Prepared as part of the National Water-Quality Assessment Program, Source Water-Quality Assessment
Abstract
Source water, herein defined as stream water collected at a water-system intake prior to water treatment, was sampled at nine community water systems, ranging in size from a system serving about 3,000 people to one that serves about 2 million people. As many as 17 source-water samples were collected at each site over about a 12-month period between 2002 and 2004 for analysis of 258 anthropogenic organic compounds. Most of these compounds are unregulated in drinking water, and the compounds analyzed include pesticides and selected pesticide degradates, gasoline hydrocarbons, personal-care and domestic-use compounds, and solvents. The laboratory analytical methods used in this study have relatively low detection levels—commonly 100 to 1,000 times lower than State and Federal standards and guidelines for protecting water quality. Detections, therefore, do not necessarily indicate a concern to human health but rather help to identify emerging issues and to track changes in occurrence and concentrations over time.
About one-half (134) of the compounds were detected at least once in source-water samples. Forty-seven compounds were detected commonly (in 10 percent or more of the samples), and six compounds (chloroform, atrazine, simazine, metolachlor, deethylatrazine, and hexahydrohexamethylcyclopentabenzopyran (HHCB) were detected in more than one-half of the samples. Chloroform was the most commonly detected compound—in every sample (year round) at five sites. Findings for chloroform and the fragrances HHCB and acetyl hexamethyl tetrahydronaphthalene (AHTN) indicate an association between occurrence and the presence of large upstream wastewater discharges in the watersheds. The herbicides atrazine, simazine, and metolachlor also were among the most commonly detected compounds. Degradates of these herbicides, as well as those of a few other commonly occurring herbicides, generally were detected at concentrations similar to or greater than concentrations of the parent compound. Samples typically contained mixtures of two or more compounds. The total number of compounds and their total concentration in samples generally increased with the amount of urban and agricultural land use in a watershed.
Annual mean concentrations of all compounds were less than human-health benchmarks. Single-sample concentrations of anthropogenic organic compounds in source water generally were less than 0.1 microgram per liter and less than established human-health benchmarks. Human-health benchmarks used for comparison were U.S. Environmental Protection Agency (USEPA) Maximum Contaminant Levels (MCLs) for regulated compounds and U.S. Geological Survey Health-Based Screening Levels for unregulated compounds. About one-half of all detected compounds do not have human-health benchmarks or adequate toxicity information for evaluating results in a human-health context.
During a second sampling phase (2004–05), source water and finished water (water that has passed through all the treatment processes but prior to distribution) were sampled at eight of the nine community water systems. Water-treatment processes differ among the systems. Specifically, treatment at five of the systems is conventional, typically including steps of coagulation, flocculation, sedimentation, filtration, and disinfection. One water system uses slow sand filtration and disinfection, a second system uses ozone as a preliminary treatment step to conventional treatment, and a third system is a direct filtration treatment plant that uses many of the steps employed in conventional treatment. Most of these treatment steps are not designed specifically to remove the compounds monitored in this study.
About two-thirds of the compounds detected commonly in source water were detected at similar frequencies in finished water. Although the water-treatment steps differ somewhat among the eight water systems, the amount of change in concentration of the compounds from source- to finished-water samples generally did not differ systematically at one or among the water systems for compounds with similar detection frequencies in source and finished water. Additionally, changes in concentration over time in source water of some compounds, for example seasonal changes in atrazine concentrations, usually were reflected in the associated finished water.
Some compounds detected in source water were removed or transformed during treatment and, therefore, were not detected in finished water. These included aromatic hydrocarbons with one or more methyl groups, 3,4-dichloroaniline (diuron degradate), the organophosphate insecticides (diazinon and malathion), and fipronil. On the basis of results for matrix spikes, decreases in concentration of these compounds or nondetections in finished water likely were due to degradation or transformation as a result of chlorine disinfection.
The annual mean concentration of all compounds detected in finished water were less than established human-health benchmarks, and concentrations of most compounds were several orders of magnitude less than human-health benchmarks. With the exception of one detection of atrazine at one site, maximum measured concentrations of all commonly detected compounds in finished water were less than established human-health benchmarks. The annual mean concentration of atrazine at this site was 0.72 microgram per liter, which is less than the MCL of 3 micrograms per liter. Most source- and finished-water samples contained mixtures of 2 or more compounds, and more than one-half of both source- and finished-water samples contained mixtures of 14 or more compounds. Degradates of commonly detected herbicides often were present at a concentration similar to or greater than of that the parent compound in both source and finished water and contributed to the number of compounds detected in mixtures.
For additional information contact:
Director, USGS South Dakota Water Science Center
U.S. Geological Survey
1608 Mt. View Rd.
Rapid City, SD 57702
(605) 394–3200
World Wide Web: http://sd.water.usgs.gov
ToxSci Advance Access originally published online on October 21, 2008
Toxicological Sciences 2009 107(1):56-64; doi:10.1093/toxsci/kfn225
Published by Oxford University Press 2008.
* Department of Molecular Biomedical Sciences, North Carolina State University, College of Veterinary Medicine, Raleigh, North Carolina 27606 † Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development ‡ Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development § National Center for Computational Toxicology, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711
1 To whom correspondence should be addressed at MD-72, Endocrinology Branch, Reproductive Toxicology Division, NHEERL, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711. Fax: (919) 541-5138. E-mail: stoker.tammy{at}epa.gov.
Received August 27, 2008; accepted October 15, 2008
Triclosan (5-chloro-2-(2,4-dichlorophenoxy)phenol) is a potentantibacterial and antifungal compound that is widely used inpersonal care products, plastics, and fabrics. Recently triclosanhas been shown to alter endocrine function in a variety of species.The purpose of this study was to determine effects of triclosanon pubertal development and thyroid hormone concentrations inthe male rat. Weanling rats were exposed to 0, 3, 30, 100, 200,or 300 mg/kg of triclosan by oral gavage from postnatal day(PND) 23 to 53. Preputial separation (PPS) was examined beginningon PND 33. Rats were killed on PND 53, organ weights were recordedand serum was collected for subsequent analysis. Triclosan didnot affect growth or the onset of PPS. Serum testosterone wassignificantly decreased at 200 mg/kg, however no effects wereobserved on androgen-dependent reproductive tissue weights.Triclosan significantly decreased total serum thyroxine (T4)in a dose-dependent manner at 30 mg/kg and higher (no observedeffect level of 3 mg/kg). Triiodothyronine (T3) was significantlydecreased only at 200 mg/kg, but thyroid stimulating hormonewas not statistically different at any dose. Liver weights weresignificantly increased at 100 mg/kg triclosan and above suggestingthat the induction of hepatic enzymes may have contributed tothe altered T4 and T3 concentrations, but it does not appearto correlate with the T4 dose-response. This study demonstratesthat triclosan exposure does not alter androgen-dependent tissueweights or onset of PPS; however, triclosan exposure significantlyimpacts thyroid hormone concentrations in the male juvenilerat.
Key Words: triclosan; puberty; thyroid hormone.
Disclaimer: The research described in this article has beenreviewed by the National Health and Environmental Effects ResearchLaboratory, U.S. Environmental Protection Agency and approvedfor publication. Approval does not signify that the contentsnecessarily reflect the views and policies of the Agency, nordoes mention of trade names or commercial products constituteendorsement or recommendation for use.
Online ISSN 1096-0929 - Print ISSN 1096-6080 Copyright © 2008 Society of ToxicologyGeoffrey M. Calvert, MD, MPH,1* Jennifer Karnik, MPH,1 Louise Mehler, PHD, MD,2 John Beckman, BS,3 Barbara Morrissey, MS,4 Jennifer Sievert, BA,5 Rosanna Barrett, MPH,6 Michelle Lackovic, MPH,7 Laura Mabee, BA,8 Abby Schwartz, MPH,9 Yvette Mitchell, MS,10 and Stephanie Moraga-McHaley, MS11
Background Approximately 75% of pesticide usage in the United States occurs in agriculture. As such, agricultural workers are at greater risk of pesticide exposure than non-agricultural workers. However, the magnitude, characteristics and trend of acute pesticide poisoning among agricultural workers are unknown.
Methods We identified acute pesticide poisoning cases in agricultural workers between the ages of 15 and 64 years that occurred from 1998 to 2005. The California Department of Pesticide Regulation and the SENSOR-Pesticides program provided the cases. Acute occupational pesticide poisoning incidence rates (IR) for those employed in agriculture were calculated, as were incidence rate ratios (IRR) among agricultural workers relative to non- agricultural workers.
Results Of the 3,271 cases included in the analysis, 2,334 (71%) were employed as farmworkers. The remaining cases were employed as processing/packing plant workers (12%), farmers (3%), and other miscellaneous agricultural workers (19%). The majority of cases had low severity illness (N 1/4 2,848, 87%), while 402 (12%) were of medium severity and 20 (0.6%) were of high severity. One case was fatal. Rates of illness among various agricultural worker categories were highly variable but all, except farmers, showed risk for agricultural workers greater than risk for non-agricultural workers by an order of magnitude or more. Also, the rate among female agricultural workers was almost twofold higher compared to males.
Conclusion The findings from this study suggest that acute pesticide poisoning in the agricultural industry continues to be an important problem. These findings reinforce the need for heightened efforts to better protect farmworkers from pesticide exposure. Am. J. Ind. Med. 51:883–898, 2008. Published 2008 Wiley-Liss, Inc.†
KEY WORDS: pesticides; surveillance; poisoning; agriculture; farmworkers
1 Division of Surveillance, Hazard Evaluations and Field Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Cincinnati, Ohio
2 Department of Pesticide Regulation, California Environmental Protection Agency, Sacramento, California
3 Public Health Institute, Oakland, California
4 Office of Environmental Assessments,Washington State Department of Health, Olympia, Washington
5 Environmental and Injury Epidemiology and Toxicology Branch, Texas Department of State Health Services, Austin,Texas
6 Florida Department of Health,Tallahassee, Florida
7 Louisiana Department of Health and Hospitals, New Orleans, Louisiana
8 Office of Environmental Public Health, Oregon Department of Human Services, Portland, Oregon
9 Division of Environmental Health, Michigan Department of Community Health, Lansing, Michigan
10 Bureau of Occupational Health, New York State Department of Health,Troy, New York
11 New Mexico Occupational Health Registry, University of New Mexico, Albuquerque, New Mexico
The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the National Institute for Occupational Safety and Health or each author's state agency.
*Correspondence to: Geoffrey M. Calvert, National Institute for Occupational Safety and Health, 4676 Columbia Parkway, R-17, Cincinnati, OH 45226. E-mail: jac6@cdc.gov Accepted 23 June 2008
DOI 10.1002/ajim.20623. Published online in Wiley InterScience
(www.interscience.wiley.com)
Published 2008 Wiley-Liss, Inc.
†This article is a US Government work and, as such, is in
the public domain in the United States of America.
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TAISEN IGUCHI AND YOSHINAO KATSU
Several nuclear receptors have recently been identified as mediators of endocrine disruption as well as steroid hormone receptors. The ubiquitous environmental contaminant tributyltin chloride (TBT) is a ligand for retinoid X receptor (RXR) in rock shell at the nanomolar level, and it acts as a ligand for both the RXR and the peroxisome proliferator-activated receptor γ in the frog Xenopus laevis and in humans. TBT, which induces imposex in marine snails and promotes adipogenesis in X. laevis and in mice, is an example of an environmental endocrine disrupter that promotes adverse effects, from the snail to mammals, through common signaling. In addition, juvenile hormone agonists used as pesticides showed endocrine- disruptive effects on parthenogenic Daphnia magna, lowering rates of reproduction, and inducing 100% male offspring. In this article, we focus on commonality in signaling through nuclear receptors and newly found endocrine disruption in D. magna.
Keywords: endocrine-disrupting chemicals, environmental estrogens, organotins, adipogenesis, nuclear receptors
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Department of Nutrition, Harvard School of Public Health, Boston, MA, USA. aascheri@hsph.harvard.edu
OBJECTIVE: Chronic, low-dose exposure to pesticides is suspected to increase the risk for Parkinson's disease (PD), but data are inconclusive. METHODS: We prospectively examined whether individuals exposed to pesticides have higher risk for PD than those not exposed. The study population comprised participants in the Cancer Prevention Study II Nutrition Cohort, a longitudinal investigation of US men and women initiated in 1992 by the American Cancer Society. Follow-up surveys were conducted in 1997, 1999, and 2001. The 143,325 individuals who returned the 2001 survey and did not have a diagnosis or symptoms of PD at baseline (1992) were included in the analyses. RESULTS: Exposure to pesticides was reported by 7,864 participants (5.7%), including 1,956 farmers, ranchers, or fishermen. Individuals exposed to pesticides had a 70% higher incidence of PD than those not exposed (adjusted relative risk, 1.7; 95% confidence interval, 1.2-2.3; p = 0.002). The relative risk for pesticide exposure was similar in farmers and nonfarmers. No relation was found between risk for PD and exposure to asbestos, chemical/acids/solvents, coal or stone dust, or eight other occupational exposures. INTERPRETATION: These data support the hypothesis that exposure to pesticides may increase risk for PD. Future studies should seek to identify the specific chemicals responsible for this association.
PMID: 16802290 [PubMed - indexed for MEDLINE]
Originally published In Press as doi:10.1074/jbc.M802210200 on September 25, 2008
J. Biol. Chem., Vol. 283, Issue 50, 34696-34703, December 12, 2008
From the Departments of ‡Neurology, §Psychiatry, and ||Neurobiology, University of California at Los Angeles David Geffen School of Medicine and the **Greater Los Angeles Veterans Administration Medical Center, Los Angeles, California 90095, and ¶Environmental Chemistry and Toxicology Laboratory, Department of Environmental Science, Policy and Management, University of California, Berkeley, California 94720-3112
The etiology of Parkinson disease (PD) is unclear but may involve environmental toxins such as pesticides leading to dysfunction of the ubiquitin proteasome system (UPS). Here, we measured the relative toxicity of ziram (a UPS inhibitor) and analogs to dopaminergic neurons and examined the mechanism of cell death. UPS (26 S) activity was measured in cell lines after exposure to ziram and related compounds. Dimethyl- and diethyldithiocarbamates including ziram were potent UPS inhibitors. Primary ventral mesencephalic cultures were exposed to ziram, and cell toxicity was assessed by staining for tyrosine hydroxylase (TH) and NeuN antigen. Ziram caused a preferential damage to TH+ neurons and elevated α-synuclein levels but did not increase aggregate formation. Mechanistically, ziram altered UPS function through interfering with the targeting of substrates by inhibiting ubiquitin E1 ligase. Sodium dimethyldithiocarbamate administered to mice for 2 weeks resulted in persistent motor deficits and a mild reduction in striatal TH staining but no nigral cell loss. These results demonstrate that ziram causes selective dopaminergic cell damage in vitro by inhibiting an important degradative pathway implicated in the etiology of PD. Chronic exposure to widely used dithiocarbamate fungicides may contribute to the development of PD, and elucidation of its mechanism would identify a new potential therapeutic target.
Received for publication, March 20, 2008, and in revised form, September 24, 2008.
* This work was supported, in whole or in part, by National Institutes of Health Grant 5 U54 ESO12078. This work was also supported by Veterans Administration Grant SW PADRREC, the National Institutes of Health Medical Scientist Training Program (to A. P. C.), a postdoctoral fellowship from the Swedish Research Council (to R. K.), and funds from the Michael J. Fox Foundation (to F. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed: Dept. of Neurology, UCLA School of Medicine, Reed Neurological Research Center, 710 Westwood Plaza, Los Angeles, CA 90095. Fax: 310-206-9819; E-mail: jbronste@ucla.edu
Full text available from jbc.org.
Ecological Applications, 18(7), 2008, pp. 1728-1742
© 2008 by the Ecological Society of America
RICK A. RELYEA1 AND NICOLE DIECKS
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15260 USA
Abstract. The field of toxicology has traditionally assessed the risk of contaminants by using laboratory experiments and a range of pesticide concentrations that are held constant for short periods of time (1-4 days). From these experiments, one can estimate the concentration that causes no effect on survival. However, organisms in nature frequently experience multiple applications of pesticides over time rather than a single constant concentration. In addition, organisms are embedded in ecological communities that can propagate indirect effects through a food web. Using outdoor mesocosms, we examined how low concentrations (10-250 lg/L) of a globally common insecticide (malathion) applied at various amounts, times, and frequencies affected aquatic communities containing zooplankton, phytoplankton, periphyton, and larval amphibians (reared at two densities) for 79 days. All application regimes caused a decline in zooplankton, which initiated a trophic cascade in which there was a bloom in phytoplankton and, in several treatments, a subsequent decline in the competing periphyton. The reduced periphyton had little effect on wood frogs (Rana sylvatica), which have a short time to metamorphosis. However, leopard frogs (Rana pipiens) have a longer time to metamorphosis, and they experienced large reductions in growth and development, which led to subsequent mortality as the environment dried. Hence, malathion (which rapidly breaks down) did not directly kill amphibians, but initiated a trophic cascade that indirectly resulted in substantial amphibian mortality. Importantly, repeated applications of the lowest concentration ( a R'R'press treatmentR^R^ consisting of seven weekly applications of 10 lg/L) caused larger impacts on many of the response variables than single R'R'pulseR^R^ applications that were 25 times as great in concentration. These results are not only important because malathion is the most commonly applied insecticide and is found in wetlands, but also because the mechanism underlying the trophic cascade is common to a wide range of insecticides, offering the possibility of general predictions for the way in which many insecticides impact aquatic communities and the populations of larval amphibians.
Key words: acetylcholine esterase inhibitor; amphibian decline; ecotoxicology; leopard frog (Rana pipiens); pesticide pulse; wood frog (Rana sylvatica).
1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD
2 Fred Hutchinson Cancer Research Center and University of Washington, Seattle, WA
3 National Institute for Occupational Safety and Health, Cincinnati, OH
Correspondence to Claudine M. Samanic, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, Room 8003, Rockville, MD 20852 (e-mail: samanicc{at}mail.nih.gov
The authors examined incident glioma and meningioma risk associated with occupational exposure to insecticides and herbicides in a hospital-based, case-control study of brain cancer. Cases were 462 glioma and 195 meningioma patients diagnosed between 1994 and 1998 in three US hospitals. Controls were 765 patients admitted to the same hospitals for nonmalignant conditions. Occupational histories were collected during personal interviews. Exposure to pesticides was estimated by use of a questionnaire, combined with pesticide measurement data abstracted from published sources. Using logistic regression models, the authors found no association between insecticide and herbicide exposures and risk for glioma and meningioma. There was no association between glioma and exposure to insecticides or herbicides, in men or women. Women who reported ever using herbicides had a significantly increased risk for meningioma compared with women who never used herbicides (odds ratio = 2.4, 95% confidence interval: 1.4, 4.3), and there were significant trends of increasing risk with increasing years of herbicide exposure (p = 0.01) and increasing cumulative exposure (p = 0.01). There was no association between meningioma and herbicide or insecticide exposure among men. These findings highlight the need to go beyond job title to elucidate potential carcinogenic exposures within different occupations.
central nervous system neoplasms; incidence; pesticides; United States
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Published Online: 11 Jul 2008
Copyright © 2008 Wiley-Liss, Inc., A Wiley Company
Mikael Eriksson 1 *, Lennart Hardell 2, Michael Carlberg 2, Måns Åkerman 3
1Department of Oncology, University Hospital, Lund, Sweden
2Department of Oncology, University Hospital, Örebro, Sweden
3Department of Pathology, University Hospital, Lund, Sweden
email: Mikael Eriksson (mikael.eriksson@med.lu.se)
*Correspondence to Mikael Eriksson, Department of Oncology, University Hospital, SE-221 85 Lund, Sweden
Funded by:
• FAS; Grant Number: 2001-0224
• Cancer-och Allergifonden
• Nyckelfonden
• Örebro University Hospital Cancer Fund
phenoxyacetic acids • MCPA • glyphosate • insecticides • impreganting agents • non-Hodgkin lymphoma
We report a population based case-control study of exposure to pesticides as risk factor for non-Hodgkin lymphoma (NHL). Male and female subjects aged 18-74 years living in Sweden were included during December 1, 1999, to April 30, 2002. Controls were selected from the national population registry. Exposure to different agents was assessed by questionnaire. In total 910 (91 %) cases and 1016 (92%) controls participated. Exposure to herbicides gave odds ratio (OR) 1.72, 95% confidence interval (CI) 1.18-2.51. Regarding phenoxyacetic acids highest risk was calculated for MCPA; OR 2.81, 95% CI 1.27-6.22, all these cases had a latency period >10 years. Exposure to glyphosate gave OR 2.02, 95% CI 1.10-3.71 and with >10 years latency period OR 2.26, 95% CI 1.16-4.40. Insecticides overall gave OR 1.28, 95% CI 0.96-1.72 and impregnating agents OR 1.57, 95% CI 1.07-2.30. Results are also presented for different entities of NHL. In conclusion our study confirmed an association between exposure to phenoxyacetic acids and NHL and the association with glyphosate was considerably strengthened. © 2008 Wiley-Liss, Inc.
Received: 4 November 2007; Accepted: 20 February 2008
Digital Object Identifier (DOI)
10.1002/ijc.23589 About DOI
Front Biosci. 2008 Jan 1;13:1240-9. Links
Costa LG, Giordano G, Guizzetti M, Vitalone A.
Dept. of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105, USA. lgcosta@u.washington.edu
Pesticides are substances widely used to control unwanted pests such as insects, weeds, fungi and rodents. Most pesticides are not highly selective, and are also toxic to nontarget species, including humans. A number of pesticides can cause neurotoxicity. Insecticides, which kill insects by targeting their nervous system, have neurotoxic effect in mammals as well. This family of chemicals comprises the organophosphates, the carbamates, the pyrethroids, the organochlorines, and other compounds. Insecticides interfere with chemical neurotransmission or ion channels, and usually cause reversible neurotoxic effects, that could nevertheless be lethal. Some herbicides and fungicides have also been shown to possess neurotoxic properties. The effects of pesticides on the nervous system may be involved in their acute toxicity, as in case of most insecticides, or may contribute to chronic neurodegenerative disorders, most notably Parkinson's disease. This brief review highlights some of the main neurotoxic pesticides, their effects, and mechanisms of action.
PMID: 17981626 [PubMed - indexed for MEDLINE]
Related ArticlesMechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. [Toxicology. 2002] Risk assessment of neurotoxic pesticides. [Acta Physiol Hung. 2000] Effects of pyrethroids on voltage-sensitive calcium channels: a critical evaluation of strengths, weaknesses, data needs, and relationship to assessment of cumulative neurotoxicity. [Toxicol Appl Pharmacol. 2004] Microbiological and biotechnological aspects of metabolism of carbamates and organophosphates. [Crit Rev Biotechnol. 1992] Pesticides and the soil fauna.
Krista A. McCoy,1,2 Lauriel J. Bortnick,2 Chelsey M. Campbell,2 Heather J. Hamlin,2 Louis J. Guillette Jr.,1,2and Colette M. St. Mary1,2
1School of Natural Resources and Environment, and 2Department of Zoology, University of Florida, Gainesville, Florida, USA
BACKGROUND: Many agricultural contaminants disrupt endocrine systems of wildlife. However,evidence of endocrine disruption in wild amphibians living in agricultural areas has been controversial. Typically, studies on the effects of pollutants on wildlife attempt to compare polluted withunpolluted sites.
OBJECTIVES: We took a novel approach to address this question by explicitly quantifying the rela-tionship between gonadal abnormalities and habitats characterized by differing degrees of agricultural activity.
METHODS: We quantified the occurrence of gonadal abnormalities and measures of gonadal func-tion in at least 20 giant toads ( Bufo marinus) from each of five sites that occur along a gradient of increasing agricultural land use from 0 to 97%.
RESULTS: The number of abnormalities and frequency of intersex gonads increased with agriculturein a dose-dependent fashion. These gonadal abnormalities were associated with altered gonadal function. Testosterone, but not 17 ß-estradiol, concentrations were altered and secondary sexualtraits were either feminized (increased skin mottling) or demasculinized (reduced forearm width and nuptial pad number) in intersex toads. Based on the end points we examined, female morphol-ogy and physiology did not differ across sites. However, males from agricultural areas had hormone concentrations and secondary sexual traits that were intermediate between intersex toads and non-agricultural male toads. Skin coloration at the most agricultural site was not sexually dimorphic; males had female coloration.
CONCLUSIONS: Steroid hormone concentrations and secondary sexual traits correlate with repro-ductive activity and success, so affected toads likely have reduced reproductive success. These reproductive abnormalities could certainly contribute to amphibian population declines occurring inareas exposed to agricultural contaminants.
KEY WORDS: amphibians, endocrine disruption, intersex, pesticides, secondary sexual traits.Environ Health Perspect 116:1526-1532 (2008). doi:10.1289/ehp.11536 available via http://dx.doi.org/ [Online 3 July 2008]
Click here to read the full article.
Sharon K. Sagiv,1 J. Kevin Nugent,2,3 T. Berry Brazelton,2 Anna L. Choi,1 Paige E. Tolbert,4 Larisa M. Altshul,1 and Susan A. Korrick 1,5
BACKGROUND: Previous literature suggests an association between organochlorines and behavioral measures in childhood, including inattention. OBJECTIVE: This study was designed to assess whether prenatal organochlorine exposure is associated with measures of attention in early infancy.
METHODS: We investigated an association between cord serum polychlorinated biphenyls (PCBs) and p,p´-dichlorodiphenyl dichloroethene (DDE) levels and measures of attention from the Neonatal Behavioral Assessment Scale (NBAS) in a cohort of 788 infants born 1993–1998 to mothers residing near a PCB-contaminated harbor and Superfund site in New Bedford, Massachusetts.
RESULTS: Medians (ranges) for the sum of four prevalent PCB congeners and DDE levels were 0.19 (0.01–4.41) and 0.30 (0–10.29) ng/g serum, respectively. For the 542 subjects with an NBAS exam at 2 weeks, we observed consistent inverse associations between cord serum PCB and DDE levels and NBAS measures of alertness, quality of alert responsiveness, cost of attention, and other potential attention-associated measures including self-quieting and motor maturity. For example, the decrement in quality of alert responsiveness score was –0.51 (95% confidence interval, –0.99 to –0.03) for the highest quartile of exposure to the sum of four prevalent PCB congeners compared with the lowest quartile. We found little evidence for an association with infant orientation, habituation, and regulation of state, assessed as summary cluster measures.
CONCLUSIONS: Our findings provide evidence for an association between low-level prenatal PCB and DDE exposures and poor attention in early infancy. Further analyses will focus on whether organochlorine-associated decrements in attention and attention-related skills in infancy persist in later childhood.
KEY WORDS: behavior, infant, organochlorines, p,p´-dichlorodiphenyl dichloroethene (DDE), poly- chlorinated biphenyls (PCBs). Environ Health Perspect 116:666–673 (2008). doi:10.1289/ehp.10553 available via http://dx.doi.org/ [Online 24 January 2008]
A Nuclear Receptors in Fish and Mammalian Cells
Miyuki Suzawa1,2, Holly A. Ingraham1,2*
1 Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, California, United States of America2 Department of Physiology, University of California San Francisco, San Francisco, California, United States of America
Atrazine
(ATR) remains a widely used broadleaf herbicide in the United States despite the
fact that this s-chlorotriazine has been linked to reproductive abnormalities in
fish and amphibians. Here, using zebrafish we report that environmentally
relevant ATR concentrations elevated zcyp19a1 expression encoding aromatase (2.2
µg/L), and increased the ratio of female to male fish (22 µg/L). ATR selectively
increased zcyp19a1, a known gene target of the nuclear receptor SF-1 (NR5A1),
whereas zcyp19a2, which is estrogen responsive, remained unchanged. Remarkably,
in mammalian cells ATR functions in a cell-specific manner to upregulate SF-1
targets and other genes critical for steroid synthesis and reproduction,
including Cyp19A1, StAR, Cyp11A1, hCG, FSTL3, LHß, INHα, αGSU, and 11ß-HSD2. Our
data appear to eliminate the possibility that ATR directly affects SF-1 DNA- or
ligand-binding. Instead, we suggest that the stimulatory effects of ATR on the
NR5A receptor subfamily (SF-1, LRH-1, and zff1d) are likely mediated by receptor
phosphorylation, amplification of cAMP and PI3K signaling, and possibly an
increase in the cAMP-responsive cellular kinase SGK-1, which is known to be
upregulated in infertile women. Taken together, we propose that this pervasive
and persistent environmental chemical alters hormone networks via convergence of
NR5A activity and cAMP signaling, to potentially disrupt normal endocrine
development and function in lower and higher vertebrates.
Full study: http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0002117
INTERNATIONAL MEETING FOR AUTISM RESEARCH
May 15, 2008; ORAL 2899
. Hertz-Picciotto
Public Health
Sciences and the M.I.N.D. Institute, University of California at Davis, Dept
PHS, Davis, CA 95616
I. N. Pessah
3 Department of Veterinary Molecular
Biosciences, University of California at Davis, M.I.N.D. Institute, One Shields
Avenue, Davis, CA 95616
R. Hansen
Pediatrics and the M.I.N.D.
Institute, University of California at Davis, 2825, 50th Street, Sacramento, CA
95817
P. Krakowiak
M.I.N.D. Institute, University of California at
Davis, 2825 50th Street, Sacramento, CA 95817
Abstract
Background: Pesticides affect a number of targets in the CNS, and
cross the placenta. One previous report suggests a link between maternal
residential proximity to commercial organochlorine pesticide exposure during
early prenatal life and the risk of autism. That study did not evaluate
individual exposures to household pesticides.
Objectives: To examine
household pesticide use during the prenatal period or early postnatal period in
relation to autism.
Methods: Participants were from the CHARGE (Childhood
Autism Risks from Genetics and the Environment study, a large population-based
case-control study in California. Autism spectrum disorders were confirmed using
the ADI and ADOS. Mothers were extensively interviewed regarding demographics,
lifestyle, and prenatal and early postnatal exposures of the child. Questions
addressed use of numerous household products, including insecticides for flies
and ants, pet shampoos, and weed control products. Interview data were available
for 333 ASD cases and 198 confirmed typically developing controls. Logistic
regression models were adjusted for family socioeconomic status. An index
exposure period was defined as three months prior to conception through the
child's first year of life.
Results: Mothers of ASD children were twice
as likely to report using pet shampoos for fleas or ticks during the index
period as compared with control mothers: adjusted Odds Ratio (aOR) = 2.0, 95%
Confidence Interval (CI) = [1.2, 3.6]. When examined by trimester, the strongest
association was during the second trimester: aOR = 2.6, 95% CI = [1.3,
6.0].
Conclusions: The higher prevalence of self-reported use of pet
shampoos by CHARGE study mothers of children with ASD could be due to reporting
bias, although many other products did not show differences. Pyrethrins have
largely replaced organophosphates for flea control, but early life exposure to
pyrethrins has been shown to compromise the blood-brain barrier in rodents,
raising concern about prenatal and early postnatal
exposures.
" … reduction of the cognitive potential of a child is a very tragic thing, and an event which has major costs to society as well as to the individual."
Carpenter, D., 2006.
International Congress Series 1287: 185– 189
Abstract.
A number of environmental contaminants are known to
cause a reduction in IQ in
children exposed prenatally or early in life. These
effects are well documented for exposure to lead, methylmercury,
polychlorinated biphenyls (PCBs), and cigarette smoke, all of which can reduce
IQ by up to 5–7 IQ points. Similar effects may result from exposure to dioxins
and some pesticides. In most or all of these situations there are also
behavioral changes as a result of exposure, including shortened attention span
and hyperactivity. Recent studies have shown that adverse effects
of
contaminants such as lead and cigarette smoke on IQ
occur at lower levels of exposure than previously thought, and that the
dose–response relationship is actually steeper at lower concentrations than
what is seen at higher levels. While adults are not as sensitive as children,
there is evidence for a rather selective loss of memory function in adults
exposed to the same substances. Our group has attempted to determine the
mechanisms whereby these effects occur using
long-term potentiation (LTP), an electrophysiological
measure known to be related to learning and memory, studied in rodent brain
slices. We find that lead and PCBs both reduce LTP whether given during
gestation and lactation or acutely applied to brain slices of unexposed
animals. Surprisingly, these very different contaminants appear to have a
similar mechanism of action, that being alteration of the activity of protein
kinase C.
[from body of text]
… Our studies lead to the somewhat surprising hypothesis that these diverse contaminants may be all acting through a common mechanism, and suggest that a target molecule may be protein kinase C. Certainly, more evidence is needed before this can be considered to be proven. However, reduction of the cognitive potential of a child is a very tragic thing, and an event which has major costs to society as well as to the individual. It is critical to both prevent exposure in the first place but also to understand how these decrements of brain function occur if one hopes to find ways to reduce and prevent the harm.
Roman, G., 2007.
Journal of the Neurological Sciences 262 :15–26
Abstract
The incidence and prevalence of autism have increased during the past
two decades. Despite comprehensive genetic studies the cause of autism
remains unknown. This review emphasizes the potential importance of
environmental factors in its causation. Alterations of cortical neuronal
migration and cerebellar Purkinje cells have been observed in autism.
Neuronal migration, via reelin regulation, requires triiodothyronine
(T3) produced by deiodination of thyroxine (T4) by fetal brain
deiodinases. Experimental animal models have shown that transient
intrauterine deficits of thyroid hormones (as brief as 3 days) result in
permanent alterations of cerebral cortical architecture reminiscent of
those observed in brains of patients with autism. I postulate that early
maternal hypothyroxinemia resulting in low T3 in the fetal brain during
the period of neuronal cell migration (weeks 8–12 of pregnancy) may
produce morphological brain changes leading to autism. Insufficient
dietary iodine intake and a number of environmental antithyroid and
goitrogenic agents can affect maternal thyroid function during
pregnancy. The most common causes could include inhibition of
deiodinases D2 or D3 from maternal ingestion of dietary flavonoids or
from antithyroid environmental contaminants. Some plant isoflavonoids
have profound effects on thyroid hormones and on the
hypothalamus–pituitary axis. Genistein and daidzein from soy (Glycine
max) inhibit thyroperoxidase that catalyzes iodination and thyroid
hormone biosynthesis. Other plants with hypothyroid effects include
pearl millet (Pennisetum glaucum) and fonio millet (Digitaria exilis);
thiocyanate is found in Brassicae plants including cabbage, cauliflower,
kale, rutabaga, and kohlrabi, as well as in tropical plants such as
cassava, lima beans, linseed, bamboo shoots, and sweet potatoes. Tobacco
smoke is also a source of thiocyanate. Environmental contaminants
interfere with thyroid function including 60% of all herbicides, in
particular 2,4-dichlorophenoxyacetic acid (2,4-D), acetochlor,
aminotriazole, amitrole, bromoxynil, pendamethalin, mancozeb, and
thioureas. Other antithyroid agents include polychlorinated biphenyls
(PCBs), perchlorates, mercury, and coal derivatives such as resorcinol,
phthalates, and anthracenes. A leading ecological study in Texas has
correlated higher rates of autism in school districts affected by large
environmental releases of mercury from industrial sources. Mercury is a
well known antithyroid substance causing inhibition of deiodinases and
thyroid peroxidase. The current surge of autism could be related to
transient maternal hypothyroxinemia resulting from dietary and/or
environmental exposure to antithyroid agents. Additional
multidisciplinary epidemiological studies will be required to confirm
this environmental hypothesis of autism.
Environmental chemicals with antithyroid effects Howdeshell [103] and Colborn [104,105] have recently reviewed the potential effects of environmental chemical agents on endocrine function—causing in particularly thyroid disruption and abnormal brain development. Low doses of toxins could become deleterious in cases of low maternal iodine [104] . Table 2 [103] provides a comprehensive list of chemical agents with effects at several levels of thyroid metabolism. More than 60% of herbicides are endocrine disruptors [104] in particular the widely used 2,4-dichlorophenoxyacetic acid (2,4-D), mancozeb, acetochlor, aminotriazole, amitrole, bromoxynil, pendamethalin, and the thioureas. Contamination of drinking water from areas rich in coal and shale by naturally occurring powerful antithyroid products such as resorcinol (1,3-dihydroxybenzene dihydroxybenzene) and the substituted resorcinol 2,4- dihydroxyacetophenone, methoxy-anthracene, phthalate esters and phthalic acid, can produce endemic goiter and hypothyroidism [106]. The developmental neurotoxicity of polychlorinated biphenyls (PCBs) and dioxins has been known since the 1990s [107,108] . Neurobehavioral alterations have been observed in newborn children exposed to PCBs including motor immaturity, hyporreflexia, and lower psychomotor scores between 6 months and 2 years of age; along with decrease in dopamine in basal ganglia and prefrontal cortex [107] . Similar dopamine alterations have been reported in children with autism [109] . These abnormalities could be mediated by disruptionof thyroid hormones by competitive binding of PCBs (structurally similar to thyroid hormones) to serum transport proteins [110] and by alterations in thyroid hormone-responsive genes in the developing brain [103–105,110–112] . Recently, Kimura-Kuroda et al. [113] demonstrated that several hydroxy- PCBs are capable of inhibiting the thyroid-hormone-dependent development of dendrites in cerebellar Purkinje cells and suggested that PCBs could be a cause of autism and other developmental disorders.
Although many authors have suggested that environmental pollutants–such as those affecting thyroid hormones– may play a role in autism [85,103–105,112,113,125] only recently Palmer and colleagues [126] , from the University of Texas at San Antonio, reported an ecological association between autism and environmental mercury pollution. This study was based on quantitative data on mercury released in the Texas environment, provided by the Agency for Toxic Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The authors correlated environmentally released mercury (per 1000 lb) with rates of autism in Texas using county (N=254) and school district (N=1184) information by means of a multilevel Poisson regression model adjusted for racial composition, socioeconomic level and urbanicity. They concluded that the risk for autism increased 6.15% per each 100 lb of environmentally released mercury (RR=1.614, 95% CI 1.487–1.752); the highest increase in relative rates of autism in school districts was for urban relative to rural (RR=4.726, 95% CI 3.8–5.9) and for suburban vs. rural districts (RR=2.547, 95% CI 2.1–3.2). Autism accounted for the increase in special education rate whereby each 100 lb of mercury released increased 4.3% the rate of special education students (RR=1.433, 95% CI 1.35–1.52) [126]. This study from our institution is one of the first to demonstrate an association between environmental pollution and autism.
Reproductive Toxicology 25 (2008) 184-191
John D. Meeker a , * , Sarena R. Ravi a , Dana B. Barr
b , Russ Hauser c , d
a Department of Environmental Health Sciences,
University of Michigan, School of Public
Health, Ann Arbor, MI, United
States
b Centers for Disease and Control and Prevention, Atlanta, GA, United
States
c Department of Environmental Health, Harvard School of Public
Health, Boston, MA,
United States
d The Fertility Center, Vincent
Memorial Obstetrics and Gynecology Service,
Massachusetts General Hospital,
Boston, MA, United States
Received 14 August 2007; received in revised
form 4 December 2007; accepted 19
December 2007
Available online 28
December 2007
Abstract
Background: Estradiol plays an important role
in male reproductive health as a germ cell
survival factor. Chlorpyrifos and
carbaryl, nonpersistent insecticides to which the general
population are
commonly exposed, were recently shown to inhibit estradiol metabolism in
vitro which could lead to altered hormone balance. Methods: Subjects (N= 322) were the male partners in couples presenting to a Massachusetts infertility clinic from years 2000-2003. 3,5,6-Trichloro-2-pyridinol (TCPY),
the major urinary metabolite of chlorpyrifos and chlorpyrifos-methyl, and 1- and 2-naphthol (1N and 2N), urinary metabolites of carbaryl and naphthalene, were measured in a spot urine sample from each subject. Estradiol, sex hormone binding globulin (SHBG), and prolactin were measured in serum collected from subjects during the same clinic visit. Results: Using multiple linear regression, an interquartile range (IQR) increase in TCPYwas
associated with a 1.36 pg/mL decline (95% confidence interval =-2.91 to -0.22) in estradiol concentration. When estradiol and TCPY were divided into quintiles, there was a dose- dependent increase in the odds of being in the lowest estradiol quintile with increasing TCPY quintiles. Conclusion: On a population level, these reductions in estradiol levels are of potential
public health importance because of widespread exposure to TCPY and its parent insecticides.
Shafer TJ, Rijal SO, Gross GW.
Neurotoxicology Division, MD-B105-05, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, United States.
Neurotoxicology. 2008 Jan 19
Types I and II pyrethroid insecticides cause temporally distinct decreases in voltage-gated sodium channel (VGSC) inactivation rates that are proposed to underlie their characteristic differences in toxicity signs. How alterations in VGSC channel function give rise to the characteristic differences in signs of pyrethroid intoxication is not completely understood, particularly those changes that occur in functional networks of interconnected neurons. To characterize better pyrethroid actions at the network level, effects of the Type I pyrethroid permethrin (PM) and the Type II pyrethroid deltamethrin (DM) on spontaneous glutamate network-dependent spikes and bursts were investigated in primary cultures of frontal cortex or spinal cord neurons grown on microelectrode arrays (MEAs). Fast GABAergic transmission was blocked by BIC, and concentration-dependent effects of DM (1nM to 5muM) and PM (10nM to 50muM) were examined. Both compounds caused concentration-dependent reductions in the network spike and burst rates. DM was more potent than PM, with IC(50) values of approximately 0.13 and approximately 4muM for inhibition of spike rate in cortical and spinal cord neurons, respectively. Both compounds decreased the percentage of spikes that occurred within a burst and increased the interspike interval within bursts. Onset of effects was rapid, but recovery from total activity loss was not readily achievable. Individual neurons responded heterogeneously; activity of most declined monophasically, but activity in others exhibited biphasic responses with increases followed by decreases in activity. In spinal cord, DM caused a greater number of biphasic responses (29%) than PM (10%). These results demonstrate that both DM and PM inhibit activity of glutamatergic networks, but with different potencies.
http://www.ncbi.nlm.nih.gov/pubmed/18304643?dopt=AbstractPlus
PMID: 18304643 [PubMed - as supplied by publisher]
University of California at Berkeley, School of Public Health, Center for Children s Environmental Health Research, Berkeley, California, USA.
PURPOSE OF REVIEW: This review summarizes the recent research on pesticide exposure and child neurobehavioral development with a focus on in-utero exposure to organochlorine and organophosphate pesticides. RECENT FINDINGS: Recent studies on in-utero exposure to the organochlorine pesticide dichlorodiphenyltrichloroethane and its breakdown product, dichlorodiphenyldichloroethene, indicate that exposure is associated with poorer infant (6 months and older) and child neurodevelopment. Yet, the studies differ on the domain of development that is affected. Research on organophosphate pesticide exposure and neurodevelopment is limited but suggests some negative association of exposure and neurodevelopment at certain ages. Two reports agree that increased levels of organophosphate exposure in utero result in greater numbers of abnormal reflexes in neonates and studies in older infants and young children also point to a negative association with development. In young children (2-3 years) two separate studies observed an increase in maternally reported pervasive developmental disorder with increased levels of organophosphate exposure. SUMMARY: Given that the literature suggests a link between organochlorine and in-utero pesticide exposure and impaired child neurodevelopment, clinicians should educate parents about prevention of exposure, especially in populations living in agricultural areas or where household use is common.
PMID: 18332717 [PubMed - as supplied by publisher]
Carpenter, D., 2006.
International Congress Series 1287: 185– 189
Abstract.
A number of environmental contaminants are known to cause a reduction in IQ in children exposed prenatally or early in life. These effects are well documented for exposure to lead, methylmercury, polychlorinated biphenyls (PCBs), and cigarette smoke, all of which can reduce IQ by up to 5–7 IQ points. Similar effects may result from exposure to dioxins and some pesticides. In most or all of these situations there are also behavioral changes as a result of exposure, including shortened attention span and hyperactivity. Recent studies have shown that adverse effects of contaminants such as lead and cigarette smoke on IQ occur at lower levels of exposure than previously thought, and that the dose–response relationship is actually steeper at lower concentrations than what is seen at higher levels. While adults are not as sensitive as children, there is evidence for a rather selective loss of memory function in adults exposed to the same substances. Our group has attempted to determine the mechanisms whereby these effects occur using long-term potentiation (LTP), an electrophysiological measure known to be related to learning and memory, studied in rodent brain slices. We find that lead and PCBs both reduce LTP whether given during gestation and lactation or acutely applied to brain slices of unexposed animals. Surprisingly, these very different contaminants appear to have a similar mechanism of action, that being alteration of the activity of protein kinase C.
[from body of text]
"Our studies lead to the somewhat surprising hypothesis that these diverse contaminants may be all acting through a common mechanism, and suggest that a target molecule may be protein kinase C. Certainly, more evidence is needed before this can be considered to be proven. However, reduction of the cognitive potential of a child is a very tragic thing, and an event which has major costs to society as well as to the individual. It is critical to both prevent exposure in the first place but also to understand how these decrements of brain function occur if one hopes to find ways to reduce and prevent the harm."
Released: 2/7/2008 12:50:58 PM
Contact Information:
U.S. Department of the Interior, U.S. Geological
Survey
Office of Communication
119 National Center
Reston, VA
20192
For several years, scientists have been working to determine why so many male smallmouth bass in the Potomac River basin have immature female egg cells in their testes - a form of intersex. They are closer to finding an answer.
Research by the U.S. Geological Survey (USGS) shows that a high incidence of intersex occurs in the Potomac watershed at sites where farming is most intense and where human population density is highest. The study also shows the greatest prevalence of this form of intersex, known as testicular oocytes (TO), occurs in the spring, just before and during the spawning season.
These results are published in the current edition of the Journal of Aquatic Animal Health.
"We collected smallmouth bass from the Shenandoah, the South Branch of the Potomac, and out of the basin for comparison," said USGS scientist Vicki Blazer, who led the study. "The fish from the sites with the highest human population density and the most farming had the highest incidences of intersex," said Blazer. "On the Shenandoah, rates of intersex were highest, ranging from 80-100 percent intersex."
Out of the Potomac basin, the most densely populated heavily farmed site had bass with a TO rate of 75 percent, where less habited sites had 14-35 percent of male bass with TO. Sites along the South Branch of the Potomac ranged from 47-77 percent; again the higher percents corresponding with increased farming and human population.
Seasonal comparisons are also striking. In the study, the USGS sampled six sites. At every site sampled, the incidence of male bass with TO was significantly higher during the spring pre-spawn to spawning period, ranging from 69-100 percent, compared to the summer post-spawn period, when it ranged from 25-67 percent.
The reproductive anomalies in the Potomac's smallmouth bass population are not readily apparent on gross examination of an affected fish -- they were discovered by accident. In 2003, scientists investigating massive fish kills and widespread lesions found many individuals with TO while looking at tissues from the testes of male fish under the microscope.
A prevalence of intersex is not unique to the Potomac basin, nor is it unique to smallmouth bass. It has been documented in other wild fish populations including spot-tail shiners in the St. Lawrence River, white suckers in Colorado, shovelnose sturgeon in the Mississippi, white perch from the Great Lakes, roach fish in the U.K and Denmark, sharp-tooth catfish in South Africa, three-spine stickleback in Germany, and barbel in Italy. It has also been noted in marine and estuarine fishes in Japan, the UK and the Mediterranean.
At many of these places, it has been associated with known or suspected endocrine disrupting compounds in wastewater effluent, which are not removed during standard sewage treatment, and in runoff from farming operations. These compounds can include estrogen from birth control pills and hormone replacements, pesticides and fertilizers used on crops, and hormones from livestock operations.
Scientists are continuing to assess the extent of TO in bass in the Potomac River system. They are examining samples collected at reference sites within and outside of the drainage basin to determine a background prevalence of TO for both smallmouth and largemouth bass, and to identify potential causes. They are also assessing the reproductive and general health of fish at sites with high and low prevalence of TO, and evaluating land use in risk assessment.
Reporters: The article "Intersex (Testicular Oocytes) in Smallmouth Bass from the Potomac River and Selected Nearby Drainages," is available by email dnoseral@usgs.gov
Studies of fish health are part of the USGS Chesapeake Bay studies, which provide integrated science for improved understanding and management of the Bay ecosystem. More information about USGS Chesapeake Bay studies, and a soon to be released report "USGS Circular 1316, "Synthesis of USGS Science for the Chesapeake Bay Ecosystem and Implications for Environmental Management," can be found at http://chesapeake.usgs.gov/.
ASAP Environ. Sci. Technol., ASAP Article,
10.1021/es702304c
Web Release Date: February 20,
2008
Chad A. Kinney,*† Edward T. Furlong,‡ Dana W. Kolpin,§ Mark R. Burkhardt,‡ Steven D. Zaugg,‡ Stephen L. Werner,‡ Joseph P. Bossio,¤ and Mark J. Benottiþ
Department of Chemistry, Colorado State University at Pueblo, 2200 Bonforte Blvd, Pueblo, Colorado 81001, National Water Quality Laboratory, U.S. Geological Survey, P.O. Box 25046, Denver Federal Center, Denver, Colorado 80225-0046, U.S Geological Survey, 400 S. Clinton St. Suite 269, Iowa City, Iowa 52240-4105, Department of Chemistry and Biochemistry, Eastern Washington University, Cheney, Washington 99004, and U.S. Geological Survey, 2045 Route 112, Building 4, Coram, New York 11727
Received for review September 14, 2007
Revised manuscript received December 21, 2007
Accepted January 7, 2008
Abstract:
Analysis of earthworms offers potential for assessing the transfer of organic anthropogenic waste indicators (AWIs) derived from land-applied biosolid or manure to biota. Earthworms and soil samples were collected from three Midwest agricultural fields to measure the presence and potential for transfer of 77 AWIs from land-applied biosolids and livestock manure to earthworms. The sites consisted of a soybean field with no amendments of human or livestock waste (Site 1), a soybean field amended with biosolids from a municipal wastewater treatment plant (Site 2), and a cornfield amended with swine manure (Site 3). The biosolid applied to Site 2 contained a diverse composition of 28 AWIs, reflecting the presence of human-use compounds. The swine manure contained 12 AWIs, and was dominated by biogenic sterols. Soil and earthworm samples were collected in the spring (about 30 days after soil amendment) and fall (140-155 days after soil amendment) at all field sites. Soils from Site 1 contained 21 AWIs and soil from Sites 2 and 3 contained 19 AWIs. The AWI profiles at Sites 2 and 3 generally reflected the relative composition of AWIs present in waste material applied. There were 20 AWIs detected in earthworms from Site 1 (three compounds exceeding concentrations of 1000 µg/kg), 25 AWIs in earthworms from Site 2 (seven compounds exceeding concentrations of 1000 µg/kg), and 21 AWIs in earthworms from Site 3 (five compounds exceeding concentrations of 1000 µg/kg). A number of compounds that were present in the earthworm tissue were at concentrations less than reporting levels in the corresponding soil samples. The AWIs detected in earthworm tissue from the three field sites included pharmaceuticals, synthetic fragrances, detergent metabolites, polycyclic aromatic hydrocarbons (PAHs), biogenic sterols, disinfectants, and pesticides, reflecting a wide range of physicochemical properties. For those contaminants detected in earthworm tissue and soil, bioaccumulation factors (BAF) ranged from 0.05 (galaxolide) to 27 (triclosan). This study documents that when AWIs are present in source materials that are land applied, such as biosolids and swine manure, AWIs can be transferred to earthworms.
John J. Spinelli 1
*†, Carmen H. Ng
1, Jean-Philippe Weber
2, Joseph M. Connors
1, Randy D. Gascoyne
1, Agnes S. Lai
1, Angela R. Brooks-Wilson 1, Nhu D. Le 1, Brian R. Berry 1, Richard P. Gallagher 1
1BC Cancer Agency,
Vancouver, British Columbia, Canada
2Centre de Toxicologie du Québec,
Sainte-Foy, Québec
email: John J. Spinelli (jspinelli@bccrc.ca)
*Correspondence to John J. Spinelli, BC Cancer Agency, 675 W. 10th Avenue, Vancouver, British Columbia, V5Z 1L3 Canada
†Fax: +604-675-8180.Funded by:
• Canadian Cancer Society through the National Cancer Institute of
Canada
• Canadian Institutes of Health Research
• Michael Smith Foundation for Health Research
Organochlorine chemicals and polychlorinated biphenyls (PCBs) have been suspected as possible risk factors for non-Hodgkin lymphoma (NHL). We investigated PCBs and organochlorine pesticides and risk of NHL in a population-based case-control study in British Columbia, Canada. Congeners of PCBs (including dioxinlike congeners) and pesticides or pesticide metabolites were measured in plasma of 422 pretreatment cases and 460 control subjects. This is so far the largest study to examine organochlorines in plasma to date. Several dioxin-like PCB congeners were associated with increased risk of NHL, including dioxin-like PCB nos. 118 and 156 with odds ratios (OR) for the highest versus lowest quartile between 1.6 and 1.8. Several non-dioxin-like congeners also showed significant associations. The PCB congener with the strongest association was no. 180 with an OR for the highest versus the lowest quartile of 1.83 (95% confidence interval = 1.18-2.84). Six pesticide analytes also showed a significant association with NHL; β-hexachlorocyclohexane, p,p´-DDE, hexachlorobenzene, mirex, oxychlordane and trans-nonachlor. The strongest association was found for oxychlordane, a metabolite of the pesticide chlordane (highest vs. lowest quartile OR = 2.68, 95% confidence interval = 1.69-4.24). Our results provide further evidence that organochlorines contribute to NHL risk. © 2007 Wiley-Liss, Inc.
American Journal of Respiratory and Critical Care Medicine Vol 177. pp. 11-18, (2008)
© 2008 American Thoracic Society
doi: 10.1164/rccm.200706-821OC
Jane A. Hoppin1, David M. Umbach2, Stephanie J. London1, Paul K. Henneberger3, Greg J. Kullman3, Michael C. R. Alavanja4 and Dale P. Sandler1
1 Epidemiology Branch and 2 Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina; 3 Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Department of Health and Human Services, Morgantown, West Virginia; and 4 Occupational Epidemiology Branch, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland
Correspondence and requests for reprints should be addressed to Jane A. Hoppin, Sc.D., NIEHS Epidemiology Branch, MD A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233. E-mail: hoppin1@niehs.nih.gov
Rationale: Risk factors for asthma among farm women are understudied.
Objectives: We evaluated pesticide and other occupational exposuresas risk factors for adult-onset asthma.
Methods: Studying 25,814 farm women in the Agricultural Health Study, we used self-reported history of doctor-diagnosed asthma with or without eczema and/or hay fever to create two case groups: patients with atopic asthma and those with nonatopic asthma.We assessed disease-exposure associations with polytomous logistic regression.
Measurements and Main Results: At enrollment (1993–1997), 702 women (2.7%) reported a doctor's diagnosis of asthma after age 19 years (282 atopic, 420 nonatopic). Growing up on a farm (61% of all farm women) was protective for atopic asthma (odds ratio [OR], 0.55; 95% confidence interval [CI], 0.43–0.70)and, to a lesser extent, for nonatopic asthma (OR, 0.83; 95%CI,0.68–1.02; P value for difference = 0.008). Pesticideuse was almost exclusively associated with atopic asthma. Anyuse of pesticides on the farm was associated only with atopicasthma (OR, 1.46; 95% CI, 1.14–1.87). This associationwith pesticides was strongest among women who had grown up ona farm. Women who grew up on farms and did not apply pesticideshad the lowest overall risk of atopic asthma (OR, 0.41; 95%CI, 0.27–0.62) compared with women who neither grew upon farms nor applied pesticides. A total of 7 of 16 insecticides,2 of 11 herbicides, and 1 of 4 fungicides were significantlyassociated with atopic asthma; only permethrin use on cropswas associated with nonatopic asthma.
Conclusions: These findings suggest that pesticides may contributeto atopic asthma, but not nonatopic asthma, among farm women.
Jarosinska, D., Gee, D., 2007. Children's environmental health and the precautionary principle. International Journal of Hygiene and Environmental Health . Article in Press.
doi:10.1016/j.ijheh.2007.07.017
Abstract
The concept of precaution has a long history in medicine and public health. The modern precautionary principle (PP), originating from environmental debates in Germany in the 1970s, has been included in many international agreements, such as the Treaty on European Union. PP is a public policy tool that justifies actions, which protect human health and the environment in face of uncertain risks. The outcome of the application of PP depends on the level, nature, and distribution of acceptable risks and on the availability of alternatives, and can range from taking no action to banning of substances or the activities of concern.
Given the complex nature and uncertainty of environmental risks to children's health, a precautionary approach is warranted. Public health professionals and clinical practitioners could adopt such an approach within the wider context of considering the environment as a source of risks to children's health. Relevant knowledge and skills are needed to enable health care professionals to address these issues. New methodological and scientific approaches are necessary to make use of scattered, but potentially relevant clinical evidence in providing ‘early warnings’ of health hazards.
Araújo AJ, Lima JS, Moreira JC, Jacob SD, Soares MD, Monteiro MC, Amaral AM, Kubota A, Meyer A, Cosenza CA, Neves CD, Markowitz S. NETT, IDT, HUCFF, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-913.
Cien Saude Colet. 2007 Mar;12(1):115-130.
A cross section study was carried out in a farming community from Nova Friburgo, Rio de Janeiro state, Brazil, to examine epidemiological, clinical and laboratory aspects of multiple exposure episodes of acute intoxication by organophosphorates either described behavioral syndromes and psychiatric disorders associated to the continued use of pesticides were diagnosed. These results indicate recurrent multiple overexposures to high concentrations of different chemicals, with serious damage to vital functions, especially considering their young age (average 35 ± 11 years old) and the productive period in their lifetime.
These results show how important it is to monitor multiple exposure to pesticides - a chain of events that may have major impacts on public health and the environment.
PMID: 17680063 [PubMed - as supplied by publisher]
Eric M. Roberts,1 Paul B. English,2 Judith K. Grether,2 Gayle C. Windham,2 Lucia Somberg,3 and Craig Wolff2
1Public Health Institute, Oakland, California, USA; 2California Department of Health Services, Richmond, California, USA; 3School of Public Health, University of California, Berkeley, California, USA
Abstract
Background: Ambient levels of pesticides ("pesticide drift") are detectable at residences near agricultural field sites.
Objective: Our goal was to evaluate the hypothesis that maternal residence near agricultural pesticide applications during key periods of gestation could be associated with the development of autism spectrum disorders (ASD) in children.
Methods: We identified 465 children with ASD born during 1996–1998 using the California Department of Developmental Services electronic files, and matched them by maternal date of last menstrual period to 6,975 live-born, normal-birth-weight, term infants as controls. We determined proximity to pesticide applications using California Department of Pesticide Regulation records refined using Department of Water Resources land use polygons. A staged analytic design applying a priori criteria to the results of conditional logistic regressions was employed to exclude associations likely due to multiple testing error.
Results: Of 249 unique hypotheses, four that described organochlorine pesticide applications—specifically those of dicofol and endosulfan—occurring during the period immediately before and concurrent with central nervous system embryogenesis (clinical weeks 1 through 8) met a priori criteria and were unlikely to be a result of multiple testing. Multivariate a posteriori models comparing children of mothers living within 500 m of field sites with the highest nonzero quartile of organochlorine poundage to those with mothers not living near field sites suggested an odds ratio for ASD of 6.1 (95% confidence interval, 2.4–15.3) . ASD risk increased with the poundage of organochlorine applied and decreased with distance from field sites.
Conclusions: The association between residential proximity to organochlorine pesticide applications during gestation and ASD among children should be further studied.
The full version of this article is available for free in HTML or PDF formats.
Zhang, S-Y, Y Ito, O Yamanoshita, Y Yanagiba, M Kobayashi, K Taya, C-M Li, A Okamura, M Miyata, J Ueyama, C-H Lee, M Kamijima and T Nakajima. Endocrinology, in press.
This version published
online on April 26, 2007
Endocrinology,
doi:10.1210/en.2006-1497
Submitted on November 13, 2006
Accepted on April
18, 2007
Mount Sinai School of Medicine, Department of Psychiatry, New York, NY, USA. Kushik.Jaga@va.gov
The literature on an association between organophosphate (OP) toxicity and depression or suicide is scarce. An interrelation exists among populations exposed to OPs, acute OP toxicity, neurobehavioral effects, depression, suicide, and fatality. Acute OP toxicity is characterized by the cholinergic syndrome with systemic and central nervous system effects. Organophosphate-induced neurobehavioral effects result in depression. A potential risk of depression and suicide exists in farm workers exposed to OPs. The sociodemographics of depression include age, gender, race, geographic region, social factors, economics, psychiatric disorders, medical conditions, and hereditary factors. Suicide is a major consequence of depression, with multiple sociodemographic risk factors. Developing countries have a higher incidence of OP toxicity, with limited information on the prevalence of depression. In these countries, the incidence of suicide is high, affecting more females. Suicide is more prevalent in rural areas, and in farming communities, commonly with ingestion of OPs. In industrialized countries,=20the incidence of OP toxicity is lower, but the prevalence of depression is higher. Suicide rates are lower in industrialized countries, affecting more males, the urban population, and farming communities. Other lethal methods of suicide, such as hanging, firearms, electrocution, and drug overdose are more common in industrialized countries. A potential risk of depression or suicide certainly exists from OP toxicity, largely depending on the epidemiology or sociodemographics of these disorders. Scientific evidence shows that the association between environmental toxicology and psychiatry has important public health implications.
PMID: 17508698 [PubMed - in process]
Vajdic CM, Fritschi L, Grulich AE, Kaldor JM, Benke G, Kricker A, Hughes AM, Turner JJ, Milliken S, Goumas C, Armstrong BK
National Centre in HIV Epidemiology and Clinical Research, University of NSW, Darlinghurst, NSW, Australia.
Pesticide exposure has been associated with non-Hodgkin lymphoma (NHL) risk in a number of studies, and two recent studies suggest that the increased risk may be confined to those with a history of asthma. We examined the interaction between occupational pesticide exposure and atopy on risk of NHL in an Australian population-based case-control study. Incident cases (n = 694) were diagnosed in New South Wales or the Australian Capital Territory between 2000 and 2001 and controls (n = 694) were randomly selected from electoral rolls and frequency-matched to cases by age, sex and State of residence. Occupational pesticide exposure was determined by an expert occupational hygienist's assessment of job-specific questionnaires administered by telephone. History of atopy (asthma, hay fever, eczema and food allergy) was self-reported. Logistic regression models included the three matching variables, ethnicity and sun exposure. The OR for NHL with substantial pesticide exposure and any history of asthma was 3.07 (95% CI 0.55-17.10) and with substantial pesticide exposure and no asthma history it was 4.23 (95% CI 1.76-10.16). The p-value for interaction was 0.29. A similar pattern of risk was observed for each of the pesticide subtypes; for asthma at various times of life; for hay fever, eczema, food allergy and any atopy, in men only and for follicular lymphomas only. Although this study had limited power, the findings do not suggest modification of the association between pesticide exposure and NHL risk by asthma or atopic disease more generally. (c) 2007 Wiley-Liss, Inc.
Maria Kouznetsova,1 Xiaoyu Huang,1 Jing Ma,1 Lawrence Lessner,1,2 and David O. Carpenter2
1Department of Epidemiology and Biostatistics, School of Public Health, and 2Institute for Health and the Environment, University at Albany, Rensselaer, New York, USA
Abstract
Background: Epidemiologic studies suggest that there may be an association between environmental exposure to persistent organic pollutants (POPs) and diabetes.
Objective: The aim of this study was to test the hypothesis that residential proximity to POP-contaminated waste sites result in increased rates of hospitalization for diabetes.
Methods: We determined the number of hospitalized patients 25–74 years of age diagnosed with diabetes in New York State exclusive of New York City for the years 1993–2000. Descriptive statistics and negative binomial regression were used to compare diabetes hospitalization rates in individuals who resided in ZIP codes containing or abutting hazardous waste sites containing POPs ("POP" sites); ZIP codes containing hazardous waste sites but with wastes other than POPs ("other" sites); and ZIP codes without any identified hazardous waste sites ("clean" sites).
Results: Compared with the hospitalization rates for diabetes in clean sites, the rate ratios for diabetes discharges for people residing in POP sites and "other" sites, after adjustment for potential confounders were 1.23 [95% confidence interval (CI), 1.15–1.32] and 1.25 (95% CI, 1.16–1.34), respectively. In a subset of POP sites along the Hudson River, where there is higher income, less smoking, better diet, and more exercise, the rate ratio was 1.36 (95% CI, 1.26–1.47) compared to clean sites.
Conclusions: After controlling for major confounders, we found a statistically significant increase in the rate of hospitalization for diabetes among the population residing in the ZIP codes containing toxic waste sites.
Key words: behavior, diabetes mellitus, dioxins, negative binomial regression, PCBs, persistent pesticides, polychlorinated biphenyls, SES, socioeconomic status, ZIP codes. Environ Health Perspect 115:75–79 (2007). [Online 18 August 2006]
Center for Environmental Health, Oakland, California, USA.
Background: By statute or regulation in the United States and elsewhere, pesticide ingredients are divided into two categories: active and inert (sometimes referred to as other ingredients, adjuvants, or coformulants). Despite their name, inert ingredients may be biologically or chemically active and are labeled inert only because of their function in the formulated product. Most of the tests required to register a pesticide are performed with the active ingredient alone, not the full pesticide formulation. Inert ingredients are generally not identified on product labels and are often claimed to be confidential business information.
Objectives: In this commentary, we describe the shortcomings of the current procedures for assessing the hazards of pesticide formulations and demonstrate that inert ingredients can increase the toxicity of and potential exposure to pesticide formulations.
Discussion: Inert ingredients can increase the ability of pesticide formulations to affect significant toxicologic end points, including developmental neurotoxicity, genotoxicity, and disruption of hormone function. They can also increase exposure by increasing dermal absorption, decreasing the efficacy of protective clothing, and increasing environmental mobility and persistence. Inert ingredients can increase the phytotoxicity of pesticide formulations as well as the toxicity to fish, amphibians, and microorganisms.
Conclusions: Pesticide registration should require full assessment of
formulations. Evaluations of pesticides under the National Environmental Policy
Act, the Endangered Species Act, and similar statutes should include impact
assessment of formulations. Environmental monitoring for pesticides should
include inert ingredients. To enable independent research and risk assessment,
inert ingredients should be identified on product labels.
PMID: 17185266
[PubMed - in process]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17185266&itool=iconabstr&itool=pubmed_DocSum
Williams MK, Barr DB, Camann DE, Cruz LA, Carlton EJ, Borjas M, Reyes A, Evans D, Kinney PL, Whitehead RD Jr, Perera FP, Matsoanne S, Whyatt RM.
Environ Health Perspect. 2006 Nov;114(11):1684-9.
Columbia Center for Children's Environmental Health, Mailman School of Public Health, Columbia University, New York, New York 10032, USA.
BACKGROUND: We previously reported widespread insecticide exposure during pregnancy among inner-city women from New York City. Here we report on a pilot intervention using integrated pest management (IPM) to reduce pest infestations and residential insecticide exposures among pregnant New York City African-American and Latina women (25 intervention and 27 control homes). METHODS: The IPM consisted of professional cleaning, sealing of pest entry points, application of low-toxicity pesticides, and education. Cockroach infestation levels and 2-week integrated indoor air samples were collected at baseline and one month postintervention. The insecticides detected in the indoor air samples were also measured in maternal and umbilical cord blood collected at delivery. RESULTS: Cockroach infestations decreased significantly (p = 0.016) after the intervention among intervention cases but not control households. Among the intervention group, levels of piperonyl butoxide (a pyrethroid synergist) were significantly lower in indoor air samples after the intervention (p = 0.016). Insecticides were detected in maternal blood samples collected at delivery from controls but not from the intervention group. The difference was significant for trans-permethrin (p = 0.008) and of borderline significance (p = 0.1) for cis-permethrin and 2-isopropoxyphenol (a propoxur metabolite). CONCLUSION: To our knowledge, this is the first study to use biologic dosimeters of prenatal pesticide exposure for assessing effectiveness of IPM. These pilot data suggest that IPM is an effective strategy for reducing pest infestation levels and the internal dose of insecticides during pregnancy.
Link to PDFhttp://pediatrics.aappublications.org/cgi/content/abstract/peds.2006-0338v1?papetoc
Nik Veldhoena, Rachel C. Skirrowb, Heather Osachoffb, Heidi Wigmoreb, David J. Clapsona, Mark P. Gundersona, Graham Van Aggelenb and Caren C. Helbinga, Corresponding Author Contact Information, E-mail The Corresponding Author
aDepartment of Biochemistry and Microbiology, P.O. Box 3055, Stn. CSC, University of Victoria, Victoria, British Columbia V8W 3P6, Canada
bPacific Environmental Science Centre, 2645 Dollarton Highway, North Vancouver, British Columbia V7H 1V2, Canada
Received 26 July 2006; revised 17 August 2006; accepted 30 August 2006. Available online 29 September 2006.
Abstract
We investigated whether exposure to environmentally relevant concentrations of the bactericidal agent, triclosan, induces changes in the thyroid hormone-mediated process of metamorphosis of the North American bullfrog, Rana catesbeiana and alters the expression profile of thyroid hormone receptor (TR) α and β, basic transcription element binding protein (BTEB) and proliferating nuclear cell antigen (PCNA) gene transcripts. Premetamorphic tadpoles were immersed in environmentally relevant concentrations of triclosan and injected with 1 × 10-11 mol/g body weight 3,5,3´-triiodothyronine (T3) or vehicle control. Morphometric measurements and steady-state mRNA levels obtained by quantitative polymerase chain reaction were determined. mRNA abundance was also examined in Xenopus laevis XTC-2 cells treated with triclosan and/or 10 nM T3. Tadpoles pretreated with triclosan concentrations as low as 0.15 ± 0.03 μg/L for 4 days showed increased hindlimb development and a decrease in total body weight following T3 administration. Triclosan exposure also resulted in decreased T3-mediated TRβ mRNA expression in the tadpole tail fin and increased levels of PCNA transcript in the brain within 48 h of T3 treatment whereas TRα and BTEB were unaffected. Triclosan alone altered thyroid hormone receptor α transcript levels in the brain of premetamorphic tadpoles and induced a transient weight loss. In XTC-2 cells, exposure to T3 plus nominal concentrations of triclosan as low as 0.03 μg/L for 24 h resulted in altered thyroid hormone receptor mRNA expression. Exposure to low levels of triclosan disrupts thyroid hormone-associated gene expression and can alter the rate of thyroid hormone-mediated postembryonic anuran development.
Keywords: Thyroid hormone; Metamorphosis; Rana catesbeiana; XTC-2; Environmental contaminant; Triclosan; Endocrine disruptor; Irgasan
Chaitali Sinhaa,
Kavita Setha,
Fakhrul Islamb,
Rajnish Kumar Chaturvedia,
Shubha Shuklaa,
Neeraj Mathurc,
N. Srivastavaa
and Ashok Kumar Agrawala,
Contact, email
aDevelopmental Toxicology Division, Industrial Toxicology Research Centre, Post Box-80, M.G. Marg Lucknow 226001, India
bDepartment of Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India
cEpidemiology Division, Industrial Toxicology Research
Centre, Post Box-80, M.G. Marg Lucknow 226001, India
Received 5 April
2005; revised 20 February 2006; accepted 28 March 2006.
Available online 13 July 2006.
Synthetic pyrethroids, besides their use in agriculture, are prevalently used in our houses as mosquito repellent (MR) in the form of aerosol, mats, coils and liquid vaporizers. Inhalation of fumes of the MR/liquid vaporizers may get entry into the brain by breaching the developing blood–brain barrier, hence deleterious to developing nervous system and can lead to long-term functional deficits. In the present study the consequence of MR exposure has further been investigated at various stages of development, evaluating free radical mediated effect pertinent to neurobehavioral and neurochemical functioning. Rat pups were exposed to pyrethroid-based MR (allethrin 3.6% w/v, 8 h/day through inhalation) during prenatal (GD1–20), postnatal (PND1–30) and perinatal (GD1–PND30) period of development and assessments were made on PND31. We observed significant oxidative stress, where an increase in lipid peroxidation and a decrease in antioxidants, glutathione, superoxide dismutase and catalase in various brain areas (cerebellum, corpus striatum, frontal cortex and hippocampus) were evident at all the exposure schedules. The hippocampus was the most affected region and further exhibited altered cholinergic functioning in the form of significant decrease in cholinergic (muscarinic) receptor binding (prenatal 32%, postnatal 35%, perinatal 38%) and inhibition in acetylcholinesterase activity (prenatal 20%, postnatal 31% and perinatal 33%). The neurochemical changes were found to accompany decrease in learning and memory performance in exposed rats, the function governed by hippocampus. The result suggests that pyrethroid-based MR inhalation during early developmental period may have adverse effect on developing nervous system causing cholinergic dysfunction leading to learning and memory deficit.
Keywords: Pyrethroid; Mosquito repellent; Oxidative stress;
Hippocampus; Cholinergic (muscarinic) receptor; Learning and memory;
Acetylcholinesterase; Development; Rats
Environmental Health Perspectives Volume 114, Number 9, September 2006 Research | Children's Health
Chensheng Lu,1 Dana B. Barr,2 Melanie Pearson,1 Scott Bartell,1 and Roberto Bravo
1Department of Environmental and Occupational Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA; 2National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia, USA
Abstract
We conducted a longitudinal study to assess the exposure of 23 elementary school–age children to pyrethroid pesticides, using urinary pyrethroid metabolites as exposure biomarkers. We substituted most of the children's conventional diets with organic food items for 5 consecutive days and collected two daily spot urine samples, first morning and before bedtime voids, throughout the 15-day study period. We analyzed urine samples for five common pyrethroid metabolites. We found an association between the parents' self-reported pyrethroid use in the residential environment and elevated pyrethroid metabolite levels found in their children's urine. Children were also exposed to pyrethroids through their conventional diets, although the magnitude was smaller than for the residential exposure. Children's ages appear to be significantly associated with pyrethroids exposure, which is likely attributed to the use of pyrethroids around the premises or in the facilities where older children engaged in the outdoor activities. We conclude that residential pesticide use represents the most important risk factor for children's exposure to pyrethroid insecticides. Because of the wide use of pyrethroids in the United States, the findings of this study are important for both children's pesticide exposure assessment and environmental public health. Key words: children's pesticide exposure, dietary exposure, PBA, permethrin, pyrethroids, residential exposure, trans-DCCA, urinary biomarker. Environ Health Perspect 114: 1419–1423 (2006) . doi:10.1289/ehp.9043 available via http://dx.doi.org/ [Online 26 April 2006]
Address correspondence to C. Lu, 1518 Clifton Rd. NE, Atlanta, GA 30322 USA. Telephone: (404) 727-2131. Fax: (404) 727-8744. E-mail: clu2@sph.emory.edu
We express our sincere appreciation to the children who participated and to their parents who greatly assisted in this study. We also thank R. Irish, K. Toepel, and P. Sande for their assistance in conducting this study, and A. Bishop, P. Restrepo, R. Walker, J. Nguyen, and D. Walden at the National Center for Environmental Health (NCEH) in the Centers for Disease Control and Prevention (CDC) for their help with sample analysis.
This study was supported by the U.S. Environmental Protection Agency (EPA) , Science to Achieve Results (STAR) program (RD-829364) , and the NCEH, CDC. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of the U.S. EPA or CDC.
The authors declare they have no competing financial interests.
Received 26 January 2006 ; accepted 26 April 2006.
Van Maele-Fabry G, Libotte V, Willems J, Lison D.
Unite de Toxicologie Industrielle et Medecine du travail, Ecole de Sante Publique, Universite Catholique de Louvain, Bruxelles, Belgium.
PURPOSE: The purpose of the present paper is to review cohort studies that examined the occurrence of prostate cancer in pesticide manufacturing workers in order to undertake a qualitative and quantitative evaluation of the risk as well as to assess the level of epidemiological evidence for each class of chemical compounds. METHODS: Following a systematic literature search, relative risk (RR) estimates for prostate cancer were extracted from 18 studies published between 1984 and 2004. All studies were summarised and evaluated for homogeneity and publication bias. As no significant heterogeneity was detected, combined RR estimators were calculated using a fixed effect model. Meta-analyses were performed both on the whole set of data and for each chemical class separately. RESULTS: The meta-rate ratio estimate for all studies was 1.28 [95% confidence interval (CI) 1.05-1.58]. After stratification by specific chemical class, consistent increases in the risk of prostate cancer were found in all groups but statistical significance was found only for accidental or non-accidental exposure to phenoxy herbicides contaminated with dioxins and furans. There was no obvious indication of publication bias. CONCLUSION: The overall meta-analysis provides additional quantitative evidence consistent with prior reviews focusing on other groups exposed to pesticides (farmers, pesticide applicators). The results again point to occupational exposure to pesticides as a possible risk factor for prostate cancer but the question of causality remains unanswered. Epidemi