many reports on the formation of dioxins from various kinds of wood upon combustion. For example, wood chips and a mixture of peat (75%) and liquid packaging board (25%) produced 0.93 and 0.130 ng/g total dioxins, respectively, upon combustion at a temperature of at least 850°C (Sinkkonen et al. 1995). However, the exact composition of these wood samples, such as the chlorine content, is not consistent among the reports. Fallen leaves were collected from the suburbs of a city and allowed to dry in the atmosphere for 2 mon. The leaves from a Konara oak tree and a cherry tree produced 10.2 and 6.37 ng/g dioxins upon combustion, respectively. The chlorine contents in the cherry tree leaves (0.074%) and in the Konara oak tree leaves (0.023%) did not correlate with total dioxin formation, suggesting that combustion temperature played a more important role in dioxin formation than the chlorine content. There is a report that chlorine

26

T. Shibamoto et al.

content less than 1% in a combustion sample did not play a role in the dioxin formation (WikstrÖm et al. 1996; Hatanaka et al. 2000). The combustion chamber temperature for the cherry tree leaves was 746°C, which was much higher than that for the Konara oak tree leaves (692°C). Generally, it is reported that the higher the combustion temperature, the less the dioxin formation (Stanmore 2004). F. Wood Impregnated with Seawater and Various Chlorides As already mentioned, various woods have been combusted in large amounts both in private homes and in city incinerators. It is well known that the chloride content of combustion samples inﬂuences the formation of dioxins. More or less, wood samples obtained from various areas are contaminated with chlorides. Therefore, it is important to determine how dioxins form from various woods in the presence of chloride in hightemperature processes such as incineration to reduce their role in environmental contamination. Figure 9 shows the results of dioxin analysis in exhaust gases formed from various kinds of wood impregnated with seawater, NaCl, chlordane, or pentachlorophenol upon combustion. This ﬁgure was constructed from the results of two studies (Yasuhara et al. 2002, 2003). The “×10” indicates that the actual values are 10 times the values shown in the ﬁgure. Table 6 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content of the

PCDDs PCDFs Coplanar PCBs

NaCl-impregnated (I) pulp 6

5

Seawater-I pine tree

X 10

5

(with bark) 4

X 10

Seawater-I cedar tree bark 4

Seawater-I cedar tree

3

X 10

(without bark)

Chlordane-I waste wood

2

2

Pentachlorophenol-I waste wood 1

0

1

1

2

3

4

5

6

7

8

9

10

11

Amount of dioxins formed (ng/g)

Fig. 9. Dioxin analysis of exhaust gases formed from combustion of wood impregnated with seawater, NaCl, chlordane, or pentachlorophenol.

Dioxin Formation

27

samples shown in Fig. 9. Bleached kraft pulp from soft wood with a chlorine content less than 0.01% was soaked in a NaCl solution for 10 min and then dried in an electric dryer at 110°C. The chlorine content of the NaCl-I bleached kraft pulp was 4.25%. Impregnating NaCl increased total dioxin formation from 0.799 ng/g (see Fig. 8) to 6.71 ng/g. Seawater-impregnated pine and cedar were prepared as follows: a log with/without bark was placed in the sea at 20 m above the bottom for 3 mon. After the seawater-impregnated log was dried for 1 mon under standard conditions, the log was cut into small chips and then incinerated under the conditions shown in Table 1. Impregnating with seawater increased the total dioxin formation from 18.0 to 116.2 ng/g for Japanese red pine and from 22.3 to 98.58 ng/g for Japanese cedar (with bark). The results indicate that any wood used for construction that comes into contact with water—such as boats, ships, houses, and piers—produces signiﬁcant amounts of dioxins on combustion and causes air contamination. For example, some logs collected near the sea contained a high level of chlorine and consequently produced relatively high levels of dioxins on combustion (Luthe et al. 1998; Pandompatam et al. 1997). Waste woods were collected from beneath a ﬂoor where chlordane had been applied as an antitermite agent (chlordane content, 19.9 µg/g). The other waste woods were collected from beneath a ﬂoor where pentachlorophenol had been applied as a preservative (pentachlorophenol content, 0.42%). The waste woods contaminated with chlordane or pentachlorophenol produced 3.5 ng/g total dioxins upon incineration. The levels of total dioxins formed were rather low due to the high combustion temperatures (800°C; refer to Table 1) applied in this experiment, suggesting that dioxin formation can be controlled by raising the combustion temperature to more than 800°C. The role of combustion temperature in dioxin formation is discussed later. G. Miscellaneous Materials Many studies have been conducted on dioxin formation from various samples burned in small-scale incinerators, in addition to the results shown in Figures 4–9. Figure 10 shows the results of dioxin analysis in exhaust gases formed from various incinerated samples. This ﬁgure was constructed from the results of four studies (Yasuhara et al. 2005a,c, 2006; Katami et al. 2004b). The “×10,” “100,” and “×1,000” indicate that the actual values are 10, 100, 1,000 times the values shown in the ﬁgure, respectively. Table 7 shows the combustion chamber conditions and concentrations of O2, CO, CO2, and Cl ion in the exhaust gases, along with the chlorine content of the samples shown in Fig. 10. One of the major sources of dioxins in the environment is the combustion of domestic waste materials. Domestic garbage is a mixture of tremendous numbers of substances, including various foods, household materials, and pet feces. For example, domestic waste, on a wet weight basis, from six

28

T. Shibamoto et al.

Newspaper alone NaCl-I NP B

TEQ

X 10

Dioxins Cl content

X 100

NaCl-I NP D

X 10

NaCl/CuCl2-I NP X 100

PVC-I NP Cardboard NaCl-I NP + fly ash

X 100

PE

X 10 X 10

PVC (in high CO conc)

X 1000

X 10 X 10

NP-NP + PVDC Pine tree Cherry tree leaves X 10

Food Sample B 0

1

2

3

4

5

6

7

8

9

Amounts of TEQ (ng-TEQ/g of sample), total dioxins formed (ng/g), and chlorine content (wt%)

Fig. 10. Dioxin analysis of exhaust gases formed from combustion of various samples.

cities in Japan consisted of 38.3% food waste, 29.4% paper, 13.2% plastic, 3.9% glass, 3.5% metal, and 2.4% textiles in 1999 (JESC 2001). There has been great concern about the large amounts of garbage produced by domestic households in the modern world. This domestic waste has been combusted in large-scale incinerators under well-controlled conditions. Public concerns in developed countries, including the United States and Japan, however, have focused on the formation of toxic dioxins during the incineration of this garbage. Dioxin contamination in the environment occurs from the combustion of waste materials, as well as from many other hightemperature processes commonly used in industrial settings (Lustenhouwer et al. 1980; Tuppurainen et al. 1998). There are some reports on dioxin formation from domestic wastes incinerated under less-controlled systems (Gullett et al. 2001) and from waste plastic combusted at various temperatures (Yoneda et al. 2002). Exhaust gases from an incinerator that contained mixtures of 67 food items—including fruits, vegetables, pasta, seafoods, meats, and processed foods and seasoned foods—were analyzed for dioxins (Katami et al. 2004b). Food sample A was a mixture of food scraps produced during food preparation and food sample B was a mixture of waste produced after eating. Food sample B produced more dioxins (29.1 ng/g) than did food sample A (18.9 ng/g), which may be due to the higher chlorine content in food sample B (1.22 wt%) than in food sample A (0.99 wt%). Also, CaCl2 content was lower in food sample B (4.0 mg/L) than in food sample A (4.7 mg/L), whereas

Dioxin Formation

29

NaCl content was higher in food sample B (5,900 mg/L) than in food sample A (5,100 mg/L). These results explain the higher formation levels of dioxins in food sample B than in food sample A. Polyvinylidene chloride (PVDC), developed by Dow Chemical in the 1930s, was initially used as a protective coating to combat corrosion on military aircraft exposed to sea spray. Later, it was used as one of the components in a copolymer, and it soon found application as a ﬁlm for wrapping food. PVDC is widely used as a thin barrier layer in multilayer sheets, ﬁlms, and tubes. Eventually, PVDC is incinerated with other domestic waste materials. PVDC was combusted with a newspaper material with no printing (NP-NP) in a small-scale incinerator to examine dioxin formation in the exhaust gas. Addition of PVDC to NP-NP increased dioxin formation from 2.22 to 58.0 ng/g; chlorine content increased from 0.0064% to 4.59%. It has been reported that the level of dioxin formation from PVDC combusted at 750°C or lower was much higher than at 800°C or higher in a quartz tubular furnace (Ohta et al. 2001). When NP was combusted with PVDC, 1.525 ng/g dioxins was formed (Katsumata et al. 2003). In the sample of electric wire coated with PVC, total PCDFs composed 85% of the total dioxins formed (38.3 ng/g) in the exhaust gas after combustion. The electric wire was composed of 37.6% copper wire and 62.4% wire coated with PVC. Therefore, the calculated value of the total dioxins without copper wire was 61.1 ng/g. In the case of PVC alone, PCDFs comprised 80% of the total dioxins formed (112 ng/g) in the exhaust gas. Based on these values, the presence of copper wire is seen to reduce dioxin formation by 30% from PCDDs, 58% from PCDFs, and 55% from the total dioxins (Yasuhara et al. 2005b). When PVC-cable sheathings were combusted, dioxins (ppm levels) were formed (Christmann et al. 1989). Other miscellaneous samples also produced appreciable amounts of dioxins upon combustion: 4.10 ng/g from a PS plastic cover for an air conditioner, 1.98 ng/g from cardboard paper, and 8.10 ng/g from lightweight coated paper. These results suggest that waste materials containing plastic materials produce dioxins in the presence of chloride upon incineration.

VI. Toxicity Equivalence Quantity in Exhaust from Incinerated Samples Dioxins are present in environmental and biological substances as extremely complex mixtures of various congeners. Some dioxins have been shown to cause toxic responses similar to those caused by 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), which is the most potent congener within these groups of compounds. Therefore, it is important to assess the risk caused by these chemicals for humans and wildlife. For this purpose, the concept of toxic equivalency factors (TEFs) has been developed and introduced to facilitate risk assessment and regulatory control of exposure to these mixtures. The method to calculate toxic equivalent (TEQ) concentrations in various

30

T. Shibamoto et al.

environmental samples, including exhaust gases from incinerators, utilized TEF values (van den Berg et al. 1998). Figure 11 shows toxicity equivalency quantity (ng-TEQ/g) of the representative samples shown in the tables. The values were obtained using the previously reported method (van den Berg et al. 1998). The “×10” indicates that the actual value is 10 times the value shown in the ﬁgure. The samples that did not contain chlorine or were not burned with chlorides exhibited low levels of TEQ values, 0.013 from NP alone and 0.073 ngTEQ/g from PE. In contrast, samples with high chlorine content, such as PVC (51.3%), gave a high level of TEQ values. Among the TEQ values from the samples reported in the 10 articles used as a core component of this review, PVC combusted in high CO content at low chamber temperature (531°C) gave the highest TEQ value of 29 ng-TEQ/g. On the other hand, when the same sample was combusted in low CO content at high temperature (633°C), the TEQ value was at the much lower level of 8.3 ngTEQ/g. NP impregnated with either organic (PVC) or inorganic (NaCl) source resulted in similar values of TEQ (3.12 ng-TEQ/g from NaCl-I NP D and 3.31 ng-TEQ/g from PVC-I NP) and dioxin formation; this may be the result of the similar chlorine content in the combustion samples (4.08% in NaCl-I NP D and 4.51% in PVC-I NP). In the U.S., emissions of dioxins from PVC burned in house ﬁres has been estimated at <1 g I-TEQ/yr (Carroll 2001).

Polyethylene terephthalate Polyvinyl chloride (PVC)

X 10

(combusted in high CO conc)

Polystyrene foam NaCl-impregnated (I) newspaper MnCl2-I newspaper (NP) PVC-impregnated NP Cedar tree wood Cherry tree fallen leaves Seawater-I cedar tree wood Chlordane-I waste wood 0.0

0.5

1.0

1.5

2.0

2.5

3.0

3.5

Toxicity equivalency quantity (ng-TEQ/g)

Fig. 11. Toxicity equivalency quantity (ng-TEQ/g) of representative samples from the samples shown in the tables.

Dioxin Formation

31

The TEQ values in general correlated with the amount of chlorine content in combustion samples and the amount of dioxin formed in exhaust gases from an incinerator. When the same sample was, however, combusted at different temperatures, the sample combusted at low temperature (NaCl-I NP D) yielded a higher TEQ value (3.12 ng-TEQ/g) than did the sample combusted at high temperature (NaCl-I NP E; refer to Table 1) (0.026 ng-TEQ/g). In the case of NaCl-I NP B (chlorine content, 0.99%), impregnating additional CuCl2 (chlorine content of sample, 1.13%) reduced the TEQ value signiﬁcantly from 1.08 to 0.62 ng-TEQ/g; nevertheless, it increased the dioxin formation in the exhaust gas from 49 to 67 ng/g. The TEQ value of the pine wood sample was calculated in ng/m3 to compare the results with the other data. When pine was combusted at below 600°C and at over 860°C, The TEQ values of its exhaust gas were 2.9 ng-TEQ/m3 and 0.0023 ng-TEQ/m3, respectively. Similar results were reported from waste wood combusted at 623°C (0.86 ng-TEQ/m3) and at 1,086°C (0.14 ng-TEQ/m3) (Ikeguchi and Tanaka 2001). NaCl-I bark (chlorine content, 0.76%) gave 3.2 ng-TEQ/m3 upon combustion (Pandompatam et al. 1997). Another report indicated that waste woods gave TEQ values of 2.7–14.4 ng-TEQ/m3 (Kolenda et al. 1994). Chlordaneand pentachlorophenol-I waste woods gave 0.34 and 0.47 ng-TEQ/m3, respectively (Yasuhara et al. 2003). These results indicate that wood samples may produce certain amounts of toxic materials with signiﬁcant TEQ values upon combustion. In fact, seven actual wood-burning facilities were found to yield 0.004–9.820 ng I-TEQ/Nm3, with the majority of values >0.1 ng ITEQ/Nm3. The highest concentrations occurred after the addition of halogenated materials (NH4Cl-hardened or PVC-coated plywood) to the input of the incinerator in this study (Kolenda et al. 1994). Samples of fallen leaves, which produced 6–10 ng/g levels of dioxins, gave TEQ values of 0.12–0.48 ng-TEQ/m3 (Katami et al. 2004a). These values are slightly higher than the maximum allowable level (0.1 ng-TEQ/m3) in the exhaust gases set by the government of Japan. Therefore, it is important to incinerate fallen leaves in well-controlled systems to minimize the formation of dioxins. Furthermore, burning fallen leaves in a homeowner’s yard or in a public park is not recommended.

VII. Dioxin Formation Mechanisms During Incineration There have been many studies on the formation of dioxins under various conditions (Kanters et al. 1996; Wikström and Marklund 2000; Iino et al. 1999, 2000). However, formation mechanisms of dioxins from waste materials upon combustion in an incinerator are not yet completely understood because many complex reaction pathways seem to be involved in the process (Huang and Buekens 1995). Some of the possible reaction mecha-

32

T. Shibamoto et al.

nisms of dioxin formation upon combustion of waste materials have been proposed in the past two decades, including high-temperature pyrosynthesis, low-temperature de novo formation from macromolecular carbon and organic or inorganic chlorine present in the ﬂy ash matrix, and formation from different organic precursors such as chlorophenols (Tuppurainen et al. 1998). It is reported that dioxins form from precursors via organic chemical reactions, such as the condensation reaction of two molecules of chlorophenols and the cyclization reaction of polychlorinated biphenyls (Luijk et al. 1994). It is also hypothesized that dioxin formation involves a radical reaction between simple carbon radicals and chloride radicals under high-temperature conditions (Stieglitz and Vogg 1987; Huang and Buekens 1995). A study on the effect of temperature on PVC combustion in a downstream tubular furnace resulted in a close correlation (R2 = 0.97) between temperature and dioxins formation (Kim et al. 2004). The effect of combustion temperatures on dioxin formation was reportedly different between the combustion chambers. Also, formation of dioxin varied in different sections of municipal waste incinerators. The amounts of dioxins were signiﬁcantly reduced when HCl was not supplied to the main combustion section, suggesting that dioxins were formed mainly in the main combustion section (Hatanaka et al. 2005). Several statistically signiﬁcant relationships between HCl emissions and the emissions of dioxins were also reported (Wagner and Green 1993). On the other hand, the addition of HCl had little or not apparent effect on the level of dioxin formation during PVDC combustion (Ohta et al. 2004). When wood chips were combusted with PVC resin or NaCl, chloride content did not inﬂuence dioxin formation at 1,000°–1,100°C but it increased it signiﬁcantly at lower temperatures (Ikeguchi and Tanaka 2001). There are several excellent reviews on dioxin formation including the role of temperature (Lustenhouwer et al. 1980; Stanmore 2004). There are generally two reactions associated with dioxin formation from waste materials based on different combustion temperatures. One reaction is a homogeneous reaction that occurs at 500°–800°C. Under these temperatures, dioxin formation and degradation may occur simultaneously in the gas phase. Possible reaction mechanisms occurring during the homogeneous reaction have been hypothesized according to general organic chemistry, including the cyclization of polychlorobiphenyls and polychlorodiphenyl ethers, the chlorination of dibenzofuran, and the dechlorination of octachloro dibenzofuran (Choudry and Hutzinger 1983; Ballschmiter et al. 1985). Most studies on dioxin formations from incinerators, including the ones discussed in Figures 4–10, were conducted at the temperatures that promote a homogeneous reaction. The other reaction is a heterogeneous reaction that occurs at 200°–400°C. Dioxins are formed on solid surfaces such as ﬂy ash and soot by some catalysis (metals) during this reaction. It has been proposed that the precursors of dioxins in this reaction are aromatic chlorides, such as chlorophenols and chlorobenzenes, and elemental

Dioxin Formation

33

carbons via de novo reaction (Addink and Olie 1995). Dioxin formation in municipal waste incineration systems was, therefore, hypothesized as a twostage process: (1) the formation of the graphitic structure of soot particles in the combustion zone (heterogeneous reaction); and (2) the conversion of the graphitic structure of soot particles to aromatic compounds, including dioxins in the postcombustion zone at high temperatures (homogeneous reaction) (Huang and Buekens 1995). From the experiment conducted using a laboratory-scale ﬂuidized-bed reactor, of which each temperature of primary and secondary combustion zones was set independently to 700°, 800°, and 900°C, it was found that dioxin concentration was reduced as the temperature of the secondary combustion zone increased. On the other hand, as the temperature of the primary combustion zone increased, the dioxins concentration also increased, suggesting that keeping the temperature of the secondary combustion zone high and primary combustion zone low reduces the release of dioxins during waste incineration (Hatanaka et al. 2001a). There are many reports suggesting that the chlorine content of combustion samples and the combustion temperature play an important role in dioxin formation in municipal incinerators (Kawabata et al. 2002, 2003; Hatanaka et al. 2001b; Procaccini et al. 2003). Figure 12 shows plots of dioxin formation against chamber temperatures. The data used are those reported in the references shown in Tables 1–7. No signiﬁcant relationship between dioxin formation and chamber temperatures was observed. However, it is obvious that dioxin formation occurred 2,000,000

Amount of Dioxins Formed (ng/kg)

200,000

A

150,000

1,500,000

100,000

1,000,000

50,000

500,000

0 400

500

600

700

800

900 1000

0 400

B

500

600

700

800

900

Temperature of Combustion Chamber (°C)

Fig. 12. Plots of dioxin formation against chamber temperatures. A. Materials incinerated with inorganic chlorides. B. Materials incinerated with organic chlorides.

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Amount of Dioxins Formed (ng/kg)

200,000

A Y = 17609X + 3688 150,000

R2

= 0.34

B Y = 15684X + 34502

1,500,000

100,000

1,000,000

50,000

500,000

0

0 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0

R2 = 0.6099

0 5 10 15 20 25 30 35 40 45 50 55 60

Chloride Content (%) Fig. 13. Relationship between chloride content of incinerated samples and dioxin formation. A. Materials incinerated with inorganic chlorides. B. Materials incinerated with organic chlorides.

at temperatures above 450°C and reduced signiﬁcantly at temperatures above 850°C. Combustion temperatures may play an important role in dioxin formation in exhaust gases from incineration of waste materials. However, the reaction occurring in an incinerator is extremely complex and there are many factors in addition to combustion temperature inﬂuencing dioxin formation. Factors involved in dioxin formation are chorine content, number of benzene rings, the level of metals in samples, and O2, CO, and HCl concentration in the combustion chamber. As already mentioned, the chloride content (%) in a combustion sample plays some role in dioxin formation (ng/kg). Figure 13 shows the relationship between chloride content in the combustion samples and dioxin formation. The data used are those reported in the references shown in Tables 1–7. This ﬁgure suggests that there is no signiﬁcant relationship between dioxin formation and chloride content in the data obtained from the references shown in Tables 1–7.

Summary There has been great concern about dioxins—polychlorinated dibenzo dioxins (PCDDs), polychlorinated dibenzo furans (PCDFs), and polychlorinated biphenyls (PCBs)—causing contamination in the environment because the adverse effects of these chemicals on human health have been known for many years. Possible dioxin contamination has received much

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35

attention recently not only by environmental scientists but also by the public, because dioxins are known to be formed during the combustion of industrial and domestic wastes and to escape into the environment via exhaust gases from incinerators. Consequently, there is a pressing need to investigate the formation mechanisms or reaction pathways of these chlorinated chemicals to be able to devise ways to reduce their environmental contamination. A well-controlled small-scale incinerator was used for the experiments in the core references of this review. These articles report the investigation of dioxin formation from the combustion of various waste-simulated samples, including different kinds of paper, various kinds of wood, fallen leaves, food samples, polyethylene (PE), polystyrene (PS), polyvinyl chloride (PVC), polyvinylidene chloride, polyethylene tetraphthalate (PET), and various kinds of plastic products. These samples were also incinerated with inorganic chlorides (NaCl, KCl, CuCl2, MgCl2, MnCl2, FeCl2, CoCl2, ﬂy ash, and seawater) or organic chlorides (PVC, chlordane, and pentachlorophenol) to investigate the role of chlorine content and/or the presence of different metals in dioxin formation. Some samples, such as newspapers, were burned after they were impregnated with NaCl or PVC, as well as being cocombusted with chlorides. The roles of incineration conditions, including chamber temperatures, O2 concentrations, and CO concentrations, in dioxin formation were also investigated. Dioxins (PCDDs, PCDFs, and coplanar-PCBs) formed in the exhaust gases from a controlled smallscale incinerator, where experimental waste samples were burned, were analyzed by gas chromatography/mass spectrometry. Formation of total PCDFs was much higher than that of PCDDs in all samples. The total PCDFs comprised 70%–90% of the total dioxin formed. The amount of total PCDFs formed ranged from 0.78 ng/g (newspaper) to 8,490 ng/g (PVC burned in high CO concentration). The amount of total PCDDs formed ranged from 0.02 ng/g (newspaper) to 430 ng/g (PVC). Coplanar PCBs were found at the lowest level of the dioxins formed. Their formation levels ranged from 0 ng/g (newspaper) to 77.6 ng/g (PVC). It is obvious that the samples with either inorganic or organic chlorides produced much more dioxins than the sample without chlorides when incinerated under similar conditions. It is not clear how inorganic and organic chloride contribute differently to dioxin formation. Among the metals examined, copper seems to have higher activity toward dioxin formation than other metals. It acted not only as a catalyst but also as a transmitter of heterogeneous chlorine. The toxicity equivalence quantity (TEQ) values generally correlated with the amount of chlorine content in the samples and the amount of dioxin formed in exhaust gases from an incinerator. When the same sample was incinerated at different temperatures, however, the sample burned at low temperature yielded a higher TEQ value than did the sample burned at high temperature. The samples that did not contain chlorine or were

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not combusted with chlorides exhibited low TEQ values. In contrast, samples with high chlorine content, such as PVC (51.3%), gave high TEQ values. Combustion temperatures may play an important role in dioxin formation in exhaust gases from the incineration of waste materials. However, no signiﬁcant relationship between dioxin formation and chamber temperatures was reported in the core articles. However, it is obvious that dioxin formation occurred at temperatures above 450°C and was reduced signiﬁcantly at temperatures above 850°C. The reaction occurring in an incinerator is extremely complex, and there are many factors in addition to combustion temperature inﬂuencing dioxin formation. Even though it is possible to hypothesize reasonable formation mechanisms of dioxins produced in exhaust gases according to the results obtained from experiments in classical chemistry, the reactions involved in an incinerator are extremely complex and heterogeneous. More detailed investigation of the many individual factors inﬂuencing dioxin formation is needed to ﬁnd ways to reduce their formation in individual and municipal incinerators.

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Gullett BK, Bruce KR, Beach LO (1990) The effect of metal catalysts on the formation of polychlorinated dibenzo-p-dioxin and polychlorinated dibenzofuran precursors. Chemosphere 20:1945–1952. Gullett BK, Bruce KR, Beach LO, Drago AM (1992) Mechanistic steps in the production of PCDD and PCDF during waste combustion. Chemosphere 25:1387–1392. Gullett BK, Lemieux PM, Lutes CC, Winterrowd CK, Winters DL (2001) Emissions of PCDD/F from uncontrolled, domestic waste burning. Chemosphere 43:721–725. Hatanaka T, Imagawa T, Takeuchi M (2000) Formation of PCDD/Fs in artiﬁcial solid waste incineration in a laboratory-scale ﬂuidized-bed reactor: inﬂuence of contents and forms of chlorine sources in high-temperature combustion. Environ Sci Technol 34:3920–3924. Hatanaka T, Imagawa T, Kitajima A, Takeuch M (2001a) Effects of combustion temperature on PCDD/Fs formation in laboratory-scale ﬂuidized-bed incineration. Environ Sci Technol 35:4936–4940. Hatanaka T, Imagawa T, Kitajima A (2001b) PCDD/Fs formation in laboratoryscale ﬂuidized-bed incineration: inﬂuence of chlorine content in low-temperature combustion. Organohalogen Compd 50:430–433. Hatanaka T, Kitajima A, Takeuchi M (2005) Role of chlorine in combustion ﬁeld in formation of polychlorinated dibenzo-p-dioxins and dibenzofurans during waste incineration. Environ Sci Technol 39:9452–9456. Huang H, Buekens A (1995) On the mechanisms of dioxin formation in combustion processes. Chemosphere 31:4099–4117. Iino F, Imagawa T, Takeuchi M, Sadakata M (1999) De novo synthesis mechanism of polychlorinated dibenzofurans from polycyclic aromatic hydrocarbons and the characteristic isomers of polychlorinated naphthalenes. Environ Sci Technol 33:1038–1043. Iino F, Imagawa T, Gullett BK (2000) Dechlorination-controlled polychlorinated dibenzofuran isomer patterns from municipal waste incinerators. Environ Sci Technol 34:3143–3147. Ikeguchi T, Tanaka M (2001) Dioxin emissions from industrial wood waste incinerators. Organohalogen Compd 50:390–393. Inui T, Otowa T, Tsutchihashi K, Takegami Y (1982) Complete oxidation of active carbon at low temperatures by composite catalysts. Carbon 20:213–217. Jay K, Stieglitz L (1991) On the mechanism of formation of polychlorinated aromatic compounds with copper(II) chloride. Chemosphere 22:987–996. JESC (2001) Fact Book: Waste Management & Recycling in Japan. Japan Environmental Sanitation Center, Tokyo, Japan, p 22. JMHW (1997) Standard method for determination of dioxins in waste management. Notiﬁcation no. 234, Japan Ministry of Health and Welfare, Tokyo, Japan. Kanters MJ, van Nispen R, Louw R, Mulder P (1996) Chlorine input and chlorophenol emission in the lab-scale combustion of municipal solid waste. Environ Sci Technol 30:2121–2126. Katami T, Ohno N, Yasuhara A, Shibamoto T (2000) Formation of dioxins from sodium chloride-impregnated newspapers by combustion. Bull Environ Contam Toxicol 64:372–376. Katami T, Yasuhara A, Okuda T, Shibamoto T (2002) Formation of PCDDs, PCDFs, and coplanar PCBs from polyvinyl chloride during combustion in an incinerator. Environ Sci Technol 36:1320–1324.

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Yasuhara A, Katami T, Shibamoto T (2006) Formation of dioxins from combustion of polyvinylidene chloride in a well-controlled incinerator. Chemosphere 62: 1899–1906. Yoneda K, Ikeguchi T, Yagi Y, Tamade Y, Omori K (2002) A research on dioxin generation from the industrial waste incineration. Chemosphere 46:1309–1319. Manuscript received April 13; accepted April 20, 2006.

Rev Environ Contam Toxicol 190:43–125

© Springer 2007

Coca and Poppy Eradication in Colombia: Environmental and Human Health Assessment of Aerially Applied Glyphosate Keith R. Solomon, Arturo Anadón, Gabriel Carrasquilla, Antonio L. Cerdeira, Jon Marshall, and Luz-Helena Sanin

Contents I. Introduction......................................................................................................... 44 II. Problem Formulation ......................................................................................... 46 A. Stressor Characterization ............................................................................. 47 B. Framework for Risk Assessment ................................................................ 59 III. Exposure Characterization................................................................................ 60 IV. Effects Characterization .................................................................................... 71 A. Glyphosate ..................................................................................................... 71 B. Glyphosate and Formulants ........................................................................ 91 C. Effects in the Field........................................................................................ 92 V. Risk Assessment ................................................................................................. 98 A. Human Health ............................................................................................... 98 B. Environment .................................................................................................. 99

Communicated by G.W. Ware. K.R. Solomon ( ) Centre for Toxicology and Department of Environmental Biology, University of Guelph, Guelph, ON, N1G 2W1, Canada A.L. Cerdeira EMBRAPA, Ministry of Agriculture, Jaguariuna, SP 13820-000, Brazil A. Anadón Departamento de Toxicología y Farmacología, Facultad de Veterinaria, Universidad Complutense de Madrid, 28040 Madrid, Spain G. Carrasquilla Hospital Universitario, Fundación Santa Fe de Bogotá, Calle 116 No. 9, Bogotá E.J.P. Marshall Marshall Agroecology Limited, 2 Nut Tree Cottages, Barton, Winscombe, Somerset, BS25 1DU, UK L.-H. Sanin Department of Public Health Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, M5S 1A8, Canada and Autonomous University of Chihuahua National Institute of Public Health, Mexico

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VI. Conclusions ....................................................................................................... A. Human Health Relevance ......................................................................... B. Ecological Relevance.................................................................................. C. Strengths and Uncertainties in the Assessment ..................................... D. Recommendations ...................................................................................... Summary ............................................................................................................ Acknowledgments ............................................................................................ References .........................................................................................................

102 103 104 104 107 107 111 112

I. Introduction It is estimated that some 200 million people worldwide use illicit drugs. Most of these drugs have natural origins, such as cannabis, cocaine, and the opiates; however, the synthetic drugs such as the amphetamines also comprise a signiﬁcant proportion of these uses (UNODC 2003). In response to the socioeconomic impacts of the production and distribution of illicit drugs, a number of individual nations, as well as multinational organizations, have initiated programs to reduce and eventually eliminate their production and distribution (UNODC 2003). Coca (Erythroxylum coca and related species) is commonly associated with the tropical regions of South America. A number of species of coca are found in South America, and various varieties grow in the wild or are cultivated in different climatic conditions. It is primarily found in regions with temperatures above 25°C and with rainfall >1000 mm/yr. Currently, it is widely cultivated in Colombia, Bolivia, and Peru, with some cultivation in Ecuador, Venezuela, Brazil, and Argentina. In 2002, it was estimated that, of the 800 t cocaine produced in Latin America, 580 t was produced in Colombia, a reduction of about 100 t from 1999 (UNODC 2003). It is estimated that, worldwide, about 14 million people abuse cocaine (UNODC 2003). Opium, morphine, and its derivative, heroin, are produced from the poppy Papaver somniferum, which is primarily grown in Asia. Global production of opium in 2002 was estimated to be 4,500 t, of which about 97 t was produced in South America; of this, 50 t was produced in Colombia (UNODC 2003). It is estimated that, globally, about 15 million people use opiates and that about 10 million of these use heroin (UNODC 2003). Similar to coca, the use of opium and morphine has historical roots in the traditional society of the producer regions but became more widely used as a human medicine when introduced to other parts of the world. Although morphine is still used for medicinal purposes, heroin use is largely illegal and its production and distribution have signiﬁcant socioeconomic impacts in producer and consumer nations. The growing and production of illicit drugs in Colombia have signiﬁcant political, social, economic, and environmental impacts. While recognizing the importance of the political, social, and economic aspects of the issue,

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this review is focused on the human health and environmental signiﬁcance of growing these crops and the control of coca and poppy through the use of the aerially applied herbicide glyphosate. It is important to recognize that the actual production of coca and poppy as well as the processing and production of cocaine and heroin involve signiﬁcant environmental impacts. Both coca and poppy are grown intensively in a process that involves the clearing of land, the planting of the crop, and its protection against pests including weeds, insects, and pathogens. Depending on the region, the clearing of the land for production purposes may have large and only slowly reversible effects on the environment. As for other forms of agricultural production, the clear-cutting of forests for the purposes of coca and poppy production reduces biodiversity, contributes to the release of greenhouse gases, increases the loss of soil nutrients, and promotes erosion of soils. Because production is illegal, it usually takes place in remote locations. As a result, clearing of land is done without government approval and with little apparent consideration for the biological and aesthetic value of the ecosystem. A number of pesticides are used in the production of illicit drugs. Herbicides may be used in the initial clearing of the land and later in the suppression of weeds. Similarly, insecticides and fungicides may be used to protect the illicit crops from pests and diseases. To increase yields, fertilizers and other nutrients may also be used. Large quantities of agrochemicals have been seized and conﬁscated as part of the program to control the production of illicit drugs (Dirección Nacional de Estupefacientes 2002). Although some of these agrochemicals are highly toxic to mammals and may have signiﬁcant environmental impacts, accurate information on the type of formulation used, amounts used, their frequency of use, and the conditions of their use is not available. Because of this, it was not possible to conduct a detailed human health and ecological risk assessment. However, the relevant toxicological and environmental properties of these substances are summarized in two separate reports, and several of these are signiﬁcant potential hazards to human health and the environment (CICAD/OAS 2004c, 2005). In addition to the use of agrochemicals in the production of coca and poppy, large amounts of chemicals are used in the processing of the raw product into reﬁned cocaine and heroin. Processing of the illicit drugs is conducted in remote locations and in the absence of occupational health and environmental regulations and controls. During and after use, these substances may be released into the environment and have signiﬁcant impacts on human and animal health and the ecosystem. The toxicological and environmental properties of these substances are summarized in a separate Tier 1 Hazard Assessment Report (CICAD/OAS 2004c). Some of these substances have potentially large environmental and human health hazards, and a subset of these is discussed in more detail in a Tier 2 Hazard Assessment Report (CICAD/OAS 2005).

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The growing of coca and poppy and the distribution of cocaine and opium/heroin in Columbia have been the focus of a national control and eradication program starting in the 1970s. The program involves a number of departments and agencies of the Colombian Government and is coordinated by the Dirección Nacional de Estupefacientes (DNE), an agency of the Ministry of the Interior and Justice. The program has three main foci: the control of production of coca and poppy, the control of the processing, puriﬁcation, and transport of the cocaine and heroin, and the seizure and forfeiture of the proﬁts of illicit drug production (Dirección Nacional de Estupefacientes 2002). The eradication program for illicit crops in Colombia is the responsibility of the Antinarcotics Directorate of the Colombian National Police (DIRANCNP), supported by data gathering from other nations such as those in North America and Europe. The DIRAN conducts regular ﬂights with aircraft that spray coca and opium poppy crops with a herbicide. The DIRAN reviews satellite imagery and ﬂies over growing regions on a regular basis to search for new coca and opium poppy growth and to generate estimates of the illicit crops through high-resolution low-altitude imagery and visual observation. The DIRAN selects the locations of the illicit crops that are to be sprayed with input from the DNE or the Government of Colombia’s Plan Colombia Ofﬁce. Several concerns have been raised about the use of glyphosate and adjuvants in the control of coca and poppy plants. These concerns range from damage to other crops to adverse effects on the environment and human health. In response to this, the Government of Colombia appointed an independent environmental auditor who reviews the spray and no-spray areas with the DIRAN and regularly monitors the results of spraying through ﬁeld checks and analysis of data from computerized spray records. The objectives of the present assessment and review are to provide a science- and data-based study of the use of glyphosate in the eradication program with a key focus on the environment and human health, to collect data for use in the assessment, and to address speciﬁc concerns that have been raised. As with all risk assessments, we have followed a framework based on those used in other jurisdictions (NRC 1986; USEPA 1992, 1998). This framework consists of a Problem Formulation, Effects and Exposure Assessment, and Risk Characterization for both humans and the environment. In conducting this review, we used data from the peer-reviewed scientiﬁc literature, from government documents, and from studies speciﬁcally conducted to address data gaps.

II. Problem Formulation Problem formulation is a key step in the risk assessment process and places the use of the substances being assessed into a local context. It is recognized

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that the growing of illicit crops such as coca and poppy, as well as the reﬁning of the cocaine and heroin, involves considerable impacts on the environment through clearing of forests and the use of a number of substances for promoting crop growth and reﬁning of the drugs. Although the identity of these substances is known, the type of formulation, the quantities used, and their manner of use is largely unknown and exposures in workers cannot be easily estimated. While the hazard of these substances is known (CICAD/ OAS 2004c, 2005), the risks cannot be estimated, as the logistics of collecting the human and environmental exposure data are very difﬁcult and not without other risks. Because of this, and as it was the initial mandate of the Panel, the focus of this risk assessment is on the use of glyphosate and adjuvants for control of the illicit crops. In this case, the locations and amounts of application are known with accuracy and environmental risk can be better estimated. In humans, there are no speciﬁc biomarkers for exposure to glyphosate that can be used to estimate historical exposures. For logistical reasons, it was not possible to measure exposures resulting from eradication spraying directly in the ﬁeld. For that reason, in epidemiology studies, indirect measures of exposures such as ecological studies, where the indicator variable or exposure is deﬁned by eradication spraying and crops production patterns, must be used. A. Stressor Characterization The potential stressors in this risk assessment are glyphosate, its formulants, and adjuvants, such as surfactants, that are added to the spray formulation to modify its efﬁcacy. The properties of glyphosate and these substances are described in the following sections. Glyphosate Glyphosate is the active ingredient of a number of herbicide formulations and is one of the most widely used pesticides on a global basis. Uses include agricultural, industrial, ornamental garden, and residential weed management. In agriculture, the use of glyphosate is increasing and use in soybeans is signiﬁcantly greater since the introduction of glyphosate-tolerant crops (Wolfenbarger and Phifer 2000). According to the U.S. National Pesticide Use Database (USNPD 2006), use in soybean increased by 330% between 1992 and 1997 and by 460% between 1997 and 2002. Other agricultural uses for glyphosate-based products include its use by farmers as a routine step in preplanting ﬁeld preparation. Nonagricultural users include public utilities, municipalities, and regional transportation departments where glyphosate is used for the control of weeds or noxious plants. The environmental and human health properties of glyphosate have been extensively reviewed (Giesy et al. 2000; Solomon and Thompson 2003; Williams et al. 2000) and by regulatory agencies (NRA 1996; USEPA 1993a, 1997, 1999; World Health

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Organization International Program on Chemical Safety 1994). The following sections highlight key issues with regard to those properties of glyphosate that are fundamental to the assessment of risks associated with the coca and poppy eradication programs in Colombia. Structure and Chemical Properties. The most common technical form of glyphosate is the isopropylamine salt (IPA), N-(phosphonomethyl) glycine isopropylamine salt (MW, 226.16; CAS number, 1071-83-6). The chemistry of glyphosate is important in determining its fate in the environment. Glyphosate (Fig. 1) is a weak organic acid comprising a glycine moiety and a phosphonomethyl moiety and closely resembles naturally occurring substances. Glyphosate is not chemically reactive, is not mobile in air or soils, does not have great biological persistence, and does not bioaccumulate or biomagnify through the food chain (CWQG 1999; Giesy et al. 2000; USEPA 1993a; Williams et al. 2000; World Health Organization International Program on Chemical Safety 1994). Glyphosate is readily ionized and, as the anion, will be strongly adsorbed to organic matter in soils of normal pH. It thus has little mobility in soils and is rapidly removed from water by adsorption to sediments and suspended particulate matter (Giesy et al. 2000).

Fig. 1. Structure of glyphosate and its major metabolic and breakdown products.

Mechanism of Action. The mechanism of action of glyphosate is via the inhibition of the enzyme 5-enolpyruvyl shikimate-3-P synthetase, an essential enzyme on the pathway to the synthesis of the aromatic amino acids in plants (Devine et al. 1993; Franz et al. 1997). This inhibition results in decreases in the synthesis of the aromatic amino acids tryptophan, phenylalanine, and tyrosine, as well as decreased rates of synthesis of protein, indole acetic acid (a plant hormone), and chlorophyll. The death of the plant is slow and is ﬁrst seen as a cessation of growth, followed by chlorosis

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and then necrosis of plant tissues. Inhibition of 5-enolpyruvyl shikimate-3-P synthetase is speciﬁc to plants. Many animals obtain their aromatic amino acids from plants and other sources and do not possess this pathway of synthesis. For this reason, glyphosate is relatively nontoxic to animals but is an effective herbicide in plants. Global and Local Registration and Use. Glyphosate has been registered since 1971 and is currently widely used as a broad-spectrum, nonselective, postemergence herbicide in a number of countries around the world (World Health Organization International Program on Chemical Safety 1994). It is rapidly translocated from the leaves of treated plants to other parts of the plant, including the growing tips of stems and roots, and to underground storage organs, such as rhizomes and tubers. It is very effective for the control of perennial weeds and is more efﬁcacious than many other nonselective herbicides that only affect the aboveground parts of the plant. Applied to soil, glyphosate shows little activity because the strong binding to soil organic matter makes it biologically unavailable for uptake by plants. Glyphosate has been used extensively in Colombia and many other countries for agricultural and other purposes for many years. Use of glyphosate in the coca and poppy spray program is shown in Table 1 and represents a relatively small fraction of the total use in Colombia. Table 1. Glyphosate use in Eradication Spraying in Colombia, 2000–2004

Year 2000 2001 2002 2003 2004

Amount sold in Colombia (L)a 7,037,500 9,473,570 NA

Amount used in the eradication of illicit crops (L)b

Percent of total amount sold

603,970 984,848 1,061,538 1,381,296 1,420,130

8.6% 10.4% 11%c 14%c 14%c

a

Data from ICA (2003). Data from Dirección Nacional de Estupefacientes (2002); Policia Nacional Dirección Antinarcóticos (2005). c Estimated from total used in 2001 but likely less than this value. b

Environmental Fate. The environmental fate of glyphosate has been extensively reviewed (CWQG 1999; Giesy et al. 2000; NRA 1996; World Health Organization International Program on Chemical Safety 1994); only key issues relevant to water and soil/sediment are summarized next. As a result of its speciﬁc physicochemical properties, glyphosate is immobile or only slightly mobile in soil. The metabolite of glyphosate,

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aminomethyl phosphoric acid (AMPA; see Fig. 1), is somewhat more mobile in soil but is rapidly broken down, resulting in minimal amounts leaching in normal agricultural soils. The strong binding of glyphosate to soil results in almost immediate loss of biological activity; however, the bound residues do break down sufﬁciently rapidly that accumulation will not occur, even over many years of regular use. Contamination of groundwater from the normal use of glyphosate is unlikely except in the event of a substantial spill or other accidental and uncontrolled release of large amounts into the environment. The high water solubility of glyphosate and its salts suggests that it would be mobile in water; however, strong and rapid binding to sediments and soil particles, especially in shallow, turbulent waters, or those carrying large loads of particulates, removes glyphosate from the water column (Tooby 1985). In normal agricultural uses, it is not expected to run off or leach into surface waters. In water, the two major pathways of dissipation are microbiological breakdown and binding to sediments (Giesy et al. 2000; World Health Organization International Program on Chemical Safety 1994). Glyphosate does not degrade rapidly in sterile water, but in the presence of microﬂora (bacteria and fungi) in water, glyphosate is broken down to AMPA (see Fig. 1) and eventually to carbon dioxide (Rueppel et al. 1977). Other metabolic pathways have been reported (Liu et al. 1991), including further degradation of AMPA to inorganic phosphate and CH3-NH3, and via sarcosine to glycine (see Fig. 1). None of these products is considered herbicidal and would not be expected to be highly toxic to aquatic organisms at concentrations that would result from ﬁeld use of glyphosate in aquatic systems. Photodegradation also may take place under ﬁeld conditions where sufﬁcient penetration of UV radiation occurs. The dissipation of glyphosate from treated foliage and from leaf litter has also been characterized. As would be expected, most of the glyphosate sprayed on the plants penetrates into plant tissues after application, but some is available for washoff for several days after application (World Health Organization International Program on Chemical Safety 1994). If the plant dies as a result of this exposure, glyphosate would be present in the dead and decaying plant tissues. Glyphosate residues in leaf litter dissipate rapidly with a time-to-50%-disappearance (DT50) of 8–9 d under temperate forestry conditions (Feng and Thompson 1990). Similar rapid dissipation from fruits and lichen has also been observed (Stiltanen et al. 1981) in north temperate regions. Under tropical conditions such as in Colombia, dissipation will likely be more rapid than in temperate regions because of higher temperatures and moisture content, which promote microbiological activity as well as chemical degradation of many pesticides. Large areas of Brazil, Colombia, and Central America share similar tropical conditions and depend heavily on herbicides such as glyphosate (Racke et al. 1997). Glyphosate has been used

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in large areas of Brazil on no-tillage crops in general and, more recently, on transgenic soybeans. Comparing the fate of pesticides in tropical and temperate conditions, Racke et al. (1997) found no evidence of particular behavior of pesticides in the tropics and concluded a greater rate of degradation occurs under tropical conditions. Formulants and Adjuvants Formulants are substances that are added to a pesticide active ingredient at the time of manufacture to improve its efﬁcacy and ease of use. These formulants serve many purposes and comprise a large range of substances, from solvents to surfactants to modiﬁers of pH. The glyphosate formulation used in Colombia includes several formulants. Adjuvants are added to formulated pesticides at the time of application and, like formulants, increase efﬁcacy, or ease of use in special situations where pests are difﬁcult to control or where nontarget effects need to be minimized. In the control program for illicit crops in Colombia, an adjuvant, Cosmo-Flux, is added at the time of spraying. The relatively large water solubility and the ionic nature of glyphosate retard penetration through plant hydrophobic cuticular waxes. For this reason, glyphosate is commonly formulated with surfactants that decrease the surface tension of the solution and increase penetration into the tissues of the plants (Giesy et al. 2000; World Health Organization International Program on Chemical Safety 1994). Surfactants in the Glyphosate Formulation. The glyphosate formulation as used in eradication spraying in Colombia contains formulants that are common to the commercial product as used in agriculture. Cosmo-Flux 411F, an agricultural adjuvant containing nonionic surfactants (a mixture of linear and aryl polyethoxylates, 17% w/v) and isoparafﬁns (83% v/v) (Cosmoagro 2004) is added to the spray solution. Adjuvants such as these are commonly added to pesticide formulations to improve efﬁcacy through several mechanisms (Reeves 1992; Tadros 1994). For example, surfactants such as the polyethoxylates in Cosmo-Flux, increase efﬁcacy through increasing target surface adherence, promoting better droplet spread, better dispersion, prevention of aggregation, and enhanced penetration of herbicides into target plant tissues through the reduction of surface tension on plants. Surfactants can also disrupt the hydrophobic wax cuticle, thus increasing the penetration of active ingredient. Base oils, such as the isoparafﬁns in Cosmo-Flux, are another class of adjuvants used in formulations. They are used primarily to aid foliar absorption of the pesticide by disrupting the waxy cuticle on the outer surface of foliage, which increases cell membrane permeability (Manthey and Nalewaja 1992).

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Coca and Poppy Control Programs The coca and poppy control programs make use of several procedures to identify, locate, and map coca and poppy ﬁelds. The initial step in this process is the use of satellite images to locate the ﬁelds. These images are provided by North American and European governments to the Government of Colombia. The images are used to locate potential areas of production. Further visual observations are made using overﬂights with observers and/or photographs from a low-altitude aerial photography aircraft, such as a Cessna Caravan, to verify the presence of coca and poppy ﬁelds. The camera used for this purpose is multispectral high resolution. Maps are generated in a Geographic Information System (GIS) and are used to produce updated coordinates for the spray pilots, as well as information for downloading into the aircraft navigation systems (Policia Nacional Dirección Antinarcóticos 2005). Field operation ofﬁces for the control program have computers and a satellite uplink for data transfer. Spray planes are equipped with high-resolution tracking equipment and Del Norte positional data recorders that display position, provide directional guidance, and store positional data and spray information on data cards for later analysis. Thus, ﬁeld locations, ﬂight paths of the spray planes, and areas where spray is released are known to within a resolution of 1–2 m. Since 1994, coca and, more recently, poppy ﬁelds have been identiﬁed and sprayed. Total areas of identiﬁed ﬁelds and the area sprayed in Colombia are shown in Fig. 2. With increasing areas sprayed, the total area planted to coca has generally decreased since 2000. Receiving Environment. Colombia is located between 4° S and 12° N of the equator. The country presents varied topography ranging from snowcapped peaks through high mountain plateaus to low-lying tropical regions. In general, coca tends to be grown at altitudes below 1,500 m and poppy at greater altitudes, usually 2,200 m. The biodiversity hotspot for the tropical Andean region includes signiﬁcant areas of Colombia (Fig. 3). The tropical Andes biodiversity region is estimated to contain 15%–17% of the world’s plant life in only 0.8% of its area. It has an area of 1,258,000 square kilometers, extends from Western Venezuela to Northern Chile and Argentina, and includes large portions of Colombia, Ecuador, Peru, and Bolivia (Centre for Biodiversity 2004). Because the diversity hotspots are mainly associated with the Andean highlands and coca is mostly grown in lower altitudes, there is only some overlap between areas of coca production and regions of high biodiversity. Poppy is grown at a greater altitude, which overlaps with the biodiversity hotspot; however, the total areas grown at this time are small (see Fig. 2). Exact areas used for coca and poppy production within the diversity hotspot are not known; however, this information would be useful for assessing total impacts of production, especially for rare and endangered plant species.

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Fig. 2. Areas planted with coca and poppy in Colombia from 1994 to 2002 as hectares (ha) (above) and as a percent of the total land area of Colombia (below).

Method of Application. All coca and poppy ﬁelds are sprayed from ﬁxedwing aircraft. The procedure described below is based on observations recorded for the AT 65, AT 802, and OV 10 aircraft. Spray planes are loaded in a special area of the tarmac (Fig. 4) at a number of bases throughout Colombia. Glyphosate and Cosmo-Flux are stored in plastic containers in a tarp-lined area protected by a berm to contain accidental spills. The areas may be in the open or covered. Glyphosate is transferred from 200-L plastic barrels to a larger plastic storage tank (Fig. 4A). Cosmo-Flux is transferred from 20-L plastic containers to a mixing tank. The required amounts of the components of the application mixture (glyphosate, Cosmo-Flux, and water from a local source) are pumped through a metering pump (Fig. 4B) into the aircraft using a table of mixing proportions to ensure the correct ratio of amounts are loaded.

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Fig. 3. Map showing the region of Colombia identiﬁed as part of the Andean Biodiversity Region.

Appropriate protective equipment is used by the mixer-loaders, who are trained in the loading procedures (Fig. 4C). The spray boom (Fig. 4D) on the aircraft is equipped with raindrop nozzles (Fig. 4E). These nozzles produce droplets with a volume mean diameter (VMD) of 300–1,500 µm and are similar to those used in forestry spraying for site preparation (Payne 1993). The aircraft spray systems are electronically calibrated to disperse a speciﬁed quantity of spray mix per hectare, compensating for variances in ground speed. These electronic spray controls are checked each day by technicians and also during the pilot’s preﬂight inspection. During actual spray operations, the pilot monitors the spray system by reading the spray pressure and ﬂow rate gauges (United States Department of State 2002). The same nozzles are used for both coca and poppy applications, but twice as many are used for the poppy applications at different boom

Glyphosate Assessment

Fig. 4. Photographs of aspects of the spray operation.

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Table 2. Application Rates of Glyphosate and Cosmo-Flux for Control of Coca and Poppy. kg AE/haa

L/ha

Glyphosate Cosmo-Flux

Coca

Poppy

Coca

Poppy

10.4 0.24

2.5 0.51

4.992

1.2

a Glyphosate acid equivalent (AE)/ha. Source: Dirección Nacional de Estupefacientes (2002).

pressures. As a result, coca and poppy applications are done separately. Currently used application rates are shown in Table 2. Each spray operation (Fig. 4F,G), which may consist of two or more spray planes, is escorted by search-and-rescue (SAR) helicopter(s) in case of an accident or incident. Spraying is only conducted in daylight hours before midafternoon to ensure that conditions are appropriate for application. If rain is imminent, visibility is poor, or wind speed is in excess of 7.5 km/hr (4 knots), spraying is not carried out. Wind speed is checked during the operation by the SAR and other helicopters with the aid of smoke generated by the spray planes. Spraying is done at about 30 m above ground and, although the ﬂight path is determined from the GIS information and the Del Norte guidance system (Fig. 4H), the actual spraying is controlled by the pilots. In personal communications with ﬁve of the pilots, it was stated that, according to spraying guidelines, ﬁelds are not sprayed if people are or soon will be present. After a spray operation, the ﬂight path of the spray planes and the areas sprayed are downloaded from the Del Norte system (Fig. 4I) and processed by GIS to show the spray patterns and calculate the areas spayed (Fig. 4J). This information is transmitted to the DIRAN where records of the spray operations are retained and used for compilation of annual reports and statistics (Dirección Nacional de Estupefacientes 2002). Frequency of Application. Frequency of application varies with local conditions and actions taken by the growers after the coca or poppy is sprayed. When coca is sprayed, some growers prune the bushes down to about 10 cm above ground in an attempt to prevent translocation of the herbicide to the roots. Sometimes these plants will recover and resprout; however, they will not yield large amounts of coca leaves for several months. If the ﬁeld is replanted to coca from seedlings, reasonable productivity may not be achieved for 4–6 mon. If the ﬁeld is replanted from cuttings, productivity may be achieved sooner. Thus, spraying of a particular coca ﬁeld may have a return frequency of about 6–12 mon.

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Being an annual, poppy is grown from seed. In the climatic conditions in Colombia, poppy ﬁelds would be harvested twice a year. If sprayed before reaching maturity and replanted immediately after spraying, they may be sprayed four times a year. Exposure Pathways in Soil, Air, Water, and Other Media. In terms of application, there are several pathways through which glyphosate and adjuvants may contact the environment (Fig. 5). Deposition on the target crop is the desired outcome; however, for purposes of assessing risks in humans and the environment, exposures that result in movement and deposition off the ﬁeld are important. Spray drift would result in movement off target and could result in adverse effects in nontarget plants and animals. Given the strong adsorption of glyphosate to soil, deposition on soil in the ﬁeld will likely not result in signiﬁcant effects on nontarget organisms; however, runoff of residues bound to soil particles may result in contamination of surface waters with sediment-bound residues. Direct deposition and spray drift may result in contamination of local surface waters with glyphosate if these are in the spray swath or drift envelope of application. Depending on the depth of water, turbulence, ﬂow, and presence of suspended particles, this would result in exposures of aquatic organisms to both glyphosate and any adjuvants present in the spray. Organisms present in the ﬁeld during spraying would be exposed to the spray droplets and receive a theoretical dose, depending on surface area exposed and body mass. Off-Target Deposition. There are two types of off-target deposition. The ﬁrst is related to incorrect application where the spray pilot initiates application too soon or turns off the spray too late, or the spray swath includes a nontarget area on one or both sides of the target ﬁeld. The second type

Fig. 5. Diagram showing exposure routes for various environmental compartments when glyphosate is used for the control of illicit crops.

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of off-target deposition is spray drift. Experience with spray equipment of the type used in Colombia suggests that spray drift will be minimal (Payne et al. 1990). Estimates of accidental overspray have been made during assessments of spray program efﬁcacy (Helling 2003). Based on site visits to 86 ﬁelds sprayed in 2002 and observations of damaged plants beyond the boundary of the area cleared and planted with coca, 22 ﬁelds showed evidence of off-ﬁeld deposition. Using the size of these areas, it was estimated that between 0.25% and 0.48% of the areas cleared for coca production were damaged by offsite spray deposition (Helling 2003). Applying this estimate to the total area of coca sprayed (see Fig. 2) and calculating upper and lower intervals, the areas potentially affected are small when compared to the total area of Colombia (Table 3). Although the areas affected by off-target drift are estimated to be small, this estimate is based on visual observations of a relatively small number of ﬁelds. These data were available only for coca, not poppy; however, the total areas planted to poppy are not large, and similar off-target deposition would be proportionately smaller than that associated with coca production. This lack of data is a source of uncertainty in the assessment. It is not logistically possible to visually inspect all sprayed ﬁelds; however, routine monitoring of the areas planted to coca and poppy that is undertaken by satellite and low-altitude imagery could be used to assess off-target deposition resulting in damage to plants. Changes in the size of sprayed ﬁelds over time could be used to extend these estimates over larger areas and increase their accuracy, although extension of the ﬁelds by growers may confound the data. The lower resolution of satellite imagery may preclude its use for this purpose; however, greater coverage by low-altitude images could facilitate this process. Table 3. Estimates of Areas Affected by Off-Target Deposition of Glyphosate in the Spraying of Coca in Colombia. Area affected by off-target deposits (ha) Year

Hectares sprayed (ha)

Lower interval (0.25%)

Upper interval (0.48%)

Upper interval as percent (%) of the total area of Colombia

1994 1995 1997 1998 1999 2000 2001 2002 2003 2004

3,871 23,915 41,861 66,029 43,111 58,074 94,152 130,364 132,817 136,551

9.7 59.8 104.7 165.1 107.8 145.2 235.4 325.9 332.0 341.4

18.6 114.8 200.9 316.9 206.9 278.8 451.9 625.7 637.5 655.4

0.0000002 0.0000010 0.0000018 0.0000028 0.0000018 0.0000024 0.0000040 0.0000055 0.0000056 0.0000057

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B. Framework for Risk Assessment The following sections outline the conceptual model and hypotheses for the assessment of the human health and environmental impact of coca and poppy production in Colombia. Conceptual Model For purposes of the risk assessment of the use of glyphosate and adjuvants in the control of poppy and coca, the conceptual model applied was that normally applied to the agricultural application of pesticides where hazard and risk are directly related to toxicity and exposure. Thus, for human health, toxicity data were compared to exposures estimated from worst case data and also from more realistic data obtained in other uses of glyphosate, such as agriculture and forestry. Because of the low frequency of spray application, exposure from this source is acute and resulting risks were compared to acute toxicity data. Toxicity data for the active ingredient, glyphosate (IPA), were obtained from the literature and from the results of acute laboratory animal tests conducted with the mixture of formulated glyphosate and Cosmo-Flux as used in the spray program in Colombia. It is possible that glyphosate used in the eradication program may contribute to exposures via the food chain and drinking water; these exposures were estimated and compared with toxicity data and exposure guidelines based on chronic toxicity for glyphosate via dietary exposures. In addition, speciﬁc human health responses were assessed in epidemiological studies conducted in Colombia. In assessing ecological risks, a similar agriculture-based approach was used. Similar to the foregoing approach, exposures were estimated from worst case models, from measurements made in other locations, and from measurements based on samples collected from the environment in Colombia. Because of the long periods between applications, ecological exposures from the spray operations are acute and were compared to acute toxicity data. Toxicity data were obtained from the literature and from laboratory-based tests on standard test organisms that were speciﬁcally conducted on the spray mixture as used in Colombia. The risk hypotheses are discussed next, and the remainder of this review focuses on tests of these hypotheses. Risk Hypotheses A large number of hypotheses were actually tested in this risk assessment; however, they were basically the same hypothesis with minor differences in the exposure and toxicity parameters. As is normal in the scientiﬁc method (Popper 1979), these hypotheses are stated as the null or negative hypothesis; thus, we attempted to falsify or disprove these hypotheses through the use of appropriate data.

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For human health, two main hypotheses were used: • Exposures to glyphosate and adjuvants as used in the poppy and coca eradication programs do not cause acute adverse effects to humans exposed via a number of routes. • The use of glyphosate and adjuvants in those locations where eradication of poppy and coca are conducted does not result in acute and chronic health outcomes that are different from other locations where glyphosate is not used or is used in other agricultural practices. For ecological effects, one main hypothesis was used: • Exposures to glyphosate and adjuvants as used in the poppy and coca eradication programs do not cause acute adverse outcomes on nontarget organisms exposed via a number of routes.

III. Exposure Characterization Exposure characterization is one of the key components of any risk assessment (NRC 1993; USEPA 1992, 1998). No measurements of farmer or pesticide applicator exposures have been made in Colombia. An assessment of pesticide use among farmers in the Amazon Basin of Ecuador has shown that paraquat and glyphosate are widely used. Risk behaviors were identiﬁed as frequent pesticide use, washing pesticide equipment in water sources used by humans, inadequate disposal of empty containers, eating and drinking during application, and using inadequate protective clothing (Hurtig et al. 2003). However, agricultural uses such as these are quite different from the aerial applications in Colombia. In the following sections, the potential for exposures in humans and the environment to glyphosate as used in the eradication program is discussed and characterized. Human Exposure In the agricultural setting, two groups are usually considered—applicators and bystanders. The group that experiences the greatest probability of exposure is the applicator group, which here includes mixer-loaders, spray plane pilots, and technicians who service the aircraft. The second group includes bystanders who may come into contact with the herbicide during application via direct deposition if they are within the spray swath, are directly exposed to spray drift, are exposed to deposits of spray when they reenter treated ﬁelds, or are exposed through the consumption of sprayed food items or contamined drinking water. Applicator Exposure. Risk to applicators was not a speciﬁc target of this assessment; however, their exposure can be characterized. Based on observations of spray operations in several locations in Colombia, a number of measures are taken to reduce potential applicator exposure (Table 4).

Table 4. Protective measures used to reduce exposure of applicators to glyphosate and formulants as used in poppy and coca eradication programs. Applicator subgroup

Spray pilot

Aircraft technician

Technology for handling of the formulation and spray mix

Use of closed-loading systems and pumps to mix and transfer glyphosate and Cosmo-Flux to the aircraft.

Not involved in mixing and loading

Protective equipment worn

Long pants, long sleeves, full rubber apron, rubber gloves, cloth hat or cap, particulate air ﬁlter and dark glasses, leather military-style boots Eye-wash station at all locations, clean water for washing hands and any contaminated surfaces, a shower in some locations

None other than normal clothing, long sleeves, long pants, jacket, and boots

Not normally involved in mixing and loading; aircraft are washed down regularly so that exposure via contaminated surfaces is reduced Short or long sleeves, shorts or long pants, boots or sneakers, cloth cap or none

Equipment used to remove contamination, should it occur

Same as is available to the mixer-loader

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Mixer-loader

Same as is available to the mixerloader

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No measures of exposure were available for mixer-loaders in Colombia; however, they are likely to be similar to those of applicators in other situations. Based on observations on forestry and agricultural applicators (Acquavella et al. 2004; and summarized in Williams et al. 2000), exposures are generally small. Peak estimated exposure in applicators from all routes was 0.056 mg/kg body weight (bw). The estimate of chronic exposure from all routes was 0.0085 mg/kg/d based on an 8-hr day and a 5-d work week. In the results of the recently published Farm Family Exposure Study, the greatest estimated systemic dose in a sample of 48 applicators was 0.004 mg/ kg bw (Acquavella et al. 2004). In Colombia, mixing and loading are done by one or two individuals wearing appropriate protective equipment. Pilots have limited opportunity for exposure and, as has been observed in other studies (Frank et al. 1985), likely experience less exposure. Exposures of mixer-loaders in Colombia are likely to be similar to those observed in agricultural applications. Exposures for spray pilots and technicians will likely also be less than for applicators. While most of the protective clothing worn by mixer-loaders is appropriate, the need for a respirator is questionable and the use of dark glasses in place of a full face shield is judged inappropriate. Dark glasses will not protect the eyes from a splash to the forehead that runs into the eyes, a vulnerable area in terms of glyphosate exposure during mixing and loading (Acquavella et al. 1999). A full face shield offers better protection. As glyphosate is not volatile, nor atomized during mixing and loading, use of a respirator offers little reduction in potential exposure and complicates the use of a full face shield. The usefulness of a respirator is judged to be small. Bystander Exposure. Bystanders can be classiﬁed into several classes, depending on their route of exposure. These are discussed in the following sections. Bystanders Directly Oversprayed. Although it is unusual for people to be present in a coca ﬁeld during application, it is possible that a person could be standing directly in the spray swath and would receive a direct application of the spray. Several scenarios could occur (Fig. 6, Table 5). The most likely is the partially clothed human with a cross-sectional area of 0.25 m2 exposed to the spray (Table 5). Given that glyphosate penetrates poorly through the skin with maximum penetration of about 2% (Williams et al. 2000), the body dose under a reasonable worst case exposure will be approximately 0.08 mg/kg bw. Bystander exposure to glyphosate was estimated as 0.0044 mg/kg bw/d for a child 1–6 yr of age (Williams et al. 2000). Exposures to glyphosate were measured in bystanders to farm applications (Acquavella et al. 2004). These studies were conducted in spouses and children not involved in applications, and frequency of measurable exposure was small, with 4% and 12% of the spouses and children, respectively, with detectable exposures based on

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Fig. 6. Illustration of human exposure scenarios. Table 5. Estimates of human exposure to glyphosate during a spray application. Exposure in mg/kg bw Scenario Partially clothed human with cross-sectional area of 0.25 m2, complete penetration Partially clothed human with cross-sectional area of 0.25 m2, 2% penetration (most likely)

Coca: 4.992 kg/ha

Poppy: 1.2 kg/ha

1.8

0.4

0.04

0.01

Assumptions: body weight, 70 kg; body surface area, 2 m2.

urinary monitoring. The maximum systemic dose estimates for spouses and children were 0.00004 mg/kg and 0.0008 mg/kg bw, respectively (Acquavella et al. 2004). If bystanders are neither directly sprayed nor reenter the ﬁeld immediately after spraying, their exposures will likely be within a factor of 10 of farm bystanders. All these measured exposures are considerably less than those estimated in Table 6, considered to be reasonable worst case values. Reentry. If a person were to reenter the sprayed ﬁeld immediately after spraying and come into contact with the treated foliage, such as when

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Table 6. Estimates of human exposure to glyphosate during reentry to treated ﬁelds. Exposure in mg/kg bw Scenario Maximum reentry exposure estimated for an adult human with a 10-hr d Maximum reentry exposure estimated for a 1- to 6-yr-old child with a 10-hr d

Coca: 4.992 kg/ha

Poppy: 1.2 kg/ha

0.013

0.003

0.259

0.062

attempting to pick leaves from sprayed coca plants, exposure to glyphosate could occur through the hands and arms. Given the area exposed, the small penetration, and the saturation of the transfer that would result once the hands were wet, total body dose is likely to be less than the reasonable worst case scenario described in Table 6. The potential for reentry exposure has been summarized by Williams et al. (2000). Reentry exposures decreased with time after application and, on day 7 after application, were 3% of those estimated for day 1. Reentry into areas of tall weeds (height, 1.5 m) resulted in 10-fold-greater exposures than in areas of short grass. Based on measurements in farmworkers, estimates of reentry exposure to glyphosate in adults ranged from 0.0000039 to 0.0026 mg/kg bw/hr of reentry time. Maximum reentry exposure for a 1- to 6-yr-old child was estimated at 0.026 mg/kg bw for a 5-hr contact period. As these estimates are based on a spray application rate of 1 kg/ha, reentry exposures under Colombian conditions are estimated to be somewhat greater (see Table 6). These numbers are also greater than the direct overspray, as the persons involved may have repeated exposures if they reenter a ﬁeld immediately after spraying. Inhalation. Because the vapor pressure of glyphosate (isopropyl ammonium salt) is low (2.1 × 10−3 mPa at 25°C) and it also has a small Henry’s law constant (4.6 × 10−10 Pa m3 mol−1) (BCPC 2003), it will not be present in air as a vapor at biologically relevant concentrations. The droplet sizes resulting from the spray application of glyphosate in Colombia are large, with a mean droplet diameter ∼1,000 µm and with very few droplets <500 µm. As such, they are unlikely to be inhaled and penetrate into the lungs. Based on measurements of glyphosate concentrations in air during applications, the maximum estimated daily dose (8 hr) resulting from inhalation of spray droplets by applicators was 0.0062 mg/kg bw (Williams et al. 2000), a value that is judged to be applicable as a maximum exposure for bystanders. Dietary and Drinking Water. Dietary and drinking water exposures to glyphosate have been estimated to be relatively small under conditions of use in North America (Williams et al. 2000) (Table 7).

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Table 7. Worst case daily human exposure estimates for glyphosate (mg/kg bw/d) Female adult Sources Drinking water Diet Wild foods Total from diet and water

Female child (1–6 yr)

Acute

Chronic

Acute

Chronic

0.000036 0.024 0.045 0.069

0.000002 0.024

0.000110 0.052 0.045 0.097

0.000004 0.052

0.024

0.052

Values extrapolated from the above (Williams et al. 2000) to the greater application rate of 4.992 kg/ha used in control of coca Drinking water Diet Wild foods Total from diet and water

0.000179 0.119 0.224 0.343

0.00001 0.119 0.224 0.293

0.00055 0.259 0.224 0.483

0.000018 0.259 0.489 0.747

The results of monitoring programs conducted by the Danish Veterinary and Food Administration from 1997 to 1999 reported on the content of glyphosate and several other pesticides in cereals produced in Denmark (Granby and Vahl 2001). Based on the residues of glyphosate in cereals, intake of glyphosate for a 60-kg adult was estimated at 0.007 mg/d. Based on a study of 51 streams in nine midwestern U.S. states, the U.S. Geological Survey (USGS) reported the presence of glyphosate and a number of other herbicides in surface waters (Battaglin et al. 2005; Scribner et al. 2003). Of a total of 154 water samples collected during 2002, glyphosate was detected in 36%, and its degradation product, aminomethylphosphonic acid (AMPA), was detected in 69%. The greatest measured concentration of glyphosate in any sample was 8.7 µg/L, and the greatest concentration of AMPA detected in the USGS study was 3.6 µg/L. More recently, glyphosate and AMPA have been detected in association with urban inputs from wastewater treatment in the U.S. Maximum concentrations of glyphosate and AMPA were 2 and 4 µg/L, respectively (Kolpin et al. 2006). Concentrations of glyphosate detected in Colombian surface waters (see following) were usually less than 25 µg/L, the detection limit. Exposures from drinking untreated surface waters in areas where spraying takes place are judged to be small and infrequent. Environmental Exposures Air. The presence of glyphosate in air is unlikely because it, and the salt forms commonly used in glyphosate formulations, have essentially

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negligible vapor pressure. Spray droplets may, however, be present in air and are the likely reason for detection of glyphosate, along with other pesticides, in rainwater in the European Union (EU) (Quaghebeur et al. 2004). From 1997 to 2001, glyphosate was only detected in rainwater in Belgium in 2001 and then with a frequency of 10% and a maximum concentration of 6.2 µg/L. Water. If water is directly oversprayed, contamination of surface waters will result (see Fig. 5). Some coca ﬁelds are located near ponds and lakes and some are near streams and rivers (Helling 2003). Although surface waters are not deliberately sprayed, some overspray of small watercourses and the edges of ponds, reservoirs, and lakes may occur. In the absence of measured concentrations immediately after spraying in surface waters located close to ﬁelds, estimates of exposure were made using worst case assumptions (Table 8) based on water depth assumptions used by the USEPA (Urban and Cook 1986) and the EU (Riley et al. 1991). Glyphosate has been detected in surface waters (see foregoing discussion on human exposures through drinking water) in a number of locations.

Table 8. Estimates of concentrations of glyphosate in surface water after a spray application. Exposure in µg/L (glyphosatea) Scenario Surface water, 2 m deep, rapid mixing and no absorption to sediments, no ﬂow Surface water, 0.3 m deep, rapid mixing and no absorption to sediments, no ﬂow Surface water, 0.15 m deep, rapid mixing and no absorption to sediments, no ﬂow Surface water, 0.15 m deep, rapid mixing and 50% absorption to sediments, no ﬂow

Coca: 4.992 kg/ha (3.69 kg AE/ha)

Poppy: 1.2 kg/ha (0.89 kg AE/ha)

185

44

1,229

296

2,473

595

1,237

297

a Note that the concentration is expressed as glyphosate acid (AE) to allow comparison to exposures used in environmental toxicity testing. In both these exposures and in the toxicity testing of Cosmo-Flux, proportional amounts are present and the exposure and toxicity values are thus directly comparable and can be used to assess the hazard of the mixture as applied in Colombia.

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Glyphosate residues have been reported in surface waters in Denmark as a result of agricultural activities. These residues were observed as part of the Pesticide Leaching Assessment Program (PLAP), a project that was intended to study leaching potential of pesticides to groundwater (Kjaer et al. 2003, 2005). PLAP was focused on pesticides used in farming and monitored leaching at six agricultural test sites representative of Danish conditions. Water from special drilled wells and from normal tile drains was analyzed for glyphosate and aminomethylphosphonic acid (AMPA, a major degradate of glyphosate). It is not clear from the report if the samples were ﬁltered before analysis; this is important as glyphosate binds strongly to organic matter in soils and can be transported in this form. The presence of macropores in soil would facilitate transport to the tile drains. In the samples from PLAP collected following glyphosate applications, there were no detections of glyphosate or AMPA that exceeded 0.1 µg/L in any of the groundwater samples taken from suction cells (1 and 2 m below the surface), the vertical wells (about 1.5–5.5 m below surface), and the horizontal wells (about 3.5 m below surface). Glyphosate residues were detected in water from tiles draining the ﬁeld and were observed primarily in the autumn. The highest measured concentrations were 5.1 µg/L for glyphosate and 5.4 µg/L for AMPA. The calculated average annual concentrations of glyphosate and AMPA in drainage water were 0.54 and 0.17 µg/L, respectively, at one location, and 0.12 and 0.06 µg/L, respectively, at a second. At a third location, glyphosate and AMPA were detected but average concentrations of both were below 0.1 µg/L. In Danish soils, degradation of glyphosate was shown to be slower in sandy soils than gravel but leaching was observed only in rounded gravel soils (StrangeHansen et al. 2004), and leachate concentrations were less than 0.1 µg/L (Fomsgaard et al. 2003). Similarly, a study on fate of glyphosate in soils showed rapid dissipation with almost total dissipation 1 mon after application (Veiga et al. 2001). Given the small organic content of gravel and the presence of macropores between the grains of gravel, movement through this matrix is not surprising. Complete degradation in other types of soil is expected. Other authors have reported glyphosate residues in surface waters in Europe (Skark et al. 1998, 2004), although the frequency of detection was not large. These authors suggested that the contamination was from application to railroad beds, environments where gravel is used and where adsorption would be expected to be minimal. This conclusion is supported by other studies on the dissipation of herbicides applied to railroad beds (Ramwell et al. 2004) and highways (Huang et al. 2004; Ramwell et al. 2002). Application of glyphosate to hard surfaces in an urban context (road edges) can give peak runoff concentrations of 650 µg/L (Ramwell et al. 2002), but only 15 µg/L from a railway trackbed (Ramwell et al. 2004). In Germany, a study

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of two catchments found that nonagricultural pesticide use contributed more than two-thirds of the whole observed pesticide load in the tributaries and at least one-third in the Ruhr River (Skark et al. 2004). Most nonagricultural pesticides were derived from runoff from domestic, industrial and railway areas. Nevertheless, in Argentina, where glyphosate-tolerant soybean is now extensively grown and regularly treated, no residues have been observed in soil or water of either glyphosate or AMPA (Arregui et al. 2004). The USGS study on midwestern U.S. streams (Battaglin et al. 2005; Scribner et al. 2003) analyzed water samples ﬁltered through a 0.7-µm ﬁlter; thus, the concentrations represent dissolved glyphosate and AMPA. Measured values in this study ranged up to 8.7 µg/L. Although the glyphosate concentrations in surface waters in other areas where it is used in agricultural and other activities are relatively small, concentrations have not been measured in Colombia. To address this uncertainty, we conducted a monitoring study to measure levels of glyphosate, AMPA, and other pesticides in surface waters. This study was conducted in ﬁve locations in Colombia representing areas where spraying of coca was planned or where other agricultural activities were undertaken and were also near the human health studies. Sites were selected for safe access as well as ease of repeated sampling and are summarized in Table 9 with further details of temperatures, rainfall, and soil characteristics from separate reports (PTG 2005a–e). To characterize concentrations of glyphosate and AMPA in surface waters, samples were taken weekly for 24 wk (CICAD/OAS 2004a). Samples, in plastic bottles, were frozen and held at −17°C until shipped to Canada for analysis using published methods (Thompson et al. 2004). The method detection limit (MDL) for the analysis was 25 µg/L. Duplicate samples were taken and one sample held in Colombia until the duplicate had been analyzed. In addition, ﬁeld-spiked samples and blanks were taken at biweekly intervals. In addition to water, sediment samples were taken at monthly intervals for analysis of glyphosate and AMPA if signiﬁcant concentrations were detected in surface waters. Appropriate ﬁeld spikes and blanks of sediment were also taken bimonthly. Quality control samples showed excellent recovery and precision of the analytical method with 98% recovery for glyphosate and 8.8% coefﬁcient of variation (CV), and 110% recovery efﬁciency for AMPA with 20% CV. Blank ﬁeld sample analyses show no coextractive interferences above the MDL for either glyphosate or AMPA at any of the sample sites. Field-spiked samples showed no signiﬁcant degradation of glyphosate during handling and transport with overall average value of 90% of expected concentrations. Results are summarized in Table 9. In all locations and on most occasions, residues of glyphosate and AMPA were present at concentrations below the MDL of 25 µg/L. On one occasion each in Valle del Cauca and Boyacá, glyphosate concentrations of 30.1 and 25.5 µg/L, respectively, were found.

Table 9. Characteristics of sampling sites for glyphosate and other pesticides in surface waters and sediments in regions of Colombia and measured values in samples collected between October 2004 and March 2005.

Site name

Location

Altitude (m)

Major crop types

3°27.642′ N 76°19.860′ W

1002

Sugar cane

Boyacá, Quebrada Paunera

5°40.369′ N 74°00.986′ W

557

Coca

Sierra Nevada, Quebrada La Otra Putumayo, Río Mansoya

11°13.991′ N 74°01.588′ W 0°43.259′ N 76°05.634′ W

407

Organic coffee

329

Coca

Nariño, Rio Sabaletas

1°27.915′ N 78°38.975′ W

15

Coca

Glyphosate and other pesticides Manual eradication, no aerial spraying of glyphosate None Aerial eradication spraying Aerial eradication spraying

Other pesticides detected (n/N) and types

1 (4%)

(3/10) 2,4-D

1 (4%)

(0/8)

0 (0%)

(0/9)

0 (0%)

(0/9)

0 (0%)

(1/8) endosulfan I, endosulfan II, endosulfan sulfate

Glyphosate Assessment

Valle del Cauca, Río Bolo

Known pesticide use

Frequency of detection of glyphosate (n of 24, %)

69

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At these sites, spraying was not carried out and the only use of glyphosate, if any, was in agriculture. These data suggest that, at the watershed level, little or no contamination of surface waters with glyphosate at signiﬁcant concentrations has resulted from the use of glyphosate in either agricultural or eradication spraying in Colombia. As concentrations in surface waters were mostly below the MDL, sediment analyses were not performed. To characterize concentrations of other pesticides in surface waters and sediments, samples of water were taken in glass bottles every 2 wk for 22 wk (CICAD/OAS 2004b). Samples were held at 4°C until shipment to Canada for analysis. Analyses were conducted at the Laboratory Services Division of the University of Guelph using standard methods (LSD 2005). Duplicate samples were held in Colombia until analyses were completed. Field spikes and blanks were taken at 5-wk intervals, as were sediment samples. Sediment blanks and spikes were taken only once. These results are also summarized in Table 9. Blanks showed no contamination of samples during storage and shipping. Spiked samples showed variable recovery, particularly for the carbamate, carbaryl. Several pesticides were detected in surface waters, which is not unexpected as pesticides are widely used in agriculture in Colombia and, based on experience in other locations, some contamination of surface waters will occur. Of interest is the detection of endosulfan (I and II) and its breakdown product, endosulfan sulfate, in samples taken at the Nariño site. Endosulfan is not registered for use in Colombia, and its detection here likely is the result of illegal use. Whether this contamination resulted from regular agricultural activity or from use in the production of coca is unknown.

Soil. Concentrations of glyphosate in the top 25 mm of soil were estimated from the application rates and ranged from 1.6 to 3.2 mg/kg for poppy use rates and from 6.7 to 13.3 mg/kg for coca, depending on assumptions about interception by the crop foliage (50%) and soil density (1.5 kg/L). Measurements could be made through the use of residue analysis; however, the more important question is the biological availability of the glyphosate, as this would determine its potential for biological effects. Although there are no direct measurements of glyphosate and AMPA concentrations available from treated coca and poppy ﬁelds in Colombia, the biological activity of any residues that may be present is judged to be small as the sprayed ﬁelds rapidly become colonized with invasive plants or are replanted to coca soon after spraying. From visual observations (Fig. 7), from observation in other uses and other locations (above), and from other reports (Helling 2003), recolonization is rapid and there have been no adverse effects observed in terms of recolonization or replanting of sprayed ﬁelds.

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Fig. 7. Photograph of coca plants near Caucasia, Colombia, replanted from cuttings in a ﬁeld sprayed with glyphosate 56 days previously.

IV. Effects Characterization A. Glyphosate Human health and environmental effects of glyphosate have been extensively reviewed (Giesy et al. 2000; Solomon and Thompson 2003; Williams et al. 2000) and by regulatory agencies (NRA 1996; USEPA 1993a, 1997, 1999; World Health Organization International Program on Chemical Safety 1994). The following sections are primarily directed to a critical analysis of original articles published since 1999 or that were not included in the earlier reviews (Giesy et al. 2000; Solomon and Thompson 2003; Williams et al. 2000). In characterizing the effects of glyphosate, it is important to distinguish between glyphosate as the active ingredient (usually glyphosate IPA salt) and the formulated product, such as Roundup. Glyphosate salts readily dissociate into the free acid, and the acid and salts are considered toxicologically equivalent. Formulations of glyphosate contain additional formulants that modify uptake of the glyphosate into plants and may alter toxicity of the mixture. In the following sections, tests conducted with the active ingredient only are referred to as “glyphosate.” Those tests where a formulation was used are referred to by the speciﬁc product name, or where this is not known, as “glyphosate formulation.” To allow easy comparison between technical product and formulations, where possible, concentrations of glyphosate have been normalized to acid equivalents (AE).

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Effects of Glyphosate on Mammals Laboratory Toxicity Studies. The toxicity of glyphosate and the formulation Roundup were reviewed by Williams et al. (2000). Glyphosate acid and its isopropylamine salt have little acute toxicity by the oral, dermal, and subcutaneous routes of exposure (Table 10). Toxicity was greatest by intraperitoneal administration. When rats and mice were given glyphosate orally or intraperitoneally, several stress symptoms, such as increased respiration, elevated rectal temperatures, and occasional asphyxial convulsions, were noted. Median lethal doses of 4,704 mg/kg bw to the rat and 1,581 mg/kg bw to the mouse orally were signiﬁcantly higher than 235 and 130 mg/kg bw, respectively, median lethal doses obtained when glyphosate was given intraperitoneally. Lung hyperemia was the major lesion noted in the glyphosate-poisoned animal (Bababurmi et al. 1978). There is limited information on acute toxicity in dogs. However, there is a retrospective study conducted of 482 glyphosate-related calls recorded at the Centre National d’Informations Toxicologiques Vétérinaires (CNITV) of France between 1991 and 1994. Only 31 cases were assessed as certain or highly probable and were linked with direct ingestion of Table 10. Acute toxicity of glyphosate and formulations in selected mammals. Species Mouse

Route Oral Subcutaneous Intraperitoneal

Rat

Oral Dermal Inhalation

Compound administereda Glyphosate Glyphosate Glyphosate saline Glyphosate saline Glyphosate saline Glyphosate saline Glyphosate Glyphosate, Roundup, glyphosate isopropylamine salt Roundup Roundup, glyphosate saline

Subcutaneous

Glyphosate saline Glyphosate saline

Rabbit

Intraperitoneal Oral Dermal

Goat

Oral

Glyphosate Glyphosate Glyphosate, Roundup, glyphosate isopropylamine salt Glyphosate, Roundup, glyphosate isopropylamine salt

Source: Smith and Oehme (1992).

LD50 (mg/kg bw) >10,000 1,538 6,250 (M) 7,810 (F) 545 (M) 740 (F) 134 >5,000 >17,000 LC50 = 3.18 mg/L (4 hr) 17,500 281 (M) 467 (F) 238 3,800 >5,000 >3,500

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glyphosate concentrates or spray in 25 dogs. The symptoms were most frequently described as vomiting, hypersalivation, and diarrhea; prostration and paresis were not common. Symptomatic treatment resulted in rapid recovery without sequelae (Burgat et al. 1998). Campbell and Chapman (2000) described the onset of clinical effects in dogs observed in several cases of poisoning as usually between 30 min and 2 hr. Recovery usually occurs over 1–2 d. Salivation, vomiting, diarrhea, irritation, and swelling of lips are common early features. Tachycardia and excitability are often present in the early stages, with the animals subsequently becoming ataxic, depressed, and bradycardic. Inappetence, pharyngitis, pyrexia, twitching, shaking, and dilated pupils are noted occasionally. Rarely, jaundice, hepatic damage, and hematuria have been reported. Eye and skin irritation are also possible. Tachypnoea occurs in glyphosate poisoning in other animals but does not appear to be a feature of glyphosate toxicity in dogs. Studies to examine the effects of chronic feeding of glyphosate to Wistar rats have measured the activity of some enzymes with a function in the pathways of NADPH generation, isocitrate dehydrogenase, glucose-6phosphate dehydrogenase, and malate dehydrogenase in liver, heart, and brain of pregnant Wistar rats and their fetuses that were exposed to glyphosate solutions of 0.5% and 1% at a dose of 0.2 and 0.4 mL/mL water during 21 d of pregnancy. Glyphosate affects these enzymes in the studied organs of pregnant rats and their fetuses (Daruich et al. 2001). Feeding Glyphosate-Biocarbo formulation at rates of 4.87 mg/kg every 2 d for 75 d resulted in leakage of the hepatic intracellular enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), suggesting irreversible damage in hepatocytes (Benedetti et al. 2004). The formulation used in this study was from Brazil, and the identity and composition of the formulants are unknown. In addition, the exposures extended over a long period and were judged inappropriate for assessing risks from acute and infrequent exposures such as may occur in eradication spraying. The effect of glyphosate on the activity of several enzymes was studied in vitro. The enzymes measured were serum acetylcholinesterase (AChE), lactate dehydrogenase (LDH), aspartate amino-transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), and acid phosphatase (AcP). Glyphosate inhibited all enzymes except AcP. IC50 values were 714.3, 750, 54.2, 270.8, and 71.4 mM for ACHE, LDH, AST, ALT, and AP, respectively (El-Demerdash et al. 2001). The most sensitive response, that of AST, was observed at 54.2 mM, equivalent to a concentration of 9,056 mg/L, a concentration that would not occur in vivo. These results do not suggest that glyphosate would have effects at concentrations lower than those previously observed. Glyphosate has not been found to be mutagenic, genotoxic, or carcinogenic. Glyphosate was not teratogenic or developmentally toxic except at large exposures (Williams et al. 2000). Some studies that were not reviewed by Williams et al. or were published after 2000 are reviewed below.

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In a study on Charles River CD-1 rats, test animals were given oral gavage doses of 0, 300, 1,000 and 3,500 mg/kg bw/d of glyphosate from day 6–19 of gestation. Control animals received 0.5% methocel. No internal or skeletal anomalies were seen at 300 and 1,000 mg/kg bw/d, although maternal toxicity was apparent at 3,500 mg/kg bw/d with soft stools, diarrhea, red nasal discharge, reduced body weight, and death by gestation day 17 (6/25). In addition, mean fetal body weights were signiﬁcantly reduced and early fetal resorption was signiﬁcantly increased at this dose (Rodwell 1980b). Female Dutch belted rabbits were given oral gavage doses of 0, 75, 175, and 350 mg/kg bw/d glyphosate from day 6–27 of gestation. Control animals received 0.5% methocel. No internal or skeletal abnormalities were seen (Rodwell 1980a). In a study from Brazil, examination of pregnant Wistar rats dosed orally with Roundup from day 6–15 of pregnancy with rates of 0, 500, 750, or 1,000 mg/kg bw glyphosate showed skeletal alteration in fetuses (15.4%, 33.1%, 42.0%, and 57.3%, respectively). There was 50% mortality of dams at 1,000 mg/kg only (Dallegrave et al. 2003). The doses were large and considerably greater than those used in an earlier study (reviewed by Williams et al. 2000). In the earlier study, a noobserved-effect-level (NOEL) of 15 mg/kg bw/d was described for fetal effects and 300 mg/kg bw/d for maternal effects. Given the very large doses used in the Dallegrave et al. (2003) and Rodwell studies (1980), their results are not surprising and do not change the assessment of teratogenic potential in Williams et al. (2000). A number of recent studies have been carried out in tissue culture. One assessed the affect of several formulated pesticides on the steroidogenesis pathway (StAR protein synthesis) in tissue cultures of mouse testicular Leydig tumor cells (Walsh et al. 2000). Exposure to the formulation at 25 mg/L in the cell culture medium caused a reduction in steroidogenesis but only for a period less than 24 hr during which there was recovery. In another study, Lin and Garry reported results of bioassays carried out in cultures of the MCF-7 breast cancer cell (Lin and Garry 2000). Results indicated that although some pesticides caused estrogen-like receptormediated effects at large exposure concentrations, both glyphosate and the Roundup formulation induced nonestrogen-like proliferation, thereby supporting the view expressed by others (Williams et al. 2000) that neither glyphosate nor Roundup is an endocrine disruptor. Studies on cells in vitro are difﬁcult to interpret as they exclude the normal pharmacokinetic and metabolic functions that would be present in whole animals; thus, these should be compared to the multigenerational study used by regulatory agencies worldwide to assess reproductive/developmental toxicity, which is the most deﬁnitive study design for the evaluation of potential endocrine modulating substances in humans and other mammals. Comprehensive reproductive and developmental toxicology studies carried out in accordance with internationally accepted protocols have demonstrated that glyphosate is not a developmental or reproductive

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toxicant and is not an endocrine disruptor (Williams et al. 2000; USEPA 1993a; World Health Organization International Program on Chemical Safety 1994). There was no evidence of neurotoxicity in a number of studies reviewed in Williams et al. (2000). Neurotoxicity was not observed in the large number of acute, subchronic, and chronic studies conducted in rodents nor was it observed in two speciﬁc neurotoxicity studies conducted in dogs. However, these studies did not assess potential effects on neurotransmitters and their metabolites in the brain and other parts of the nervous system, measures of response used in current testing protocols for neurotoxicity. Some reports on the immunotoxicity of glyphosate appear in the literature. Female CD-1 mice exposed to Roundup at concentrations up to 1.05% in drinking water for 21 d showed no change in immune function (Tlymphocyte and macrophage-dependent antibody response) when, on day 21 of the exposure period, they were inoculated with sheep erythrocytes (Blakley 1997). In an in vitro study on cytokine production by human peripheral blood mononuclear cells, glyphosate had only a slight effect at the greatest concentration tested (1,000 µM = 226,000 µg/L) (Nakashima et al. 2002). Results of both studies suggest that glyphosate does not affect immune response in mammals at realistic exposure concentrations. However, studies in ﬁsh suggest that that there may be some immunotoxic effects. Short exposures to Roundup (10 min at a concentration of 100,000 µg/L) in carp (Cyprinus carpio) and European catﬁsh (Silurus glanis) caused a decrease in metabolic and phagocytic activity as well as proliferative response (Terech-Majewska et al. 2004). In contrast to these effects at large concentrations, responses on splenic antibody plaque-forming cells in the ﬁsh Tilapia nilotica were reported at concentrations of 1.65 × 10−2 µM (= 4.4 µg/L). As responses of the immune system are difﬁcult to interpret in terms of survival of individuals or the population, they are not formally used in assessment of pesticides by regulatory agencies. Toxicokinetics of glyphosate were reviewed by Williams et al. (2000). Between 15% and 36% of ingested glyphosate is absorbed through the intestinal tract and only about 2% via the skin. Excretion of unabsorbed glyphosate is via the feces, but the absorbed glyphosate is excreted via the urine with only a small amount of metabolism. Whole-body half-lives were biphasic, with an initial half-life of 6 hr and a terminal elimination half-life of 79–337 hr in rats (Williams et al. 2000). Clearance from most tissues was rapid but was cleared more slowly from the bone, possibly because of ionic binding to bone calcium (Williams et al. 2000). Glyphosate is clearly not bioaccumulated, and any absorbed dose is excreted in the urine relatively rapidly. Cases of Human Poisoning. A number of anecdotal reports of human poisoning with glyphosate and its formulations have been published. In some cases, these are reports of a single event and an observed response.

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In one, toxic pneumonitis was observed after exposure to a glyphosate formulation (Pushnoy et al. 1998). However, no information was provided to demonstrate how airborne exposure could have occurred and the results are at odds with the known inhalation toxicity of the formulation (Williams et al. 2000) and tests done on the product as used in Colombia (see following). In another case, a man accidentally sprayed himself with an unidentiﬁed formulation of glyphosate (Barbosa et al. 2001). He developed skin lesions 6 hr after the accident but these responded to routine treatment. However, 1 mon later, the patient presented with a case of symmetrical Parkinsonism syndrome. This is an isolated case, and it is impossible to conclude anything about causality as the disease may have already been present but asymptomatic. In a similar case, a 78-yr-old woman presented with extensive chemical burns in legs and trunk caused by an accidental contact with a glyphosate formulation. These lesions disappeared, without consequences, a month later (Amerio et al. 2004). Acute intoxication information has been documented in two case-series studies, from Taiwan, China, where glyphosate formulations were apparently used for attempted suicide (Chang et al. 1999; Lee et al. 2000). The ﬁrst paper analyzed 15 intentional intoxications with glyphosate formulation and found that 68% of the patients presented esophageal, 72% gastric, and 16% duodenal injuries. Esophageal injury was the most serious injury but was minor in comparison with that caused by strong acids. Lee et al. (2000) analyzed 131 suicide attempts in southern Taiwan. The most common symptoms were sore throat and nausea; the fatality rate was 8.4%. In this study, 20.5% presented respiratory symptoms and more than half of them needed intubations. The authors propose that direct damage to the airway passage occurs and mention that the surfactant in the formulation (POEA MON 0818) may be responsible for the toxicity. In many cases, the exact doses consumed by persons attempting suicide are not known, and it is difﬁcult to interpret these ﬁndings in the context of bystander and other accidental exposures, which are usually many orders of magnitude less. It is, however, interesting to note the low fatality rate compared to what has been reported from other pesticides such as paraquat and the organophosphorus insecticides (Krieger 2001). It is well known that the older formulations of glyphosate that contained the surfactant POEA (MON 0818) in larger amounts were eye irritants. Goldstein et al. (2002) analyzed 815 glyphosate-related “calls” to the Pesticide Illness Surveillance Program (PISP), most of them involving eye irritation (399), skin (250), upper airway (7), and combinations of these. Of the 187 systemic cases, 22 (12%) had symptoms deﬁnitely related to exposure to formulations of glyphosate. Again, this is not surprising as the formulation of glyphosate is acidic, similar to strong vinegar, and the surfactant is an eye irritant. In other studies on eye and skin irritation reviewed in Williams et al. (2000), none of the reported exposures resulted in permanent

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change to the structure or function of the eye. Based on these ﬁndings, it was concluded that the potential for severe ocular effects in users of Roundup herbicides is extremely small. This observation is consistent with the minimal ocular and dermal effects observed with the formulation of glyphosate used in Colombia (see below). Human Epidemiology Studies. A number of studies in the recent epidemiology literature have attempted to address the issue of glyphosate exposure and disease incidence in humans. Epidemiology studies on pesticides commonly suffer from two sources of error. Possibly the most important of these is the error in assigning exposures. Exposures in the studied population are never measured directly and it is common to use surrogates for exposures such as areas treated with pesticides, number of applications, and/or number of years of application. Studies have shown that these surrogates are susceptible to signiﬁcant errors (Arbuckle et al. 2004). Similar conclusions have been put forward by others (Arbuckle et al. 2005; Harris et al. 2002; Solomon et al. 2005b). A second possible source of error is the fact that the populations that are studied (farmers and professional applicators) typically use many pesticides. Thus, any substance-speciﬁc responses and causality are difﬁcult to ascertain. Cancer Studies. The work of Hardell et al. (2002) presented a pooled analysis of two case-control studies, one on non-Hodgkin’s lymphoma (NHL) (Hardell and Eriksson 1999) and another related to a hairy cell leukemia (HCL), a rare subtype of NHL. The 1999 study employed a casecontrol study design based on a total of 442 subjects; however, only 4 cases and 3 controls, or less than 1% of the overall study subjects, reported the use of glyphosate. The conclusions are thus based on small numbers and the conﬁdence interval (CI) reported for exposure to glyphosate was 0.4–13, showing a lack of statistical conﬁdence. In their pooled analysis, Hardell et al. (2002) reported a positive association with use of glyphosate [odds ratio (OR) 3.04, 95% CI of 1.08–8.52] when analyzed using univariate statistics with the highest risk for exposure during the latest decade before diagnosis. However, the OR was reduced when using multivariate statistics (OR 1.85, 95% CI of 0.55–6.20). In addition, the study was based on a small number of cases and controls (8/8) and lacked power to differentiate linkages. De Roos et al. (2005) evaluated associations between glyphosate exposure and cancer incidence in the Agricultural Health Study (AHS), a prospective cohort study of 57,311 licensed pesticide applicators in Iowa and North Carolina. Among private and commercial applicators, 75.5% reported having ever used glyphosate, of which >97% were men. In their analysis, glyphosate exposure was deﬁned as (a) ever personally mixed or applied products containing glyphosate, (b) cumulative lifetime days of use, and (c) intensity-weighted cumulative exposure. Glyphosate exposure was not associated with incidence of 12 common cancer types [the relative risk (RR)

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included 1 in all cases]; however, the RR for multiple myeloma incidence was 2.6 (95% CI of 0.7–9.4 based on 32 cases of the total of 2,088 cancers), prompting the authors to suggest that this should be followed up in future studies. Overall, there is no strong evidence to link glyphosate exposure to increased risk of cancer. Taken with the lack of any evidence of genotoxicity or carcinogenicity of glyphosate in laboratory studies (Williams et al. 2000), it is highly unlikely that glyphosate is carcinogenic in humans. Neurological Effects. A recent study on farmers in the Red River Valley in Minnesota (USA), reported on the link between glyphosate and attention deﬁcit disorder and attention deﬁcit hyperactivity disorder (ADD/ ADHD) in children of farmers who applied it (Garry et al. 2002). They reported an OR of 3.6 (95% CI, 1.3–9.6); however, the study suffered from several potential sources of error. The authors noted the lack of uniform diagnostic neurobehavioral information related to ADD/ADHD and that their study identiﬁed 14 cases of ADD/ADHD among 1,532 live births, a frequency that was actually considerably lower than background rates of ADD/ADHD which had previously been reported by researchers in Canada and the U.S. Notwithstanding, while Garry et al. (2002) concluded that their study showed a tentative association between ADD/ADHD and the use of glyphosate, they also noted that other experimental evidence did not support this conclusion, including that glyphosate was not genotoxic and that little, if any, evidence of neurotoxicity has been associated with exposure to glyphosate, except in cases of intentional oral overdose. Finally, the authors expressed concern that their tentative conclusions could be explained by random chance alone and stated the need for further detailed neurodevelopmental studies to resolve these outstanding issues. Overall, there appears to be little evidence to support a link between glyphosate exposure and neurobehavioral problems in children of exposed applicators. Reproductive Outcomes. Several papers have reported on the relationship between adverse reproductive outcomes and the use of glyphosate. In a study in Ontario, Canada, Arbuckle et al. (2001) observed a moderate increase in the risk of late abortions associated with preconception exposure to glyphosate (OR = 1.7, 95% CI, 1.0–2.9). Another study in Ontario, part of the Ontario Farm Family Health Study, reported a positive association (decrease in fecundability of 20%, ratio range = 0.51–0.80) when both spouses participated in activities where they could be exposed to pesticides. This ﬁnding was observed for 6 of 13 pesticide categories, 1 of which was glyphosate (Curtis et al. 1999). The study was based on 2,012 planned pregnancies. There was no strong or consistent pattern of associations of pesticide exposure with time to pregnancy (TTP). For exposure intervals in which only the men participated in pesticide activities or in which neither men nor women participated in pesticide activities but pesticides had been

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used on the farm, conditional fecundability ratios ranged from 0.75 to 1.50, with no apparent consistency among pesticide classes, chemical families, or active ingredients. Again, although this study did suggest a linkage between pesticide exposure and fecundability, there is no evidence from laboratory studies that glyphosate is a reproductive toxicant at exposures that would be expected in humans (Williams et al. 2000). Overall, there is little epidemiological evidence to link glyphosate to any speciﬁc diseases in humans. This conclusion is supported by laboratory toxicity studies. However, responses related to reproductive outcomes such as fecundability measured through time to pregnancy offer a useful measure of possible effects that can be applied in situations such as Colombia where other health data are difﬁcult to gather. With this in mind, a preliminary study was designed to gather human epidemiological data in several regions in Colombia. These regions were the same as those selected for the surfacewater sampling (see Table 9). The design and results are summarized in the following section; a detailed report is given in a separate document (Sanin 2005). Human Health Effects – Time to Pregnancy. A speciﬁc study was conducted to elucidate possible effects on reproductive health from exposure to glyphosate and adjuvants by assessing fertility/fecundability among women resident in different areas of the country with different pesticide use patterns. The design was cross-sectional with retrospective collection of data and is equivalent to a retrospective cohort. The study population consisted of 600 women of reproductive age in each of ﬁve different areas (see Table 9). The independent variable in the study was exposure to glyphosate for control of illicit crops, measured through use information from the region as indicated in Table 9. Possible confounders or independent predictors of reproductive variables in study the were also considered (Sanin 2005; Solomon et al. 2005a). The distribution of pregnancies in relation to time to pregnancy (TTP) (Fig. 8) was different among the ﬁve regions. In previous work in Colombia (Idrovo et al. 2005), the percentage of pregnancies for ﬁrst month was about 30%, small compared with data from developed countries. In this case, Valle del Cauca had very small initial percentage and Boyacá had larger values for the 1st and 12th months (Fig. 8). The mean for 12 mon in developed countries is 85%–90%. In the crude analyses, longer TTP was associated with a number of factors such as region, older maternal age, ethnic group, irregular menstrual cycles, and irregular partner relationship. Previous visits to a physician for problems related with fertility, X-rays taken in the year before pregnancy (YBP), and coffee consumption in the YBP also were associated with longer TTP. Coffee consumption had a signiﬁcant test for trend, but the odds ratio (OR) was not signiﬁcant. Maternal overweight was associated with a longer TTP. A tendency to longer TTP was observed among those

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Fig. 8. Time to pregnancy (TTP) in the ﬁve study regions in Colombia.

engaged in some waged work and with higher education. Paternal unemployment or self-employment was associated with longer TTP. No other paternal data were related with the TTP. In the ﬁnal multivariate model, the main predictor of TTP was the region adjusted by irregular relationship with partner and maternal age at ﬁrst pregnancy. Boyacá had the minimal risk and was the reference region; Nariño, Sierra Nevada, and Putumayo had slightly greater risk. The greatest risk was in the Valle del Cauca region. There was no association between TTP and use of herbicides in the control of illicit crops in the regions studied. The reason(s) for the increased risk for longer TTP in the Valle del Cauca region, where sugar cane is grown, is not known. In this study, the increased risk in Valle del Cauca cannot be attributed to exposure to pesticides alone because Sierra Nevada, where organic crops are grown, also showed a statistically signiﬁcant difference from the reference location where pesticides are used (Boyacá). This study was designed to test hypotheses related to the use of glyphosate in eradication spraying, and the data cannot be used to identify causality associated with other risk factors. To test this question in Valle del Cauca or any other region, a new study would have to be designed and conducted. Some of the factors associated with higher TTP that were identiﬁed should be included in any future studies.

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Effects of Glyphosate in Nontarget Organisms in the Environment The mechanism of action of glyphosate is via the disruption of the shikimate metabolic pathway that leads to the synthesis of aromatic compounds in numerous microorganisms and plants. Glyphosate translocates to active growing tissues; this is particularly effective in most plants because its degradation is slow. Thus, the herbicide moves throughout the plant before symptoms are noticed. The shikimate pathway is absent from mammals (Eschenburg et al. 2003; Roberts et al. 1998, 2002). However, toxic effects of the compound on, for example, nonmammalian aquatic organisms, have been observed at large concentrations. These effects are discussed in more detail below. A common question in conducting risk assessments in tropical regions and other nontemperate regions is the paucity of toxicity data for “tropical species.” It is true that most of the test species used in toxicity testing, particularly of pesticides, are “temperate species” largely because of the location of testing laboratories that are able to conduct guideline toxicity tests under Good Laboratory Practice (GLP). Except for a few substances with deﬁned mechanisms of action, there is no reason to believe that organisms from tropical regions are inherently more or less sensitive than organisms from temperate regions. It is well known that DDT and some of the pyrethroids become more toxic at lower temperatures (Dyer et al. 1997); however, the mechanisms here are well understood and do not apply to glyphosate. Comparison of responses of tropical and temperate organisms to a number of pesticides other than DDT has shown that there are no signiﬁcant differences in sensitivity (Maltby et al. 2005). With this in mind, we used the rich data set of toxicity values that have accumulated in the literature for glyphosate and its formulations. Effects in Nontarget Terrestrial Animals. The potential environmental effects of glyphosate and Roundup were extensively reviewed in 1999 (Giesy et al. 2000). Additional papers have appeared since then. Soil Invertebrates. The effects of glyphosate and formulations on earthworms have been reviewed (Giesy et al. 2000) and risks were judged to be essentially negligible. A recent study on the earthworm Eisenia fetida reported that, although a commercial formulation of glyphosate was not directly toxic to the earthworms, it did cause effects on locomotory activity that may be detrimental to the earthworms (Verrell and Van Buskirk 2004). The formulation used in the study was Ortho Groundclear Total Vegetation Killer, which contains 5% by volume glyphosate as the isopropylamine salt (IPA). In this study, the authors applied 82 mL of a 1 : 4 solution of Groundclear to 2 L of soil in a plastic box, an amount much greater than would be applied under normal agricultural uses or in the control of illicit crops. Assuming that the boxes of soil were cubes, the area of the surface would

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be 12.6 × 12.6 cm or 159 cm2. This being so, the application rate was equivalent to 518 kg glyphosate/ha, a totally unrealistic application rate and 100 times more than that used in the control of coca. This study was seriously ﬂawed, and the results are not applicable to any ﬁeld use of glyphosate. Soil Microorganisms. Glyphosate and its formulations have little effect on soil microorganisms (Giesy et al. 2000). Because the symbiotic soil and root-associated microorganisms may be partially dependent on the plant for nutrients, the death or injury of the plant will affect the organisms associated with it. Similarly, death of the plants will release organic matter and nutrients into the soil, affecting soil microorganisms similarly to the application of compost or fertilizer. This response, as reported for glyphosate formulation and its effects on grass (Tenuta and Beuchamp 1995), would also occur with other herbicides and with mechanical control of plants. Effects have been demonstrated in hydroponically grown plants exposed through the watering solution; however, this route of exposure is not relevant to ﬁeld conditions where glyphosate would bind strongly to soil particles and not be biologically available. Effects on symbiotic microbiota have also been demonstrated in glyphosate-tolerant plants treated at 10 times normal ﬁeld application rates, but these are not relevant exposures as the studies were done in vitro and in the absence of soil (Mårtensson 1992). Some effects on metabolism of phenolic substances in symbiotic bacteria in glyphosate-tolerant soybeans have been shown; however, these changes did not alter nitrogenase activity (Hernandez et al. 1999). Microbial systems in soil are complex, and considerable variation can be expected among tests and among soil types. More-recent studies on the effects of glyphosate on microbiological activity in soils have shown an increase in microbiological activity, mainly in fungi, which are likely using the glyphosate as a source of carbon, nitrogen, and phosphorus (Araujo et al. 2003; Haney et al. 2002; Laatikainen and Heinonen-Tanski 2002). These changes in microbiological activity are not judged to be deleterious. The effects of several fungicides and herbicides on the growth of the ectomycorrhizal fungi Lactarius deliciosus, strain LDF5, and Pisolithus tinctorius, strains 30AM, 3SR, and Mx, in pure culture have been studied. Glyphosate (formulation unspeciﬁed) at concentrations of 0, 1, 10, 100, and 1,000 mg/kg soil had no effect (Diaz et al. 2003). Some 64 strains of ectomycorhizal fungi were tested against the most common pesticides used in forestry in Finland. Glyphosate did not produce strong inhibition in any of the strains, most were unaffected, and some were stimulated by 1 mg/L Roundup Bio in agar (Laatikainen and Heinonen-Tanski 2002). Laboratory tests on four species of entomopathogenic fungi have shown that glyphosate has no effect, but a range of formulated products did have fungicidal properties, especially RoundUp Ready-To-Use (Morjan and Pedigo 2002). In fact, as fungi and bacteria have the shikimate pathway, this suggests the potential use of shikimate pathway inhibitors for the beneﬁcial control of

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fungal pathogens and apicomplexan parasites, such as Toxoplasma gondii, Plasmodium falciparum, and Cryptosporidium parvum (Roberts et al. 1998, 2002). Analysis of all lines of evidence for effects of glyphosate and its formulations on soil microorganisms indicates that adverse effects would be unlikely as a result of application at normal ﬁeld rates. Any minor effects to communities, such as described above, would be expected to disappear rapidly (Giesy et al. 2000; World Health Organization International Program on Chemical Safety 1994). After reviewing several studies conducted in many climates, in different soils over the past 10 years, and under various cropping systems, Motavalli et al. (2004) have concluded that, so far, glyphosate and its formulations have no relevant effect on nutrient transformations by microbes. However, they point out that this topic needs further study, as not every situation has been adequately researched. Further, because of lack of bioavailability on soils, adverse effects on beneﬁcial soil fungi and bacteria are unlikely to occur under ﬁeld conditions. Glyphosate binds strongly to soil particles and would not be available for uptake by microorganisms, many of which are actually inside the plant tissues. The fact that seeds will readily germinate in soils soon after treatment with glyphosate and that nitrogen-ﬁxing Roundup Ready soybeans grow and develop high yields despite treatment with glyphosate demonstrates the practical insigniﬁcance of these effects under actual use conditions. Terrestrial Invertebrates. As glyphosate is a nonselective herbicide, it will cause habitat alteration, which also results from a number of human activities in the production of food and ﬁber. Most important is the clearing of land for agricultural production. Whether this is through slash-and-burn processes as used in the initial preparation of coca and poppy ﬁelds or the application of herbicides such as glyphosate and paraquat, also used in coca production, the effects on nontarget species are the same. Use of cultural or mechanical controls, or herbicides, to remove plants will have effects on organisms that normally use these plants for food or shelter. After applying glyphosate formulation at double the recommended application rates, no effects were observed in microarthropods in soil (Gomez and Sagardoy 1985). Because weed species compositions and densities are directly affected by glyphosate, indirect effects are more likely to occur. Jackson and Pitre (2004b) found that populations of adult Cerotoma trifurcata, adult Spissistilus festinus, larvae of Plathypena scabra, and the caterpillar of Anticarsia gemmatalis were unaffected by glyphosate formulation, but populations of adult Geocoris punctipes, a homopoteran insect predator, were decreased. This effect was caused by reduced weed densities after herbicide treatment. Populations of green cloverworm (Hypena scabra) were evaluated on soybean glyphosate-resistant varieties, with and without exposure to glyphosate [glyphosate acid Roundup Ultra at 2.48 kg equivalent per hectare (AE/ha)], and no differences among treatments

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were detected on developmental time and survivorship (Morjan and Pedigo 2002). Weed management systems, more than glyphosate, that allowed more weeds to grow generally had higher insect population densities (Buckelew et al. 2000). Effects of glyphosate and associated cultural practices can affect arthopods indirectly. In studies conducted in the U.K., indirect effects of glyphosate were observed in the spider Lepthyphantes tenuis, caused by habitat alteration and related to death of plants and decreasing height of vegetation. Applications of glyphosate had only a within-season indirect habitat effect on L. tenuis as ﬁeld margins sampled 16 mon after an application of 360 g glyphosate AE/ha showed no detrimental effects (Bell et al. 2002; Haughton et al. 2001). Tests of the fecundity and mortality of Geocoris punctipes (Say), exposed to glyphosate as Roundup on soybean found no effects over 10-d posttreatment. Exposure of G. punctipes eggs to Roundup Ultra spray had no effect on egg hatch (Jackson and Pitre 2004a). Some reductions in numbers of this species 3 wk after treatment probably reﬂect weed removal (Jackson and Pitre 2004b). Similarly, studies on populations of leaf litter invertebrates in areas of Australia where Roundup Biactive was sprayed at 1–1.4 kg/ha for the control of an invasive weed showed no signiﬁcant effects 4 mon after spraying (Lindsay and French 2004). Variability in treated and untreated areas was large and suggested that the nature of the vegetative community and its structure and the postspray weather may also be important. In agriculture, these effects are part of the risk assessment related to integrated pest management (IPM), and potential effects on beneﬁcial organisms are weighed in the risk–beneﬁt equation. In conclusion, there is little evidence of any direct effect of glyphosate on insects in the ﬁeld or in natural environments. Terrestrial Vertebrates. Technical glyphosate, formulated glyphosate (above), and glyphosate mixed with Cosmo-Flux (see below) are not acutely toxic to mammals via several routes of exposures. Although wild mammals have not been speciﬁcally tested with the mixture as used in Colombia, data from these laboratory studies suggest that they would be insensitive and not directly affected by a direct overspray. Birds are not susceptible to glyphosate. In studies on bobwhite quail (Colinus virginianus) and mallard duck (Anas platyrhynchos), acute oral LD50 values of >4,640 and >4,640 mg/kg bw have been reported (USEPA 2001). Again, direct effects of formulated glyphosate or glyphosate plus Cosmo-Flux are judged to be very unlikely. Indirect effects on terrestrial wildlife have been reported with the use of glyphosate in agriculture and forestry. Alteration of habitat is more of an issue in semiwild areas such as forests where herbicides may be used to control competing vegetation and allow conifers to grow and mature more rapidly. In these cases, short-term effects on birds and other wildlife do

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occur; however, these populations usually recover in 2–3 yr (Kimball and Hunter 1990; Santillo et al. 1989a,b), and even the vegetation recovers in less than 10 yr (BC Ministry of Forests 2000; Boateng et al. 2000). Normally, in these uses, the actual areas treated are relatively small and are surrounded by or adjacent to untreated areas that can act as refugia or sites for repopulation by animals that have moved away because of the changes in habitat. As new vegetation develops to replace that controlled by the herbicide, the habitat will again become usable by these animals (Giesy et al. 2000; World Health Organization International Program on Chemical Safety 1994). Glyphosate is widely used for vegetation management, including the restoration of native plant communities where exotic or invasive species are controlled (Hartman and McCarthy 2004). The use of glyphosate for “conifer release” from competition has minimal effects on wildlife and can be used to enhance biodiversity if used for spot and patch treatments (Sullivan and Sullivan 2003). A review of management of northern U.S. forests, including the use glyphosate, indicated no adverse ecological effects (Lautenschlager and Sullivan 2002). However, the impacts of vegetation removal by manual clearance and glyphosate application in conifer plantations had effects on bird communities in British Columbia, mediated by the removal of deciduous plants. Where the herbicide was used, number of bird species declined, total number of individuals increased, and common species dominated. Populations of residents, short-distance migrants, ground gleaners, and conifer nesters increased signiﬁcantly after herbicide treatment. Deciduous nesters and foliage gleaners increased in abundance (nonsigniﬁcantly) in control and manually thinned areas. Warbling vireos (Vireo gilvus), which are deciduous specialists, declined in treated areas and may be particularly susceptible to the indirect effects of glyphosate plant removal (Easton and Martin 1998; 2002). Nevertheless, control of Cirsium arvense (Canada thistle) using wick application of glyphosate in wildfowl areas can enhance plant diversity that beneﬁts water birds (Krueger-Mangold et al. 2002). However, the broadspectrum activity of glyphosate means that accidental overspray of rare nontarget plant species during control of invasive plants will cause damage (Matarczyk et al. 2002). Beneﬁcial Insects. Glyphosate is not considered toxic to honeybees, with a reported LD50 of >100 µg/bee (USEPA 2001), however, the formulation, with the adjuvant Cosmo-Flux, as used in Colombia may have different toxicity because of the added surfactants. To test this hypothesis, toxicity testing of a mixture of a commercial formulation of glyphosate and the surfactant Cosmo-Flux 411F was conducted to determine the acute contact toxicity to honey bees (Apis mellifera L.) (Stantec 2005a), following standard test guidelines (OECD 1998a; USEPA 1996a). The mixture of glyphosate and Cosmo-Flux 411F was not toxic via acute contact exposure to honeybees (i.e., did not cause mortality or stress effects in bees within 48-hr

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of treatment) at concentrations equal to or less than 63.9 µg AE/bee. These results are similar to those for glyphosate and formulations from the USEPA ECOTOX data base (USEPA 2001) and show that the formulated product as used in Colombia is not hazardous to bees or, by extrapolation, to other beneﬁcial insects. Effects in Aquatic Animals. Several extensive reviews of the effects of glyphosate on aquatic organisms have concluded that glyphosate presents an essentially negligible risk to aquatic organisms (Giesy et al. 2000; Solomon and Thompson 2003; World Health Organization International Program on Chemical Safety 1994). Several publications reported on the effects of glyphosate and several of its formulations in frogs. The acute toxicity of technical-grade glyphosate acid, glyphosate isopropylamine, and three glyphosate formulations to Australian frog species was measured by Mann and Bidwell (1999). Acute toxicity was observed for adults of one species and tadpoles of four species of southwestern Australian frogs in 48-hr static/ renewal tests. The 48-hr LC50 values for Roundup herbicide (MON 2139) tested against tadpoles of Crinia insignifera, Heleioporus eyrei, Limnodynastes dorsalis, and Litoria moorei ranged between 8,100 and 32,200 µg/L (2,900 and 11,600 µg AE/L, whereas the 48-hr LC50 for Roundup herbicide tested against adult and newly metamorphosed C. insignifera ranged from 137,000 to 144,000 µg/L (49,400–51,800 µg AE/L). These values were different, depending on the type of dilution water (lake or tap water). For the purposes of this risk assessment, the most sensitive stage was used. Touchdown herbicide (4 LC-E) tested against tadpoles of C. insignifera, H. eyrei, L. dorsalis, and L. moorei was slightly less toxic than Roundup with 48-hr LC50 values between 27,300 and 48,700 µg/L (9,000 and 16,100 µg AE/L, respectively). Roundup Biactive (MON 77920) was practically nontoxic to tadpoles of the same four species, producing 48-hr LC50 of 911,000 µg/ L (328,000 µg AE/L) for L. moorei and >1,000,000 µg/L (>360,000 µg AE/L) for C. insignifera, H. eyrei, and L. dorsalis. Technical glyphosate isopropylamine salt was practically nontoxic, producing no mortality among tadpoles of any of the four species over 48-hr, at concentrations between 503,000 and 684,000 µg/L (343,000 and 466,000 µg AE/L). The toxicity of technicalgrade glyphosate acid (48-hr LC50, 81,200–121,000 µg AE/L) is likely to be caused by acid intolerance. Slight differences in species sensitivity were evident, with L. moorei tadpoles showing greater sensitivity than those of the other four species. Adult and newly emergent metamorphs were less sensitive than tadpoles. A series of studies on frogs was conducted with several formulations of glyphosate in relation to its use in forestry in Canada (Chen et al. 2004; Edginton et al. 2004; Thompson et al. 2004; Wojtaszek et al. 2004). Using a formulation of glyphosate (Vision) containing glyphosate and ethoxylated tallowamine surfactant (POEA), LC50 values as low as 880 µg AE/L were reported for tadpoles of Xenopus laevis, Bufo americanus, Rana clamitans,

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and Rana pipiens (Edginton et al. 2004). Embryo stages were less sensitive than older larvae, and toxicity was affected by the pH of the exposure medium, although not in a consistent manner. For the purposes of this assessment, values obtained at the most sensitive pH and for the most sensitive stage were used. In a related study on the toxicity of the Vision formulation of glyphosate to the zooplankton organism Simocephalus vetulus and tadpoles (Gosner stage 25) of Rana pipiens, interactions between pH and food availability were reported (Chen et al. 2004). Both high pH (7.5 vs. 6.5) and food deprivation increased the toxicity of this formulation. As only two concentrations were tested (750 and 1,500 µg AE/L), LC50 values could not be determined. Field studies conducted on larvae of R. clamitans and R. pipiens with Vision showed that, in the presence of natural factors such as sediment and environmentally relevant pH, toxicity of the formulation was reduced compared with laboratory observations (Wojtaszek et al. 2004). The authors reported 96-hr LC50 values ranging from 2,700 to 11,500 µg AE/L (Wojtaszek et al. 2004). Although they used a formulation of glyphosate containing the more-toxic surfactant POEA, the results conﬁrm that, in the presence of sediments, reduction in the bioavailability of glyphosate (and formulants) occurs, further reducing risks, a conclusion reached for this forestry use (Thompson et al. 2004) but which is equally relevant to the use of glyphosate in Colombia. These observations are consistent with the rapid dissipation of both glyphosate and the POEA surfactant in the presence of sediments (Tsui and Chu 2004; Wang et al. 2005). Toxicity of a number of glyphosate formulations to frogs (R. clamitans, R. pipiens, Rana sylvatica, and Bufo americanus) was reported (Howe et al. 2004); these included Roundup Original, glyphosate technical, the POEA surfactant used in some glyphosate-based herbicides, and ﬁve newer formulations of glyphosate. As expected, the most toxic of the materials was the POEA surfactant, followed by Roundup Original, Roundup Transorb, and Glyfos AU. No signiﬁcant acute toxicity was observed with glyphosate technical material [96-hr LC50 > 17,900 µg/L(AE)]. LC50 values for Roundup Original in R. clamitans, R. pipiens, and R. sylvatica were 2,200, 2,900, and 5,100 µg AE/L, respectively; these values were used in this risk assessment. Several other formulations of glyphosate were also tested in R. clamitans (Roundup Biactive, Touchdown, and Glyfos BIO) and were essentially nontoxic with LC50 values >57,000 µg AE/L. In a study on Rana cascadae, a 48-hr LC50 for Roundup (52% IPA) of 3,200 µg AI/L (2,336 µg AE/L) was reported using static exposures in glass tanks (Cauble and Wagner 2005). In a chronic exposure study with the same formulation over a 43-d period in glass tanks without sediment using a 7-d static renewal exposure with nominal concentrations of 730 and 1,460 µg AE/L, the authors found a number of effects such as decreasing time to death, increased mortality (8.6% and 51% at 730 and 1,460 µg AE/L,

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respectively), increased time to metamorphosis, and decreased weight of metamorphs. The relevance of these observations to exposures under ﬁeld conditions must be considered. Under ﬁeld conditions, glyphosate and its surfactants have been shown to bind strongly to sediments, which rapidly reduces concentrations, resulting in reduced toxicity. Thus, under use conditions in the ﬁeld, exposures longer than the 48–96-hr used in acute tests are extremely unlikely. As no sediments were present in the glass tanks of this study, the chronic exposures used are not representative of what occurs in the ﬁeld and are not applicable to the risk assessment for amphibians. In a study of several commercial pesticide formulations in leopard frogs (Rana pipiens), green frogs (R. clamitans), bullfrogs (Rana catesbeiana), the American toad (B. americanus), and gray tree frogs (Hyla versicolor), effects of Roundup and interactions with other pesticides were reported (Relyea 2004). The Roundup used in this study contained the more-toxic POEA surfactant. Survival and growth over a 16-d period were not signiﬁcantly affected by the glyphosate formulation at 1,000 µg AE/L but some species were affected at 2,000 µg AE/L. Some interactions were observed between glyphosate and other pesticides such as the insecticides diazinon, carbaryl, and malathion. One paper reported that a glyphosate formulation containing POEA was highly toxic to tadpoles of several species of frogs exposed under realistic conditions in small (1,000-L) ﬁeld microcosms (Relyea 2005a). The tadpoles (wood frog, Rana sylvatica; leopard frog, Rana pipiens; American toad, Bufo americanus; gray tree frog, Hyla versicolor; and the spring peeper, Pseudacris crucifer) were exposed to 3,800 µg AE/L commercial glyphosate (unspeciﬁed) applied directly to the surface of the water. Application rate was equivalent to 16 kg AE/ha, an unrealistic value. At this concentration, glyphosate formulated with POEA would be expected to be lethal to tadpoles. The discussion in the paper that suggests that use of glyphosate may have adverse effects on frogs more generally is thus based on a ﬂawed study design and is not supported by other data, as already discussed. In a laboratory study (Relyea 2005b) in which juvenile terrestrial stages of three different species (R. sylvatica, B woodhousii folweri, and H. versicolor) were exposed to direct applications of formulated glyphosate at 1.6 mg active ingredient (AI)/m2 (1.2 mg AE/m2) in plastic tubs, 79% mortality was observed after only 24-hr. The volume of formulation (6.9 mL) used to spray the tubs and the concentration of glyphosate (1.9%, IPA assumed) suggest that actual exposures were much greater than stated (91 mg AE/ tub). Clearly, there were errors in the description of the methods, and the results of the study are uninterpretable. Effects on other nontarget aquatic organisms have also been reported. In studies on the toxicity of glyphosate to several aquatic algae and zooplankton, Tsui and Chu (2003) showed that technical glyphosate was considerably less toxic than Roundup, which is formulated with the POEA surfactant. LC50 and EC50 values for technical glyphosate ranged from 5,890 to 415,000 µg AE/L. In tests conducted in the presence of sediment (Tsui

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and Chu 2004), they showed that biological availability of glyphosate was signiﬁcantly reduced by binding to sediment. The reduction in concentration in pore water resulting from the sediments was proportional to the amount of organic carbon in the sediments. Tests on the ﬁsh Oreochromis niloticus (Nile tilapia) exposed for 3 mon to sublethal concentrations (5,000 and 15,000 µg/L) of glyphosate as Roundup caused signiﬁcant damage to gill, liver, and kidney tissue. The structural damage could be correlated to the signiﬁcant increase (P ≤ 0.05) in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities in the second and third months of exposure. The results indicated that long-term exposure to Roundup at large, although at sublethal concentrations, had caused histopathological and biochemical alterations of the ﬁsh (Jiraungkoorskul et al. 2003). Because technical glyphosate was not tested, the contribution of surfactants to this response cannot be judged. In studies on the freshwater mussel Utterbackia imbecillis, a commercial formulation of Roundup was reported to have little toxicity (24-hr LC50 of 18,300 µg/L and a NOEC of 10,040 µg/L–7,442 µg AE/L) to larval mussels (Conners and Black 2004). In studies on genotoxicity in these mussels, there was no signiﬁcant difference in response between the control and mussel larvae treated at one-fourth the NOEC, ≈2,500 µg/L (1,850 µg AE/L). Response of total free amino acid proﬁles of snails to glyphosate exposures has been studied (Tate et al. 2000), showing that exposure of the aquatic snails (Pseudosuccinae columella) to technical glyphosate at nominal concentrations of 1,000–10,000 µg/L led to increased egg laying and increased amino acid concentrations in tissues. Technical glyphosate was not particularly toxic with a 24-hr LC50 of 98,900 µg/L (72,200 µg AE/L). The effect on egg laying and amino acid concentrations was stimulative rather than adverse, but the authors speculate that it could lead to increases in incidence of diseases for which the snails are intermediate hosts. Increases in parasites may affect organisms in the environment. Similar stimulation was observed in the rotifer Brachionus calyciﬂorus in which growth rates and sexual and asexual reproduction were stimulated in the presence of glyphosate (formulation unknown) at ≥4,000 µg/L (growth) and ≥2,000 µg/L for reproduction and resting egg production (Xi and Feng 2004). Again, although stimulatory and not “adverse”, the authors point out that increases in one species may affect other species indirectly. In a study on grazing of the alga Scenedesmus spp. by the aquatic crustacean Daphnia pulex, technical glyphosate was shown to have no adverse effect, although it appeared to stimulate algae growth (Bengtsson et al. 2004). This stimulation was suggested to be caused by release of nitrogen and phosphorus from glyphosate metabolism by Daphnia. Similar stimulation was also seen in the effects of glyphosate (Rodeo, glyphosate IPA without surfactants) on the primary productivity of a natural phytoplankton algal assemblage dominated by species of diatoms and a dinoﬂagelate (Schaffer and Sebetich 2004). A 60% increase in productivity as measured

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by assimilation of 14CO2 was observed at concentrations of 125, 1,250, and 12,500 µg/L, with no apparent concentration response. The authors speculate that the increase was caused by the release of nitrogen and phosphorus from the breakdown of glyphosate. Effects of Glyphosate on Terrestrial Plants There are differences in glyphosate uptake between different coca species and between young and mature plants of Erythroxylum coca and E. novogranatense (Ferreira and Reddy 2000). Absorption through the leaf is greater in young plants of both species and greater in E. novogranatense. Earlier studies showed that control of regrowth was better in E. novogranatense for equivalent rate of glyphosate (Ferreira et al. 1997). This study also indicated that defoliation of E. coca 24-hr before application resulted in no signiﬁcant effect of glyphosate (applied up to 6.7 kg AI/ha) on regrowth. This result conﬁrms that, as for other plants, uptake via the leaves is the major route of penetration into the plant. A study on the control of the perennial weed pepperweed (Lepidium latifolium) has shown better control with glyphosate following mowing. The mechanism is via the better movement of glyphosate to roots from leaves lower in the canopy. Following mowing, the leaf distribution and the spray deposition are closer to the ground, giving better basipetal translocation to roots and better subsequent control (Renz and DiTomaso 2004). In forestry situations with an aerial application, spray deposition is typically much greater higher in the canopy (Thompson et al. 1997). Studies of glyphosate efﬁcacy on annual weeds indicated that application during the day (0900 and 1800) gives best control (Martinson et al. 2002; Miller et al. 2003). Resistance to glyphosate is known for an increasing number of species, including Conyza canadensis (Mueller et al. 2003), Illinois waterhemp (Amaranthus rudis and A. tuberculatus) (Patzoldt et al. 2002), Eleusine indica (Baerson et al. 2002), Lolium multiﬂorum (Perez and Kogan 2003), and Lolium rigidum (Neve et al. 2003a,b). Rates of evolution of resistance in the latter species are dependent on herbicide use patterns as part of crop production. Nontarget impacts of glyphosate on seed germination and growth characteristics of the F1 generation of treated wild plant species have been reported. Blackburn and Boutin (2003) noted effects on 7 of 11 species tested with 1%, 10%, or 100% of a 0.89 kg AI/ha label rate of glyphosate formulated as Roundup solution sprayed near seed maturity. Effects of glyphosate drift on rice seed germination were reported by Ellis et al. (2003), and May et al. (2003) noted reduced seed production in alfalfa in the year following applications 1.760 kg AI/ha for Cirsium arvense control. Nevertheless, applications at 0.420 kg AE/ha on susceptible soybean had adverse effects on sprayed plants but not on progeny (Norsworthy 2004). Subtle adverse effects of glyphosate on pollen viability and seed set in

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glyphosate-resistant cotton were noted by Pline et al. (2003). Pollen viability of glyphosate-resistant corn was also signiﬁcantly reduced by glyphosate applied at 1.12 kg AI/ha, but yield and seed set were not signiﬁcantly affected (Thomas et al. 2004). These data indicate that drift might cause subtle ecological changes to plant communities associated with changes in plant recruitment. However, this would be signiﬁcant only for communities largely made up of monocarpic plant species (those that ﬂower once and die, especially annuals) dependent on seeds for recruitment. B. Glyphosate and Formulants There are a number of formulations of glyphosate on the market that may contain a number of surfactants and other formulants (Giesy et al. 2000; Solomon and Thompson 2003; Williams et al. 2000). Normally, this would not be an issue in the risk assessment of a pesticide; however, in the case of glyphosate IPA, the active ingredient has little toxicity to nontarget organisms, thus making the surfactant toxicity more important for risk assessment. For example, tests on Ca2+-activated ATPase and cholinesterase (ChE) activities in the nervous system of the slug Phyllocaulis soleiformis showed no effects of pure glyphosate IPA. An effect noted with the formulation Gliz 480CS was caused by nonglyphosate components of the formulation (da Silva et al. 2003). Technical-grade glyphosate at concentrations of 52 mM (870 mg/L) did not affect the protozoan Tetrahymena thermophila or the parasite Ichthyophthirius multiﬁliis. However, the commercial formulation Glyphosate was up to 100 times more toxic, reﬂecting data for ﬁsh species and other aquatic invertebrates and caused by surfactants in the formulation (Everett and Dickerson 2003). Because the spray solution as used in the control of coca and poppy in Colombia contains surfactants as part of the glyphosate formulation as well as additional surfactants (Cosmo-Flux) added to the spray mix, the toxicity of the formulants and the adjuvants may interact to change the toxicity of the mixture. For this reason, standardized toxicity tests for mammals and environmental nontarget organisms were conducted with the spray mixture itself, as discussed next. Effects of Formulated Glyphosate and Cosmo-Flux on Mammals Two series of mammalian toxicity tests on the formulation of glyphosate and Cosmo-Flux were conducted. One set was conducted in the U.S. (Springborn 2003a–g) under good laboratory practices (GLP) and using quality control assurance as appropriate for regulatory decision making. The other studies (Immunopharmos 2002a–j) were conducted in Colombia, also in compliance with GLP and according to USEPA guidelines. These studies were reviewed in detail (Solomon et al. 2005a), and a number of conclusions were drawn for the mixture glyphosate and Cosmo-Flux sprayed on either poppy or coca.

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• The acute oral and dermal LD50 was >5,000 mg/kg bw in the rat. Therefore, this formulation is considered as practically nontoxic orally. • The acute inhalation LC50 was >2.60 mg/L in the rat. In one study, the rats showed breathing abnormalities after exposures at 2.6 mg/L for 4-hr. This value for the test substance is considered as potentially harmful for durations of exposure of the order of 4-hr. In two other studies, the mixture was shown to be not harmful at exposures up to 20 mg/L for 4-hr. Exposures via inhalation in these studies were via small droplets. Exposures via inhalation under ﬁeld conditions will be smaller as the droplets are larger and less easily inhaled. • The formulation is considered to be a slight and moderate irritant to the skin and eyes of the rabbit. The calculated primary irritation index for the test article was 0.25. Based on these observations, the hazards to humans via application or bystander exposures are considered small and are limited to slight to moderate skin and eye irritation. These responses will be reduced if the affected areas are rinsed shortly after exposure to remove contamination. It was also concluded that the addition of the adjuvant Cosmo-Flux to glyphosate did not change the toxicological properties of the glyphosate formulation to mammals. Effects of Formulated Glyphosate and Cosmo-Flux on Nontarget Aquatic Organisms A base set of toxicity data is required for all pesticide registrations. For freshwater environments, the set normally makes use of a cold-water ﬁsh, such as rainbow trout ﬁngerlings (Onchorynchus mykiss); a warm-water ﬁsh, such as fathead minnows (Pimephales promelas); an invertebrate such as the water ﬂea (Daphnia magna); and an alga, such as Selanastrum capricornutum. Recognized guidelines were used for the tests (OECD 1984a,b, 1992; USEPA 1996b), which were conducted under the principles of GLP (OECD 1998b). These are standard test organisms, have been used for testing glyphosate itself and several other formulations, and thus are useful for comparison purposes. To reduce the requirement for animals in the testing, one combination of glyphosate and Cosmo-Flux, the combination for poppy (see Table 2), was selected. The results of these tests are summarized in Table 11. C. Effects in the Field Duration of Effects In tropical forest situations, similar to some locations in coca eradication programs, there are limited data on vegetation recovery following glyphosate application. Nevertheless, there are a number of studies of successional patterns following land clearance and for tree gaps. Forest clearance has

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Table 11. Toxicity values obtained from toxicity tests conducted on a mixture of glyphosate and Cosmo-Flux.

Test species

Common name

Selenastrum

Algae, based on cell numbers, area under the growth curve, and growth rate Water ﬂea, mortality Rainbow trout, mortality Fathead minnow, mortality

Daphnia magna Onchorynchus mykiss Pimephales promelas a

96-hr LC50/EC50 in µg/L (as glyphosate AE)

Reference

2,278–5,727a

Stantec (2005e)

4,240 (3,230–5,720)b

Stantec (2005b)

1,847 (1,407–2,425)b

Stantec (2005d)

4,600 (1,805–11,700)b

Stantec (2005c)

Greatest and smallest effect measures in the study. LC50/EC50 and 95% conﬁdence Interval.

b

been a historical feature of the development of agriculture across the globe (Boahene 1998; Matlack 1997). In Central America, agricultural intensiﬁcation and forest clearance in Mayan and other cultures has been determined from the pollen record (Clement and Horn 2001; Curtis et al. 1998; Goman and Byrne 1998). Patterns of successional change (recovery) in Neotropical forests have been reviewed by Gauriguata and Ostertag (2001). The authors noted that “the regenerative power of Neotropical forest vegetation is high, if propagule sources are close by and land use intensity before abandonment has not been severe.” However, they also caution that recovery is heavily dependent on interactions between site-speciﬁc factors and land use, “which make it extremely difﬁcult to predict successional trajectories in anthropogenic settings.” In relation to the eradication program, patterns of vegetation recovery will be dependent on size of plot, location of plot in relation to surrounding vegetation types, and local anthropogenic management, i.e., subsequent cultivation activities. A study of tree regeneration in dry and humid selectively logged Bolivian tropical forests indicated that tree release with glyphosate in logging gaps had no signiﬁcant impact on target tree species growth (Pariona et al. 2003). Although glyphosate controlled vegetation for a limited period, there were problems with the recruitment of commercial trees in logging gaps, suggesting a silvicultural need for site preparation treatments and more judicious seed tree retention. Glyphosate has been widely used for controlling deciduous understory vegetation in managed northern forests, so-called conifer-release

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treatments (Lautenschlager and Sullivan 2002). Recovery of the deciduous herb and shrub layers occurs over 2–3 yr in general and the tree layer over 10 yr. Often, total structural diversity is unaffected by glyphosate treatments after 1 yr. Forest Clearance and Soils. The impacts of forest clearance on soil fertility are generally well understood. Typically, tropical forest soils are fragile, being nutrient poor and subject to leaching. Tree clearance can quickly result in loss of nutrients, change in pH, and therefore change in element availability to plants (McAlister et al. 1998). Such conditions often allow only shifting cultivation under subsistence production, so-called slash-andburn agriculture. Studies in Jamaican forests have shown that cultivations result in large amounts of soil erosion compared with secondary forest. An agroforestry treatment with Calliandra calothyrsus contour hedges reduced erosion and increased rainfall inﬁltration within the hedges (McDonald et al. 2002). As coca is a shrub, typically grown in rows, it might be argued that soil and water changes associated with forest clearance may be less than for annual crops such as maize, but clearly both have signiﬁcant adverse effects on primary forest sites. Although vegetation recovery may be rapid in eastern North America, research has led to the surprising conclusion that 19th-century agricultural practices decreased forest ﬂoor nutrient content and C : N and C : P ratios and increased nitriﬁer populations and net nitrate production, for approximately a century after abandonment (Compton and Boone 2000). The level of agricultural intensity, in terms of cultivation and fertilizer use, may have signiﬁcant long-term impact on soils. Effects on Associated Fauna. In an area of highly disturbed tropical dry forest in Cordoba Department, northern Colombia, small mammals were censused by live-trapping, running from secondary growth forest into agricultural areas (Adler et al. 1997). The results suggested the disturbed habitat supports a small mammal fauna of low diversity. However, several of the species appear to have beneﬁted from forest clearance and agricultural activities and may occasionally reach extremely high numbers, although populations were not stable. A similar effect on reduced diversity of termites with increasing disturbance has been shown in dry forest in Uganda (Okwakol 2000). Changes in bird populations of a eucalypt forest in Australia following clear-felling indicate that full recovery may take up to 70 yr (Williams et al. 2001). Although some species are adapted to disturbed conditions and can utilize agricultural land and secondary forest, there are many species associated with primary forest only, for example, the great argus pheasant in Indonesian tropical forests (Nijman 1998). With much of Colombia associated with extremely high biodiversity, there are very many endemic plant

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and animal species associated with national parks and in all likelihood with areas where coca and poppy are grown. Studies on the impacts of vegetation change caused by glyphosate use on associated fauna in northern environments are available for some species. For example, following the application of glyphosate in clear-cut forest areas in Maine (USA), the use by moose (Alces alces) of treated and untreated areas was compared 1–2 yr and 7–11 yr postapplication (Eschenburg et al. 2003; Eschholz et al. 1996). At 1 and 2 yr posttreatment, tracks of foraging moose were 57% and 75% less abundant on treated than untreated clear-cuts (P = 0.013). However, at 7–11 yr posttreatment, tracks of foraging moose (P = 0.05) and moose beds (P = 0.06) were greater on treated than untreated clear-cuts. Less foraging activity at 1–2 yr posttreatment appeared to be the result of reduced browse availability, because conifer cover for bedding was similar on treated and untreated clear-cuts. The authors hypothesized that the greater counts of tracks of foraging moose on older treated clear-cuts were the result of increased foraging activity on sites with more abundant conifer cover (Eschholz et al. 1996; Raymond et al. 1996); i.e., tree cover had returned sufﬁciently after 10 yr. Studies of responses of small mammals to vegetation control with glyphosate in similar environments (Sullivan et al. 1998) indicated that vegetation recovery 2–3 yr after treatment was sufﬁcient to return population dynamics to expected ranges. Spot applications of glyphosate to reduce invasive ground ﬂora in forests can have the beneﬁcial effect of opening up the ground layer and encouraging spring ephemeral species to establish larger populations. Carlson and Gorchov (2004) reported this effect when controlling Alliaria peteolata, an invasive biennial plant. The impact of glyphosate on the target species was only for a single season. Recovery from Effects. Glyphosate, as a well-translocated herbicide, affects most plant species if sufﬁcient herbicide can penetrate plant tissues, particularly leaves. Effects typically result in plant death over 2–3 wk, although species with extensive storage organs, e.g., long rhizomes, large size, or particularly impenetrable leaf surfaces, may survive. A small dose of glyphosate can result in growth abnormalities in plants, most typically localized accelerated branching. If the dose of herbicide is insufﬁcient to cause death, it has been proposed that plant ﬁtness may also be reduced, such that if there is competition with other plants, death may result indirectly, though there is little published evidence for this. The effect of glyphosate is limited to the plants that receive spray at the time of application, as the herbicide is rapidly adsorbed onto soil and root uptake does not occur. The broad spectrum of plant species controlled and the pattern of foliar uptake, together with the safety of the compound, have led to widespread use of the herbicide for total vegetation control, in preharvest weed control in annual crops, and for the control of perennial plants.

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Recovery of treated areas is dependent on the initial level of control, the quantities of material (and the methods used) for plant regeneration and the environmental conditions of the site. Plants have a variety of adaptations for regenerating, with some life forms showing a range of methods, while others have only a single strategy. Monocarpic species, typically annuals, have seeds for recruitment of the next generation. Polycarpic species may also produce seeds, but many also have a variety of vegetative means of regenerating, such as rhizomes, bulbs, corms, and runners. Patterns of secondary succession, the resultant plant communities over time, reﬂect the plant–environment interactions and the opportunities for regeneration provided by the local species pool. Seeds in the soil or those that can reach a site from the surroundings, together with vegetative fragments, will establish initially. Continued agricultural operations, such as cutting or soil disturbance, will have a major inﬂuence on the species that survive. In most situations, vegetation recovery is rapid, with ruderal and pioneer plant species establishing within weeks of application. In tropical forests, similar to some of the locations of the coca eradication programs, there are limited published data on vegetation recovery following glyphosate application. Nevertheless, there are a number of studies of successional patterns following land clearance and for tree gaps. Secondary succession (forest recovery) has become more common in some forest areas, for example, in Puerto Rico (Chinea 2002). Forest recovery is generally fairly rapid, but recovery of the full complement of forest species can take many years (>30 yr), and the effects of bulldozing for initial clearance can reduce diversity of native species and enhance establishment of nonnative species. Comparisons of different aged plots (2–40 yr) in the Bolivian Amazon forests have contributed to the knowledge of secondary succession (Pena-Claros 2003). Not surprisingly, it takes longer for the forest canopy to achieve similar diversity to mature forest compared with the understory and subcanopy communities. In relation to the eradication program, patterns of vegetation recovery will be dependent on size of plot, location of plot in relation to surrounding vegetation types, and local anthropogenic management, i.e., subsequent cultivation activities. Nevertheless, it should be noted that naturally occurring tree gaps (20–460 m2) are an important component of overall forest diversity, providing opportunities for understory and subcanopy species and regeneration of canopy species in the modiﬁed light climate (Martins and Rodrigues 2002; Martins et al. 2004). In Brazilian varzea (white-water) forests, natural patterns of succession are affected by both light and local ﬂooding (Wittmann et al. 2004). The patch scale of eradication applications of glyphosate may or may not be at the scale of natural forest gap dynamics; this deserves further study. In the high Andes alpine paramo habitats, patterns of succession were described by Sarmiento et al. (2003). Following cultivation, usually for potato, patterns of secondary succession were such that, after 12 yr, species

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diversity of the undisturbed paramo had still not been attained. The characteristic paramo life forms, sclerophilous shrubs (e.g., Baccharis prunifolia, Hypericum laricifolium) and giant rosettes (e.g., Espeletia schultzii), appear very early and gradually increase in abundance during succession (Sarmiento et al. 2003). In situations of agricultural expansion over large areas in Europe and North America, there is evidence that, where the proportion of remaining ancient habitat is small, subsequent forest recovery on abandoned agricultural land can be extended over long time periods (Vellend 2003). It is unlikely that habitat fragmentation and intensity of agriculture will combine to provide such a scenario in the coca eradication areas. Effects on the successional patterns of vegetation in northern temperate and boreal forest situations are that woody and herbaceous species are most reduced by glyphosate (Bell et al. 1997). In a study in British Columbia, species richness, diversity, and turnover of the herb, shrub, and tree layers were not signiﬁcantly (P > 0.10) different between mechanical and glyphosate spray cut stump treatments and a control. Similarly, the structural diversity of herb, shrub, and tree layers were also not signiﬁcantly different (P > 0.10) between treatments and control. By opening the canopy and decreasing the dominance of the deciduous tree layer, both manual and cut-stump treatments showed greater total structural diversity (herb, shrub, and tree layers combined) relative to the control. However, differences in total structural diversity between treatments and control were, for the most part, not signiﬁcant (P > 0.10). Therefore, these vegetation management treatments affected only the volume of the targeted deciduous tree layer and did not adversely affect species richness, diversity, turnover, or structural diversity of the plant community. These results may be applicable to other temperate forest ecosystems where conifer release is practiced in young plantations (Lindgren and Sullivan 2001). Herb biomass and cover usually recover to untreated values within 2–3 yr of conifer release treatment (Sullivan 1994). Meanwhile, the reduced competition on target conifers allows enhanced growth with little adverse effect on plant diversity (Sullivan et al. 1996, 1998). Nevertheless, some plant groups may take longer to recover from glyphosate application. For example, cryptogams (ferns) may take longer than 5 yr to recover in boreal forest situations (Newmaster and Bell 2002), probably reﬂecting longer generation times and poor dispersal. Reviewing the effects of glyphosate use in forestry, Sullivan and Sullivan (2003) noted that single applications of glyphosate control much of the vegetation that receives spray, but recovery is generally rapid and within the range of natural disturbances. Overall, the experience of glyphosate use in northern temperate forests is that vegetation and fauna recover over 2–3 yr following a single coniferrelease treatment. With generally rapid plant growth under tropical conditions, available data conﬁrm this scenario for Colombian conditions.

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In comparison, land clearance for agriculture, or coca/poppy production, is a much more environmentally damaging operation, impacting adversely on soils in particular. Land clearance for illicit crops is already a threat to the conservation of bird species diversity in Colombia (Álvarez 2002). Although there are legitimate scientiﬁc questions as to the effects of (a) the spatial scale of individual glyphosate applications and (b) the return frequency of eradication treatments, ﬁeld operational factors set these parameters. Spray areas reﬂect the patch scale of coca and poppy growing, averaging 1–2 ha each in a total of ∼150,000 ha. Reapplication frequencies are generally greater than 6 mon for coca and greater than 3 mon for poppy and, bearing in mind the molecule is biologically unavailable in the soil and soil-bound residues have a half-life of 14–32 d, the environmental impacts are no greater than single applications.

V. Risk Assessment The risk assessment was conducted by comparing estimated exposures to effect values for glyphosate from speciﬁc toxicity studies, from the literature, and from regulatory guidelines such as those established by the USEPA (1993b). The estimated exposures used were those calculated for the use of glyphosate for eradication spraying in Colombia. A. Human Health From an assessment of the results of toxicity testing of the formulation of glyphosate and Cosmo-Flux as used in Colombia, it was concluded that the addition of Cosmo-Flux to the spray mixture did not affect toxicity of the glyphosate to mammals. For this reason, it was possible to compare the toxicity of glyphosate and its formulations to exposures estimated under conditions of use in Colombia. Exposures for the assessment were taken from Tables 5–7. The greatest values were taken as reasonable worst case for a hazard assessment. These results are shown in Table 12 and illustrated in Fig. 9. In comparing the exposure and effect concentrations, a margin of exposure approach was used. Thus a number greater than 1 (in Table 12) means that the exposure was less than criterion value or the exposure (or dose) that caused the response in the toxicology study. From these data, it is clear that potential exposures to glyphosate and Cosmo-Flux do not present a risk to human bystanders. In all cases, the margin of exposure for the most sensitive endpoint in laboratory animal studies with glyphosate was greater than 100, a conservative value often used to account for uncertainty in risk assessments of this type. As well, estimated worst case exposures were below the reference dose (RfD) established for glyphosate by the USEPA. The toxicity values used in both these approaches were derived from chronic exposures where the animals were dosed over extended time periods. They are thus

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Table 12. Summary of reasonable worst case estimated exposures of humans to glyphosate resulting from use in the eradication of coca and poppy in Colombia and margins of exposure.

Exposure value (mg/kg) Source of exposure Direct overspray Reentry Inhalation Diet and water Worst case total exposure from all sources

Coca

Poppy

Coca

Poppy

0.04 0.26 0.01 0.75 1.05

0.01 0.06 0.01 0.18 0.26

4,918 676 28,226 234 167

20,417 2,804 28,226 972 680

Exposure value (mg/kg) Source of exposure Direct overspray Reentry Inhalation Diet and water Worst case total exposure from all sources

Margin of exposure compared to the most sensitive NOEL (175 mg/kg bw)

Margin of exposure for the U.S. EPA RfD (2 mg/kg bw/d)

Coca

Poppy

Coca

Poppy

0.04 0.26 0.01 0.75 1.05

0.01 0.06 0.01 0.18 0.26

56 8 323 2.7 1.9

233 32 323 11.1 7.8

additionally protective of short and infrequent exposures that would occur during the use of glyphosate in the eradication spray program. Some exposure values were close to the inhalation toxicity value, but as already discussed, droplet size is large and inhalation will be less than in the laboratory animal studies as well as the droplet size used in agriculture, from which the potential inhalation exposure was derived. B. Environment The acute toxicity data for formulated glyphosate in aquatic animals from Solomon and Thompson (2003) were combined with some of the new data for amphibians described above and are displayed graphically as a point of reference for characterizing the toxicity of glyphosate plus Cosmo-Flux as

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Fig. 9. Illustration of acute toxicity values in laboratory mammals for glyphosate plus Cosmo-Flux, the no-observed-effect-level (NOEL) from the most sensitive chronic study in laboratory animals, and the reference dose (RfD) (glyphosate) and the estimated worst case acute exposures that may be experienced under conditions of use in Colombia.

used in Colombia (Fig. 10). The graph is presented as a cumulative frequency distribution in a manner similar to that used in probabilistic risk assessments for pesticides (Solomon and Takacs 2002). The combination of formulated glyphosate and Cosmo-Flux, as used in Colombia, is more toxic to the aquatic organisms tested than formulations of glyphosate without the addition of surfactants and/or adjuvants, which is not altogether surprising. The toxicity of glyphosate itself to aquatic organisms is very small (Solomon and Thompson 2003) but, when mixed with some surfactants and adjuvants, this toxicity can be increased. The toxicity of Cosmo-Flux was not tested on its own; however, from experience with other adjuvants, it clearly contributes to the increased toxicity of the mixture. It is interesting to note that larval amphibians appear to be more susceptible to glyphosate formulations than other aquatic animals. The reason for this is likely the surfactants in the formulation of Roundup, as already discussed, as other formulations of glyphosate are less toxic to amphibians (Howe et al. 2004). Assessment of the environmental risks of glyphosate and Cosmo-Flux to aquatic organisms was based on toxicity data from the literature and from studies conducted on the mixture of formulated glyphosate and Cosmo-Flux as used in Colombia. When the toxicity values for the mixture as used in Colombia are compared with the range of estimated exposures

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that would result from a direct overspray of surface waters (see Table 8), it is clear that aquatic animals and algae in some shallow water bodies may be at risk (see Fig. 10). Although the overlap of the range of estimated exposure concentrations with the toxicity values for green alga and rainbow trout suggest that there may be increased risk in situations where an accidental overspray will occur, this would have to be in a location where a shallow water body is close enough to the coca ﬁeld that it is accidentally oversprayed, that it is less than 30 cm deep, and that it is not ﬂowing. Water ﬂow would likely result in rapid hydraulic dilution to concentrations below the threshold of biological activity, so organisms in ﬂowing water would not be at great risk. It was not possible to determine the actual frequency of these risks, as data on proximity of surface water to coca ﬁelds are not available. Based on the toxicity data with formulated Roundup in amphibians, this group of organisms may be at risk; however, speciﬁc testing in amphibians has not been conducted on the glyphosate plus Cosmo-Flux as used in Colombia. Based on the toxicity data for honeybees, glyphosate and Cosmo-Flux is not acutely toxic via contact exposure to honeybees. It caused no mortality

Fig. 10. Cumulative frequency distribution of toxicity values for glyphosate technical, formulated glyphosate (Roundup) in all aquatic organisms and in ﬁsh and the toxicity values in four aquatic species for glyphosate and Cosmo-Flux 411 mixture as used in Colombia.

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or stress effects in bees in the normal 48-hr period after treatment at concentrations equal to or less than 63.9 mg AE/bee, showing that the formulated product is not directly hazardous to bees or, by extrapolation, to other beneﬁcial insects. Although no acute or chronic data are available on wild animals, extrapolation of the mammalian data discussed earlier and reports in the literature support the conclusion that glyphosate and Cosmo-Flux will not have adverse direct effects on wild mammals or birds. Indirect effects through habitat alteration are possible. However, it is unlikely that the coca and poppy ﬁelds are signiﬁcant habitats for wildlife. Human activities related to cultivation, pest control, and harvesting will be more disruptive to wildlife, and death of the coca bushes or the poppy plants as a result of spraying with glyphosate will not add an additional stressor. In fact, if the sprayed area is not replanted and allowed to naturalize, this new successional habitat may be more attractive to birds and mammals than an old-growth forest. Given that coca and poppy ﬁelds are usually located in remote areas and are often surrounded by natural habitats, sources for recolonization or alternate habitats will be close by. Some habitat alteration will result from accidental oversprays that affect nontarget vegetation; however, as already discussed, these areas are small in relation to the sprayed ﬁelds (<0.48%), represent a very small proportion of the total habitat available (<<0.001%), and will undergo rapid recolonization and succession to habitats suitable for wildlife.

VI. Conclusions Risks associated with the use of glyphosate and Cosmo-Flux in the coca and poppy eradication program in Colombia are related to the total impacts of coca and poppy production discussed in the section on Problem Formulation. There are a number of other activities associated with the production of cocaine and heroin that result in risks to human health and the environment. Data are not available to quantify all these risks, but some of them may be estimated on the basis of other knowledge and expert judgment, which was done using an adaptation of a risk prioritization scheme used in ecological risk assessment (Harwell et al. 1992). For purposes of ranking human health hazards, the intensity score ranged from 0 to 5, with 5 being a severe effect such as a physical injury or toxicity. The recovery score also ranged from 0 to 5 and was based on the potential for complete recovery from the adverse effect. Frequency was based on an estimate of the proportion (%) of the total number of persons involved in coca and poppy cultivation, production, and the reﬁnement of cocaine and heroin. The score for impact was the product of the individual scores and the percent impact is based on the sum of the impact scores. A similar procedure to that described above was used for ranking ecological risks associated with the cycle of coca and poppy production.

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The intensity score was ranked from 0 to 5, with 5 being most intense, such as the total destruction of the habitat by clear-cutting and burning a natural area. Intensity of effects in this case also included off-ﬁeld effects such as on nontarget animals and plants. Recovery time in this scheme is the estimated time for the impacted area to recover to a state similar to the initial condition. In the case of clear-cutting and burning, it is recognized that succession will begin immediately; however, full recovery to a mature and diverse tropical forest may take considerably more than the 60 yr estimated here. Similarly, in the absence of cultivation, it was estimated that invasive and competitive species will displace coca and poppy in several years, and an estimate of 4 yr was used in this case. Given the need to apply fertilizer and pesticides frequently because of utilization of nutrients and resurgence of pests, the recovery time for these ecological impacts was judged to be small. The scores were multiplied to give the impact score, and the percent impact was based on the sum of the impact scores. A. Human Health Relevance Based on all the evidence and information presented here, we concluded that the risks to humans and human health from the use of glyphosate and Cosmo-Flux in the control of coca and poppy were minimal (Table 13). Acute toxicity of the formulated product and Cosmo-Flux to laboratory animals was very low, the likely exposures were low, and the frequency of exposures was low. When these risks are compared with other risks associated with clearing of land, the uncontrolled and unmonitored use of other pesticides (many of them more toxic to humans than glyphosate, CICAD/

Table 13. Potential human health impacts of the cycle of coca or poppy production in the Colombian environment. Impacts Clear cutting and burning Planting the coca or poppy Fertilizer inputs Pesticide inputs Eradication spray Processing and reﬁning

Intensity score

Recovery score

Frequency (%)

Impact score

Impact (%)

5

3

3

45

16.7

0

1

100

0

0.0

0

0.5

10

0

0.0

5

3

10

150

55.6

0

0

10

0

0.0

5

3

5

75

27.8

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OAS 2005) to protect the coca and poppy, and exposures to substances used in the reﬁning of the raw product into cocaine and heroin, they are essentially negligible. B. Ecological Relevance Based on evidence and data discussed above and results of a number of speciﬁc studies conducted speciﬁcally for this assessment, we concluded that the risks to the environment from the use of glyphosate and CosmoFlux in the control of coca and poppy were small in most circumstances (Table 14). Risks of direct effects in terrestrial wildlife such as mammals and birds were judged to be negligible, as were those to beneﬁcial insects such as bees. Moderate risks to some aquatic wildlife may exist in some locations where shallow and static water bodies are located in close proximity to coca ﬁelds and are accidentally oversprayed. However, when taken in the context of the environmental risks from other activities associated with the production of coca and poppy, in particular, the uncontrolled and unplanned clearing of pristine lands in ecologically important areas for the purposes of planting the crop, the added risks associated with the spray program are small. Table 14. Potential environmental impacts of the coca or poppy production cycle in the Colombian environment. Intensity score

Impacts Clear cutting and burning Planting the coca or poppy Fertilizer inputs Pesticide inputs Eradication spray Processing and reﬁning

Recovery time (years)

Impact score

Impact%

5

60

300

96.9

1

4

4

1.3

1 5

0.5 0.5

0.5 2.5

0.2 0.8

1

0.5

0.5

0.2

2

1

2

0.6

C. Strengths and Uncertainties in the Assessment This assessment has both strengths and uncertainties, as discussed in the following sections; these lie in the exposure and effects characterizations and, because they are used in the risk characterization, are also reﬂected in the risk assessment. Uncertainties are inherent in all risk assessments and, in some cases, can be easily addressed though additional data collection or

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speciﬁc studies. Recommendations for additional studies and data collection are addressed in the ﬁnal section. Exposures Human Exposures. Human exposures to glyphosate were estimated from extensive and well-documented studies in other jurisdictions and are judged to be accurate with respect to bystanders who are directly oversprayed. Exposures were judged to be small and, in all cases, considerably below thresholds of concern. Application rates of glyphosate used for coca control are greater than those used in conventional agriculture, suggesting that experience and exposures measured under these conditions may not be applicable to bystander exposures in eradication spraying in Colombia. While this may be true, the margins between exposures doses at which chronic effects may occur are great enough to provide a wide margin of safety to bystanders. Less information is available regarding the likelihood of exposure upon reentry to coca ﬁelds immediately after spraying; this relates to the anecdotal evidence that picking of leaves or pruning of plants immediately after they are sprayed with glyphosate will “save” the plants. Exposures under these conditions are unmeasured, but are estimated to be below the USEPA reference dose. Environmental Exposures. Applications of glyphosate are well characterized using state-of-the-art equipment. Locations of application and areas sprayed are well documented and measured with resolutions only equaled in some applications in forestry in other jurisdictions. Mixing and application rates are well characterized, and the probability of application of amounts of glyphosate and Cosmo-Flux greater than those speciﬁed is small. Concentrations in soil and water that may result from an accidental overspray also have high certainty. The environmental behavior of glyphosate is well characterized and, under the conditions of use, it will not persist, accumulate, or biomagnify. Analyses of surface waters and sediments in one watershed where eradication spraying was carried out did not reveal the presence of signiﬁcant concentrations of glyphosate, conﬁrming the conclusion based on its properties that it is not mobile in the environment. Residues of glyphosate were infrequently detected in areas where eradication spraying was not conducted but where glyphosate use was known to occur in agriculture. Given that considerably more glyphosate is used in agriculture and other noneradication uses (∼85%), this further conﬁrms that glyphosate is not sufﬁciently mobile to result in signiﬁcant contamination of surface waters in Colombia, regardless of the use pattern. Uncertainties in the exposure characterization lie in lack of precise measurements of the proximity of sprayed ﬁelds to surface waters and the proportion of treated areas that are in close proximity. Sampling of the surface

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waters only took place for 24 wk, and only ﬁve locations were sampled. Although two of these were scheduled to be sprayed, only one was treated during the sampling period. For logistical reasons, it was also not possible to sample close to application sites. Had sampling been conducted at more sites closer to the sprayed ﬁelds and over a longer time period, residues may have been detected more frequently. Effects Effects in Humans. The database of glyphosate effects is large and its risks to humans and the environment have been extensively reviewed and assessed in a number of national and international jurisdictions as well as in the open scientiﬁc literature. In all cases, glyphosate poses little risk. However, some of the studies on which these assessments are based were conducted before the reﬁnement of testing guidelines and the availability of new and more sensitive methods of analysis and effect characterization, such as those based on alteration in the concentrations of neurotransmitters and their metabolites in the central nervous system. In the process of reassessment and reregistration, older studies will be replaced with newer tests using current guidelines. Given the large and expanding use of glyphosate in agriculture, priorities for updating the database will likely be high. Changes in the regulatory status of glyphosate should be monitored and any newly identiﬁed risks included in an updated risk assessment. There is considerable literature on the epidemiology of pesticides and possible effects on human health. As a result of recent work, it is clear that many epidemiology studies are confounded by the use of poor and inaccurate surrogates for exposures to pesticides. We also conducted a preliminary epidemiological study to assess possible linkages between the use of glyphosate and adverse human health outcomes; this study recognizes that, for clear logistical reasons, no measures of exposure were available for the various groups enrolled in the study, other than the use of glyphosate for eradication spraying in the region. The results do not suggest that there is an association between the use of glyphosate in the eradication program and time to pregnancy (TTP) as a reproductive outcome. A somewhat greater risk for longer TTP was observed in one region (Valle del Cauca) where eradication spraying is not conducted, but it was not possible to identify any speciﬁc factors that may have been responsible for this observation. Environmental Effects. The environmental toxicology database for glyphosate is relatively large, and its effects in nontarget organisms are well known or can be extrapolated. Glyphosate itself is essentially nontoxic to nontarget organisms. However, there are a number of formulations of glyphosate in the marketplace that contain many different surfactants and/or adjuvants. It is also known that it is the surfactants that determine the toxicity of the

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formulation and are more toxic than technical glyphosate itself. Because of this, several toxicity tests were conducted with the formulated product of glyphosate plus Cosmo-Flux used in the Colombian program; this reduced uncertainty with respect to toxicity to beneﬁcial insects, such as the honeybee, and to aquatic organisms. Recent studies have reported that frogs are among the more-sensitive aquatic organisms to formulations of glyphosate such as Roundup and Vision. We did not conduct toxicity studies in amphibians with the mixture of glyphosate plus Cosmo-Flux, and this is a source of some uncertainty for ecological risks for frogs. Confounding Risks Through the Tier 1 and Tier 2 hazard assessments of the other substances used in the production and reﬁning of cocaine and heroin (CICAD/OAS 2004c, 2005), we recognize that some of these substances present a signiﬁcantly greater hazard to both humans and the environment than does the mixture of glyphosate and Cosmo-Flux used in the program. Exacerbating these hazards is the lack of information about the conditions of their use. Because of the lack of speciﬁc data on use and exposure, it was not possible to conduct detailed risk assessments for these substances. From anecdotal evidence and observations in other locations, it is clear that, in most cases, these substances are used without adequate safety training, without adequate protective equipment, without suitable disposal methods, and without supervision, which represents a signiﬁcant and serious potential risk to humans and the environment. D. Recommendations We have identiﬁed a number of uncertainties in our review of the data and, from these, make the following recommendations. These recommendations are grouped into two classes, recommendations to retain current practices that were judged to be essential or useful (Table 15) and recommendations related to new activities or data collection which will address key uncertainties identiﬁed in our study (Table 16). As already noted, risk assessments require review and reevaluation from time to time. Thus, our recommendations include the updating of this risk assessment as additional data become available.

Summary The production of coca and poppy as well as the processing and production of cocaine and heroin involve signiﬁcant environmental impacts. Both coca and poppy are grown intensively in a process that involves the clearing of land in remote areas, the planting of the crop, and protection against pests such as weeds, insects, and pathogens. The aerial spray program to control coca and poppy production in Colombia with the herbicide glyphosate is

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Table 15. Recommendations for the continuance of current practices in the coca and poppy eradication program in Colombia.

Practice Mixer-loader, worker, and environmental protection in the storage, mixing, and loading operations. Use of state-of-art application technology. Replace the respirator worn by the mixer-loader with a full face shield to reduce the potential for splashed material to run down the face into the eyes. Use of glyphosate in the eradication program.

Beneﬁt of continuance

Ranking of importance (5 = most important)

Protection of the humans and the environment from excessive exposures.

5

Accurate records of location and areas sprayed. This recommendation is procedures modiﬁcation of current that will reduce the risk of splashes of concentrated formulation into the eyes.

5

The risk of this product to humans and the environment is judged to be smaller than any currently available alternatives. However, if new candidate products become available, their use should be considered only after an appropriate risk assessment has been conducted.

5

4

conducted with modern state-of-the-art aircraft and spray equipment. As a result of the use of best available spray and navigation technology, the likelihood of accidental off-target spraying is small and is estimated to be less than 1% of the total area sprayed. Estimated exposures in humans resulting from direct overspray, contact with treated foliage after reentry to ﬁelds, inhalation, diet, and drinking water were small and infrequent. Analyses of surface waters in ﬁve watersheds showed that, on most occasions, glyphosate was not present at measurable concentrations; only two samples had residues just above the method detection limit of 25 µg/L. Concentrations of glyphosate in air were predicted to be very small because of negligible volatility. Glyphosate in soils that are directly sprayed will be tightly bound and biologically unavailable and have no residual activity. Concentrations of glyphosate plus CosmoFlux will be relatively large in shallow surface waters that are directly

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Table 16. Recommendations for the collection of new data and information in the coca and poppy eradication program in Colombia.

Recommendation Conduct a study to identify risk factors associated with time to pregnancy (TTP).

Including proximity to surface waters in Geographic Information System (GIS) analysis of locations and areas of coca and poppy ﬁelds. Identify mixtures of glyphosate and adjuvants that are less toxic to aquatic organisms than the currently used mixture. The priority of this recommendation would depend on the results of the GIS analysis. Testing of the glyphosateCosmo-Flux formulation for toxicity to amphibians. Use of GIS to quantify areas of coca and poppy production in biodiversity hotspots.

Beneﬁt of new data This is a recommendation resulting from the observation of increased risk of longer TTP in one region of Colombia (Valle del Cauca) where eradication spraying was not carried out. The study should be considered for prioritization in the general human health research programs conducted in Colombia. Better indication of likely frequency of contamination of these habitats; this would help to better quantify the risks to aquatic organisms in shallow-water nonﬂowing habitats. Reduction in possible environmental impacts to nontarget organisms in shallow surface water environments.

Ranking of importance (5 = most important) 3

2

2

Decrease in uncertainty regarding the toxicity to amphibians.

2

Better quantiﬁcation of proportion of regions identiﬁed as important sources of biodiversity that are being adversely impacted because of clear-cutting and planting of coca and poppy.

2

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Table 16. Continued

Recommendation Use of GIS to quantify size of ﬁelds planted to coca and poppy and track these over time to judge extent of environmental impact as well as recovery. Review the regulatory status of glyphosate on a regular basis.

Measurement of exposures to glyphosate in bystanders to sprays and reentry into sprayed ﬁelds. This recommendation would follow selection of new formulations and mixtures of adjuvants that have less environmental toxicity.

Beneﬁt of new data Allow more-accurate quantiﬁcation of potentially impacted areas as well as recovery when these ﬁelds are abandoned. Ensure that new testing and toxicity data on glyphosate are included in the risk assessment of its use in eradication spraying in Colombia. Better characterization of exposures under conditions of use in Colombia.

Ranking of importance (5 = most important) 2

2

1

oversprayed (maximum instantaneous concentration of 1,229 µg AE/L in water 30 cm deep); however, no information was available on the number of ﬁelds in close proximity to surface waters, and thus it was not possible to estimate the likelihood of such contamination. The formulation used in Colombia, a mixture of glyphosate and CosmoFlux, has low toxicity to mammals by all routes of exposure, although some temporary eye irritation may occur. Published epidemiological studies have not suggested a strong or consistent linkage between glyphosate use and speciﬁc human health outcomes. An epidemiology study conducted in Colombia did not show any association between time to pregnancy in humans and the use of glyphosate in eradication spraying. The mixture of glyphosate and Cosmo-Flux was not toxic to honeybees. The mixture was, however, more toxic to the alga Selenastrum, the cladoceran Daphnia magna, fathead minnow, and rainbow trout than formulated glyphosate (Roundup) alone. Studies on the use of glyphosate in agriculture and forestry have shown that direct effects on nontarget organisms other

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than plants are unlikely. Indirect effects on terrestrial arthropods and other wildlife may be the result of habitat alteration and environmental change brought about by the removal of plants by glyphosate. Because of the lack of residual activity, recovery of glyphosate-treated areas in Colombia is expected to be rapid because of good plant growth conditions. However, return to the conditions of tropical old-growth forest that existed before clear-cutting and burning may take hundreds of years, not from the use of glyphosate but because of the clear-cutting and burning, which are the primary cause of effects in the environment. The risk assessment concluded that glyphosate and Cosmo-Flux did not present a signiﬁcant risk to human health. In the entire cycle of coca and poppy production and eradication, human health risks associated with physical injury during clear-cutting and burning and the use of pesticides for protection of the illicit crops were judged to be considerably more important than those from exposure to glyphosate. For the environment, direct risks from the use of glyphosate and Cosmo-Flux to terrestrial mammals and birds were judged to be negligible. Moderate risks could occur in aquatic organisms in shallow surface waters that are oversprayed during the eradication program. However, the frequency of occurrence and extent to which this happens are unknown as data on the proximity of surface waters to coca ﬁelds were not available. Considering the effects of the entire cycle of coca and poppy production and eradication, clear-cutting and burning and displacement of the natural ﬂora and fauna were identiﬁed as the greatest environmental risks and are considerably more important than those from the use of glyphosate for the control of coca and poppy.

Acknowledgments This review is based on a report (Solomon et al. 2005a) prepared for the Inter-American Drug Abuse Control Commission (CICAD) section of the Organization of American States (OAS) in response to requests from the Governments of Colombia, the United Kingdom, and the United States. The request was to conduct a science-based risk assessment of the human health and environmental effects of the herbicide, glyphosate, used for the control of the illicit crops coca and poppy in Colombia. With an international panel of experts and activities in several countries, a study of this nature requires good coordination and organization. We are deeply indebted to Mr. Jorge Rios and Ms. Adriana Henao of the CICAD ofﬁce for their excellent work in organizing meetings, teleconferences, and ﬁeld trips. They served the authors well and frequently worked well beyond the call of duty. We are also very grateful for the contributions of the Colombian Field Team. Unfortunately, we cannot name these individuals; however, we extend our most grateful thanks to all of you for all the hard work and the personal risks that you took on behalf of data collection for this project.

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Field visits to Colombia by the authors were facilitated and coordinated by the staff of the Ministry of Foreign Affairs, and we were afforded protection by the National Police (Antinarcoticos). We offer our grateful thanks to Brigadier General Luis Gómez, his staff, the pilots, technicians, and the “Junglas” commandos for aiding us in our observations and sampling and for tolerating our scientiﬁc curiosity in the face of other priorities. At all times, we were given free and unfettered access to information, were allowed to take photographs freely, and were always treated with respect and in a most professional manner. The panel members are indebted to Drs. Lesbia Smith, Angus Crossan, Richard Brain, and also to the many students in the Toxicology Program at the University of Guelph for their work on the separate reports on Tier 1 and Tier 2 hazard assessment of other substances used in the production and reﬁning of cocaine and heroin. These data are presented in separate reports (CICAD/OAS 2004c, 2005).

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Index

Abiotic degradation, sulfonamides, 187:80 Acceptor/donor spectral overlap (illus), 182:8 Acephate, water-sediment degradation proﬁle, 187:168 Acetamiprid, aerobic aquatic metabolism (diag.), 187:207 Acetamiprid, water-sediment degradation proﬁle, 187:201 Acetochlor, water-sediment degradation proﬁle, 187:179 Acibenzolar-S-methyl, water-sediment degradation proﬁle, 187:199 Acrolein, water-sediment degradation proﬁle, 187:199 Activated carbon, metal remediation, water, 188:73 Activated charcoal, adsorbable organic halides measurement, 185:74 Activated sludge, PFOS effects, 186:143 Activated sludge treatment, paper production efﬂuent, 185:84 Acute hemorrhagic conjunctivitis, enterovirus related, 186:22 Acute lead exposure, effects, 185:94 Acute toxicity, arsenic, 184:112 Acute toxicity, glyphosate, 190:72, 100 Acute toxicity, PBDE congeners, 183:73 Adenovirus, diarrhea cause, 186:4 Adenovirus, incidence by age, 186:26 Adenovirus infection, drinking waterrelated, 186:9 Adenovirus, waterborne enteric disease, children, 186:36 Adenoviruses, enteric, described, 186: 8 Adsorbable organic halides (AOX), paper production, 185:74

Adsorption capacities, sorbents metal remediation, water, 188:71 Adsorption, ionizable pesticides in soils, 188:149 ff. Adsorption mechanisms, soil, 188:166, 168 Adults blood lead levels, Brazil, 184:85, 87 AEATF task force, 186:110 Aerial application, glyphosate illicit crops, Colombia, 190:43 ff. Aerial transport of pesticides, 181:1 ff. Africa, mercury contamination, 181: 156 Age differences, children’s blood lead, 185:105 Age effect, human nail element content, 185:147 Agitation leaching (gold), using cyanide, 183:25 Agricultural Handlers Exposure Assessment Database (AHED), 186:113 Agricultural pesticide drift, 181:1 ff. Agricultural Reentry Exposure Task Force (ARTF), 186:112, 116 Agrowaste remediation, heavy metals in water, 188:59 ff. Agrowastes, metal remediation, water, 188:67 AHED (Agricultural Handlers Exposure Assessment Database), 186:113 AHETF task force, 186:110, 113 Air, effect on element content human nails, 185:153 Air levels, pollutants in S. America, 185:8 Alachlor/metolachlor photodegradation pathways (diagram), 182:64

127

128

Index

Alachlor, microcosm degradation proﬁle, 187:218 Alachlor, water-sediment degradation proﬁle, 187:178 Alaska, gold mining mercury beach sediments, 181:166 Alcohol consumption, effects nail/ element studies, 185:150 Aldicarb, water-sediment degradation proﬁle, 187:187 Aldrin in foods, S. America, 185:22 Aldrin, marine mammals, 184:4 Aldrin, use in S. America, 185:2 Algae bioassays, Reconquista River, 185:54 Algae, mercury contamination, Chile, 183:6, 8 Algicide, simazine, 189:1 Alkaline chlorination, wastewater cyanide removal, 183:26 Allolobophora icterica, earthworm biomarkers, 188:100 Allolobophora spp. (earthworms), heavy metal bioassays, 186:82 Alpha-cypermethrin, water-sediment degradation proﬁle, 187:172 Alteromonas luteoviolaceus, Q1 source, 188:18 Aluminum, in human nails, 185:162 Aluminum inﬂuence on sorption, ionisable pesticides, 188:197 Amalgamation (mercury), ecotoxicological aspects, 181: 143 Amalgamation, gold with mercury, 181:143 Amazon River, mercury contamination, 181:143 Amide chemical structures, 182:139 Amide herbicide photodegradation, on glass, 182:43 Amide herbicide photodegradation, on plants, 182:75 Amide herbicide photodegradation, on soils, 182:63 Amides, fate in water-sediment systems, 187:177 Amitraz, water-sediment degradation proﬁle, 187:202

Amitrole, water-sediment degradation proﬁle, 187:196 Amphibian gonadal abnormalities, before 1945 (table), 187:119 Amphibians gonadal anomalies, chemical exposure, 187:103 ff. Amphibians, pesticide effects, 187:7 Analytical instruments used in nail/ element studies, 185:148 Analytical methods, arsenic, 184:122 Analytical methods, free cyanide, 183:39 Analytical procedures, human nail elements, 185:146 Andean Biodiversity Region, Colombia (map), 190:54 Androgenic substances, paper production contaminants, 185:76 Androgens from progesterone, paper production, 185:77 Androgens produced from progesterone (illus.), 185:77 Anilazine, water-sediment degradation proﬁle, 187:197 Anilide chemical structures, 182:139 Anilide herbicide photodegradation, on glass, 182:43 Anilide herbicide photodegradation, on soils, 182:63 Anilides, fate in water-sediment systems, 187:177 Animal bioassays, Reconquista River, 185:54 Animal manure, metal remediation, water, 188:68 Animals, geophagous (table), 183:118 Anti-ChE pesticides, earthworm effects, 188:96 Antimony, aquatic environment hazard, 188:61 Antimony, in human nails, 185:161 Antimony, potential health effects, 188:63 Aporrectodea calignosa, earthworm biomarkers, 188:89 Aporrectodea nocturna, earthworm biomarkers, 188:100 Aporrectodea tuberculata, earthworm biomarkers, 188:91

Index Applied risk analysis, exposure monitoring, 186:107 ff. Apporectodea spp. (earthworms), heavy metal bioassays, 186:82 Aquatic ecosystems, pesticide effects, 187:6 Aquatic invertebrates, pesticide effects, 187:9 Aquatic invertebrates, PFOS toxicity (table), 186:147 Aquatic macrophytes, PFOS effects, 186:145 Aquatic microbes, pesticide effects, 187:18 Aquatic plants, pesticide effects, 187:17 Aquatic toxicology, paper production, 185:75 AQUATOX, pesticide impact aquatic organisms model, 187:160 AQUIRE, EPA amphibian lethality database, 187:7 Argentina, Reconquista River pollution, 185:35 ff. Argentina rivers pollution, 185:36 Argentina, urban population percentage, 185:35 Arsanilic acid, toxicity, 184:110 Arsenic acid (AsV), structure Arsenic acid, herbicide, 184:104 Arsenic, acute toxicity, 184:112 Arsenic, agricultural chemicals sources, 184:103 Arsenic, agricultural sustainability Bangladesh, 189:78 Arsenic, air content, 184:102 Arsenic, analytical methods food, 184:121 Arsenic, analytical methods Mexican foods, 181:75 Arsenic, aquatic environment hazard, 188:60, 63 Arsenic, atmospheric levels, 184:102 Arsenic, ATP formation inhibition, 184:111 Arsenic, Bangladesh agriculture, 189:65 Arsenic, Bangladesh foods, 189:71, 73 Arsenic, Bangladesh soil & crops, 189:67 Arsenic behavior, soil, 189:44

129

Arsenic, bioavailability, 184:120, 125 Arsenic, bioavailability, plant species, 184:132 Arsenic, bioavailability, rhizosphere interactions, 184:132 Arsenic, bioavailability, soil adsorption, 184:132 Arsenic, bioavailability, soil factors, 184:131 Arsenic, capillary electrophoresis speciation, 184:124 Arsenic chemistry, 184:104 Arsenic chemistry, in crops, 189:48 Arsenic chemistry, in foods, 189:60 Arsenic chemistry, in soil, 189:44 Arsenic chemistry, iron plaque anaerobic soil, 189:48 Arsenic chemistry, marine plants, 189:64 Arsenic chemistry, seafoods, 189:64 Arsenic chemistry, soil rhizosphere, 189:48 Arsenic, Chinese coal contamination, 189:92 Arsenic, Chinese coal distribution (map), 189:93 Arsenic, Chinese coal hazard, 189:92 Arsenic, chronic toxicity, 184:112 Arsenic, citric acid cycle effects, 184:110 Arsenic compounds, chemical structures, 184:105 Arsenic, derivitization methods (table), 184:126 Arsenic, drinking water guidelines, 184:114 Arsenic, energy metabolism inhibition, 184:110 Arsenic, environmental transfer pathways, 184:108 Arsenic, enzyme systems inactivation, 184:110 Arsenic, EPA Maximum Permissible Conc drinking water, 184:101 Arsenic, epidemic in China, 189:94 Arsenic, food recommended guidelines, 184:114 Arsenic, food safety guidelines Bangladesh, 189:79

130

Index

Arsenic, gas chromatography speciation, 184:124 Arsenic, grain yield effects, 189:57 Arsenic, groundwater chemistry, 184:105 Arsenic, groundwater contamination, India, 184:97 Arsenic, groundwater levels, global, 184:102 Arsenic, groundwater major health concern, 189:43 ff. Arsenic, health effects indoor Chinese coal burning, 189:89 ff. Arsenic, human exposure Bangladesh, 189:75 Arsenic, human exposure guidelines, 189:76 Arsenic, human exposure management, 189:77 Arsenic, human exposure pathway, 184:115, 117 Arsenic, human food intake (table), 184:119 Arsenic, hydride generation detection, 184:123 Arsenic, hydroponics effects plants, 189:55 Arsenic III (AsIII), plant uptake, 189:50 Arsenic III (AsIII), soil, 189:45 Arsenic, in food chains, 184:116 Arsenic, in human nails, 185:162 Arsenic, industrial sources, 184:103 Arsenic, irrigation water, 189:65 Arsenic, irrigation water plant effects, 189:58 Arsenic LD50s, lab animals, 184:112 Arsenic, liquid chromatography speciation, 184:123 Arsenic, major compounds in human exposure, 184:116 Arsenic, mechanisms of toxicity, 184:110 Arsenic, methylated species in plants, 189:52 Arsenic, modes of toxic action, 184:110, 113 Arsenic movement, groundwater & soil to crops, 189:43 ff.

Arsenic, oxidation states, 184:104 Arsenic oxyanions, 184:104 Arsenic, phytoxicity levels, 184:114 Arsenic, plant accumulation, 189:51 Arsenic, plant metabolism, 189:51 Arsenic, plant tolerance, 189:54 Arsenic, plant toxicity, 184:113 Arsenic, plant translocation, 189:51 Arsenic, pyruvate oxidation inhibition, 184:110 Arsenic, redox conditions, 189:45 Arsenic, Redox potential, groundwater (diagram), 184:106 Arsenic, removal from foods, methods, 184:121 Arsenic, role of soil iron hydroxides, 189:44 Arsenic, seafood main dietary source, 184:115 Arsenic, seawater content, 184:101 Arsenic, smelting & mining sources, 184:103 Arsenic, soil chemistry, 184:107 Arsenic, soil content, global, 184:101 Arsenic, soil cycles, 184:108 Arsenic, soil microorganisms effect, 189:47 Arsenic, soil organic matter effect, 189:47 Arsenic, soil pH effect, 189:47 Arsenic, soil speciation, 184:120 Arsenic, soil transformations (diagram), 184:108 Arsenic sources, anthropogenic, 184:103 Arsenic sources, environmental, 184:99 Arsenic sources, geogenic, 184:99 Arsenic sources, igneous rocks, 184:100 Arsenic sources, sedimentary rocks, 184:100 Arsenic sources, soils & sediments, 184:100 Arsenic speciation, deﬁned, 184:119 Arsenic speciation, foods, 189:60 Arsenic speciation in biological systems, 184:97 ff. Arsenic, speciation methods, 184:122, 126 Arsenic speciation, rice, 189:61, 72

Index Arsenic speciation, soil, 189:45 Arsenic speciation toxicity, 184:97 ff. Arsenic species, relative toxicity plants, 189:53 Arsenic, spiked soil tests AsIII/AsV, 189:57 Arsenic tolerance, plants & iron plaque, 189:49 Arsenic, total intake from foods (table), 184:119 Arsenic, toxic effects humans & animals, 184:111 Arsenic, toxic effects plants, 184:113 Arsenic, toxic effects plants, 189:52 Arsenic, toxic effects soil microorganisms, 189:59 Arsenic toxicity, 184:97 ff. Arsenic toxicity, chemical forms, 184:109 Arsenic toxicity, species dependent, 184:120 Arsenic trioxide, major form industryproduced, 184:103 Arsenic, uptake in plants, 189:50 Arsenic V (AsV), phosphate analogue, 189:47 Arsenic V (AsV), plant uptake, 189:50 Arsenic V (AsV), soil, 189:45 Arsenic, vegetable concentrations (table), 184:118 Arsenic, volatile forms, 184:108 Arsenic, volatilization from soil, 189:48 Arsenic, water cycles, 184:108 Arsenic, water speciation, 184:120 Arsenic, WHO recommended value, drinking water, 184:101 Arsenic, wood preservative sources, 184:104 Arsenical herbicides, 184:104 Arsenical insecticides, 184:104 Arsenical pesticides, 184:104 Arsenicosis, pandemic Bangladesh, 184:97 Arsenious acid (AsIII), structure, 184:105 Arsenobetaine (AsB), in foods, 189: 60 Arsenobetaine (AsB), relative toxicity, 184:98, 105

131

Arsenocholine (AsC), relative toxicity, 184:98, 105 Arsenopyrite, arsenic-bearing mineral, 184:99 ARTF (Agricultural Reentry Exposure Task Force), 186:110, 112, 116 Arthrobacter aurescens, simazine degrader, 189:15 Aryloxyalkanoate herbicide chemical structures, 182:136 As-III, arsine, 184:104 AsB (arsenobetaine), relative toxicity, 184:98, 105 AsC (arsenocholine), relative toxicity, 184:98, 105 Aseptic meningitis, entovirus-related, 186:21 AsIII (arsenious acid), relative toxicity, 184:98, 104, 107 AsO, elemental arsenic, 184:104 Assessment endpoints, enteric viral diseases, children, 186:37 Astigmate bioassays, DDTcontaminated soils, 186:89 Astrovirus, diarrhea cause, 186:4 Astroviruses, described, 186:10 Asulam, water-sediment degradation proﬁle, 187:188 AsV (arsenic acid), relative toxicity, 184:98, 104, 107 Atmosopheric pesticide studies, regulatory considerations, 181:24 Atmospheric arsenic, 184:102 Atmospheric inversion layer, lead pollution, 185:100 Atmospheric lead, Brazil, 184:69 Atmospheric lead pollution, gasoline, 185:99 Atmospheric lead, seasonal variation, 185:104 Atmospheric lead, working environment limits, Brazil, 184: 90 Atmospheric mercury, 181:145 Atmospheric oxygen species, 182:29 ATP formation inhibition, arsenic, 184:111 Atrazine, adsorption coefﬁcient, 188:190

132

Index

Atrazine effects, gonads ﬁsh/frogs, 187: 114 Atrazine, ionisable herbicide, 188:150, 156 Atrazine, water-sediment degradation proﬁle, 187:197 Avermectin, chemical structures, 182: 156 Avoidance behavior, earthworm test (diag.), 188:101 Avoidance behavior, earthworms, chemicals (table), 188:98 Azadirachtin, chemical structure, 182: 156 Azocyclotin, microcosm degradation proﬁle, 187:220 Azole chemical structures, 182:151 Azole herbicide photodegradation, in solvents, 182:55 Azole herbicide photodegradation, on glass, 182:45 Azole herbicide photodegradation, on soils, 182:67 Azole herbicide photodegradaton, on plants, 182:75 Azole herbicides, fate in watersediment systems, 187:195 Azoxystrobin, water-sediment degradation proﬁle, 187:175 B-lymphocyte function, children deﬁcient, 186:2 BAFs, see Bioaccumulation factors, 186:143 Bagasse, metal remediation, water, 188:68, 72 Baikal seals, epizootics, 184:2 Baleen whales, organohalogen contaminants, 184:2 Bangladesh, arsenic situation agriculture, 189:65 Bangladesh, food & water consumption, 189:74 Bark (wood), metal remediation, water, 188:73 Bat kills, cyanide, 183:35 BCFs, see Bioconcentration factors, 186:140

BDE-153, dominant PBDE tissue congener, 183:60 BDE-47, dominant PBDE tissue congener, 183:60 BDE-47, high levels in ﬁsh eaters, 183:64 BDE-47, PBDE congener breast cancer patients, 183:60 Beluga whale blubber PHCs (table), 184:24 Beluga whales, 184:7 Benalaxyl, water-sediment degradation proﬁle, 187:180 Benchmarks, PFOS aquatic organisms, 186:160 Benfuracarb photodegradation (diagram), 182:42 Benomyl, earthworm avoidance, 188:98 Bentazone, adsorption coefﬁcient, 188:189 Bentazone, water-sediment degradation proﬁle, 187:203 Bentonite, metal remediation, water, 188:73 Benzo(a)pyrene, earthworm response, 188:90 Benzoylurea chemical structures, 182:140 Benzoylurea herbicides, fate in watersediment systems, 187:189 Bermellon, mercury ore type, 183:1 Berylium, in human nails, 185:161 Beta-cyﬂuthrin, water-sediment degradation proﬁle, 187:172 Beta-sitosterol, reduced ﬁsh steroids, 185:76, 82 BFRs (brominated ﬂame retardants, 188:25 Biethylene (butadiene), 189:132 Bifenox, water-sediment degradation proﬁle, 187:200 Bioaccumulation factors (BAFs), 186:140 Bioaccumulation, lead Brazil, 184:61 Bioaccumulation, methylmercury ﬁsh, 189:108 Bioassays, in ecological risk assessment, 186:75

Index Bioavailability, arsenic species, 184:125 Bioavailability of soil contaminants, parameters considered, 186:92 Biobio, Chilean industrial region (map), 183:7 Bioconcentration factors, PFOS, 186:138, 140 Biodegradation, PFOS, 186:136 Bioﬁlm, sediment cover, 187:140 Biological oxygen demand (BOD), paper production, 185:73 Biological oxygen demand (BOD), Reconquista River, 185:44, 52 Biomagniﬁcation, methylmercury ﬁsh, 189:108 Biomarker responses, earthworms, pollutants (table), 188:90 Biomarker, trace element exposure, human nails, 185:141 ff. Biomarkers, butadiene exposure, 189:142 Biomarkers, chloroprene exposure, 189:155 Biomarkers, human exposure to pollutants, 189:109 Biomarkers, isoprene exposure, 189:162 Biomarkers, standardized toxicity tests, earthworms, 188:104 Biomass (living), metal remediation, water, 188:65 Biomass (nonliving), metal remediation, water, 188:66, 72 Biomass, alcohol production, 189:25 ff. Biomass ion-exchange, heavy metals, 188:67, 72 Biotransformation, sulfonamides in mammals, 187:79 Bioturbation, pesticide water-sediment studies, 187:214 Bird kills, cyanide, 183:32 Bird mortality, sodium cyanide (table), 183:34 Birds, geophagous (table), 183:121 Birds, PFOS toxicity, 186:154, 158, 166 Birds, pollutant levels in S. America, 185:20 Birds, wetland, pesticide effects, 187:21

133

Bismuth, in human nails, 185:161 Bisphenol A effects, gonads ﬁsh/frogs, 187:114 Bitertanol, water-sediment degradation proﬁle, 187:196 Bivinyl (butadiene), 189:132 Black bindweed (Fallopia convolvulus), copper bioassays, 186:87 Black liquor, paper production, 185:73 Bleaching, organic stream contaminant source, 185:72 Blood lead, adults, 185:110 Blood lead, affected children, 185:110 Blood lead, animals, 185:110 Blood lead, changes with age, 185:121 Blood lead, children, 185:102 Blood lead, correlation with head hair lead, 185:123, 125 Blood lead levels, adults, Brazil, 184:85, 87 Blood lead levels, age distribution, 185:118 Blood lead levels, chickens, Brazil, 184:79 Blood lead levels, children, Brazil, 184:83 Blood lead levels, control populations, Brazil, 184:88 Blood lead levels, Mexico, 181:67, 69, 71, 77, 81, 92, 98 Blood lead levels vs age, 185:112 Blood lead levels vs. industrial sites, Brazil, 184:86 Blood lead levels vs. lead recycling plant, Brazil, 184:89 Blood lead levels vs. mining areas, Brazil, 184:87 Blood lead reference values, Brazil, 184:88 Blood lead, seasonal changes, 185:122 Blood lead, symptoms vs age, 185:111 Blood pesticide levels, Uruguay, 181:125, 127, 129, 130 BOD (biological oxygen demand), paper production, 185:73 BOD (biological oxygen demand), Reconquista River, 185:44, 52 Body burdens, lead, Brazil, 184:81

134

Index

Body surface area, pesticide exposure, 186:121 Body weight average, pesticide exposure, 186:121 Bornholm disease, entovirus related, 186:23 Boron, in human nails, 185:161 Boscalid, water-sediment degradation proﬁle, 187:181 Bottlenose dolphins, epizootics, 184:2 Brazil, air lead contamination regulations, 184:67 Brazil environmental lead contamination, 184:59 ff. Brazil, lead ore reserve estimates, 184:60 Brazil lead problems, 184:59 ff. Brazil, lead production, imports, exports, 184:60 Brazil, mercury contamination table, 181:147 Brazilian legislation, maximum lead permitted in foods, 184:77 Breast cancer patients, BDE-47 (PBDE congener), 183:60 Breast feeding, reduces infant diarrhea, 186:5 Brittle nails, effect on element content, 185:151 Brominated anizoles, 188:34 Brominated ﬂame retardants (BFRs), 188:25 Brominated HNPs, most abundaant, 188:4 Brominated phenols, 188:34 Brominated phenoxyanisoles (MeOBDEs), 188:23 Brominated phenoxyanisoles, analytical aspects, 188:28 Brominated phenoxyanisoles, environmental distribution, 188: 29 Brominated phenoxyanisoles, related compounds, 188:31 Bromodibenzo-dioxins, chemical structures, 188:32 Bromoindoles, 188:42 Bromoindoles, chemical structures, 188:42

Bromophenols, analytical aspects, 188:36 Bromophenols, chemical structures, 188:35 Bromophenols, environmental distribution, 188:37 Bromoquinones, chemical structures, 188:34 Bromoxynil, microcosm degradation proﬁle, 187:217 Bromoxynil, water-sediment degradation proﬁle, 187:164 Brown algae, metal remediation, water, 188:65 Brownstock, paper production, 185:71, 73 Bufo arenarum (toad), bioassay organism, 185:55 Bufo bufo, gonadal abnormalities, 187:104 Butachlor, earthworm response, 188:91 Butadiene,1-3-, toxicology, 189:131 ff. Butadiene, carcinogenicity, 189:136 Butadiene, chronic inhalation studies, 189:136 Butadiene, cytochrome P450 oxidation, 189:137 Butadiene, detoxiﬁcation mechanisms, 189:140 Butadiene diepoxide, potent genotoxicity, 189:139 Butadiene epoxide metabolites, genotoxicity, 189:139 Butadiene, exposure biomarkers, 189:142 Butadiene, genotoxicity, 189:145 Butadiene, hematopoietic toxicity, 189:135 Butadiene, human epidemiology, 189:148 Butadiene, industrial uses, 189:133 Butadiene, kinetics, 189:137 Butadiene, Known to be a Human Carcinogen, 189:149 Butadiene, metabolic scheme (chart), 189:138 Butadiene, metabolism, 189:137 Butadiene, motor vehicle production, 189:134

Index Butadiene, multisite carcinogen in mice, 189:136 Butadiene, mutagenicity, 189:145 Butadiene, number workers exposed, 189:133 Butadiene, occupational exposure, 189:133 Butadiene, other chemical names, 189:132 Butadiene, photodegradation rates, 189:134 Butadiene, physicochemical properties, 189:132 Butadiene, Probably Carcinogenic to Humans, 189:149 Butadiene, risk assessment, 189:150 Butadiene, toxicity, 189:134 Butadiene toxicology, 189:131 ff. Butadiene, worker exposure leukemia, 189:149 Butadiene, world production, 189:133 Butadiene-1,3 (butadiene), 189:132 Butafenacil, water-sediment degradation proﬁle, 187:185 Butamifos, water-sediment degradation proﬁle, 187:168 By-catch delphinoid PHC studies, 184:35 Cacodylic acid, structure, 184:105 Cadmium, analytical methods Mexican foods, 181:75 Cadmium, aquatic environment hazard, 188:61, 63 Cadmium content, Reconquista River, 185:46 Cadmium, earthworm biomarkers, 188:87 Cadmium, in human nails, 185:161 Calcium arsenate, insecticide, 184:104 Calcium, dietary need, geophagy, 183:117 Calcium, in human nails, 185:161 Calcivirus, diarrhea cause, 186:4 Calcivirus, genera/strains, table, 186:12 Calciviruses, described, 186:11 Calciviruses, incidence by age, 186:26 Calciviruses, waterborne enteric disease, children, 186:36

135

California Pesticide Illness Surveillance Program, 186:57 ff. California, pyrethroid illnesses, 186: 57 ff. California Roller, uniform pesticide applicator, 186:117 California sea lions, reproductive impairment PHCs, 184:9 Canada, mercury contamination, 181:158 Cancer studies, glyphosate, 190:77 Capillary electrophoresis, arsenic speciation, 184:124 Captan, water-sediment degradation proﬁle, 187:184 Carbamate chemical structures, 182:141 Carbamate photodegradation, in solvents, 182:52 Carbamate photodegradation, on glass, 182:42 Carbamate photodegradation, on plants, 182:73 Carbamate photodegradation, on soils, 182:62 Carbamates, fate in water-sediment systems, 187:186 Carbaryl, earthworm response, 188:90 Carbaryl, microcosm degradation proﬁle, 187:219 Carbaryl, water-sediment degradation proﬁle, 187:187 Carbendazim, adsorption coefﬁcient, 188:187, 190 Carbendazim, earthworm avoidance, 188:98 Carbofuran, earthworm response, 188:91 Carbofuran, microcosm degradation proﬁle, 187:219 Carbon cycle, organic matter role, 188:128 Carbon dioxide (CO2) emissions, S. America, 185:6 Carbon in pulp, gold precipitation, 183:22 Carbosulfan, microcosm degradation proﬁle, 187:219 Carboxylic acids, fate in watersediment systems, 187:170

136

Index

Carboxylic esters, fate in watersediment systems, 187:170 Carbutamide, physicochemical properties, 187:77 Carcinogenicity, PBDEs, 183:78 Carfentrazone-ethyl, microcosm degradation proﬁle, 187:220 Carfentrazone-ethyl, water-sediment degradation proﬁle, 187:200 Carpropamid, water-sediment degradation proﬁle, 187:178 Carson River watershed (Nevada), mercury contamination, 181:142, 160 CAS numbers, pesticides, 181:28, 134 CAS numbers, pesticides, 188:205 Caspian seals, epizootics, 184:2 Cellulose, wood composition amount, 185:70 Central tendency statistic, pesticide exposure, 186:121 Ceramics, lead content, Mexico, 181: 67 Ceramics, lead oxide glazing, 181:68 Ceramics, lead-glazed, major health hazard, 181:38 Cetaceans, HDBPs body burdens, 188:15 Cetaceans, organohalogen contaminants, 184:1 ff. ChE inhibitors, restricted entry interval determining, 186:115 Chemic/physical properties, PFOS, 186:135 Chemical exposure, gonadal anomaly, 187:103 ff. Chemical names, pesticides, 188:205 Chemical oxygen demand (COD), paper production, 185:73 Chemical oxygen demand (COD), Reconquista River, 185:44, 52 Chemical/physical properties, endosulfan, 183:102 Chemical/physical properties, soil health indicators, 188:135 Chemical/physical properties, sulfonamides (table), 187:71 Chemical structures, amides, 182:139 Chemical structures, anilides, 182:139

Chemical structures, arsenic species, 184:105 Chemical structures, azoles, 182:151 Chemical structures, benzoylureas, 182:140 Chemical structures, bromodibenzodioxins, 188:32 Chemical structures, bromoindoles, 188:42 Chemical structures, bromophenols, 188:35 Chemical structures, bromoquinones, 188:34 Chemical structures, carbamates, 182:141 Chemical structures, HDBPs (ﬁgure), 188:10 Chemical structures, MeO-BDEs (ﬁgure), 188:24 Chemical structures, miscellaneous fungicides, 182:152 Chemical structures, miscellaneous herbicides, 182:152 Chemical structures, miscellaneous insecticides, 182:152 Chemical structures, miscellaneous rodenticides, 182:152 Chemical structures, organochlorine pesticides, 182:146 Chemical structures, organophosphorus pesticides, 182:148 Chemical structures, pesticide, directory, 182:130 Chemical structures, phenoxy herbicides, 182:136 Chemical structures, pyrethroids, 182:137 Chemical structures, Q1 (ﬁgure), 188:17 Chemical structures, sulfonylureas, 182:144 Chemical structures, triazines, 182:151 Chemical structures, ureas, 182:140 Chemiluminescence, described, 182: 25 Children, diarrheal disease numbers, 186:4 Children, enteric viral infection risks, 186:1 ff.

Index Children enteric viruses, hospital admissions, 186:7 Children, environmental risks, 186:2 Children, immunocompromised diseases, enterovirus-related, 186:24 Children lead exposure, 185:101 Children, spleen immature marginal zone compartment, 186:2 Children’s blood lead, age differences, 185:105 Children’s blood lead, chelation treated, 185:112 Children’s blood lead levels, Brazil, 184:83 Children’s blood lead, seasonal variation, 185:104 Children’s Exposure Factors Handbook (EPA), pesticide, 186:124 Chile, map of, 183:3 Chile, mercury contamination, 183:1 ff. Chile, regional map of, 183:5 Chilean government, mercury contamination limits, 183:14 China, largest global coal producer/ consumer, 189:90 China, mercury contamination, 181:156 Chinese coal, arsenic hazard, 189:92 Chinese coal, indoor burning health effects, 189:89 ff. Chitosan, metal remediation, water, 188:73 Chlordane, use in S. America, 185:4 Chlordanes in foods, S. America, 185:22 Chlordanes, marine mammals, 184:4 Chlorimuron-ethyl, photoinduced rearrangement (diagram), 182:57 Chlorinated insecticides, sediment levels in S. America, 185:16 Chlorinated insecticides, soil levels in S. America, 185:10 Chlorinated insecticides, use in S. America, 185:2 Chlorinated insecticides, water levels in S. America, 185:13 Chlorine derivatives, pulp bleaching, 185:72

137

Chlorine, in human nails, 185:161 Chlornitrofen (CNP), water-sediment degradation proﬁle, 187:200 Chloroprene, exposure biomarkers, 189:155 Chloroprene, genotoxicity, 189:155 Chloroprene, human epidemiology, 189:156 Chloroprene, industrial uses, 189:150 Chloroprene, kinetics, 189:152 Chloroprene, metabolic scheme (chart), 189:154 Chloroprene, metabolism, 189:152, 154 Chloroprene, physical properties, 189:133 Chloroprene, physicochemical properties, 189:150 Chloroprene, risk assessment, 189:157 Chloroprene, toxicity, 189:151 Chloroprene toxicology, 189:131 ff. Chloroprene, worker exposure, 189: 151 Chloroprene, world production, 189:150 Chlorpropham, water-sediment degradation proﬁle, 187:187 Chlorpropham, water-sediment degradation proﬁle, 187:187 Chlorpyrifos, earthworm response, 188:91 Chlorpyrifos, microcosm degradation proﬁle, 187:216 Chlorpyrifos-methyl, microcosm degradation proﬁle, 187:216 Chlorsulfuron, adsorption coefﬁcient, 188:185, 189 Chlorsulfuron, anaerobic aquatic metabolism (diag.), 187:194 Chlorsulfuron, water-sediment degradation proﬁle, 187:191 Chromium, aquatic environment hazard, 188:62, 63 Chromium content, Reconquista River, 185:46 Chromium, removal from water, lignocellulose, 188:70 Chronic lead exposure, children effects, 185:94 Chronic toxicity, arsenic, 184:112

138

Index

CICAD (Inter-American Drug Abuse Control Commission), 190:113 Cigarette smoke, effects on nail/ element studies, 185:150 CIMMYT-Bangladesh, arsenic research, 189:70 Cinidon-ethyl, water-sediment degradation proﬁle, 187:184 cis/trans isomerization, photoinduced pyrethroids, 182:40 Citric acid cycle effects, arsenic, 184:110 Clams, mercury contamination, Chile, 183:7 Classic chlorinated contaminants, 188:2 Clay inﬂuence on sorption, ionisable pesticides, 188:196 Clays, metal remediation, water, 188: 73 Clays, photophysical/photochemical processes, 182:27 Climatic properties, ionisable compounds adsorption, 188:163 Clofentezine, water-sediment degradation proﬁle, 187:204 Cloransulam-methyl, anaerobic aquatic metabolism (diag.), 187:183 Cloransulam-methyl, water-sediment degradation proﬁle, 187:181 Clothianidin, water-sediment degradation proﬁle, 187:202 Clusters of lead exposure, 185:108 CNP (chlornitrofen), water-sediment degradation proﬁle, 187:200 CO2 (carbon dioxide) emissions, S. America, 185:6 Coal burning, indoors without chimneys, 189:91 Coal burning, trace element dispersal, 189:90 Cobalt, in human nails, 185:162 Cobaltite, arsenic-bearing mineral, 184:99 Coca eradication, Colombia, 190:43 ff. Coca eradication, glyphosate, 190:43 ff. Coca production, environmental impacts (Colombia), 190:104 Coca production, human health impacts (Colombia), 190:103

Cocaine, from Erythroxylum coca (coca), 190:44 Cocaine, global production, 190:44 Cocaine usage, global numbers, 190:44 Coco production, control recommendations (Colombia), 190:108 Coconut husks, metal remediation, water, 188:72 COD (chemical oxygen demand), paper production, 185:73 COD (chemical oxygen demand), Reconquista River, 185:44, 52 Collembola, copper bioassays, 186:87 Collembola, heavy metal bioassays, 186:83 Combined upper-bound exposure factors, pesticide, 186:123 Combustion chamber conditions, dioxin formation, 190:5 ff. Conjugation, pesticides/watersediment, 187:147, 154 Contaminated sites, pollutants in S. America, 185:7 Contaminated soil, ecological risk assessment, 186:73 ff. Contaminated soils, earthworm avoidance, 188:97 Contaminated soils, realistic assessment, 188:108 Continuous-ﬂow water-sediment apparatus (diag.), 187:155 Copper chloride, earthworm response, 188:91 Copper, earthworm biomarkers, 188: 87 Copper, in human nails, 185:161 Copper, potential health effects, 188:63 Copper-contaminated soils, risk assessment, 186:85 Copper-contaminated soils, screening levels, 186:85 Corn ethanol, input costs, 189:28 Corn fermentation/distillation, energy inputs, 189:28 Corn production, energy inputs, 189:26 Corn use in ethanol production, 189:26 Cosmo-Flux®, glyphosate adjuvant, 190:51, 91

Index Costs of enteric viral infections in children, 186:29 Crassostrea corteziensis (oyster), lead levels, 181:58 Crassostrea virginica (oyster), lead levels, 181:57 Cricket bioassays, DDT-contaminated soils, 186:89 CropLife America (formerly NACA), 186:113 Cuticular fruit/leaf waxes, composition (table), 182:89 Cyanatryn, microcosm degradation proﬁle, 187:219 Cyanidation process, gold extraction, 183:22 Cyanide annual use, North America, 183:22 Cyanide, bird kills, 183:32 Cyanide contamination, water management issues, 183:40 Cyanide, drinking water contamination, 183:35 Cyanide effects, aquatic plants, 183:30 Cyanide effects, ﬁsh, 183:29 Cyanide effects, terrestrial ﬂora, 183: 36 Cyanide, ﬁsh kills, 183:28 Cyanide hazards, aquatic ecosystems, 183:28 Cyanide hazards, gold mining, 183: 21 ff. Cyanide leaching (gold mining), wildlife mortality, 183:25 Cyanide leaching, gold mining, 181:142 Cyanide levels in water/sediments, downstream mining, 183:24 Cyanide, livestock kills, 183:36 Cyanide losses from soils, routes, 183:27 Cyanide losses from water, routes, 183:31 Cyanide mitigation techniques, 183:37 Cyanide persistence, alkaline conditions, 183:25 Cyanide, plant germination inhibition, 183:37 Cyanide releases, gold mining, accidents, 183:24

139

Cyanide, respiration inhibition higher plants, 183:37 Cyanide water remediation, impoundments, 183:26 Cyanide water remediation, microbial oxidation, 183:26 Cyanide, wildlife protection, 183:32 Cyanide-laced sludge releases, accidents, 183:23 Cyanide-resistant yeasts, 183:27 Cyanide-tolerant ﬁsh, 183:30 Cyanofos, water-sediment degradation proﬁle, 187:166 Cyazofamid, water-sediment degradation proﬁle, 187:181 Cyclanilide, water-sediment degradation proﬁle, 187:180 Cyclodiene insecticides, use in S. America, 185:2 Cyﬂuthrin, dislodgeable foliar residue illnesses, 186:65 Cyﬂuthrin, illnesses described, 186:64 Cyﬂuthrin-β, water-sediment degradation proﬁle, 187:172 Cyhalofop-butyl, water-sediment degradation proﬁle, 187:171 Cyhalothrin-λ, illnesses described, 186:66 Cyhalothrin-λ, microcosm degradation proﬁle, 187:218 Cyhalothrin-λ, water-sediment degradation proﬁle, 187:173 CYP isoenzymes, induction, marine mammals, 184:7 Cypermethrin photodegradation (diagram), 182:53 Cypermethrin-α, water-sediment degradation proﬁle, 187:172 Cyromazine, water-sediment degradation proﬁle, 187:197 Cytochrome P-450 oxidation, simazine, 189:17 Cytochrome P450 induction, marine mammals, 184:7 2,4-D, adsorption coefﬁcient, 188:184, 193 2,4-D, ionizable herbicide, 188:150, 154 2,4-D, soil half-life, 188:201

140

Index

2,4-D water-sediment degradation proﬁle, 187:171 2,4,DB, water-sediment degradation proﬁle, 187:171 Daphnia magna, aquatic pesticide monitoring, 187:12 DBDE (decabromodiphenyl ether), dermal toxicity, 183:74 DBDE (decabromodiphenyl ether), oral toxicity, 183:73, 75 DDE o,p-, water-sediment degradation proﬁle, 187:171 DDT biomagniﬁcation, cat kills, 187:5 DDT in foods, S. America, 185:22 DDT, marine mammals, 184:3 DDT, microcosm degradation proﬁle, 187:217 DDT o,p-, water-sediment degradation proﬁle, 187:114 DDT side effects, mosquito control, 187:5 DDT, use in S. America, 185:4 DDT, water-sediment degradation proﬁle, 187:163 DDT-contaminated soils, bioassays, 186:89 DDT-contaminated soils, risk assessment, 186:88 Decabromodiphenyl ether (DBDE), toxicity, 183:73 Decline curves, pesticide photodegradation, soil, 182:35 Degradation pathways, simazine, 189:8 Delphinapterus leucas (beluga whale), 184:7 Delphinoid blubber PBDEs (table), 184:28 Delphinoid blubber PCBs, hemispheres compared (ﬁg.), 184:33 Delphinoid blubber PHCs, freeranging (table), 184:37 Delphinoid blubber PHCs, in vitro assays, 184:39 Delphinoid liver, perﬂuorinated compounds (table), 184:26 Delphinoid populations, free-ranging, 184:35 Delphinoid studies, dead animal sampling, 184:35

delta-aminolevulinic acid, urine lead indicator, 185:101 Deltamethrin, microcosm degradation proﬁle, 187:217 Deltamethrin, water-sediment degradation proﬁle, 187:172 Demethylation, methylmercury in organisms, 189:108 Dendrobaena octaedra, earthworm biomarkers, 188:99 Dental ﬂuorosis, case photos China, 189:97 Derivitization methods, arsenic (table), 184:126 Dermal absorption, pesticide exposure, 186:122 Dermal dosimetry, pesticides, 186:113 Desmedipham, water-sediment degradation proﬁle, 187:187 Diallate, soil half-life, 188:201 Diarrhea-associated hospitalizations, ethnicity, 186:5 Diarrheal diseases, children numbers, 186:4 Diarrheal diseases, leading cause childhood morbidity, 186:4 Diazinon, earthworm response, 188:93 Diazinon, water-sediment degradation proﬁle, 187:167 Dicamba, water-sediment degradation proﬁle, 187:163 Dicarboximide herbicide photodegradation, in solvents, 182:54 Dicarboximide herbicide photodegradation, on glass, 182:43 Dicarboximide herbicide photodegradation, on soils, 182: 63 Dicarboximides, fate in water-sediment systems, 187:177, 183 Dichlobenil, water-sediment degradation proﬁle, 187:164 Dichlorprop, ionisable herbicide, 188:150 Dieldrin in foods, S. America, 185:22 Dieldrin, marine mammals, 184:4 Dieldrin residues, beef, Uruguay, 181:120

Index Dieldrin residues, butter, Uruguay, 181:125 Dieldrin, use in S. America, 185:2 Dietary supplements, effect human nail element content, 185:159 Diethofencarb, water-sediment degradation proﬁle, 187:187 Diffusion coefﬁcients, pesticides in soils (table), 182:92 Diffusion, pesticide soil adsorption, described, 187:144 Diﬂubenzuron, water-sediment degradation proﬁle, 187:190 Dimethenamid, water-sediment degradation proﬁle, 187:179 Dimethenamid-P, water-sediment degradation proﬁle, 187:179 Dimethoate, earthworm avoidance, 188:98 Dimethylarsenic acid (DMA), in soil, 189:45 Dimethylarsinic acid (DMA), relative toxicity, 184:98, 105, 107 Diniconazole, photoinduced isomerization, 182:45 Dinotefuran, water-sediment degradation proﬁle, 187:202 Dioxin analysis, incinerator exhaust, 190:13 Dioxin collection, incinerator exhaust, 190:12 Dioxin congeners in incinerator exhaust (table), 190:17 Dioxin formation, combustion temperature effect, 190:2 Dioxin formation, impregnated wood incineration, 190:10, 26 Dioxin formation mechanisms, incineration, 190:31 Dioxin formation, newspaper incineration, 190:5, 15, 18 Dioxin formation, plastics incineration, 190:7, 21 Dioxin formation, PVC incineration, 190:8, 22 Dioxin formation, waste incineration, 190:1 ff. Dioxin formation, wood/leaves incineration, 190:9, 24

141

Dioxin recovery efﬁciencies, incinerator exhaust, 190:14 Dioxins (PCDDs), S. America pollutants, 185:5 Dioxins, air levels in S. America, 185:9 Dioxins, deﬁned, 190:1 Dioxins, marine mammals, 184:4 Dioxins, paper production contaminants, 185:75 Dioxins, soil levels in S. America, 185:11 Dioxins, waste incineration, 190:1 ff. Dioxins, water levels in S. America, 185:11 DIRAN-CNP, Colombian antinarcotics program, 190:46 Dirty Dozen persistent pollutants, 188:2 Dislodgeable foliar residue, 186:112 Dislodgeable residue studies, pyrethroids, 186:65 Disodium methanearsonate (DSMA), herbicide, 184:104 Dissolved organic carbon (DOC), composition in freshwater, 187:137 Dissolved organic matter (DOM), sulfonamide sorption, 187:88 Dissolved oxygen (DO), Reconquista River, 185:44 Diterpenoid carboxylic acids (resin acids), paper production, 185:85 Divinyl (butadiene), 189:132 DMA (cacodylic acid), 184:105 DMA (dimethylarsenic acid), in soil, 189:45 DMA (dimethylarsinic acid), relative toxicity, 184:98, 107 DO (dissolved oxygen), Reconquista River, 185:44 DOC (dissolved organic carbon), composition in freshwater, 187:137 Dollar costs of enteric viral infections, children, 186:29 Dolphin blubber PHCs (table), 184:12 Dolphin liver, perﬂuorinated compounts (table), 184:27 Dolphins, epizootics, 184:2 Dolphins, pollutant levels in S. America, 185:19

142

Index

Dolphins, scientiﬁc names (table), 184: 12 DOM (dissolved organic matter), sulfonamide sorption, 187:88 Dose-response models, enteric viral infection, 186:33 Drawida willsi, earthworm biomarkers, 188:91 Drift, pesticides atmospheric, 181:1 ff. Drinking water, arsenic recommended guidelines, 184:114 Drinking water, cyanide contamination, 183:35 Drinking water, element content human nails effect, 185:153 Drinking water, enteric viral infections, children, 186:31 Drinking water intake by age, 186:32 Drinking water, maximum lead permitted, Brazil, 184:79 Earthworm avoidance, contaminated soils, 188:97 Earthworm avoidance, two-chamber test (diag.), 188:97, 101 Earthworm behavior, pollutants (diag.), 188:116 Earthworm biological responses, pollutants (diag.), 188:116 Earthworm biomarker responses, pollutants (table), 188:90 Earthworm biomarkers, ecological risk assessment, 188:85 ff. Earthworm biomarkers, ecological survey, 188:106 Earthworm biomarkers, ﬁeld studies, 188:101, 105 Earthworm biomarkers, lab soil tests, 188:102, 105 Earthworm biomarkers, simulated ﬁeld studies, 188:103, 106 Earthworm biomarkers, standardized toxicity tests, 188:104 Earthworm biomarkers, test exposure conditions, 188:111 Earthworm skin, contaminant uptake indicator, 188:85 Earthworm standard, described, 188:109

Earthworm tests, lysosomal membrane stability, 188:88 Earthworm tests, neutral red retention assay (NRR), 188:88 Earthworms (Eisenia andrei), zinc bioassays, 186:80 Earthworms (Eisenia fetida), heavy metal bioassays, 186:82 Earthworms, anti-ChE pesticide effects, 188:96 Earthworms, avoidance behavior, chemicals (table), 188:98 Earthworms, bioindicators soil pollution, 188:85 ff. Earthworms, biomonitors of remediation , 188:112 Earthworms, ecotoxicological test organisms, 188:87 Earthworms, PFOS uptake/toxicity, 186:142 Earthworms, simazine toxicity, 189:2 Earthworms, soil ecosystem contribution, 188:95 Ecological risk assessment (ERA), earthworm biomarkers, 188:85 ff. Ecological risk assessment, contaminated soil, 186:73 ff. Ecological risk assessment, deﬁned, 186:74 Ecologically Acceptable Concentration, pesticide, 187:3 Economic impact, enteric viral infections, 186:28 Ecosystem long-term effects, pesticide exposure, 187:28 Ecotoxicological impacts of soil pollutants, microﬂora monitors, 188:127 ff. Ecotoxicology, PFOS, 186:143 ff. Efﬂuent water, maximum lead permitted, Brazil, 184:79 Eisenia andrei (earthworms), zinc bioassays, 186:80 Eisenia andrei, earthworm biomarkers, 188:86 Eisenia fetida (earthworms), heavy metal bioassays, 186:82 Eisenia fetida, earthworm biomarkers, 188:86

Index Emission proﬁles, photosensitizers (table), 182:86 Emission regulation, air lead, Brazil, 184:67 Enargite, arsenic-bearing mineral, 184:99 Enchytraeus crypticus (pot worm), zinc bioassays, 186:80 Endocrine disruption, paper production contaminants, 185:81 Endocrine disruption, PHCs, marine mammals, 184:9 Endocrine disruptors, described, 185:81 Endocrine effects, PBDEs, 183:82 Endocrine-active chemicals, gonadal effects, 187:109 Endocrine-active compounds effects, gonads ﬁsh/frogs, 187:111 Endocrine-disrupting chemicals, deﬁned, 187:109 Endosulfan, α-enriched insect toxicity, 183:107 Endosulfan, α-isomer residue problems, 183:111 Endosulfan, β-enriched desirability, 183:110 Endosulfan, β-enriched insect toxicity, 183:107, 108 Endosulfan, chemical/physical properties, 183:102 Endosulfan, commercial synthesis, 183:109 Endosulfan diol, structure, 183:100 Endosulfan:endosulfate residues, ratios, 183:109 Endosulfan, environmental fate, 183:104 Endosulfan environmentally derived products, structures, 183:100 Endosulfan, GABA-gated chloride channel binding, 183:101 Endosulfan in foods, S. America, 185:22 Endosulfan, insecticidal properties, ﬁeld, 183:106 Endosulfan isomers, different vapor pressures, 183:102 Endosulfan isomers, half-lives, 183:104 Endosulfan isomers, residues, 183:99 ff.

143

Endosulfan isomers, structures, 183: 100 Endosulfan isomers, toxicity, 183:99 ff. Endosulfan, mode of action, 183:101 Endosulfan synthesis, α-/β-isomer ratios, 183:109 Endosulfan technical, insect toxicity, 183:107 Endosulfan, toxicity, 183:101 Endosulfan, toxicity aquatic invertebrates, 183:102 Endosulfan, toxicity ﬁsh, 183:102 Endosulfan, water-sediment degradation proﬁle, 187:163 Endosulfan-α, structure, 183:100 Endosulfan-β, structure, 183:100 Endosulfate:endosulfan residues, ratios, 183:109 Endosulfate, endosulfan residue animal fat, 183:110 Endosulfate isomers, structures, 183:100 Endrin in foods, S. America, 185:22 Endrin, marine mammals, 184:4 Endrin, use in S. America, 185:2 Energy inputs, corn production, 189: 26 Energy inputs, fermentation/ distillation, 189:28 Enteric adenoviruses 40 & 41, described, 186:9 Enteric viral diseases, children, waterborne, 186:35 Enteric viral infection, children, social factors, 186:32 Enteric viral infection, dose-response models, 186:33 Enteric viral infections, children, 186: 1 ff. Enteric viral infections, economic impact, 186:28 Enteric viral infectious dose, children, 186:33 Enteric virus infections, incidence by age, 186:25 Enterovirus illness, described 18 Enterovirus illnesses in children, table, 186:25 Enterovirus, incidence by age, 186:27

144

Index

Enterovirus infestations, symptoms in children, 186:19 Enterovirus related rheumatoid arthritis, 186:25 Enteroviruses, described, 186:16 Enteroviruses, incubation periods, 186:16 Enteroviruses, perinatal/neonatal infections, 186:19 Enteroviruses, waterborne enteric disease, children, 186:38 Environmental concentrations, sulfonamides (table), 187:91 Environmental lead contamination, Brazil, 184:59 ff. Environmental lead, Mexico, lack of data, 181:38 Environmental lead, Mexico problems, 181:37 ff. Environmental lead samples, homes, 185:109 EPA controls, paper production efﬂuent guidelines, 185:83 Epidemiology, PBDEs, 183:83 Epoxiconazole, microcosm degradation proﬁle, 187:220 ERA (Ecological risk assessment), earthworm biomarkers, 188:85 ff. Erythrene (butadiene), 189:132 Erythroxylum coca (coca), cocaine source, 190:44 Esfenvalerate, water-sediment degradation proﬁle, 187:173 Estradiol 17β-, effects, gonads ﬁsh/ frogs, 187:111 Eteroviruses (human), serotypes (table), 186:17 Ethanol, annual production, 189:30 Ethanol as gasoline additive, 189:25 ff. Ethanol production, by-products, 189:30 Ethanol production, cornland use, 189:30 Ethanol production, cropland use, 189:31 Ethanol production, economic costs, 189:29 Ethanol production, energy costs, 189:25 ff.

Ethanol production, energy return, 189:33 Ethanol production, environmental impacts, 189:32 Ethanol production, federal subsidies, 189:29 Ethanol production, food security, 189:34 Ethanol production, food vs fuel issue, 189:35 Ethanol production, for vehicle fuel, 189:25 ff. Ethanol production, net energy yield, 189:29 Ethanol production, sugarcane, 189:31 Ethinyl estradiol 17α-, effects, gonads ﬁsh/frogs, 187:112 Ethofumesate, water-sediment degradation proﬁle, 187:204 Ethoxysulfuron, water-sediment degradation proﬁle, 187:193 Etofenprox photodegradation (diagram), 182:41 European Union pesticide risk assessment, 187:1 ff. Evaluation of nervous system effects, lead exposure, 185:123, 126 EXAMS, pesticide physicochemical/ degradative proﬁles model, 187:161 Exanthems (skin eruptions), entovirus related, 186:21 Exhaust gas temperatures, incineration, 190:4 Exposure databases (pesticide), applied risk analysis, 186:107 ff. Exposure, enteric viral infections, children, 186:31 ff. Exposure estimates, PBDEs, 183:86 Exposure Factors Handbook (EPA), pesticide, 186:124 Exposure monitoring databases, 186:107 ff. Exposure monitoring in risk analysis, 186:107 ff. Extractable organic halides (EOX), paper production, 185:74 Extreme case, pesticide exposure, 186:120

Index Famoxadone, water-sediment degradation proﬁle, 187: 184 Febril illness, nonspeciﬁc, entovirus related, 186:21 Fecal pollution, Reconquista River, 185:51, 53 Fecal-oral agent exposure, children, 186:4 Federal subsidies, ethanol production, 189:29 Fenamidone, water-sediment degradation proﬁle, 187:203 Fenbuconazole, water-sediment degradation proﬁle, 187:196 Fenhexamid, water-sediment degradation proﬁle, 187:180 Fenitrooxon, water-sediment degradation proﬁle, 187:167 Fenitrothion, microcosm degradation proﬁle, 187:216 Fenitrothion, water-sediment degradation proﬁle, 187:166 Fenpropathrin, water-sediment degradation proﬁle, 187:172 Fenthion, microcosm degradation proﬁle, 187:216 Fenthion, water-sediment degradation proﬁle, 187:166 Fentrazamide, water-sediment degradation proﬁle, 187:178 Fenvalerate, water-sediment degradation proﬁle, 187:173 Fermentation/distillation, energy inputs, 189:28 Ferric hydroxide, role in soil arsenic level, 184:107 Field metabolic rate (FMR), deﬁned, 183:125 Fingernails, biomarker of trace element exposure, 185:141 ff. Fingernails vs toenails, trace element content, 185:163 Fipronil, microcosm degradation proﬁle, 187:219 Fipronil, photodegradation pathways, 182:48 Fipronil, water-sediment degradation proﬁle, 187:204

145

Fish bioassays, paper mill efﬂuent, 185:69 Fish consumption, nail/element content effect, 185:150 Fish consumption rate, versus hair mercury content, 189:107 ff. Fish, endosulfan toxicity, 183:102 Fish, females masculinized, paper production efﬂuent, 185:75 Fish gonadal anomalies, chemical exposure, 187:103 ff. Fish kills, cyanide, 183:28 Fish, mercury contamination, Chile, 183:10 Fish, methylmercury biomagniﬁcation, 189:108 Fish, morphological effects, paper production efﬂuent, 185:75 Fish, pesticide effects, 187:8 Fish, PFOS toxicity (table), 186:150, 163 Fish, pollutant levels in S. America, 185:19 Flame retardants, PBDEs, 183:56 Flofencet, adsorption coefﬁcient, 188:184 Florasulam, water-sediment degradation proﬁle, 187:181 Fluazifop, adsorption coefﬁcient, 188:184 Fluazinam, water-sediment degradation proﬁle, 187:200 Fludioxinil, water-sediment degradation proﬁle, 187:203 Flufenacet, aerobic aquatic metabolism (diag.), 187:182 Flufenacet, water-sediment degradation proﬁle, 187:180 Flumetsulam, adsorption coefﬁcient, 188:185, 189, 193 Flumetsulam, ionisable herbicide, 188:156 Flumioxazin, water-sediment degradation proﬁle, 187:184 Fluorescence wavelengths of pesticides (table), 182:80 Fluorine, Chinese coal hazard, 189:96 Fluorine, dental ﬂuorosis in China, 189:97

146

Index

Fluorine, epidemic in China, 189:96 Fluorine health effects, indoor Chinese coal burning, 189:89 ff. Fluorine, in human nails, 185:162 Fluoxastrobin, degradation pathways (illus), 187:177 Fluoxastrobin, water-sediment degradation proﬁle, 187:176 Flupyrsulfuron-methyl, aerobic aquatic metabolism (diag.) 195 Flupyrsulfuron-methyl, water-sediment degradation proﬁle, 187:192 Flupysulfuron-methyl, ionisable herbicide, 188:154 Fluridone, adsorption coefﬁcient, 188: 187, 190 Fluridone, ionisable herbicide, 188:158 Fluridone, microcosm degradation proﬁle, 187:220 Fluridone, water-sediment degradation proﬁle, 187:205 Fluroxypyr, water-sediment degradation proﬁle, 187:171 Flurtamone, water-sediment degradation proﬁle, 187:202 FMR (ﬁeld metabolic rate), deﬁned, 183:125 Folsomia candida (springtails), zinc bioassay, 186:79 Food , maximum permitted lead levels, Brazil, 184:77 Food, arsenic recommended guidelines, 184:114 Food, element content human nails effect, 185:153 Foods, pollutant levels in S. America, 185:20, 22 Foramsulfuron, water-sediment degradation proﬁle, 187:192 Free cyanide, analytical methods, 183: 39 Freundlich isotherm model, metal remediation, water, 188:74 Frog limb malformations, pesticide effect, 187:7 Fruit ﬂy bioassays, DDT-contaminated soils, 186:89 Fruit/leaf waxes, composition (table), 182:89

Fungicide chemical structures, miscellaneous, 182:152 Fungicide imports, amounts, Uruguay, 181:118 Furans (PCDFs), S. America pollutants, 185:5 Furans, air levels in S. America, 185:9 Furans, marine mammals, 184:4 Furans, paper production contaminants, 185:75 Furans, soil levels in S. America, 185: 11 Furans, water levels in S. America, 185:11 GABA-gated chloride channel binding, endosulfan, 183:101 Gamasite bioassays, DDTcontaminated soils, 186:89 Gambusia holbrooki, masculinized females, paper production contaminants, 185:75 Gas chromatography, arsenic speciation, 184:124 Gas chromatography electron ionization mass spectrometry (GC/ EI-MS), 188:6 Gas chromatography electron-capture negative ion mass spectrometry (GC/ECNI-MS), 188:4 Gasahol use, Brazil, 184:71 Gasohol production, global, 189:25 ff. Gasoline ethanol content, Brazil, 184: 71 Gasoline lead, air contamination, Brazil, 184:67 Gasoline lead content, Brazil, 184:71 Gasoline, lead use, Mexico, 181:42 Gasoline, leaded, atmospheric pollution, 185:99 Gastrointestinal infection risk, children, 186:2 GC/ECNI-MS (gas chromatog. electron-capture neg. ion mass spect), 188:4 GC/ECNI-MS, organobromine detection, 188:4 GC/EI-MS (gas chromatog. electron ionization mass spect), 188:6

Index GC/EI-MS, organobromine detection, 188:5 Generic exposure databases (pesticide), development, 186:113 Generic pesticide exposure data bases, 186:107 ff. Genotoxicity, butadiene, 189:145 Genotoxicity, chloroprene, 189:155 Genotoxicity, isoprene, 189:162 Geogenic (natural) arsenic sources, 184:99 Geophagous animals (table), 183:118 Geophagous terrestrial birds (table), 183:121 Geophagous terrestrial mammals (table), 183:118 Geophagous terrestrial reptiles (table), 183:120 Geophagy, absorption of contaminants, 183:126 Geophagy, calcium dietary need, 183:117 Geophagy, contaminants terrestrial vertebrates, 183:115 ff. Geophagy, deﬁned, 183:115 Geophagy, estimating daily soil ingestion, 183:124 Geophagy, incidental/accidental, 183:123 Geophagy, intentional, 183:116 Geophagy, pharmacology, 183:122 Geophagy, reasons for, 183:115 Geophagy, sodium dietary need, 183:116 Geophagy, soil ingestion by animals, 183:115 ff. Germanium, in human nails, 185:161 Glass, pesticide photodegradation studies, 182:36 Global distillation, PHCs, 184:3 Global transport, PHCs, 184:3 Globicephala macrorhyncus (shortﬁnned pilot whale), 184:7 Globicephala melas (long-ﬁnned pilot whale), 184:7 GLP (Good Laboratory Practices), 186:109 Glyphosate, acute toxicity laboratory animals, 190:100

147

Glyphosate, acute toxicity selected mammals, 190:72 Glyphosate, adsorption coefﬁcient, 188:188, 192 Glyphosate, aerial application air levels, 190:65 Glyphosate, aerial application, environmental effects, 190:43 ff. Glyphosate, aerial application, health effects, 190:43 ff. Glyphosate, aerial application methods, 190:53 Glyphosate, aerial application risk hypotheses, 190:59 Glyphosate, aerial applicator exposure, 190:60 Glyphosate, aerial off-target deposition, 190:57 Glyphosate, application method to coca & poppy, 190:53 Glyphosate, application rates for coca & poppy, 190:56 Glyphosate, bystander exposure aerial application, 190:62 Glyphosate, cancer studies, 190:77 Glyphosate, coca & poppy control programs, 190:52 Glyphosate, coca eradication, 190: 43 ff. Glyphosate, conceptual model, illicit crop control, 190:59 Glyphosate/Cosmo-Flux®, toxicity ﬁsh, 190:93 Glyphosate, effects aquatic animals, 190:86 Glyphosate, effects beneﬁcial insects, 190:85 Glyphosate, effects nontarget animals, 190:81 Glyphosate, effects on mammals, 190:72 Glyphosate, effects soil invertebrates, 190:81 Glyphosate, effects soil microorganisms, 190:82 Glyphosate, effects terrestrial invertebrates, 190:83 Glyphosate, effects terrestrial plants, 190:90

148

Index

Glyphosate, effects terrestrial vertebrates, 190:84 Glyphosate, environmental exposure, 190:105 Glyphosate, environmental fate, tropics, 190:49 Glyphosate, epidemiology studies, 190:77 Glyphosate, exposure pathways, soil, air, water, 190:57 Glyphosate, formulants and adjuvants, 190:51 Glyphosate, global/Colombian registration & use, 190:49 Glyphosate, human exposure, 190: 105 Glyphosate, human exposure, 190:60, 63, 65 Glyphosate, human exposure coca/ poppy control, 190:99 Glyphosate, human exposure protective measures, 190:61 Glyphosate, human health assessment, 190:43 ff. Glyphosate, human health effects, 190:79, 106 Glyphosate, human poisoning, 190:75 Glyphosate, illicit crop eradication, Colombia, 190:43 ff. Glyphosate, in soil after application, 190:70 Glyphosate, in surface water after application, 190:66, 69 Glyphosate, inhalation exposure, 190:64 Glyphosate, ionisable herbicide, 188:160 Glyphosate, mechanism of action, 190:48 Glyphosate, microcosm degradation proﬁle, 187:217 Glyphosate, neurological effects, 190:78 Glyphosate, physico/chemical properties, 190:48 Glyphosate, plant recovery from effects, 190:95 Glyphosate, poppy eradication, 190: 43 ff.

Glyphosate, reentry exposure, treated ﬁelds, 190:63 Glyphosate, reproductive effects, 190:78 Glyphosate, risk assessment, 190:98 Glyphosate, spray-droplet characteristics, 190:54 Glyphosate, surfactants in formulations, 190:51 Glyphosate, time to pregnancy studies, Colombia, 190:79 Glyphosate, use in Colombian eradication spraying, 190:49 Glyphosate, use in forest clearance, 190:94 GnRH (gonadotropic-releasing hormone), PME ﬁsh effects, 185:69 Gold contamination, by mercury, Chile, 183:14 Gold heap leaching, using cyanide, 183:21 Gold mining, current procedures, 181:141 Gold mining, cyanide extraction procedure, 183:22 Gold mining, cyanide hazards, 183: 21 ff. Gold mining, cyanide leaching process, 181:142 Gold mining history, mercury role, 181:140 Gold mining mercury, Alaskan beach sediments, 181:166 Gold mining mercury, human hazard, 181:139 ff. Gold mining methods, Brazil, 181:145 Gold mining sites, U.S., 183:23 Gold mining, using mercury, 183:2, 13 Gold vat leaching, using cyanide, 183:23 Gold yields, heap vs vat leaching, 183:23 Gonadal abnormalities (ﬁsh/frogs), suggested terminology, 187:117 Gonadal abnormalities, amphibians, before 1945 (table), 187:119 Gonadal abnormalities, terminology, 187:103 ff.

Index Gonadal anomalies based on gross morphology, 187:106 Gonadal anomalies based on histology, 187:107 Gonadal anomalies, frogs, photos, 187:108 Gonadal anomalies in ﬁsh, terminology, 187:103 ff. Gonadal anomaly terminology, 187: 103 ff. Gonadal deformities, terminology (table), 187:106 Gonadal dysgenesis, abnormalities, deﬁned, 187:124 Gonadosomatic index (GSI), PME ﬁsh effects, 185:69 Gonadotrophs (GtH), PME ﬁsh effects, 185:69 Gonadotropic-releasing hormone (GnRH), PME ﬁsh effects, 185:69 Good Agricultural Practice, pesticide application, 187:4 Good Laboratory Practices (GLP), 186:109, 114 Grasshopper effect, PHCs, 184:3 Grey seals, epizootics, 184:2 Groundwater, arsenic content, global, 184:102 Groundwater contamination, simazine, 189:5, 12 Groundwater drawdown, sink hole formation, 183:41 Group A rotavirus, endemic worldwide, 186:6 Group B rotavirus, adult diarrhea source, 186:6 GSI (gonadosomatic index), PME ﬁsh effects, 185:69 GtH (gonadotrophs), PME ﬁsh effects, 185:69 Hafnium, in human nails, 185:161 Hair, bioindicator of mercury exposure, 189:107 ff. Hair, biomarker of mercury exposure, 189:109 Hair, growth rate, 189:109 Hair lead, blood lead correlation, 185:123, 125

149

Hair mercury content, versus ﬁsh consumption rate, 189:107 ff. Hair mercury, correlated with blood mercury, 189:108 Hair-mercury, different populations, 189:114 Halichoerus grypus, epizootics, 184:2 Halogen isotope abundances (table), 188:7 Halogenated dimethyl bipyrolles, global detection, 184:3 Halogenated dimethyl bipyrroles (HDBPs), 188:9 Halogenated monoterpenes, analytical aspects, 188:41 Halogenated monoterpenes, environmental distribution, 188: 41 Halogenated monoterpenes, mixed (MHC-1), 188:40 Halogenated natural products (HNPs), 188:2 Halogenated pollutants, 188:2 Halogenated products, natural marine, 188:1 ff. Haloxifop, adsorption coefﬁcient, 188:184 Harbour porpoises, 184:10 Harbour seals, epizootics, 184:2 Harp seals, 184:9 Hazard, assessment, PFOS, 186:157 Hazard characterization, PBDEs, 183:85 HCB (hexachlorobenzene), marine mammals, 184:3 HCB (hexachlorobenzene), use in S. America, 185:4 HCB in foods, S. America, 185:22 HCH (hexachlorocyclohexane), 184:4 HCH in foods, S. America, 185:22 HCH isomers, Arctic seawater concentrations, 184:4 HCHs (hexachlorocyclohexanes), water levels in S. America, 185:13 HDBPs (halogenated dimethyl bipyrroles), 188:9 HDBPs, analytical aspects, 188:13 HDBPs, body burdens, cetaceans/ marine birds, 188:15

150

Index

HDBPs, chemical structures (ﬁgure), 188:10 HDBPs, concentrations marine environment (table), 188:16 HDBPs, environmental distribution, 188:15 Head hair lead, blood lead correlation, 185:123, 125 Health risk assessment, PBDEs, 183:85 Health risks in children, enteric viral infections, 186:1 ff. Heap leaching (gold), using cyanide, 183:21 Heap leaching, affected resources, 183:41 Heavy metal exposure, human nail biomarkers, 185:141 ff. Heavy metals, aquatic environment hazard, 188:60 Heavy metals content, Reconquista River, 185:45 Heavy metals, remediation, water, 188:59 ff. Heavy metals, removal from water, plants, 188:59 ff. Heavy metals, water quality criteria (table), 188:64 Hepatic dysfunction, paper production contaminants, 185:78 Hepatitis A incidence, by age, table, 186:13 Hepatitis A, incubation period, 186:13 Hepatitis A sources, table, 186:13 Hepatitis A virus, described, 186:12 Hepatitis A virus, incidence by age, 186:26 Hepatitis A virus, waterborne enteric disease, children, 186:37 Hepatitis A, water-transmitted, 186:14 Hepatitis E, incubation period, 186:15 Hepatitis E, leading illness agent, developing countries, 186:15 Hepatitis E virus, described, 186:15 Hepatitis E virus, incidence by age, 186:27 Hepatitis E virus, waterborne enteric disease, children, 186:37 Hepatitis E, young & middle-aged adults, 186:15

Hepatitis viruses, 186:12 ff. Heptachlor, marine mammals, 184:4 Heptachlor, use in S. America, 185:4 Heptachloromethyl bipyrrole (Q1), 188:17 Heptachlors in foods, S. America, 185:22 Herbicide abiotic degradation, simazine, 189:14 Herbicide biodegradation, simazine, 189:15 Herbicide chemical structures, miscellaneous, 182:152 Herbicide imports, amounts, Uruguay, 181:117 Herbicide management practices, simazine, 189:10 Herbicide soil half-lives, simazine, 189:3 Herbicides, groundwater contamination, 189:5 Herbicides, metabolized to sulfonamides, 187:68 Hermaphroditism, deﬁned, 187:106, 115 Heroin, from Papaver somniferum (poppy), 190:44 Heroine usage, global numbers, 190: 44 Herpangina, entovirus related, 186:20 Herpetofauna, wetland, pesticide effects, 187:24 Hexachlorobenzene (HCB), use in S. America, 185:4 Hexachlorocyclohexane (HCH), 184:4 Hexachlorocyclohexanes (HCHs), water levels S. America, 185:13 High-resolution mass spectrometry (HRMS), 188:8 HNPs (halogenated natural products), 188:2 HNPs, annual cycle, 188:45 HNPs, biosynthesis, 188:44 HNPs, mass spectrometric investigations, 188:4 HNPs, novel discoveries, 188:2 HNPs of environmental concern, 188:9 HNPs, physicochemical parameters, 188:14

Index HNPs, resembling chlorinated POPs, 188:43 HNPs, unknown, 188:44 Hormone disruption, paper production efﬂuents, 185:81 Hospital admissions, children enteric viruses, 186:7 Household paints, lead content, 185:98 HRMS (high-resolution mass spectrometry), 188:8 Human adipose, PBDE monitoring, 183:59, 61 Human blood, PBDE monitoring, 183:60, 63 Human brain damage, methylmercury, 189:108 Human enteroviruses, serotypes, table, 186:17 Human epidemiology, butadiene, 189:148 Human epidemiology, chloroprene, 189:156 Human epidemiology, isoprene, 189:164 Human exposure databases (pesticide), risk analysis, 186:107 ff. Human exposure pathway, arsenic, 184:115, 117 Human fat, pesticide residues, Uruguay, 181:130, 131 Human foods, pollutant levels S. America, 185:20, 22 Human lead exposure, Brazil, 184:59 ff. Human lead exposure, Brazil, 184:77 Human lead exposure, Chile, 185:93 ff. Human mercury contamination, Chile, 183:11 Human milk, PBDE monitoring, 183:64 Human nail biomarkers of element exposure, 185:141 ff. Human nails, age effect on element content, 185:147 Human nails, analytical instruments used in element studies, 185:148 Human nails, contamination effect on element content, 185:152 Human nails, desiccation after washing, 185:146

151

Human nails, dietary supplement effects element content, 185: 159 Human nails, digestion for analysis, 185:146 Human nails, drinking water effect on element content, 185:153 Human nails, element correlation other samples, 185:160 Human nails, element interaction element content, 185:158 Human nails, element levels health risk, 185:155 Human nails, element levels vs exposure period, 185:155 Human nails, element levels vs health status, 185:155 Human nails, element speciation uptake effect, 185:159 Human nails, elemental analysis quality control, 185:147 Human nails, elemental analytical methods, 185:146 Human nails, environmental exposure, 185:152 Human nails, essential element accumulation, 185:165 Human nails, exposure and sampling times, 185:144 Human nails, ﬁngernails vs toenails element content, 185:163 Human nails, food effect element content, 185:153 Human nails, genetic variation effect element content, 185:151 Human nails, multielement effects, 185:157 Human nails, nail character effect element content, 185:151 Human nails, normal vs brittle nail effect element content, 185:151 Human nails, nutritional element determination, 185:155 Human nails, occupational effect element content, 185:154 Human nails, regional effect element content, 185:151 Human nails, sampling procedures, 185:144

152

Index

Human nails, sex effect element content, 185:147 Human nails, time/season effect element content, 185:151 Human nails, toxic element accumulation, 185:165 Human nails, toxic element determination, 185:157 Human nails, trace element analysis, 185:143 Human nails, trace elements studied, 185:147 Human nails, urban/rural gradients element content, 185:154 Human nails vs blood, trace element content, 185:164 Human nails vs hair, trace element content, 185:163 Human nails vs multiple tissues, element content, 185:164 Human nails vs urine, trace element content, 185:164 Human nails, washing/cleaning methods, 185:145 Human pesticide exposure risk analysis, 186:107 ff. Human poisoning, glyphosate, 190:75 Human tissue insecticide residues, S. America, 185:21, 25 Humans, chlorinated insecticide residues, S. America, 185:21, 25 Humans, PCB residues, S. America, 185:25 Humic substances effects, pesticide photolysis, soil, 182:18, 23 Humic substances, photophysical/ photochemical processes (diagram), 182:24 Hunted delphinoid PHC studies, 184:35 Hydride generation, arsenic speciation, 184:123 Hydrogen peroxide, cyanide tailings mitigation, 183:38 Hydrolysis, pesticides/water-sediment, 187:147, 153 Hydrolysis, PFOS, 186:136 Hydrolysis products, sulfonamides, 187:83

Hydrophobic sorption, ionisable compounds, 188:167, 176 Hydroponics, arsenic effects plants, 189:55 Hydroxides, photophysical/ photochemical processes, 182:28 Hydroxyl radical, reactions with pesticides (table), 182:88 Hydroxyl radicals, importance in photooxidation, 181:15 Hyla versicolor tadpole mortality, carbaryl/predator, 187:7 Illicit crop eradication, Colombia, 190:43 ff. Imazapyr, adsorption coefﬁcient, 188:187, 191 Imazapyr, ionisable herbicide, 188:158 Imazaquin, adsorption coefﬁcient, 188:187, 191 Imazaquin, ionisable herbicide, 188:158 Imazethapyr, adsorption coefﬁcient, 188:188, 191 Imazethapyr, ionisable herbicide, 188:160 Imazomox, water-sediment degradation proﬁle, 187:203 Imidacloprid, earthworm avoidance, 188:100 Imidacloprid, water-sediment degradation proﬁle, 187:201 Imidazolinone herbicides, ionisable, 188:150 Imidazolinones, adsorption coefﬁcient, 188:191 Imide herbicide photodegradation, on plants, 182:75 Immunochemical assays, marine mammals, 184:7 Immunocompromised children diseases, enterovirus related, 186:24 Immunoglobulin A, combating viral interic infection, 186:2 Immunotoxicity, PBDEs, 183:80 Impregnated wood incineration, dioxin formation, 190:10, 26 In vitro assays, PHCs, delphinoids, 184:39

Index Incineration, dioxin formation, 190:1 ff. Incineration, dioxin formation mechanisms, 190:31 Incineration dioxin gas toxicity, 190:29 Incinerator conditions, dioxin formation, 190:5 ff. Incinerator diagram, experimental, 190:3 Incinerator exhaust, dioxin analysis, 190:13 Incinerator exhaust, dioxin collection, 190:12 Incinerator exhaust gas toxicity, 190:29 Incinerator gas toxicity, 190:29 Incinerator temperature measurements, 190:4 Indicators, soil health/quality (table), 188:131 Indoor coal burning, health effects China, 189:89 ff. Industrial lead sites vs. blood levels, Brazil, 184:86 Industrial waste incineration, dioxin formation, 190:1 ff. Infants, dehydration risk, 186:3 Inhalation exposure, pesticides, 186:113 Insecticide chemical structures, miscellaneous, 182:152 Insecticide illnesses (pyrethroid), California, 186:57 ff. Insecticide imports, amounts, Uruguay, 181:118 Insecticide levels, Reconquista River, 185:47 Instrumental analysis used in nail/ element studies, 185:148 Inter-American Drug Abuse Control Commission (CICAD), 190:113 Interferon-α, deﬁcient in infant lungs, 186:2 Interic virus infections, incidence U.S., 186:28 Intersex, gonadal abnormalities, deﬁned, 187:123 Intersex gonads, deﬁned, 187:107, 109 Intussusception, adenovirus associated, 186:9 Inversion layer, atmospheric lead pollution, 185:100

153

Invertebrates, PFOS effects, 186:146 Iodine, in human nails, 185:162 Iodosulfuron, water-sediment degradation proﬁle, 187:191 Ion-exchange, biomass, heavy metals, 188:67, 70 Ionic strength, ionisable compounds adsorption, 188:164 Ionisable compounds degradation, soil pH, 188:198 Ionisable herbicides, chemical properties, 188:155, 157, 159 Ionisable herbicides, chemical structures, 188:154 Ionisable herbicides, listed, 188:150 Ionisable herbicides, phenols, 188:183 Ionisable herbicides, sulfonylureas, 188:183 Ionisable herbicides, surface water contaminants, 188:150 Ionisable pesticides, adsorption coefﬁcients (table), 188:184 Ionisable pesticides, chemical characteristics, 188:150 Ionisable pesticides, soil adsorption, 188:149 ff. Ionisable pesticides, use patterns, 188:150 Ionisation, pesticides, described, 188:151 Ioxynil, water-sediment degradation proﬁle, 187:164 Iprodione, photoinduced rearrangement, 182:66 Iprodione, water-sediment degradation proﬁle, 187:185 Iprovalicarb, water-sediment degradation proﬁle, 187:188 IQ levels, lead-exposed children, Mexico, 181:93 Iron hydroxides, role in soil arsenic, 189:45 Iron, in human nails, 185:162 Iron oxides inﬂuence on sorption, ionisable pesticides, 188:197 Iron plaque, role in plant arsenic tolerance, 189:49 Iron plaque, roots wetland plants, 189:49

154

Index

Irradiance spectra, photolysis light sources (diagram), 182:31 Isoenzymes (CYP), induction, marine mammals, 184:7 Isoprene, exposure biomarkers, 189:162 Isoprene, genotoxicity, 189:162 Isoprene, human epidemiology, 189:164 Isoprene, industrial uses, 189:158 Isoprene, kinetics, 189:160 Isoprene, metabolic scheme (chart), 189:160 Isoprene, metabolism, 189:160 Isoprene, physical properties, 189: 133 Isoprene, physicochemical properties, 189:158 Isoprene, toxicity, 189:159 Isoprene toxicology, 189:131 ff. Isoprene, world production, 189:158 Isoproturon, water-sediment degradation proﬁle, 187:190 Isoxaben, photoinduced rearrangement (diagram), 182:44 Isoxaﬂutole, water-sediment degradation proﬁle, 187:202 Jazzercise study, children’s pesticide exposure, 186:117 Killer whale blubber PHCs (table), 184:18 Killer whales, 184:11 Kinetic analysis, pesticide photodegradation, 182:31, 34 Kinetic analysis, pesticide watersediment designs, 187:159 Koc (soil adsorption coefﬁcients), pesticides (chart), 187:142 Kraft pulping, paper production, 185: 71 Kresoxim-methyl, water-sediment degradation proﬁle, 187:175 Laboratory equipment, pesticide photolysis, 181:21 Laboratory pesticide water-sediment systems, 187:162, 165

Lahontan Reservoir (Nevada), mercury contamination, 181:142, 160 lambda-cyhalothrin, illnesses described, 186:66 lambda-cyhalothrin, microcosm degradation proﬁle, 187:218 lambda-cyhalothrin, water-sediment degradation proﬁle, 187:173 Langmuir isotherm model, metal remediation, water, 188:74 LD50s, arsenic lab animals, 184:112 Lead acetate, earthworm response, 188:93 Lead aerosols, Mexico City, 181:44, Lead aerosols, San Luis Potosi, Mexico, 181:46 Lead air contamination, Brazil, 184:66 Lead, air contamination Mexico, 181: 43 Lead, analytical methods Mexican foods, 181:75 Lead, aquatic organisms, Mexico, 181:57 Lead bioaccumulation, aquatic animals, Brazil, 184:62 Lead bioaccumulation, plants, Brazil, 184:62 Lead, bivalves coasts of Mexican Paciﬁc, 181:58 Lead, blood levels adults, Mexico, 181: 79 Lead, blood levels children, Mexico, 181:81, 84, 92, 93, 95, 98 Lead, blood levels children, Mexico City, 181:73, 81, 82 Lead, blood levels lead-glazing potters, 181:69 Lead, blood levels, Mexico City, 181:71 Lead, blood levels, rural Mexican women, 181:67 Lead, body burdens, Brazil, 184:81, 84 Lead, ceramics, Mexico, 181:67 Lead, children’s body burdens, Brazil, 184:82, 84 Lead, coastal areas, Gulf of California, 181:56 Lead, coastal areas Mazatlán, Sinaloa, Mexico, 181:55

Index Lead, coastal areas Mexican Paciﬁc, 181:56 Lead, coastal lagoons Gulf of Mexico, 181:55, Lead, Coatzacoalcos River Mexico, 181:53 Lead, coloring pencil levels, source comparison, 181:65 Lead contamination, aquatic organisms, Brazil, 184:65 Lead contamination, ﬁsh, Brazil, 184:64 Lead contamination, food containers, Brazil, 184:81 Lead contamination, homes, 185:109 Lead contamination, maximum permitted in food, Brazil, 184:77 Lead contamination, school articles, Brazil, 184:81 Lead contamination, sediments, Brazil, 184:74, 76 Lead contamination, soil, Brazil, 184:70 Lead contamination sources, Brazil, 184:66 Lead contamination, surface waters, Brazil, 184:74 Lead contamination, underground water, Brazil, 184:70 Lead, dog tissues, Mexico City, 181:60 Lead, drinking water, Mexico, 181:65 Lead, dust & soil, Mexico, 181:46 Lead, dust samples, Ciudad Juárez, Mexico, 181:47 Lead, earthworm biomarkers, 188:87 Lead, earthworm response, 188:90 Lead encephalopathy, lead exposure, 185:94 Lead, environmental problems Mexico, 181:37 ff. Lead exports, Brazil, 184:62 Lead exposure, acute effects, 185:94 Lead exposure, children’s toys, 185:127 Lead exposure, chronic effects, 185:94 Lead exposure clusters, 185:108 Lead exposure, effects during pregnancy, 185:95 Lead exposure, evaluating nervous system effects, 185:123 Lead exposure, food contamination, 185:127

155

Lead exposure, general population, Mexico, 181:70 Lead exposure, human, Brazil, 184:59, 77 Lead exposure, humans Chile, 185:93 ff. Lead exposure, lead in soil, 185:129 Lead exposure, lead ore storage, 185:120 Lead exposure, neurological effects, age differences, 185:115 Lead exposure, prevention recommendations, 185:130 Lead exposure, primary lead sources, 185:96 Lead exposure, toxic wastes, 185:120 Lead, ﬁsh canned & fresh, Mexico, 181:76 Lead, food contamination, examples, 185:96 Lead, foods in Mexico, 181:74 Lead, general population exposure, Mexico, 181:70 Lead, horse tissues, Mexico City, 181:60 Lead house dust contamination, Brazil, 184:66 Lead, house dusts, Mexico City, 181: 64 Lead, household paints content, 185:97 Lead, human bones, Mexico, 181:87 Lead, human hair, Mexico, 181:86 Lead, human levels, Mexico, 181:77 Lead, human lungs, Mexico, 181:89 Lead, human milk, Mexico, 181:85, 88 Lead in hair, correlation with blood lead, 185:123,125 Lead, in human nails, 185:161 Lead in urine, tetraethyl lead exposure indicator, 184:90 Lead, in wheat ﬂour, 185:108, 110 Lead, industrial uses, Mexico, 181:41 Lead, IQ levels of exposed children, Mexico, 181:93 Lead, Lerma River, Mexico, 181:53 Lead, marine environment, Mexico, 181:54 Lead, marine organisms, Mexican Paciﬁc, 181:58

156

Index

Lead, maximum permitted levels drinking water, Brazil, 184:79, 80 Lead, maximum permitted levels foods, Brazil, 184:77 Lead, Mexican tobacco, 181:66 Lead, Mexico pollution by Met Mex Peñoles, 181:90 Lead, migratory birds from Lerma Valley, Mex., 181:61 Lead, milk, Mexico, 181:76 Lead, moss from trees, Mexico City, 181:63 Lead, mother blood vs umbilical cord, 181:80 Lead, neurological damage to children, Mexico, 181:91 Lead, occupational exposure, Mexico, 181:68 Lead ore concentrates, urban contamination, 185:113 Lead oxide, pottery glazing process, 181:68 Lead, oysters, Gulf of Mexico, 181:57 Lead, pigeon tissues, Mexico City, 181:60, Lead poisoning, children Mexico, 181:72 Lead, pollution by Met Mex Peñoles, Mexico, 181:90 Lead, potential health effects, 188:63 Lead problems, Brazil, 184:59 ff. Lead production, Brazil, 184:60 Lead production, export/import, Mexico, 181:41 Lead production, Mexico, 181:39 Lead, rural exposure, Mexico, 181:66 Lead, San Juan River, Mexico, 181:51 Lead smelting, dust contamination, Mexico, 181:48 Lead, soil irrigated w/ Mexico City waste water, 181:51 Lead, soil of Torreón, Coahuila, Mexico, 181:49 Lead, soil playgrounds, Torreón, Coahuila, Mexico, 181:49 Lead sources, human exposure, 185:96 Lead, street dust, Mexico City, 181:50 Lead sulﬁde, lead ore, urban contamination, 185:113

Lead, suspended particles, Torreón, Coahuila, Mex., 181:46 Lead, tree leaves, Mexico City, 181: 62 Lead, turtle eggs, Mexico, 181:62 Lead, umbilical cord blood, Mexico, 181:80 Lead, urban exposure Mexico, 181:63 Lead use, historical, 185:94 Lead uses, Mexico, 181:41 Lead, water & sediment levels, Mexico, 181:51 Lead, working environment limits, Brazil, 184:90 Lead-glazed ceramics, leaching levels, 181:64 Lead-glazed ceramics, major health hazard, 181:38 Lead-producing cities, Mexico, 181:40 Leaded gasoline, air regulations, Brazil, 184:67 Leaded gasoline, historical annual usage, 185:107 Leaded gasoline, human lead exposure, 185:96 Leaded gasoline, lead content history, 185:107 Legacy pesticides, described, 187:2 Leukemia, butadiene worker exposure, 189:149 LGC-42153, water-sediment degradation proﬁle, 187:192 Light source types, photodegration studies, 182:31 Lignin, metal remediation, water, 188:68, 72 Lignin, wood composition amount, 185:70 Lignocellulosic waste, metal remediation, water, 188:67, 72 Lindane, water-sediment degradation proﬁle, 187:163 Linuron, water-sediment degradation proﬁle, 187:190 Liquid chromatography, arsenic speciation, 184:123 Liver somatic index (LSI), PME ﬁsh effects, 185:69 Livestock kills, cyanide, 183:36

Index Living biomass, metal remediation, water, 188:65 Lixiviants, ore leaching solutions, 183:39 Llimpi, mercury ore type, 183:1 LOAELs, PBDEs rodents, 183:79 Low birth weight, risk factor infant gastroenteritis, 186:6 LSI (liver somatic index), PME ﬁsh effects, 185:69 Lumbricus rubellus, earthworm biomarkers, 188:89 Lumbricus spp. (earthworms), heavy metal bioassays, 186:82 Lumbricus terrestris, earthworm biomarkers, 188:94 Lux bacteria-based bioassay, described, 186:76 Lymnea stagnalis (snail), simazine toxicity, 189:2 Lysosomal membrane stability, earthworm tests, 188:88 Magnesium arsenate, insecticide, 184:104 Magnesium, in human nails, 185:162 Malathion, earthworm response, 188: 91 Malathion, water-sediment degradation proﬁle, 187:167 Malnourished world population percentage, 189:35 Mammal kills, cyanide, 183:35 Mammals, geophagous (table), 183:118 Mammals, wetland, pesticide effects, 187:18 Manure, metal remediation, water, 188:68 Marine brown algae, metal remediation, water, 188:65 Marine halogenated products, 188:1 ff. Marine mammal blubber PCBs, (ﬁgure), 184:29 Marine mammal tissue contaminants, 184:1 ff. Marine mammals, halogenated contaminates, methods, 184:11 Marine mammals, pollutant accumulation pattern, 184:6

157

Marine mammals, pollutant biotransformation, 184:6 Marine mammals, reproductive impairment PHCs, 184:9 Masculinized female ﬁsh, paper production efﬂuent, 185:75 Maximally exposed individual, pesticide exposure, 186:120 Maximum absorption wavelengths of pesticides (table), 182:85 Maximum Permissible Concentration (EPA), arsenic drinking water, 184:101 Maximum permitted drinking water levels, Brazil, 184:79 Maximum permitted food levels, lead, Brazil, 184:77 Maximum rate/maximum number, pesticide applications, 186:123 Maximum reﬂectance wavelength spectra of pesticides (table), 182:85 MCPA, ionisable herbicide, 188:150, 154 Mecoprop, ionisable herbicide, 188:150, 154 Mecoprop-P, water sediment degradation proﬁle, 187:171 MeO-BDEs (brominated phenoxyanisoles), 188:23 MeO-BDEs, analytical aspects, 188:28 MeO-BDEs, chemical structures (ﬁgure), 188:24 MeO-BDEs, environmental distribution, 188:29 MeO-BDEs, natural sources, 188:25 Mercury, air contamination, gold melting, 183:14 Mercury, Amazon River contamination, Brazil, 181:143 Mercury, aquatic life protection criteria, 181:179 Mercury biomagniﬁcation, mammals, 181:176 Mercury, bird protection criteria, 181:180 Mercury, blood levels, 181:147 Mercury, Brazilian river contamination, 181:147

158

Index

Mercury, Chilean environmental contamination, 183:6 Mercury, Chilean sources, 183:2 Mercury concentrations, abiotic & biota materials, 181:146 Mercury contamination, Africa, 181:156 Mercury contamination, Brazil (table), 181:147 Mercury contamination, Canada, 181:158 Mercury contamination, Chile, 183:1 ff. Mercury contamination, Chilean government limits, 183:14 Mercury contamination, China, 181: 156 Mercury contamination, ﬂoodplain sediments, wildlife hazard, 181:166 Mercury contamination, mitigation, Brazil, 181:154 Mercury contamination, near Brazilian gold mines, 181:147 Mercury contamination, near historic gold mining, U.S., 181:161 Mercury contamination, Philippines, 181:156 Mercury contamination, Siberia, 181:158 Mercury contamination, small mining sources, Chile, 183:15 Mercury contamination, South America, 181:154 Mercury contamination, U.S., 181:159, 161 ff. Mercury, criteria to protect selected natural resources, 181:179 Mercury, crop protection criteria, 181:179 Mercury, daily human exposure estimates, 189:112 Mercury effects, aquatic organisms, 181:168 Mercury effects, birds, 181:165, 168, 172 Mercury effects, earthworms, 181:177 Mercury effects, ﬁsh, water temperature, 181:171 Mercury effects, freshwater ﬁsh, 181:168

Mercury effects, mammals, 181:168, 175 Mercury effects, proposed safety criteria, 181:178 Mercury effects, reproduction aquatics, 181:170 Mercury, estuarian contamination, Chile, 183:6 Mercury exposure, hair as bioindicator, 189:107 ff. Mercury exposure, humans, Chile, 183:11 Mercury fungicides, poisonings in Iraq, 189:121 Mercury, gold mining history, 181:140 Mercury, hair content versus ﬁsh consumption, 189:107 ff. Mercury, hair levels Alaska, 189:118 Mercury, hair levels Amazonia, 189: 116 Mercury, hair levels Arabia, 189:119 Mercury, hair levels Asian populations, 189:115 Mercury, hair levels Cambodia, 189:120 Mercury, hair levels correlate with blood levels, 189:108 Mercury, hair levels from different populations, 189:114 Mercury, hair levels Spain, 189:119 Mercury, hair levels Sweden, 189:117 Mercury, hair levels Tanzania, 189:120 Mercury, hazards to environment, 181:139 ff. Mercury, hazards to humans, 181: 139 ff. Mercury, human blood levels, Chile, 183:12 Mercury, human contamination, Chile, 183:11 Mercury, human exposure case studies, 189:113 Mercury, human exposure estimates, 189:112 Mercury, human exposure workplaces, 189:110 Mercury, human health protection criteria, 181:180 Mercury, human tissue residues, 181:147

Index Mercury, in gold concentrates, Chile, 183:14 Mercury, in human nails, 185:161 Mercury, in sea water, Chile, 183:8 Mercury, inorganic history, 189:110 Mercury, lethal effects, 181:167 Mercury, mammal protection criteria, 181:180 Mercury methylation, in river sediments, 181:145 Mercury, mutagen, teratogen, carcinogen, 181:143 Mercury, no beneﬁcial biological function, 181:139 Mercury phytoremediation, ﬂoating plants, 181:152 Mercury, poisonings in Iraq, 189:121 Mercury, potential health effects, 188:63 Mercury residues, air (U.S.), 181:163 Mercury residues, birds (U.S.), 181:161 Mercury residues, rivers (U.S.), 181: 160 Mercury residues, wildlife (U.S.), 181:161 Mercury, sediments protection criteria, 181:179 Mercury, sewage contamination, Chile, 183:14 Mercury, soil contamination, Chile, 183:14 Mercury, sources & release rates, 181:144 Mercury, sublethal effects, 181:167 Mercury vapor, binding to hair, 189:109 Mercury vapor, long range transport, 189:110 Mercury, wildlife & ﬁsh cycles, 181:143 Mesocosm studies, pesticides, 187:2 Mesocosm vs microcosm pesticide fate comparisons, 187:210 Mesocosms, pesticide fate systems, 187:208 Mesotrione, adsorption coefﬁcient, 188:186, 189 Mesotrione, ionisable herbicide, 188:156 Mesotrione, water-sediment degradation proﬁle, 187:202

159

Met Mex Peñoles, lead pollution, Mexico, 181:90 Metal oxides, photophysical/ photochemical processes, 182:28 Metal removal from water, plants, 188:59 ff. Metalaxyl, water-sediment degradation proﬁle, 187:179 Metalaxyl-M, water-sediment degradation proﬁle, 187:180 Methamidophos, water-sediment degradation proﬁle, 187:168 Methoxychlor, microcosm degradation proﬁle, 187:217 Methoxychlor, water-sediment degradation proﬁle, 187:164 Methoxyfenozide, water-sediment degradation proﬁle, 187:201 Methyl isothiocyanate, photolysis pathway, 181:14 Methyl mercury, environmental contamination, 183:8 Methyl parathion, microcosm degradation proﬁle, 187:216 Methyl parathion, water-sediment degradation proﬁle, 187:166 Methylmercury, bioaccumulation ﬁsh, 189:108 Methylmercury, biomagniﬁcation ﬁsh, 189:108 Methylmercury, blood vs hair levels, 189:113 Methylmercury, demethylation in organisms, 189:108 Methylmercury effects, fruitﬂy, 181:177 Methylmercury, hair follicle incorporated, 189:109 Methylmercury, hair samples, 189:109 Methylmercury, history, 189:110 Methylmercury, human brain damage, 189:108 Methylmercury, Minamata Disease Japan, 189:113 Methylmercury, most toxic form of mercury, 181:143 Methylmercury, naturally occurring compound, 189:107 Metolachlor/alachlor photodegradation pathways, 182:64

160

Index

Metolachlor, microcosm degradation proﬁle, 187:218 Metolachlor, water-sediment degradation proﬁle, 187:179 Metribuzin, adsorption coefﬁcient, 188:186, 190 Metribuzin, microcosm degradation proﬁle, 187:220 Metsulfuron-methyl, adsorption coefﬁcient, 188:185, 189 Metsulfuron-methyl, ionisable herbicide, 188:154 Metsulfuron-methyl, water-sediment degradation proﬁle, 187:191 Mexico, lead environmental problems, 181:37 ff. Mexico, lead production, 181:39, 40 MFO (mixed-function oxidase), PME ﬁsh effects, 185:69 MFO, effects of paper production efﬂuent, 185:79 MHC-1 (mixed halogenated monoterpenes), 188:40 Microbes, zinc bioassays, 186:81 Microbial indicators, categories soil health, 188:138 Microbial indicators, soil health, 188:136 Microbial oxidation, cyanide water remediation, 183:26 Microcosm vs mesocosm pesticide fate comparisons, 187:210 Microcosms, pesticide fate systems, 187:208 Microorganisms, metabolize industrial pollutants, 185:84 Microtox bioassay, described, 186:76 Migratory bird mortality, cyanide water contamination, 183:34 Migratory Bird Treaty Act, cyanide pond protection, 183:34 Minamata Disease in Japan, methylmercury poisoning, 189:113 Mining lead sites vs. blood levels, Brazil, 184:87 Mirex in foods, S. America, 185:22 Mirex, marine mammals, 184:4 Mirex, use in S. America, 185:4 MITC, photolysis pathway, 181:14

Mite (predatory) bioassays, DDTcontaminated soils, 186:89 Mixed gonadal tissue, gonadal abnormalities, deﬁned, 187:123 Mixed sex, gonadal abnormalities, deﬁned, 187:123 Mixed-function oxidase (MFO), PME ﬁsh effects, 185:69 Mixed-function oxidases (MFOs), paper production effects, 185:79 MMA (monomethylarsenic acid), in soil, 189:45 MMA (monomethylarsonic acid), relative toxicity, 184:98, 107 MMAA (monomethylarsonic acid), soil mobility, 184:107 Mode of action, arsenic, 184:110 Mode of action, endosulfan, 183:101 Mode of action, pyrethroids, 186:58 Mode of action, simazine, 189:4 Model systems, pesticide phodegradation, soil surfaces, 182:35 Model systems, pesticide photodegradation, on plants, 182:35, 47 Modiﬁed California Roller, pesticide applicator, 186:118 Molybdenum, in human nails, 185:161 Monodontid blubber PHCs (table), 184:24 Monomethylarsenic acid (MMA), in soil, 189:45 Monomethylarsine oxide, toxicity, 184:110 Monomethylarsonic acid (MMA), relative toxicity, 184:98, 107 Monosodium methanearsonate (MSMA), herbicide, 184:104 Morphine, from Papaver somniferum (poppy), 190:44 Morphological effects (ﬁsh), paper production efﬂuent, 185:75 Mosquito control, DDT side effects, 187:5 Mussel lead contamination, Brazil, 184:64 Mussel, mercury contamination, Chile, 183:6

Index Mussel Watch pollutant data, S. America, 185:18 Mutagenicity, butadiene, 189:145 Mutagenicity, PBDEs, 183:80 Myocarditis, enterovirus related, 186:23 Mysticeti, baleen whales, 184:2 NACA (National Agricultural Chemicals Association, 186:113 Nail biomarkers, advantages of use, 185:142 Naled, water-sediment degradation proﬁle, 187:167 Naproanilide, microcosm degradation proﬁle, 187:218 Naproanilide, water-sediment degradation proﬁle, 187:180 Narwhal blubber, PHCs (table), 184: 25 National Agricultural Chemical Association (NACA), 186:113 National University of Luján, river pollution studies, 185:40 Natural halogenated products (HNPs), 188:1 ff. Naturally occurring halogenated products, 188:1 ff. Nematodes, zinc bioassays for soil, 186:81 Nervous system effects evaluation, lead exposure, 185:123 Net panels, cyanide pond wildlife protection, 183:38 Neurological effects, lead exposure vs age, 185:113, 116 Neurotoxicity, PBDEs, 183:80 Neutral red retention assay (NRR), earthworms, 188:88 Newspaper incineration, dioxin formation, 190:5, 15, 18 NH4 pollution, Reconquista River, 185:52 NICA-Donnan model, metal remediation, water, 188:74 Niccolite, arsenic-bearing mineral, 184:99 Nickel, aquatic environment hazard, 188:61 Nickel, in human nails, 185:161

161

Niclosamide, water-sediment degradation proﬁle, 187:180 Nicosulfuron, adsorption coefﬁcient, 188:185, 189 Nitric acid, gold/mercury amalgam separation, 183:14 Nitrogen cycle, organic matter role, 188:128 Nonspeciﬁc febrile illness, enterovirus related, 186:21 Nontarget invertebrates, pesticide effects, 187:25 Nontarget plants, pesticide effects, 187:26 Nonylphenol 4-tert-, effects, gonads ﬁsh/frogs, 187:113 Norwalk virus, diarrhea cause, 186:4 Novel HNPs, annual discovery numbers, 188:2 Nut husks (ground), metal remediation, water, 188:68 Nutritional element determination, human nails, 185:155 OBDE (octabromodiphenyl ether), dermal toxicity, 183:74 OBDE (octabromodiphenyl ether), oral toxicity, 183:73, 76 Occupational exposure, element content human nails effect, 185:154 Occupational exposure, lead, Mexico, 181:68 Occupational exposure, mercury, Chile, 183:11 Occupational exposure, PBDEs, 183:67, 69 Occupational exposure, pesticides, Uruguay, 181:128 Octabromodiphenyl ether (OBDE), toxicity, 183:73 Octanol/water partitioning, PFOS, 186:137 Octylphenol 4-tert-, effects, gonads ﬁsh/ frogs, 187:113 Odontoceti whales, 184:2 Open pit mining, land disturbance, 183:40 Opiate usage, global numbers, 190:44

162

Index

Opium, from Papaver somniferum (poppy), 190:44 Opium, global production, 190:44 ORETF task force, 186:110 Organic halides, paper production efﬂuent, 185:73 Organic pollutants in South America, 185:2 ff. Organic solvents, pesticide photodegradation media, 182:47 Organobromines, GC/ECNI-MS detection , 188:4 Organochlorine contaminants in whales, 184:1 ff. Organochlorine pesticides, chemical structures, 182:146 Organochlorine photodegradation, in solvents, 182:49 Organochlorine photodegradation, on glass, 182:37 Organochlorine photodegradation, on plants, 182:69 Organochlorine photodegradation, on soils, 182:58 Organochlorines, fate in watersediment systems, 187:162 Organohalogen contaminants in cetaceans, 184:1 ff. Organomercurial fungicides, poisonings in Iraq, 189:121 Organometal compounds, aquatic environment hazard, 188:61 Organophosphates, fate in watersediment systems, 187:165 Organophosphates, oxon formation, 181:13 Organophosphorus ester photodegradation, in solvents, 182:49 Organophosphorus ester photodegradation, on glass, 182:37 Organophosphorus ester photodegradation, on plants, 182:70 Organophosphorus ester photodegradation, on soils, 182: 58 Organophosphorus pesticides, chemical structures, 182:148

Orpiment, arsenic-bearing mineral, 184:99 ortho, para-DDE, effects, gonads ﬁsh/ frogs, 187:114 ortho, para-DDT, effects, gonads ﬁsh/ frogs, 187:114 Outdoor Residential Exposure Task Force (pesticide), 186:118 Ovotestis, deﬁned, 187:107, 109, 121 Oxadiargyl, water-sediment degradation proﬁle, 187:200 Oxasulfuron, water-sediment degradation proﬁle, 187:193 Oxidation, pesticides/water-sediment, 187:146, 152 Oxon formation, organophosphate photooxidation, 181:13 Oxyanions, arsenic, 184:104 Oxydemeton-methyl, water-sediment degradation proﬁle, 187:167 Oxygen deligniﬁcation, paper production efﬂuent, 185:84 Oxygen species, atmospheric, 182: 29 Oysters, lead content, Gulf of Mexico, 181:57 Ozone, reactions with pesticides (table), 182:88 Paints, human lead exposure, 185:96 Palm pressed ﬁbers, metal remediation, water, 188:72 Pantanal wetlands, mercury contamination, 181:152 Papaver somniferum (poppy), heroin source, 190:44 Paper making, history, 185:67 Paper manufacture impact on aquatic environment, 185:67 ff. Paper mill efﬂuent (PME), ﬁsh effects, 185:69 Paper mill efﬂuent (PME), stream release, 185:68 Paper production, aquatic toxicology, 185:75 Paper production, chemical outputs, 185:72 Paper production contaminants, morphological effects, 185:75

Index Paper production contaminants, organic halides, 185:73 Paper production contaminants, resin acids, 185:85 Paper production efﬂuent, EPA guidelines, 185:83 Paper production efﬂuent, extended cooking , 185:84 Paper production, environmental impacts, 185:72 Paper production process, 185:70 ff. Paper production, reproductive effects aquatics, 185:80 Paper production, steroid effects aquatics, 185:80 Paper pulp efﬂuent, effect aquatic environment, 185:68 Paralysis, enterovirus related, 186:18 Parathion, photooxidation, 181:13 Parathion, successive photoreduction, dimerization (diagram), 182:50 Parathion, water-sediment degradation proﬁle, 187:166 Paris green, insecticide, 184:104 PBBs (polybrominated biphenyls), 188:2 PBDEs (polybrominated diphenyl ethers), 183:55 ff. PBDEs (polybrominated diphenyl ethers), 188:2 PBDEs, adipose tissue retention, 183:72 PBDEs, annual production, 183:56 PBDEs, BDE-153 dominant tissue congener , 183:60 PBDEs, BDE-47 dominant tissue congener, 183:60 PBDEs, biological effects humans, 183:71 PBDEs, blood/serum levels occupationally exposed, 183:69 PBDEs, body burden outliers, 183:66, 68 PBDEs, carcinogenicity studies, 183:78 PBDEs, chronic toxicity, 183:78 PBDEs, commercial uses, 183:56 PBDEs, congener acute toxicity, 183: 73 PBDEs, congeners, 183:56

163

PBDEs, delphinoid blubber (table), 184:28 PBDEs, eight congeners in blood, 183:62 PBDEs, endocrine effects, 183:82 PBDEs, environmental release, 183:57 PBDEs, epidemiology, 183:83 PBDEs, exposure estimates, 183:86 PBDEs, exposure margin of safety, 183:86 PBDEs, ﬂame retardant additives, 183:55 PBDEs, hazard characterization, 183:85 PBDEs, health risk assessment, 183:85 PBDEs, hexa- & hepta-BDE adipose levels, 183:59 PBDEs, human absorption/metabolism, 183:71 PBDEs, human adipose tissue levels, 183:59 PBDEs, human blood levels, 183:60, 63 PBDEs, human plasma/serum levels, 183:63 PBDEs, human tissue levels, 183:58 PBDEs, immunotoxicity, 183:80 PBDEs, inhalation particulate phase, 183:71 PBDEs, inhalation toxicity, 183:74 PBDEs, isomers, 183:56 PBDEs, levels human adipose tissue (table), 183:61 PBDEs, levels human milk, 183:64 PBDEs, levels in cancer patients, 183:59 PBDEs, LOAEL rodents, 183:79 PBDEs, mammalian toxicity, 183:71 PBDEs, milk levels/adipose levels, 183:64 PBDEs, mutagenicity, 183:80 PBDEs, neurotoxicity, 183:80 PBDEs, occupational exposure types, 183:67, 69 PBDEs, polybrominated diphenyl ethers, marine mammals, 184:3 PBDEs, prenatal/postnatal exposure, 183:66 PBDEs, public exposure, routes, 183:58 PBDEs, regulatory control, 183:84

164

Index

PBDEs, repeated-dose studies, 183:75 PBDEs, reproductivity toxicity, 183:81 PBDEs, risk assessment, 183:87 PBDEs, See polybrominated diphenyl ethers, 183:55 ff. PBDEs, skin sensitization, 183:75 PBDEs, structure similarity to PCBs, 183:56 PBDEs, teratogenicity, 183:81 PBDEs, U.S. manufacturers, 183:57 PBDEs, use in plastic/textile products, 183:58 PBDEs, workplace monitoring, 183:67, 69 PBPK (physiologically based pharmacokinetic) models, 189:141 PBTs (persistent bioaccumulative & toxic chemicals), 188:2 PCBs (polychlorinated biphenyls), 190:1 PCBs (polychlorinated biphenyls), use in S. America, 185:5 PCBs, air levels S. America, 185:8 PCBs, delphinoid blubber hemispheres compared (ﬁg.), 184:33 PCBs, dolphins, 184:2 PCBs effects, gonads ﬁsh/frogs, 187:114 PCBs, gull eggs S. America, 185:20 PCBs marine mammal blubber (ﬁgure), 184:29 PCBs, marine mammals, 184:3 PCBs, sediment levels S. America, 185:17 PCBs, soil levels S. America, 185:11 PCBs, water levels S. America, 185:15 PCDD (dioxins), paper production efﬂuent, 185:75 PCDD (dioxins), S. America pollutants, 185:5 PCDDs (polychlorinated dibenzo-pdioxins), 190:1 PCDF (furans), paper production efﬂuent, 185:75 PCDF (furans), S. America pollutants, 185:5 PCDFs (polychlorinated dibenzofurans), 190:1 PCNB, microcosm degradation proﬁle, 187:217

PCNs (polychloronapthalenes), 188:2 Peanut hulls, metal remediation, water, 188:68 Peat moss, metal remediation, water, 188:73 PeBDE (pentabromodiphenyl ether), dermal toxicity, 183:74 PeBDE (pentabromodiphenyl ether), oral toxicity, 183:73, 76 Pendimethalin, water-sediment degradation proﬁle, 187:201 Penicillium steckii, simazine degrading, 189:16 Pentabromodiphenyl ether (PeBDE), toxicity, 183:73 Pentachlorophenol, water-sediment degradation proﬁle, 187:163 Pentylphenol 4-tert-, effects, gonads ﬁsh/frogs, 187:114 Peñoles (Mex Met), lead pollution, Mexico, 181:90 Perﬂuorinated alkyl acids (PFAAs), 186:133 Perﬂuorinated compounds, delphinoid liver (table), 184:26 Perﬂuorooctanesulfonate (PFOS), ecotoxicological evaluation, 186:133 ff Perﬂuorooctanesulfonate, see PFOS, 186:133 ff. Perinatal lead exposure, effects, 185: 95 Permethrin, water-sediment degradation proﬁle, 187:172 Persistent bioaccumulative & toxic chemicals (PBTs), 188:2 Persistent organic pollutants (POPs), 188:2 Persistent organic pollutants (POPs) in South America, 185:1 ff. Persistent organohalogen contaminants (PHCs), physicochemical properties, 184:2 Personal protective equipment (PPE), pesticide workers, 186:110 Pesticide application, Good Agricultural Practice, 187:4 Pesticide behavior, adsorptiondesorption soil, 187:141

Index Pesticide behavior, air-water interfaces, 187:139 Pesticide behavior in water-sediment systems, 187:133 ff. Pesticide chemical structures, directory, 182:130 Pesticide container disposal policy, Uruguay, 181:130 Pesticide degradation, abiotic processes, 187:145 Pesticide degradation, biotic processes, 187:151 Pesticide degradation proﬁles, microcosm systems, 187:215 Pesticide dermal dosimetry, 186:113 Pesticide distribution, water-sediment controlling factors, 187:136 Pesticide drift, 181:1 ff. Pesticide effects, amphibians, 187:7 Pesticide effects, aquatic invertebrates, 187:9 Pesticide effects, aquatic microbes, 187:18 Pesticide effects, aquatic plants, 187:17 Pesticide effects, community/species assemblage, 187:33 Pesticide effects, ﬁsh, 187:8 Pesticide effects, habitat/resource modiﬁcation, 187:28 Pesticide effects, local extinction & reduced biodiversity, 187:29 Pesticide effects, nontarget invertebrates, 187:25 Pesticide effects, nontarget plants, 187:26 Pesticide effects, populations, 187:32 Pesticide effects, quantitative tools, population analysis, 187:39 Pesticide effects, recovery/ recolonization, 187:30 Pesticide effects, wetland birds, 187:21 Pesticide effects, wetland herpetofauna, 187:24 Pesticide effects, wetland mammals, 187:18 Pesticide exposure, body surface area, 186:121 Pesticide exposure, body weight, 186:121

165

Pesticide exposure databases, applied risk analysis, 186:107 ff. Pesticide exposure, dermal absorption, 186:122 Pesticide exposure, ecosystem longterm implications, 187:28 Pesticide exposure estimates from generic data, 186:119 Pesticide exposure, respiration rate, 186:122 Pesticide exposure risk analysis, 186:107 ff. Pesticide exposure, transferable residue, 186:122 Pesticide exposures derived from generic databases (table), 186:124 Pesticide fate, atmospheric, 181:1 ff. Pesticide fate in air, assessment ﬂowchart, 181:26 Pesticide fate, water-sediment lab systems, 187:162, 165 Pesticide generic exposure databases, development, 186:113 Pesticide Handlers Exposure Database (PHED), 186:110 Pesticide imports, class distribution, Uruguay, 181:117 Pesticide imports, value, Uruguay, 181:115 Pesticide inhalation exposure, 186:113 Pesticide ionisation, described, 188: 151 Pesticide long-term effects, risk, 187: 1 ff. Pesticide management practices, simazine, 189:10 Pesticide occupational exposure, Uruguay, 181:128 Pesticide photodegradation, atmospheric oxygen species, 182:29 Pesticide photodegradation, in foliar/ topical application (table), 182:120 Pesticide photodegradation, in solvents (table), 182:101 Pesticide photodegradation, kinetic analysis, 182:31, 34 Pesticide photodegradation, light sources (exptl), 182:31

166

Index

Pesticide photodegradation, model systems, plants, 182:36 Pesticide photodegradation, model systems, soil, 182:35 Pesticide photodegradation, on clay thin-layers (table), 182:105 Pesticide photodegradation, on glass, 182:36 Pesticide photodegradation, on glass/ silica gel (table), 182:94 Pesticide photodegradation, on plants, 182:69 Pesticide photodegradation, on soil & clays, 182:56 Pesticide photodegradation, photochemical processes, 182:5 Pesticide photodegradation, photophysical processes, 182:3 Pesticide photodegradation, typical decline curves (diagram), 182: 35 Pesticide photolysis, atmospheric, 181:10 Pesticide photolysis, gas-phase sampling, 181:23 Pesticide photolysis, gas-phase spectra, 181:24 Pesticide photolysis, lab equipment designs, 181:21 Pesticide photolysis, light sources, 181:23 Pesticide photolysis on plants, controlling factors, 182:10 Pesticide photolysis on plants, environmental factors, 182:10 Pesticide photolysis on plants, formulation effect, 182:12 Pesticide photolysis on soil, controlling factors, 182:17 Pesticide photolysis on soil, environmental factors, 182:19 Pesticide photolysis on soil, humic substances effects, 182:18 Pesticide photolysis on soil, mass transport in soil, 182:19 Pesticide photolysis on soil, photic depth in soil, 182:21 Pesticide photolysis on soil, soil component effects, 182:17

Pesticide photolysis on soil, soil properties, 182:22 Pesticide photolysis, surfactant effects, 182:12 Pesticide photoreactions on soils (diagram), 182:23 Pesticide poisonings, clinical cases, Uruguay, 181:127, 129 Pesticide properties, ionisable compounds adsorption, 188:164 Pesticide reactions with active oxygen species (table), 182:88 Pesticide reactions with hydroxyl radical (table), 182:88 Pesticide reactions with ozone (table), 182:88 Pesticide reactions with singlet oxygen (table), 182:88 Pesticide regulations, Uruguay, 181:113, 116 Pesticide residue tolerances, foods, Uruguay, 181:119 Pesticide residues, agricultural crops, Uruguay, 181:119 Pesticide residues, blood, Uruguay, 181:125, 127, 129 Pesticide residues, drinking water, Uruguay, 181:121 Pesticide residues, environmental, Uruguay, 181:121, 124 Pesticide residues, foods, Uruguay, 181:122 Pesticide residues, human fat, Uruguay, 181:130 Pesticide residues, humans, S. America, 185:21, 25 Pesticide residues, lemon oils, Uruguay, 181:125 Pesticide residues, sewage efﬂuents, Uruguay, 181:122 Pesticide restrictions, Uruguay, 181:115 Pesticide risk assessment, conservation biology vantage, 187:34 Pesticide risk assessment, ecological vantage, 187:31 Pesticide risk assessment, Europe, 187:1 ff. Pesticide risk, human health, Uruguay, 181:127

Index Pesticide transport/distribution, watersediment system (diag.), 187:134 Pesticide usage, Uruguay, 181:111 ff. Pesticide vapor pressure vs water solubility, 181:9 Pesticide waste disposal, Uruguay, 181:122 Pesticide water-sediment experimental designs, 187:155 Pesticides, airborne fate, 181:1 ff. Pesticides, airborne hydroxyl removal, 181:15 Pesticides, aquatic ecosystem effects, 187:6 Pesticides, atmospheric removal, 181:7 Pesticides, CAS numbers (table), 188:205 Pesticides, CAS numbers, 181:28, 134 Pesticides, chemical names (table), 188:205 Pesticides, chemical names, 181:28, 134 Pesticides, common names, 181:28, 134 Pesticides, disposal of outdated, Uruguay, 181:130 Pesticides, ecosystem effects, 187:4 Pesticides, experimental photolysis in air, 181:12 Pesticides, fate in mesocosms, 187:208 Pesticides, fate in microcosms, 187:208 Pesticides, fate in water-sediment systems, 187:162, 165 Pesticides, gas-phase oxidative rates, 181:19 Pesticides, impacts on nontargets, 187: 4 Pesticides in water-sediment systems, 187:133 ff. Pesticides, indirect effects, 187:5, 7 Pesticides, listed as hazardous air pollutants, 181:27 Pesticides, long-term effect assessment, 187:2 Pesticides manufactured in Uruguay, 181:115 Pesticides, off-target movement, 181:1 ff. Pesticides, oxidative rate estimations, 181:20 Pesticides, photolysis, 182:2 ff.

167

Pesticides, photoreaction types (diagram), 182:7 Pesticides, sediment levels S. America, 185:17 Pesticides, soil adsorption coefﬁcients (Koc) (chart), 187:142 Pesticides, soil diffusion coefﬁcients (table), 182:92 Pesticides, soil levels S. America, 185:11 Pesticides, sunlight photodegradation, 182:2 ff. Pesticides, surface water contaminants, 188:150 Pesticides, usage in S. America, 185: 2 Pesticides, used in cocaine/heroin production, 190:45 Pesticides, UV absorption proﬁles, 182:3 Pesticides, volatilization, 181:4 Pesticides, water levels S. America, 185:12 Pesticides, water-sediment conjugation, 187:147, 154 Pesticides, water-sediment degradation processes, 187:145 Pesticides, water-sediment hydrolysis, 187:147, 153 Pesticides, water-sediment oxidation, 187:146, 152 Pesticides, water-sediment photolysis, 187:150 Pesticides, water-sediment redox reactions, 187:148 Pesticides, water-sediment reduction, 187:146, 153 Petroleum hydrocarbons, earthworm avoidance, 188:98 PFAAs, see Perﬂuorinated alkyl acids, 186:133 PFAs, perﬂuorinated acids, marine mammals, 184:3 PFOS, aquatic hazard assessment, 186:160 PFOS, aquatic plant benchmark, 186:161 PFOS, aquatic toxicity benchmarks, 186:160

168

Index

PFOS, bioaccumulaction factors for plants, 186:143 PFOS, bioconcentration factors, 186:138, 140 PFOS, biodegratation, 186:136 PFOS, bird tissue residues, 186:166 PFOS, bird toxicity benchmarks, 186:165 PFOS, chemical structure, 186:134 PFOS, critical body burden, ﬁsh, 186:162 PFOS, ecotoxicology, 186:143 ff. PFOS, effects activated sludge, 186:143 PFOS, effects aquatic macrophytes, 186:145 PFOS, effects invertebrates, 186:146 PFOS, effects phytoplankton, 186:143 PFOS, environmental fate, 186:135 PFOS, environmental persistence, 186:133 PFOS, ﬁsh bioconcentration factors, 186:140 PFOS, hazard assessment, 186:157 PFOS, hydrolysis, 186:136 PFOS, octanol/water partitioning, 186:137 PFOS, perﬂuorooctane sulfonates, marine mammals, 184:3 PFOS, photolysis, 186:136 PFOS, physico/chemical properties, 186:135 PFOS salts, 186:135 PFOS, See Perﬂuorooctanesulfonate, 186:133 ff. PFOS, soil adsorption/desorption, 186:138 PFOS, terrestrial invertebrates benchmark, 186:165 PFOS, terrestrial plants benchmark, 186:164 PFOS, terrestrial toxicity benchmarks, 186:164 PFOS, thermal stability, 186:137 PFOS toxicity, amphibians, 186:151 PFOS toxicity, aquatic invertebrates (table), 186:147 PFOS toxicity, birds, 186:154, 158, 166 PFOS toxicity, ﬁsh (table), 186:150, 163

PFOS toxicity, terrestrial invertebrates, 186:152 PFOS toxicity, terrestrial plants, 186:152 PFOS toxicity, terrestrial vertebrates, 186:154 PFOS, uptake terrestrial plants, 186:142 PFOS, uses, 186:134 pH inﬂuence on degradation, ionisable compounds, 188:199 pH inﬂuence on sorption, ionisable pesticides, 188:192 pH inﬂuence, soil adsorption, 188:175, 180 Pharmacology of geophagy, 183:122 PHC studies, delphinoids, 184:11 PHCs, “grasshopper” effect, 184:3 PHCs (Persistent Organohalogen Contaminants), physicochemical properties, 2 PHCs, beluga whale blubber (table), 184:24 PHCs, delphinoid blubber, in vitro assays, 184:39 PHCs, dolphin blubber (table), 184:12 PHCs, free-ranging delphinoids’ blubber (table), 184:37 PHCs, global transport, 184:3 PHCs, killer whale blubber (table), 184:18 PHCs, monodontid blubber (table), 184:24 PHCs, narwhal blubber (table), 184:25 PHCs, phocoenid blubber (table), 184:20 PHCs, pilot whale blubber (table), 184:19 PHCs, porpoise blubber (table), 184: 20 PHCs, sources & spatial distribution, 184:4 PHCs, spatial trends, marine mammals, 184:29, 36 PHCs, temporal trends, marine mammals, 184:34, 36 PHED (Pesticide Handlers Exposure Database), 186:110, 112 PHED task force, 186:110, 112

Index Phenmedipham, water-sediment degradation proﬁle, 187:188 Phenoxy acid herbicides, ionisable, 188:150 Phenoxy herbicide chemical structures, 182:136 Phenoxy herbicides, photodegradation on soils, 182:61 Phenoxyalkanoate herbicides, photodegradation on soils, 182:61 Phenoxyalkanoic acids, fate in watersediment systems, 187:170 Phenoxyalkanoic esters, fate in watersediment systems, 187:170 Phenyl ring opening, via oxidation (diag.), 187:152 Philippines, mercury contamination, 181:156 Phoca caspica (Caspian seal), epizootics, 184:2 Phoca groenlandica (harp seal), 184:9 Phoca hispida (ringed seal), 184:5 Phoca sibirica (Baikal seal), epizootics, 184:2 Phoca vitulina (harbour seal), seal epizootics, 184:2 Phocoena phocoena (harbour porpoise), 184:10 Phocoenid blubber PHCs (table), 184:20 Phorate, microcosm degradation proﬁle, 187:217 Phorate, photooxidation, 181:13 Phosphate, analogue of Arsenic V, 189:47 Phosphates, fate in water-sediment systems, 187:169 Phosphorescence lifetime, pesticides, 182:4 Phosphorescence wavelength spectra, pesticides (table), 182:80 Phosphorodithioates, fate in watersediment systems, 187:169 Phosphorothioates, fate in watersediment systems, 187:165 Phosphorothiolates, fate in watersediment systems, 187:169 Phosphorous cycle, organic matter role, 188:128

169

Photic depth, pesticide photolysis on soil, 182:21 Photochemical processes, pesticide photodegradation, 182:5 Photodegradation, amide herbicides on glass, 182:43 Photodegradation, amide herbicides on plants, 182:75 Photodegradation, amide herbicides on soils, 182:63 Photodegradation, anilide herbicides on glass, 182:43 Photodegradation, anilide herbicides on soils, 182:63 Photodegradation, azole herbicides in solvents, 182:55 Photodegradation, azole herbicides on glass, 182:45 Photodegradation, azole herbicides on plants, 182:75 Photodegradation, azole herbicides on soils, 182:67 Photodegradation, carbamates in solvents, 182:52 Photodegradation, carbamates on glass, 182:42 Photodegradation, carbamates on plants, 182:73 Photodegradation, carbamates on soils, 182:62 Photodegradation, dicarboximide herbicides in solvents, 182:54 Photodegradation, dicarboximide herbicides on glass, 182:43 Photodegradation, dicarboximide herbicides on soils, 182:63 Photodegradation, imide herbicides on plants, 182:75 Photodegradation of pesticides, atmospheric oxygen species, 182:29 Photodegradation, organochlorines in solvents, 182:49 Photodegradation, organochlorines on glass, 182:37 Photodegradation, organochlorines on plants, 182:69 Photodegradation, organochlorines on soils, 182:58

170

Index

Photodegradation, organophosphorus esters in solvents, 182:49 Photodegradation, organophosphorus esters on glass, 182:38 Photodegradation, organophosphorus esters on plants, 182:70 Photodegradation, organophosphorus esters on soils, 182:58 Photodegradation, pesticides, 182:2 ff. Photodegradation, pesticides in foliar/ topical application (table), 182: 120 Photodegradation, pesticides in organic solvents, 182:47 Photodegradation, pesticides in plant model systems, 182:47 Photodegradation, pesticides in solvents (table), 182:101 Photodegradation pesticides, light sources (exptl), 182:31 Photodegradation, pesticides on clay thin-layers (table), 182:105 Photodegradation, pesticides on glass, 182:36 Photodegradation, pesticides on glass/ silica gel (table), 182:94 Photodegradation, pesticides on plants, 182:69 Photodegradation, pesticides on plants, environmental factors (illus), 182:11 Photodegradation, pesticides on soil & clays, 182:56 Photodegradation, phenoxy herbicides on soils, 182:61 Photodegradation products, sulfonamides, 187:80, 83 Photodegradation, pyrethroids in solvents, 182:51 Photodegradation, pyrethroids on glass, 182:39 Photodegradation, pyrethroids on plants, 182:73 Photodegradation, pyrethroids on soils, 182:61 Photodegradation, triazine herbicides on glass, 182:45 Photodegradation, triazine herbicides on soils, 182:67

Photodegradation, urea herbicides in solvents, 182:55 Photodegradation, urea herbicides on glass, 182:44 Photodegradation, urea herbicides on plants, 182:75 Photodegradation, urea herbicides on soils, 182:66 Photoinduced rearrangement, pesticides, 182:40, 44, 57, 66, 68 Photoionization, atmospheric pesticides, 181:11 Photolysis chamber, soil studies (diagram), 182:33 Photolysis chambers, pesticide photodegration studies, 182:32 Photolysis light sources, 182:31 Photolysis on plants, illumination conditions, 182:10 Photolysis, pesticides, 182:2 ff. Photolysis, pesticides in air experimental, 181:12 Photolysis, pesticides/water-sediment, 187:150 Photolysis, PFOS, 186:136 Photolysis, simazine, 189:15 Photooxidative rearrangement, pesticides, 182:40, 44, 57, 66, 68 Photophysical pathways, energy state diagram, 182:4 Photophysical processes, pesticide photodegradation, 182:3 Photoreactions, pesticides (diagram), 182:7 Photosensitizer wavelength emission proﬁles (table), 182:86 Physeter macrocephalus (sperm whaled), 184:9 Physicochemical parameters, HNPs, 188:14 Physicochemical properties, simazine, 189:2 Physicochemical properties, sulfonamides (table), 187:71 Physiologically Based Pharmacokinetic (PBPK) Models, 189:141 Phytoplankton, PFOS effects, 186:143 Phytoplankton, Reconquista River, 185:49

Index Phytoremediation, mercury & ﬂoating plants, 181:152 Picloram, water-sediment degradation proﬁle, 187:163 Picolinafen, water-sediment degradation proﬁle, 187:181 Picoxystrobin, water-sediment degradation proﬁle, 187:175 Pilot whale blubber PHCs (table), 184:19 Pilot whales, 184:7 Pinnipeds, organohalogen contaminants, 184:1ff. Pit lakes (gold mining), cyanide retention, 183:46 Pit lakes (gold mining), environmental effects, 183:45 Pit lakes (gold mining), perpetual management, 183:47 Plankton, mercury contamination, Chile, 183:6 Plant leaf anatomy (diagram), 182:13 Plant model systems, pesticide photodegradation, 182:36, 47 Plant remediation, alternative to chemical technology, 188:64 Plant remediation, heavy metals in water, 188:59 ff. Plant tolerance, arsenic, 189:54 Plant wax chemistry, 182:14 Plant waxes, UV absorption spectra, 182:15 Plasma retinol reduction, PHCs marine mammals, 184:10 Plastics incineration, dioxin formation, 190:7, 21 Pleurodynia, entovirus related, 186: 23 PME (paper mill efﬂuent), stream release, 185:68 Poliovirus, probability of infection, different routes, 186:39 Poliovirus, tapwater exposure, children, 186:39 Pollutant input, S. America, 185:2 ff. Pollutant ranges in sediments, S. America, 185:15 Pollutant ranges in soils, S. America, 185:10

171

Pollutant ranges in water, S. America, 185:13 Pollutants, soil health impact, 188:141 Polybrominated biphenyls (PBBs), 188:2 Polybrominated diphenyl ethers (PBDEs), 188:2 Polybrominated diphenyl ethers (PBDEs), human tissue levels, 183:55 ff. Polychlorinated biphenyls (PCBs), 190:1 Polychlorinated biphenyls (PCBs), usage S. America, 185:5 Polychlorinated dibenzo-p-dioxins (PCDDs), 190:1 Polychlorinated dibenzofurans (PCDFs), 190:1 Polychlorinated furans, marine mammals, 184:4 Polychlorinated HNP (Q1), 188:4, 17 Polychloronapthalenes (PCNs), 188:2 Polyethylene balls, pond coverage duck repellent, 183:37 Polyhalogenated compounds, contaminants, 188:1 ff. Polyvinyl chloride (PVC) incineration, dioxin formation, 190:8, 22 Polyvinyl chloride incineration, dioxin formation, 190:2 Poppy eradication, Colombia, 190:43 ff. Poppy eradication, glyphosate, 190:43 ff. Poppy, opium, morphine, heroin source, 190:44 Poppy production, control recommendations (Colombia), 190:108 Poppy production, environmental impacts (Colombia), 190:104 Poppy production, human health impacts (Colombia), 190:103 POPs (persistent organic pollutants), 188:2 POPs (see Persistent organic pollutants), 185:1 ff. POPs, soil levels in S. America, 185:9 Porpoise blubber PHCs (table), 184:20

172

Index

Porpoise liver, perﬂuorinated compounds (table), 184:26 Porpoises, pollutant levels S. America, 185:19 Pot worm (Enchytraeus crypticus), zinc bioassays, 186:80 Potassium, in human nails, 185:162 PPE (Personal protective equipment), 186:21 Predatory mite bioassays, DDTcontaminated soils, 186:89 Predicted environmental concentrations, sulfonamides (table), 187:91 Pregnancy, lead exposure effects, 185:95 Primisulfuron, adsorption coefﬁcient, 188:185, 189 Probability of infection, poliovirus different routes, 186:39 Prochloraz, adsorption coefﬁcient, 188:190 Prochloraz, ionisable herbicide, 188:158 Prochloraz, photoinduced rearrangement, 182:68 Profenofos, water-sediment degradation proﬁle, 187:167 Progesterone, androgens from, paper production, 185:77 Prometryn, ionisable herbicide, 188: 156 Propargite, water-sediment degradation proﬁle, 187:199 Propiconazole, adsorption coefﬁcient, 188:190 Propiconazole, water-sediment degradation proﬁle, 187:196 Propineb, water-sediment degradation proﬁle, 187:190 Proposed mercury criteria, resource protection, 181:178 Propoxycarbazone, water-sediment degradation proﬁle, 187:193 Propyzamide, water-sediment degradation proﬁle, 187:178 Prostigmate bioassays, DDTcontaminated soils, 186:89 Prosulfuron, adsorption coefﬁcient, 188:189

Prosulfuron, water-sediment degradation proﬁle, 187:191 Prothioconazole, water-sediment degradation proﬁle, 187:196 Pulp bleaching, paper production, 185:71 Pulp efﬂuent, effects on aquatic environment, 185:68 Pulp processing, paper production, 185:71 Pulping methods, paper production, 185:70 PVC (polyvinyl chloride) incineration, dioxin formation, 190:8, 22 Pymetrozine, water-sediment degradation proﬁle, 187:204 Pyraclostrobin, water-sediment degradation proﬁle, 187:176 Pyraﬂufen-ethyl, water-sediment degradation proﬁle, 187:200 Pyrene, earthworm response, 188:91 Pyrethroid chemical structures, 182:137 Pyrethroid illnesses, California, 186: 57 ff. Pyrethroid illnesses, group vs individual, California, 186:60 Pyrethroid photodegradation, in solvents, 182:51 Pyrethroid photodegradation, on glass, 182:39 Pyrethroid photodegradation, on plants, 182:73 Pyrethroid photodegradation, on soils, 182:61 Pyrethroid photoinduced cis/trans isomerization, 182:40 Pyrethroid-related illnesses, California, table, 186:60 Pyrethroids, exposure symptoms (human), table, 186:61 Pyrethroids, fate in water-sediment systems, 187:170 Pyrethroids, illness & use report data, California, 186:59 Pyrethroids, illness episodes, California, 186:62 Pyrethroids, mode of action, 186:58 Pyrethroids, symptom array & exposure route, 186:61

Index Pyrethroids, Types I & II, described, 186:57 Pyrethroids, use violations, 186:62 Pyridate, water-sediment degradation proﬁle, 187:199 Pyriproxyfen, water-sediment degradation proﬁle, 187:203 Pyruvate oxidation inhibition, arsenic, 184:110 Q1, (heptachloromethyl bipyrrole), 188:17 Q1, Alteromonas luteoviolaceus production, 188:18 Q1, analytical aspects, 188:19 Q1, chemical structures (ﬁgure), 188:17 Q1, concentrations marine environment (table), 188:22 Q1, environmental distribution, 188: 20 Q1, identical to U3, 188:18 Q1, important polychlorinated HNP, 188:4, 17 Q1, reference standard available, 188:19 QWASFI, pesticide water-airsediment-ﬁlm interaction model, 187:160 Radium, in human nails, 185:161 Rana pipiens, gonadal abnormalities, 187:104 Rana sylvatica, trematode infection vs pesticide exposure, 187:7 Raphidocellis subcapitata (alga), aquatic pesticide monitoring, 187:12 RATL, Canadian reptile/amphibian lethality database, 187:7 Realistic upper bound, pesticide exposure, 186:120 Recommendations, lead exposure prevention, 185:130 Reconquista River, a “dead river”, 185: 57 Reconquista River, abiotic parameters, 185:42 Reconquista River, analytical portrait, 185:42

173

Reconquista River, biotic parameters, 185:49 Reconquista River description, 185:37 Reconquista River, fecal pollution, 185:51, 53 Reconquista River, heavy metal levels, 185:45 Reconquista River, insecticide levels, 185:47 Reconquista River, microbiology, 185:51 Reconquista River, N-NH4 pollution, 185:52 Reconquista River of Argentina, highly polluted, 185:35 ff. Reconquista River, physiocochemical parameters, 185:42 Reconquista River, pollution details, 185:39 Reconquista River, toxicity bioassays, 185:53 Reconquista River, turbidity, 185:48 Reconquista River, University of Luján studies, 185:40 Reconquista River, water quality chemical indexes, 185:48 Reconquista River, water sample analyses, 185:43 Red Book (National Academy of Science), 186:108 Red shrimp, mercury contamination, Chile, 183:9 Redox conditions, arsenic soil role, 189:45 Redox potential, arsenic (diagram), 184:106 Redox reactions, pesticides/watersediment, 187:148 Redtop grass (Agrostis stolonifera), copper-tolerant, 186:87 Reduced biodiversity & species extinction, pesticide effects, 187:29 Reduction, pesticides/water-sediment, 187:146, 153 Reentry Worker Exposure, 186:114 Regulatory control, PBDEs, 183:84 Regulatory guidelines, pesticide water-sediment designs (table), 187:157

174

Index

REI (Restricted entry intervals), 186:114 Reproductive effects, paper production efﬂuent, 185:78 Reproductive impairment, PHCs, marine mammals, 184:9 Reproductive toxicity, PBDEs, 183: 81 Reptiles, geophagous (table), 183:120 Residential pesticide exposure duration, 186:123 Residue tolerances, pesticide foods, Uruguay, 181:119 Residue transferability (pesticide), to ﬁeld workers, 186:114 Resin acids (diterpenoid carboxylic acids), paper production, 185:85 Resmethrin, photooxidative rearrangement (diagram), 182:40 Respiration inhibition, cyanide higher plants, 183:37 Respiration rate, pesticide exposure, 186:122 Respiratory illness, enterovirus-related, 186:21 Restricted entry intervals (REI), 186:114 Rheumatoid arthritis, enterovirusrelated, 186:25 Rice husks, metal remediation, water, 188:68 Rice straw, metal remediation, water, 188:68 Rimsulfuron, adsorption coefﬁcient, 188:185, 189 Ringed seals, 184:5 Río Uruguay, pesticide contamination levels, 181:126 Risk assessment, contaminated soil, 186:73 ff. Risk assessment, ecological, earthworm biomarker, 188:85 ff. Risk assessment endpoints, enteric viral diseases, children, 186:38 Risk assessment, enteric viral infection, children, 186:33 Risk assessment, PBDEs, 183:87 Risk assessment, pesticides Europe, 187:1 ff.

Risk characterization, enteric viruses water/children, 186:38 Rivers, mercury contamination, Chile, 183:9 Rodent kills, cyanide, 183:35 Rodenticide chemical structures, miscellaneous, 182:152 Rotavirus, diarrhea cause, 186:4 Rotavirus gastroenteritis, incidence vs children age, 186:6 Rotavirus, greatest agents of infant gastroenteritis, 186:6 Rotavirus Group A, endemic worldwide, 186:6 Rotavirus Group B, adult diarrhea source, 186:6 Rotavirus, incidence by age, 186:25 Rotavirus, most common viral diarrhea pathogen, 186:4 Rotavirus prevalence, by country, 186:8 Rotavirus, waterborne enteric disease, children, 186:36 Roundup® herbicide, effects on frogs, 190:87 Ruthenium, in human nails, 185:161 Safe level, pesticide foliar residue, 186:115 Safety criteria, mercury hazard prevention, 181:178 Salicylic acid, adsorption coefﬁcient, 188:184 Santiago, Chile, atmospheric lead pollution, 185:100 Sawdust (wood), metal remediation, water, 188:72 Scientiﬁc names, dolphins (table), 184:12 Seafood, arsenic main dietary source, 184:115 Seals, harbour, epizootics, 184:2 Seasonal variation, children’s blood lead, 185:104 Seaweed, metal remediation, water, 188:72 Secondary sexual characteristics, paper production efﬂuent, 185:81 Sediment contamination, lead, Brazil, 184:74, 76

Index Sediment lead criteria, Canada, 184:75 Sediments, physical properties, 187:138 Segmented gonads, abnormalities, deﬁned, 187:124 Selenium, Chinese coal contamination, 189:98 Selenium, Chinese coal hazard, 189:98 Selenium, epidemic in China, 189:98 Selenium health effects, indoor coal burning, 189:89 ff. Selenium, in human nails, 185:161 Selenium, potential health effects, 188:63 Selenium, species in nature, 189:98 Selenosis, case photos China, 189:99 Sex reversal, amphibians, deﬁned, 187:106 Shell Chemical Co., cyclodiene insecticides S. America, 185:3 Shellﬁsh, pollutant levels S. America, 185:18 Sherwin Williams, paint lead contents, 185:98 Siberia, mercury contamination, 181:158 Silthiofam, water-sediment degradation proﬁle, 187:178 Silver, in human nails, 185:161 Simazine, abiotic degradation, 189:14 Simazine, agricultural management practices, 189:10 Simazine, air behavior, 189:13 Simazine, algicide, 189:1 Simazine, annual use volume, 189:1 Simazine, available formulations, 189:2 Simazine, biodegradation, 189:15 Simazine, chemical name, 189:1 Simazine, chemical structure, 189:3 Simazine, chemical synthesis method, 189:4 Simazine, chemodynamics, 189:4 Simazine, crustacean toxicity, 189:1 Simazine, degradation pathways, 189:8 Simazine, earthworm toxicity, 189:2 Simazine, groundwater contamination California, 189:5 Simazine herbicide, chemistry and fate, 189:1 ff. Simazine, hydrolysis, 189:14

175

Simazine, in rainfall, 189:13 Simazine, ionisable herbicide, 188:150, 156 Simazine metabolism, cytochrome P450 oxidation, 189:17 Simazine, mode of action, 189:4 Simazine, orchard management, 189:10 Simazine, oxidation, 189:14 Simazine, pesticide management practices, 189:10 Simazine, photolysis, 189:15 Simazine, physicochemical properties, 189:2 Simazine, precipitation, 189:13 Simazine, proprietary names, 189:2 Simazine, snail toxicity, 189:2 Simazine, soil behavior, 189:4 Simazine, soil half-life, 188:201 Simazine, soil half-lives, 189:3 Simazine, soil runoff characteristics, 189:9 Simazine, soil sorption, 189:4, 6 Simazine, sorption to organic matter, 189:7 Simazine, surface water contamination, 189:12 Simazine, toxicity to crustacean, 189:1 Simazine, toxicity to earthworms, 189:2 Simazine, water behavior, 189:11 Simazine, water quality criteria, 189:13 Singlet oxygen, reactions with pesticides (table), 182:88 Sink holes, groundwaster drawdown, 183:41 Sitosterol-β, reduced ﬁsh steroids, 185:76, 82 Smoking, effects nail/element studies, 185:150 Snails, simazine toxicity, 189:2 Sodium cyanide, bird mortality (table), 183:34 Sodium cyanide, use in gold mining, 183:21 Sodium, dietary need, geophagy, 183:116 Sodium hydroxide, pulp bleaching, 185:72 Soil adsorption, anion exchange, 188:170, 176

176

Index

Soil adsorption, bound residues, 188:174 Soil adsorption, cation (water) bridging, 188:173, 176 Soil adsorption, cation exchange, 188:171, 176 Soil adsorption, charge transfer, 188:171, 176 Soil adsorption coefﬁcients (Koc), pesticides (chart), 187:142 Soil adsorption, compound basicity, 188:177 Soil adsorption, hydrophobic sorption, 188:167 Soil adsorption, hydrophobicity, 188:177 Soil adsorption, ionic exchange, 188:170, 176 Soil adsorption, ionisable compounds, 188:160 Soil adsorption, ionisable pesticide behavior prediction, 188:175 Soil adsorption, ionisable pesticides, 188:149 ff. Soil adsorption, ligand exchange, 188:172, 176 Soil adsorption, mechanisms (table), 188:176 Soil adsorption mechanisms, 188:166 Soil adsorption, pH inﬂuence, 188:175, 180 Soil adsorption, van der Waals interactions, 188:168, 176 Soil clay inﬂuence on sorption, ionisable pesticides, 188:196 Soil components inﬂuence on sorption, ionisable pesticides, 188:193 Soil contaminants, realistic assessment, 188:108 Soil contamination, lead, Brazil, 184:70, 73 Soil, daily amount ingested (geophagy), 183:125 Soil, diet fraction (geophagy), 183: 124 Soil diffusion coefﬁcients, pesticides (table), 182:92 Soil, effect on element content human nails, 185:153

Soil, geophagous contaminant absorption, 183:126 Soil health assessment, soil microﬂora monitors, 188:127 ff. Soil health concept, 188:128 Soil health indicators, chemical/ physical properties, 188:135 Soil health indicators, microbial, 188:136 Soil health measurement, 188:130 Soil health, microbial activity, 188:139 Soil health, microbial functional stability, 188:140 Soil health monitoring, microﬂora, 188:127 ff. Soil health, pollutant impact, 188:141 Soil health/quality indicators (table), 188:131 Soil ingestion, by vertebrates (geophagy), 183:115 ff. Soil ingestion, daily estimates (geophagy), 183:124 Soil lead, 185:129 Soil levels, pollutants S. America, 185:9 Soil microbial biomass vs biodiversity, 188:137 Soil microﬂora, soil health assessment, 188:127 ff. Soil microorganisms, affect arsenic availability, 189:47 Soil microorganisms, arsenic toxicity, 189:59 Soil organic matter, affect arsenic availability, 189:47 Soil organic matter inﬂuence on sorption, ionisable pesticides, 188:194 Soil organic matter, solid description, 188:195 Soil organic matter, water-dissolved description, 188:195 Soil pH, affect arsenic availability, 189:47 Soil pH, ionisable compounds degradation, 188:198 Soil pH, measurement techniques, 188:152 Soil photolysis chamber (diagram), 182:33

Index Soil pollutants, earthworm behavior (diag.), 188:116 Soil properties, ionisable compounds adsorption, 188:162 Soil properties, pesticide photolysis on soil, 182:22 Soil quality, deﬁned, 188:129 Soil risk assessment, earthworm biomarkers, 188:85 ff. Soil sorption and degradation processes, linkage, 188:201 Soil sorption, measurement, 188:160 Soil surface models, pesticide photodegradation, 182:35 Soil surface structure (illus), 182:19 Soils, arsenic content, global, 184:101 SOM (soluble organic matter), sulfonamide sorption, 187:88 Songbird kills, cyanide, 183:33 Sorbent adsorption capacities, metal remediation, water, 188:71 Sorption and degradation processes, linkage, 188:201 South America, air pollutant levels, 185:9 South America, bird pollutant levels, 185:20 South America, contaminated sites as pollutant sources, 185:7 South America, ﬁsh pollutant levels, 185:19 South America, mercury contamination, 181:154 South America, persistent organic pollutants, 185:2 ff. South America, pollutant input, 185:2 South America, shellﬁsh pollutant levels, 185:18 South America, soil pollutant ranges, 185:10 South America, underrepresented in pollutant information, 185:2 South America, water pollutant levels, 185:13 Spatial trends, PHCs marine mammals, 184:29, 36 Speciation, deﬁned, 184:120 Speciation methods, arsenic, 184:122, 126

177

Species extinction & reduced biodiversity, pesticide effects, 187: 29 Spectral irradiance, photolysis studies light sources (diagram), 182:31 Spectral overlap, acceptor/donor (illus), 182:8 Sperm whales, 184:9 Spinosad, water-sediment degradation proﬁle, 187:205 Spinosyn, aerobic aquatic metabolism (diag.), 187:208 Spinosyn, chemical structures, 182: 156 Spirodiclofen, water-sediment degradation proﬁle, 187:199 Spiroxamine, water-sediment degradation proﬁle, 187:204 Spleen, children, immature marginal zone compartment, 186:2 Springtail bioassays, DDTcontaminated soils, 186:89 Springtails (Folsomia candida), zinc bioassay, 186:79 Springtails, copper bioassays, 186:86 Springtails, heavy metal bioassays, 186:83 Standardized test procedures, contaminated soils, 186:75 Stenella coeruleoalba (striped dolphin), epizootics, 184:2 Steroid effects, gonads ﬁsh/frogs, 187:111 Steroid-binding protein (SBP), paper production contaminants, 185: 81 Steroids, paper production efﬂuent effects, 185:78 Stockholm Convention on Persistent Organic Pollutants, 184:4 Stranded delphinoid PHC studies, 184:35 Stratiﬁcation, pesticide water-sediment studies, 187:213 Striped dolphins, epizootics, 184:2 Strobin analogues, fate in watersediment systems, 187:174 Study methods, contaminates marine mammals, 184:11

178

Index

Subdivision U (EPA), pesticide exposure monitoring history, 186:112 Sugar-beet pulp, metal remediation, water, 188:70, 72 Sugar-cane bagasse, metal remediation, water, 188:68, 72 Sugarcane, ethanol production, 189:31 Sulfabenzamide, physicochemical properties, 187:75 Sulfacetamide, physicochemical properties, 187:76 Sulfadiazine, physicochemical properties, 187:74 Sulfadimethoxine, physicochemical properties, 187:74 Sulfadimidine, physicochemical properties, 187:71 Sulfadoxine, physicochemical properties, 187:78 Sulfamerazine, physicochemical properties, 187:76 Sulfameter, physicochemical properties, 187:77 Sulfamethoxazole, physicochemical properties, 187:72 Sulfamethoxypyridazine, physicochemical properties, 187:75 Sulfanilamide, physicochemical properties, 187:73 Sulfapyridine, physicochemical properties, 187:72 Sulfentrazone, adsorption coefﬁcient, 188:193 Sulﬁte pulping, paper production, 185:71 Sulfometuron, adsorption coefﬁcient, 188:185 Sulfonamide antibiotics, average physicochemical properties, 187:78 Sulfonamide antibiotics, estimated usage, 187:69 Sulfonamide veterinary drugs, environmental contaminants, 187:67 ff. Sulfonamides, abiotic degradation, 187:80 Sulfonamides, biotransformation in mammals, 187:79

Sulfonamides, biphasic biotransformation, 187:79 Sulfonamides, DOM sorption, 187:88 Sulfonamides, environmental concentrations (table), 187:91 Sulfonamides, general chemical structure (illus.), 187:71 Sulfonamides, herbicide metabolites, 187:68 Sulfonamides, hydrolysis products, 187:84 Sulfonamides, in environment, 187:67 ff. Sulfonamides, in manure fertilizer, 187:69 Sulfonamides, photodegradation products, 187:80, 83 Sulfonamides, physicochemical properties (table), 187:71, 78 Sulfonamides, predicted environmental concentrations, 187:89 Sulfonamides, residues in ground/ surface waters, 187:86 Sulfonamides, residues in manure, 187:84 Sulfonamides, residues in soil, 187: 85 Sulfonamides, soil sorption, 187:87 Sulfonamides, SOM sorption, 187:88 Sulfonylurea chemical structures, 182:144 Sulfonylurea herbicides, fate in watersediment systems, 187:189 Sulfonylurea herbicides, ionisable, 188:150 Sulfosulfuron, water-sediment degradation proﬁle, 187:192 Sulfur cycle, organic matter role, 188:128 Sulfur dioxide, wastewater cyanide removal, 183:26 Sunlight intensity, pesticide photolysis, 181:10 Sunlight photodegradation, pesticides, 182:2 ff. Surface water contaminants, ionisable herbicides, 188:150 Surface water contamination, lead, Brazil, 184:74

Index Surface water contamination, simazine, 189:12 Surface water lead limits, Brazil, 184:75 Surfactant effects, pesticide photolysis, plants, 182:13 Sururu mytella falcata (mussel), lead content, Brazil, 184:64 Symptoms, pyrethroid-related illnesses, table 61 Synthetic pyrethroid illnesses, California, 186:57 ff. T-cell helper function, children deﬁcient, 186:2 Tadpole assays, polluted streams, 185:55 Tantalum, in human nails, 185:162 Tapwater intake by age, 186:32 TCPM, tris(4-chlorophenyl)methane, 184:3 TCPMe, tris(4-chlorophenyl)methanol, 184:3 Tebufenozide, water-sediment degradation proﬁle, 187:201 Tebupirimfos, water-sediment degradation proﬁle, 187:167 Teﬂon sheets, pesticide photodegradation studies, 182:44 Temporal trends, PHCs marine mammals, 184:34, 36 Tepraloxydim, water-sediment degradation proﬁle, 187:204 TEQ (toxicity equivalent) emissions, S. America, 185:6 Teratogenicity, PBDEs, 183:81 Terbutryn, adsorption coefﬁcient, 188:186, 190 Terbutryn, ionisable herbicide, 188:158 Terbutryn, water-sediment degradation proﬁle, 187:197 Terminology, gonadal abnormalities, 187:117 Terrestrial birds, geophagous (table), 183:121 Terrestrial ﬂora, cyanide effects, 183:36 Terrestrial mammals, geophagous (table), 183:118 Terrestrial reptiles, geophagous (table), 183:120

179

Test earthworm, described, 188:109 Test exposure conditions, earthworm biomarkers, 188:111 Testicular dysgenesis, deﬁned, 187: 106 Testicular oocytes, deﬁned, 187:107, 109, 122 Testicular oogenesis, deﬁned, 187:107 Testis-ova, deﬁned, 187:107 Testosterone effects, gonads ﬁsh/frogs, 187:112 Testosterone-binding, paper production efﬂuent, 185:81 Tetrabromophenoxyanisoles, chemical structures, 188:24 Tetraethyl lead, air contamination, Brazil, 184:67 Tetraethyl lead exposure, lead in urine indicator, 184:90 Tetraethyl lead, gasoline content Mexico, 181:42 Theoretical upper-bound estimate (TUBE), pesticide exposure, 186:119 Thermomechanical pulping, paper production, 185:71 Thiabendazole, water-sediment degradation proﬁle, 187:203 Thiacloprid, aerobic aquatic metabolism (diag.), 187:207 Thiacloprid, water-sediment degradation proﬁle, 187:201 Thiamethoxam, water-sediment degradation proﬁle, 187:202 Thifensulfuron-methyl, water-sediment degradation proﬁle, 187:191 Thiobencarb, water-sediment degradation proﬁle, 187:187 Thiourea, cyanide substitute leaching method, 183:39 Thyroid hormone reduction, PHCs marine mammals, 184:10 Tilapia rendalis, lead contamination, Brazil, 184:64 Tissue residues, insecticides, S. America, 185:21, 25 TNT, earthworm avoidance, 188:99 Toenails, biomarker trace element exposure, 185:141, 148

180

Index

Tolclofos-methyl, water-sediment degradation proﬁle, 187:166 Toothed whales, organohalogen contaminants, 184:2 Total suspended solids (TSS), paper production, 185:74 Toxaphene, marine mammals, 184:4 Toxaphene, use in S. America, 185:4 Toxicity bioassays, Reconquista River, 185:53 Toxicity equivalence, incinerator exhaust, 190:29 Toxicity equivalent (TEQ) emissions, S. America, 185:6 Toxicity, PFOS, animals & plants, 186:143 ff. TOXSWA, pesticide water-sediment lab studies model, 187:161 Trace element dispersal, coal burning, 189:90 Trace element exposure, human nail biomarkers, 185:141 ff. Trace elements, coal, 189:91 Trace elements, human nails, 185: 161 Trace metals, downstream mining, 183:24 Tralomethrin, microcosm degradation proﬁle, 187:218 Transfer coefﬁcient (pesticides), to ﬁeld workers, 186:114 Transferable turf residue, pesticide, 186:118 TRIAD system, sediment quality, described, 186:96 Triasulfuron, water-sediment degradation proﬁle, 187:191 Triazine chemical structures, 182:151 Triazine herbicide photodegradation, on glass, 182:45 Triazine herbicide photodegradation, on soils, 182:67 Triazine herbicides, 189:2 Triazine herbicides, fate in watersediment systems, 187:195, 198 Triazine herbicides, ionisable, 188:150 Triazines, adsorption coefﬁcient, 188:190

Triazinones, adsorption coefﬁcient, 188:190 Tribufos, water-sediment degradation proﬁle, 187:168 Triclopyr, adsorption coefﬁcient, 188:188, 192 Triclopyr, ionisable herbicide, 188:160 Triclopyr, microcosm degradation proﬁle, 187:216 Triﬂoxystrobin, water-sediment degradation proﬁle, 187:175 Triﬂoxysulfuron sodium, watersediment degradation proﬁle, 187: 192 Triﬂuralin, microcosm degradation proﬁle, 187:219 Triﬂuralin, photooxidative dealkylation, 181:14 Triﬂuralin, water-sediment degradation proﬁle, 187:201 Trinexapac-ethyl, water-sediment degradation proﬁle, 187:199 Tropospheric oxidation, kinetics, 181: 17 Tropospheric pesticide residues, sources, 181:4 Tropospheric pesticides, fate processes, 181:8 Tropospheric photooxidation, principles, 181:15 Tropospheric transport of pesticides, 181:1 ff. TSS (total suspended solids), paper production, 185:74 TUBE (theoretical upper-bound estimate), pesticide exposure, 186: 119 Tungsten, in human nails, 185:162 Turf, transferable pesticide residue, 186:118 Tursiops truncatus (bottlenose dolphin), epizootics, 184:2 Two-chamber test system, earthworm avoidance, 188:97 Type I pyrethroids, described, 186:57 Type II pyrethroids, described, 186:57 Tyrian purple, marine mollusk source, 188:42

Index U3, identical to Q1, 188:18 Underground water contamination, lead, Brazil, 184:70, 73 United States, mercury contamination, 181:159 Urea chemical structures, 182:140 Urea herbicide photodegradation, in solvents, 182:55 Urea herbicide photodegradation, on glass, 182:44 Urea herbicide photodegradation, on plants, 182:75 Urea herbicide photodegradation, on soils, 182:66 Urea herbicides, fate in water-sediment systems, 187:189 Urine delta aminolevulinic acid, lead exposure indicator, 185:101 Urine, tetraethyl lead, human exposure indicator, 184:90 Uruguay, map, 181:112 Uruguay, pesticide regulations, 181:113 Uruguay, pesticide usage, 181:111 ff. UV absorption proﬁles, pesticides, 182: 3 UV-B radiation, glass absorption, 182:10, 14 Vapor pressure vs water solubility, pesticides, 181:9 Vat leaching (gold), using cyanide, 183: 23 Vertebrate soil ingestion (geophagy), 183:115 ff. Veterinary antibiotics, worldwide total usage, 187:67 Veterinary drug occurrence, different environments (illus.), 187:70 Veterinary drugs, sulfonamides in the environment, 187:67 ff. Vinylethylene (butadiene), 189:132 Viral diarrhea, causal organisms, 186:4 Viral protein 4, children’s inability to cleave virulent strain, 186:5 VOCs (volatile organic compounds), paper production, 185:73 Volatile organic compounds (VOCs), paper production, 185:73

181

Waste incineration, dioxin formation mechanisms, 190:31 Waste incineration, dioxin production, 190:1 ff. Wastewater cyanide removal, alkaline chlorination, 183:26 Water, arsenic content, global, 184:101 Water hyacinth, cyanide removal technology, 183:38 Water intake by age, 186:32 Water quality chemical indexes, Reconquista River, 185:48 Water quality criteria, heavy metals (taable), 188:64 Water quality criteria, simazine, 189: 13 Water/sediment cyanide levels, downstream mining, 183:24 Water/sediment trace metals, downstream mining, 183:24 Water temperature, mercury effects, 181:171 Water-sediment pesticide degradation processes, 187:145 Water-sediment, pesticide kinetic analysis, 187:159 Water-sediment pesticide lab studies, designs (table), 187:157 Water-sediment systems, pesticide behavior, 187:133 ff. Waterborne enteric viral diseases, children, 186:35 Waxes, fruit/leaf composition (table), 182:89 Weight-of-evidence (WOE), ecotoxicological term, 188:86 Whale halogenated contaminates, study methods, 184:11 Whales, organochlorine contaminants, 184:1 ff. Wheat bran, metal remediation, water, 188:72 WHO pesticide toxicity categories, 181:114 WHO recommended value, arsenic drinking water, 184:101 Whole-body dosimetry, pesticides, 186:113

182

Index

Wildlife effect, water reduction & riparian habitat, 183:44 Wildlife mortality, cyanide/gold leaching, 183:25 Wildlife protection, cyanide, 183:32, 37 WOE (weight-of-evidence), ecotoxicological term, 188:86 Wood bark, metal remediation, water, 188:73 Wood/leaves incineration, dioxin formation, 190:9,24 Wood processing methods, paper production, 185:70 Worker reentry exposure database, 186:116 Worst case, pesticide exposure, 186:120 Yttrium, in human nails, 185:161 Zalophus californianus (California sea lion), 184:10 Zeolite, metal remediation, water, 188:73 Zinc, aquatic environment hazard, 188:62

Zinc chloride, earthworm response, 188:91 Zinc content, Reconquista River, 185:46 Zinc, earthworm biomarkers, 188: 87 Zinc, in human nails, 185:161 Zinc protoporphyrine (ZPP), blood lead measure, 185:111 Zinc-contaminated soils, risk assessment, 186:77 Zinc-contaminated soils, screening levels, 186:78 Zinc-contaminated soils, The Netherlands, 186:78 Zinc-contaminated soils, United Kingdom, 186:81 Zooplankton, Reconquista River, 185:51 Zoxamide, water-sediment degradation proﬁle, 187:178 ZPP (zinc protoporphyrine), blood lead measure, 185:111 Zwitterionic compounds, adsorption coefﬁcient, 188:191

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