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Effect of Endocrine Disruptor Pesticides: A Review

Wissem Mnif, Aziza Ibn Hadj Hassine, Aicha Bouaziz and 3 more

International Journal of Environmental Research and Public Health · 2011 · Review · CC BY

doi:10.3390/ijerph8062265

Abstract

Endocrine disrupting chemicals (EDC) are compounds that alter the normal functioning of the endocrine system of both wildlife and humans. A huge number of chemicals have been identified as endocrine disruptors, among them several pesticides. Pesticides are used to kill unwanted organisms in crops, public areas, homes and gardens, and parasites in medicine. Human are exposed to pesticides due to their occupations or through dietary and environmental exposure (water, soil, air). For several years, there have been enquiries about the impact of environmental factors on the occurrence of human pathologies. This paper reviews the current knowledge of the potential impacts of endocrine disruptor pesticides on human health.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 17, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Since the discovery of DDT in 1939, numerous pesticides (organochlorides, organophosphates, carbamates) have been developed and used extensively worldwide with few guidelines or restrictions. In industrialized countries, the Green Revolution of the 1960s significantly increased agricultural productivity by increasing the cultivated surfaces, mechanization, planting of hybrid crops with higher yields, and pest control. This fight requires the massive use of pesticides, which are hazardous chemicals designed to repel or kill rodents, fungi, insects, and “weeds” that undermine intensive farming. The main effects of pesticides represent a great benefit for human health. Indeed, they help control agricultural pests (including diseases and weeds) and plant disease vectors, human and livestock disease vectors and nuisance organisms, and organisms that harm other human activities and structures (gardens, recreational areas, etc.). Moreover, they insure increased food production, a safe and secure food supply, and other secondary benefits. However, many first generation pesticides have been found to be harmful to the environment. Some of them can persist in soils and aquatic sediments, bioconcentrate in the tissues of invertebrates and vertebrates, move up trophic chains, and affect top predators.

Rachel Carson’s book “Silent Spring”, published in 1962, first drew attention to the hazard of the widespread extensive use of pesticides for the environment (namely birds) and also for human health. The book resulted in big modifications to the US national policy on pesticides, leading to a national ban on DDT and certain other pesticides.

Worldwide consumption of pesticides for agricultural use is constantly increasing, rising from 0.49 kg/ha in 1961 to 2 kg/ha in 2004 (see various web sources, such as for example http://ec.europa.eu/agriculture/envir/report/fr/pest_fr/report.htm#fig6; http://faostat.fao.org/site/424/default.aspx#ancor; http://www.goodplanet.info/eng/Food-Agriculture/Pesticides/Pesticides/(theme/266)), and humans and wildlife are today continuously exposed to a number of pesticides via the environment (surface water, ground water, soil), food and drinking water.

The World Health Organization (WHO) has reported that roughly three million pesticide poisonings occur annually, resulting in 220,000 deaths worldwide. In some cases, it has been suggested that diseases such as cancer, allergies, neurological disorders and reproductive disorders may be connected to pesticide exposure.

This article focuses on pesticides that act as endocrine disruptors, and reviews the available information about the exposure and effects of such pesticides, as well as human biomonitoring for human health risk assessment.

Effects of Endocrine Disruptor Pesticides

Many chemicals that have been identified as endocrine disruptors are pesticides. About 105 substances can be listed, and most of them are shown in Table 1. Of these, 46% are insecticides, 21% herbicides and 31% fungicides; some of them were withdrawn from general use many years ago but are still found in the environment (ex. DDT and atrazine in several countries).

EDCs act mainly by interfering with natural hormones because of their strong potential to bind to estrogen or androgen receptors as shown in Table 1. In particular, EDCs can bind to and activate various hormone receptors (AR, ER, AhR, PXR, CAR, ERR) and then mimic the natural hormone’s action (agonist action). EDCs may also bind to these receptors without activating them. This antagonist action blocks the receptors and inhibits their action. Finally, EDCs may also interfere with the synthesis, transport, metabolism and elimination of hormones, thereby decreasing the concentration of natural hormones. For example, thyroid hormone production can be inhibited by some ten endocrine disruptor pesticides (amitrole, cyhalothrin, fipronil, ioxynil, maneb, mancozeb, pentachloronitro-benzene, prodiamine, pyrimethanil, thiazopyr, ziram, zineb, not shown in Table 1).

At the environmental level, wildlife is particularly vulnerable to the endocrine disrupting effects of pesticides. Effects linked to endocrine disruption have been largely noted in invertebrates, reptiles, fish, birds and mammals as reviewed by Mnif et al.. Most of them are linked to exposure to organochlorine pesticides (OC) and affect the reproductive function. For example, a study on Daphnia magna has shown that endosulfan sulphate disrupts the ecdysteroidal system (regulating processes such as molting and embryonic development) and juvenile hormone activity (regulating the sex ratio) of crustaceans. Another example is the influence of linuron on reproductive hormone production, testosterone production in rats being significantly reduced after in utero exposure to linuron, whereas progesterone production was not affected.

At the human level, endocrine disruptor pesticides have also been shown to disrupt reproductive and sexual development, and these effects seem to depend on several factors, including gender, age, diet, and occupation.

Age is a particularly sensitive factor. Human fetuses, infants and children show greater susceptibility than adults. Much of the damage caused by EDC occurs during gametogenesis and the early development of the fetus. However, the effects may not become apparent until adulthood. Moreover, fetuses and infants receive greater doses due to the mobilization of maternal fat reserves during pregnancy and breastfeeding. Infants are extremely vulnerable to pre and postnatal exposure to endocrine disruptor pesticides, resulting in a wide range of adverse health effects including possible long-term impacts on intellectual function and delayed effects on the central nervous system functioning.

Likewise, residential proximity to agricultural activity is a factor often described to explain developmental abnormalities in epidemiological studies of low birth weight, fetal death, and childhood cancers. Additionally, a higher prevalence of cryptorchidism and hypospadias was found in areas with extensive farming and pesticide use and in sons of women working as gardeners. Recently, a relation has been reported between cryptorchidism and persistent pesticide concentration in maternal breast milk. The impact of endocrine disruptor pesticides on fertility has also been discussed.

Based on the epidemiological studies since 2000, the study concluded that pesticide exposure may affect spermatogenesis leading to poor semen quality and reduced male fertility. Furthermore, an increasing number of epidemiological studies tend to link environmental exposure to pesticides and hormone-dependent cancer risks. High levels of PCBs, DDE, and DDT have been found in fat samples from women with breast cancer. The risk of breast cancer is said to be four times greater in women with increased blood levels of DDE ]. One of the latest epidemiological studies performed in Spain between 1999 and 2009 shows that among a total of 2,661 cases of breast cancer reported in the female population, 2,173 (81%) were observed in areas of high pesticide contamination. Moreover, it was also suggested that women with hormone responsive breast cancer have a higher DDE body burden than women with benign breast disease. Similar studies have revealed correlations between damage to the immune system and increased amounts of organochlorine residues in certain cancerous tissues. Numerous other studies support the hypothesis that pesticide exposure influences the risk of breast cancer, but few of them are really conclusive due to some inconsistent data across the study. Further research is required to explore long-term follow-up beginning in early life, with opportunities for exposure measurement at critical periods of vulnerability. Moreover, improvements are needed in the cohort sample size and standardization of exposure assessments methods. Finally, researchers also need to consider simultaneous co-exposures to these substances and other chemicals and whether they may act in an additive, synergistic, or antagonistic manner.

There may also be a connection between pesticide exposure and prostate cancer. Various studies have consistently demonstrated a higher risk in agricultural populations than in the general population. For example, pesticides (in particular DDT) were associated with a statistically significant higher rate of prostate cancer among farmers (exposed to organochloride pesticides) in a multi-site case-control study carried out in five rural areas between 1990–92 in Italy. Several studies in the USA and Sweden showed that farmers and commercial pesticide applicators have a slightly and/or significantly higher rate of prostate cancer than the general population.

Several meta-analyses, cohort studies and case-control studies on the risk of prostate cancer in populations exposed occupationally or professionally to pesticides have been conducted in recent years (and reference therein). They all showed a significantly higher risk of prostate cancer estimated at between 10 and 40%, the higher values being for professional exposure. Quite recently, a study analyzed the relationship between exposure to chlordecone (organochloride pesticide extensively used for more than 30 years in the French West Indies to control the banana root borer) and the risk of prostate cancer. It showed a significant increase in the risk of prostate cancer with increasing plasma chlordecone concentrations and supported the hypothesis that exposure to environmental estrogens may increase the risk of prostate cancer.

However, in spite of these outcomes, the hypothesis that such excess risk is related to the use of pesticides has not yet been formally demonstrated. Various other factors have been suggested to explain the increase in prostate cancer in agricultural or rural populations, such as dietary issues, contact with infectious agents via livestock, dust, tobacco and chemical products. Rigorous studies with larger cases that accurately and objectively estimate pesticide exposures and consider gene-environment interactions are needed to determine a potential relationship between pesticides and prostate cancer.

Biomonitoring for Human Exposure Assessment

Exposure to pesticides can occur via numerous pathways, including household use of pesticide products, dietary exposure to pesticide residues, and exposure to agricultural drift. Biological monitoring studies indicate that pesticide exposures are widespread in the human population. Dietary exposure comes from residues in fruits, vegetables, and from contaminated meat, fish, rice and dairy products. The European Commission estimated that, in 2005, consumer intake was always below the acceptable daily intakes (ADI) for long-term exposures. Several recent studies also show the difference between EDI and ADI. However, according to the European report, the acute reference dose (a parameter for high short-term intakes, usually in one day or one meal) was exceeded for some pesticides in different vegetables and fruits and 26.7% of samples show residues of more than one pesticide, with a significant upward trend as compared to previous years. Food intake is not the only exposure pathway for the general population. Living near sites where pesticides are used, manufactured or disposed of may significantly increase environmental exposure through inhalation and contact with air, water and soil.

Human exposure to pesticides is assessed by measuring the levels of pesticides in human samples such as breast milk, maternal blood and serum, urine and sometime umbilical cord blood. Improvements in analytical techniques have made it possible to detect pesticides and their metabolites at trace levels (from milligrams per kilogram to femtograms per kilogram in some laboratories) in almost all human samples. Table 1 reports the detection of pesticides in human samples.

Most of these studies show evidence of higher levels of pesticides in the exposed population (for example due to their occupation or geographical location) than in non-exposed control people. For example, a relation was established between employment in agriculture of Spanish women during pregnancy and serum levels of organochlorine endocrine disruptor pesticides, including DDT and isomers (despite their being banned in Spain since 1977). Also, higher levels of DDTs and HCHs were found in maternal milk and blood samples in Chinese provinces than in developed or industrialized countries. Finally, higher concentrations of several pesticides were also found in urine and plasma of pregnant Israeli women compared to other populations of pregnant women in the United States and the Netherlands.

Pesticide metabolites are also monitored in human samples because they can be representative of a global contamination. This is particularly true for organophosphorus compounds. Alkyl phosphates have been reported in human samples (urine, hair) as representative of exposure to organophosphate pesticides, and some authors have observed a significant difference in the levels of total dialkyl phosphates among exposed and no exposed groups.

Discussion and Perspectives

Endocrine disruptor pesticides are widely used for agricultural, municipal, home and medical purposes worldwide. Humans are exposed to these compounds, and due to their toxic properties, the consequences of this exposure on human hormoel-dependent pathologies are being established. Most risk assessment studies and some epidemiologic studies have looked at the exposure and toxicology of a single compound. However, two other considerations must be included: the presence of pesticide by-products and the cumulative exposure to pesticides multiresidue.

It is undisputed that in some cases, pesticide by-products can exhibit greater harmful effects than their parent compounds. For example, one study showed that, at the organism level, the only sublethal effect seen was an increase in heart rate at low concentration and a decrease at higher concentration with the use of aldicarb-sulfoxide but not with aldicarb. Another study reported that the oxons of methyl-parathion, chlorpyrifos and diazinon were 15 to 10 times more toxic (to sperm DNA) than their corresponding parent compounds. As another example, in vitro studies confirmed that 2,4-dichlorophenoxyacetic acid (2,4-D), a commonly used organophosphate herbicide promoting the proliferation of androgen-sensitive cells, is a known estrogen receptor ligand. Vinclozolin degrades to several metabolites in the soil, in the plants and in animal organisms. Two hydrolytic degradation products, 2-[[(3,5- dichlorophenyl)-carbamoyl]oxy]-2-methyl-3-butenoic acid and 3′,5″-dichloro-2-hydroxy-methylbut-3-enalide, have been identified as anti-androgenic compounds that mediate the adverse effects of vinclozolin.

Furthermore, the combined actions of pesticides also need also to be addressed in the risk assessment process because mixtures of these substances may cause higher toxic effects than those expected from the single compounds. For example an equimolar mixture of three pesticides (deltamethrin, methiocarb, and prochloraz) suppressed androgen receptor (AR) activation in vitro. Also, under the additional presence of simazin and tribenuronmethyl, weight changes of the adrenal gland and alterations in gene expression of AR-associated genes were observed in vivo in castrated testosterone-treated rats. The question of the combined effect of mixtures of contaminants has attracted the attention of the scientific community. Predictive approaches are generally based on the mathematical concepts of Concentration Addition (CA) and Independent Action (IA), both predicting the toxicity of a mixture based on the individual toxicities of the mixture components (e.g., and references therein). Recently, a review showed that some other models could be useful as tools to assess combined tissue doses and to help predict potential interactions including thresholds for such effects.

Finally, the impact of synthetic pesticides, due in particular to an excessive use (including environmental pollution and implications to human health) have led to modifications in agricultural practices and various national and international regulations limiting their use. Further limitations and/or bans should be sought, along with alternative solutions that are safer and non-toxic to the environment and humans. One such alternative is so called “natural pesticides” that are not synthetically produced, but are derived from nature such as botanicals pesticides (pyrethrum, limonene, and many others), microbial/biological agents (microbes, parasites) and inorganic minerals (boric acid, limestone, diatomaceous earth). These solutions are generally assumed to be less toxic for human health than synthetic pesticides and could represent an interesting alternative. But their usefulness is actually questionable because some such pesticides are not potent enough to control pests but at the same time do exhibit adverse effects for human health (i.e. “natural pyrethroids”). Further studies are needed on the occurrence, fate and impact of such pesticides on the ecosystem and public health.

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    Not in our library10.1097/00001648-199709000-00011

  60. 60.

    Carbone P, Giordano F, Nori F, Mantovani A, Taruscio D, Lauria L, Figà-Talamanca I. Cryptorchidism and hypospadias in the Sicilian district of Ragusa and the use of pesticides. Reprod. Toxicol. 2006;22:8-12.

    Not in our library10.1016/j.reprotox.2006.01.006

  61. 61.

    Weidner IS, Moller H, Jensen TK, Skakkebæk NE. Cryptorchidism and hypospadias in sons of gardeners and farmers. Environ. Health Perspect. 1998;106:793-796.

    Not in our library10.1289/ehp.98106793

  62. 62.

    Skakkebæk NE, Rajpert-De Meyts E, Main KM. Testicular dysgenesis syndrome, an increasingly common developmental disorder with environmental aspects. Hum. Reprod. 2001;16:972-978.

    Not in our library10.1093/humrep/16.5.972

  63. 63.
    Persistent Pesticides in Human Breast Milk and Cryptorchidism · 2006
    No notice
  64. 64.

    Roeleveld N, Bretveld R. The impact of pesticides on male fertility. Curr. Opin. Obstet. Gynecol. 2008;20:229-233.

    Not in our library10.1097/gco.0b013e3282fcc334

  65. 65.

    McKinlay R, Plant JA, Bell JNB, Voulvoulis N. Endocrine disrupting pesticides, Implications for risk assessment. Environ. Int. 2008;34:168-183.

    Not in our library10.1016/j.envint.2007.07.013

  66. 66.

    PPDB: Pesticide Properties DataBase.

    Not in our library

  67. 67.

    Kim DO, Lee SK, Jeon TW, Jin CH, Hyun SH, Kim EJ, Moon GI, Kim JA, Lee ES, Lee BM, et al. Role of metabolism in parathion-induced hepatotoxicity and immunotoxicity. J. Toxicol. Environ. Health A. 2005;68:2187-2205.

    Not in our library10.1080/15287390500180549

  68. 68.

    Panuwet P, Prapamontol T, Chantara S, Thavornyuthikarn P, Montesano MA, Whitehead R, Barr DB. Concentrations of urinary pesticide metabolites in small-scale farmers in Chiang Mai Province; Thailand. Sci. Total Environ. 2008;407:655-668.

    Not in our library10.1016/j.scitotenv.2008.08.044

  69. 69.
    Semen quality in relation to biomarkers of pesticide exposure. · 2003
    No notice
  70. 70.

    Singh AK. Acute effects of acephate and methamidophos and interleukin-1 on corticotropin-releasing factor (CRF) synthesis in and release from the hypothalamus in vitro. Comp. Biochem. Physiol. C Toxicol. Pharmacol. 2002;132:9-24.

    Not in our library10.1016/s1532-0456(02)00020-0

  71. 71.

    Inoue S, Saito T, Mase H, Suzuki Y, Takazawa K, Yamamoto I, Inokuchi S. Rapid simultaneous determination for organophosphorus pesticides in human serum by LC–MS. J. Pharm. Biomed. Anal. 2007;44:258-264.

    Not in our library10.1016/j.jpba.2007.01.036

  72. 72.

    Rollerová EE. Interaction of acetochlor with estrogen receptor in the rat uterus. Acetochlor—possible endocrinemodulator? Gen. Physiol. Biophys. 2000;19:73-84.

    Not in our library

  73. 73.
    Exposure to the herbicide acetochlor alters thyroid hormone-dependent gene expression and metamorphosis in Xenopus Laevis. · 2002
    No notice
  74. 74.

    Mikamo E, Harada S, Nishikawa J, Nishihara T. Endocrine disruptors induce cytochrome P450 by affecting transcriptional regulation via pregnane X receptor. Toxicol Appl. Pharmacol. 2003;193:66-72.

    Not in our library10.1016/j.taap.2003.08.001

  75. 75.

    Klotz D, Arnold SF, McLachlan JA. Inhibition of 17 beta-estradiol and progesterone activity in human breast and endometrial cancer cells by carbamate insecticides. Life Sci. 1997;60:1467-1475.

    Not in our library10.1016/s0024-3205(97)00098-2

  76. 76.

    Lemaire G, Terouanne B, Mauvais P, Michel S, Rahmani R. Effect of organochlorine pesticides on human androgen receptor activation in vitro. Toxicol. Appl. Pharmacol. 2004;196:235-246.

    Not in our library10.1016/j.taap.2003.12.011

  77. 77.

    Cruz S, Lino C, Silveira MI. Evaluation of organochlorine pesticide residues in human serum from an urban and two rural populations in Portugal. Sci. Total Environ. 2003;317:23-35.

    Not in our library10.1016/s0048-9697(03)00334-6

  78. 78.

    Botella B, Crespo J, Rivas A, Cerrillo I, Olea-Serrano MF, Olea N. Exposure of women to organochlorine pesticides in Southern Spain. Environ. Res. 2004;96:34-40.

    Not in our library10.1016/j.envres.2003.10.001

  79. 79.

    Nasir K, Bilto YY, Al-Shuraiki Y. Residues of chlorinated hydrocarbon insecticides in human milk of Jordanian women. Environ. Pollut. 1998;99:141-148.

    Not in our library10.1016/s0269-7491(97)00195-4

  80. 80.

    Cooper R, Stoker TE, Tyrey L, Goldman JM, McElroy WK. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Toxicol. Sci. 2000;53:297-307.

    Not in our library10.1093/toxsci/53.2.297

  81. 81.

    Sanderson JT, Seinen W, Giesy JP, van den Berg M. 2-Chloro-s-triazine herbicides induce aromatase (CYP19) activity in H295R human adrenocortical carcinoma cells, a novel mechanism for estrogenicity? Toxicol. Sci. 2000;54:121-127.

    Not in our library10.1093/toxsci/54.1.121

  82. 82.
    Atrazine-induced hermaphroditism at 0.1 ppb in American leopard frogs (Rana pipiens): laboratory and field evidence. · 2003
    No notice
  83. 83.

    Thibaut R, Porte C. Effects of endocrine disrupters on sex steroid synthesis and metabolism pathways in fish. J. Steroid Biochem. Mol. Biol. 2004;92:485-494.

    Not in our library10.1016/j.jsbmb.2004.10.008

  84. 84.

    Curwin BD, Hein MJ, Sanderson WT, Striley C, Heederik D, Kromhout H, Reynolds SJ, Alavanja MC. Urinary Pesticide Concentrations Among Children; Mothers and Fathers Living in Farm and Non-Farm Households in Iowa. Ann. Occup. Hyg. 2007;51:53-65.

    Not in our library10.1093/annhyg/mel062

  85. 85.

    Barr DB, Barr JR, Maggio VL, Whitehead RD, Sadowski MA, Whyatt RM, Needham LL. A multi-analyte method for the quantification of contemporary pesticides in human serum and plasma using high-resolution mass spectrometry. J. Chromatogr. B Analyt. Technol. Biomed. Life Sci. 2002;778:99-111.

    Not in our library10.1016/s0378-4347(01)00444-3

  86. 86.

    Morinaga H, Yanase T, Nomura M, Okabe T, Goto K, Harada N, Nawata H. A benzimidazole fungicide; benomyl; and its metabolite; carbendazim; induce aromatase activity in a human ovarian granulose-like tumor cell line (KGN). Endocrinology. 2004;145:1860-1869.

    Not in our library10.1210/en.2003-1182

  87. 87.

    Kim IY, Shin JH, Kim HS, Lee SJ, Kang IH, Kim TS, Moon HJ, Choi KS, Moon A, Han SY. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. J. Reprod. Dev. 2004;50:245-255.

    Not in our library10.1262/jrd.50.245

  88. 88.

    Ostrea EM, Bielawski DM, Posecion NC, Corrion M, Villanueva-Uy E, Bernardo RC, Jin Y, Janisse JJ, Ager JW. Combined analysis of prenatal (maternal hair and blood) and neonatal (infant hair; cord blood and meconium) matrices to detect fetal exposure to environmental pesticides. Environ. Res. 2009;10:116-122.

    Not in our library10.1016/j.envres.2008.09.004

  89. 89.

    Trosken EE, Scholz K, Lutz RW, Volkel W, Zarn JA, Lutz WK. Comparative assessment of the inhibition of recombinant human CYP19 (aromatase) by azoles used in agriculture and as drugs for humans. Endocr. Res. 2004;30:387-394.

    Not in our library10.1081/erc-200035093

  90. 90.

    Okubo T, Yokoyama Y, Kano K, Soya Y, Kano I. Estimation of estrogenic and antiestrogenic activities of selected pesticides by MCF-7 cell proliferation assay. Arch. Environ. Contam. Toxicol. 2004;46:445-453.

    Not in our library10.1007/s00244-003-3017-6

  91. 91.

    Goad R, Goad J, Atieh B, Gupta R. Carbofuran-Induced endocrine disruption in adult male rats. Toxicol. Mech. Methods. 2004;14:233-239.

    Not in our library10.1080/15376520490434476

  92. 92.

    Barr DB, Ananth CV, Yan X, Lashley S, Smulian JC, Ledoux TA, Hore P, Robson MG. Pesticide concentrations in maternal and umbilical cord sera and their relation to birth outcomes in a population of pregnant women and newborns in New Jersey. Sci. Total Environ. 2010;408:790-795.

    Not in our library10.1016/j.scitotenv.2009.10.007

  93. 93.

    Tessier D, Matsumura F. Increased ErbB-2 tyrosine kinase activity; MAPK phosphorylation; and cell proliferation in the prostate cancer cell line LNCaP following treatment by select pesticides. Toxicol. Sci. 2001;60:38-43.

    Not in our library10.1093/toxsci/60.1.38

  94. 94.

    Röllin HB, Sandanger TM, Hansen L, Channa K, Odland JØ. Concentration of selected persistent organic pollutants in blood from delivering women in South Africa. Sci. Total Environ. 2009;408:146-152.

    Not in our library10.1016/j.scitotenv.2009.08.049

  95. 95.

    Kang JH, Park H, Chang YS, Choi JW. Distribution of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) in human serum from urban areas in Korea. Chemosphere. 2008;73:1625-1631.

    Not in our library10.1016/j.chemosphere.2008.07.087

  96. 96.

    Schinas V, Leotsinidis M, Alexopoulos A, Tsapanos V, Kondakis XG. Organochlorine pesticide residues in human breast milk from southwest Greece, associations with weekly food consumption patterns of mothers. Arch. Environ. Health. 2000;55:411-417.

    Not in our library10.1080/00039890009604039

  97. 97.

    Tanabe S, Kunisue T. Persistent organic pollutants in human breast milk from Asian countries. Environ. Pollut. 2007;146:400-413.

    Not in our library10.1016/j.envpol.2006.07.003

  98. 98.

    Polder A, Thomsen C, Lindström G, Løken KB, Skaare JU. Levels and temporal trends of chlorinated pesticides; polychlorinated biphenyls and brominated flame retardants in individual human breast milk samples from Northern and Southern Norway. Chemosphere. 2008;73:14-23.

    Not in our library10.1016/j.chemosphere.2008.06.002

  99. 99.

    Devanathan G, Subramanian A, Someya M, Sudaryanto A, Isobe T, Takahashi S, Chakraborty P, Tanabe S. Persistent organochlorines in human breast milk from major metropolitan cities in India. Environ. Pollut. 2009;157:148-154.

    Not in our library10.1016/j.envpol.2008.07.011

  100. 100.

    Jarrell JF, Villeneuve D, Franklin C, Bartlett S, Wrixon W, Kohut J, Zouves CG. Contamination of human ovariam follicular fluid and serum by chlorinated organic compounds in three Canadian cities. Can. Med. Assoc. J. 1993;148:1321-1327.

    Not in our library

  101. 101.

    Tapiero HT, Nguyen BG, Tew KD. Estrogens and environmental estrogens. Biomed. Pharmacother. 2002;56:36-44.

    Not in our library10.1016/s0753-3322(01)00155-x

  102. 102.

    Fang H, Tong W, Branham WS, Moland CL, Dial SL, Hong H, Xie Q, Perkins R, Owens W, Sheehan DM. Study of 202 natural; synthetic; and environmental chemicals for binding to the androgen receptor. Chem. Res. Toxicol. 2003;16:1338-1358.

    Not in our library10.1021/tx030011g

  103. 103.

    Vinggaard A, Breinholt V, Larsen JC. Screening of selected pesticides for oestrogen receptor activation in vitro. Food Addit. Contam. 1999;16:533-542.

    Not in our library10.1080/026520399283678

  104. 104.

    Kang HG, Jeong SH, Cho JH, Kim DG, Park JM, Cho MH. Chlropyrifos-methyl shows anti-androgenic activity without estrogenic activity in rats. Toxicology. 2004;199:219-230.

    Not in our library10.1016/j.tox.2004.02.025

  105. 105.

    Chen H, Xiao J, Hu G, Zhou J, Xiao H, Wang X. Estrogenicity of organophosphorus and pyrethroid pesticides. J. Toxicol. Environ. Health A. 2002;65:1419-1435.

    Not in our library10.1080/00984100290071243

  106. 106.

    McCarthy AR, Thomson BM, Shaw IC, Abella AD. Estrogenicity of pyrethroid insecticide metabolites. J. Environ. Monit. 2006;8:197-202.

    Not in our library10.1039/b511209e

  107. 107.

    Hardt J, Angerer J. Biological monitoring of workers after the application of insecticidal pyrethroids. Int. Arch. Occup. Environ. Health. 2003;76:492-498.

    Not in our library10.1007/s00420-003-0451-8

  108. 108.

    Tapiero HT, Nguyen BG, Tew KD. Estrogens and environmental estrogens. Biomed. Pharmacother. 2002;56:36-44.

    Not in our library10.1016/s0753-3322(01)00155-x

  109. 109.
    Xenoestrogen-Induced ERK-1 and ERK-2 Activation via Multiple Membrane-Initiated Signaling Pathways · 2004
    No notice
  110. 110.

    Qu W, Suri RPS, Bi X, Sheng G, Fu J. Exposure of young mothers and newborns to organochlorine pesticides (OCPs) in Guangzhou; China. Sci. Total Environ. 2010;408:3133-3138.

    Not in our library10.1016/j.scitotenv.2010.04.023

  111. 111.

    Fujii Y, Haraguchi K, Harada KH, Hitomi T, Inoue K, Itoh Y, Watanabe T, Takenaka K, Uehara S, Yang HR, et al. Detection of dicofol and related pesticides in human breast milk from China; Korea and Japan. Chemosphere. 2011;82:25-31.

    Not in our library10.1016/j.chemosphere.2010.10.036

  112. 112.

    Foster W, Chan S, Platt L, Hughes C. Detection of endocrine disrupting chemicals in samples of second trimester human amniotic fluid. J. Clin. Endocrinol. Metab. 2000;85:2954-2957.

    Not in our library10.1210/jcem.85.8.6850

  113. 113.

    Tsatsakis AM, Tzatzarakis MN, Tutudaki M. Pesticide levels in head hair samples of Cretan population as an indicator of present and past exposure. Forensic Sci. Int. 2008;176:67-71.

    Not in our library10.1016/j.forsciint.2007.07.017

  114. 114.

    Pathak R, Ahmed RS, Tripathi AK, Guleria K, Sharma CS, Makhijani SD, Banerjee BD. Maternal and cord blood levels of organochlorine pesticides, Association with preterm labor. Clin. Biochem. 2009;42:746-749.

    Not in our library10.1016/j.clinbiochem.2008.11.007

  115. 115.

    Manabe M, Kanda S, Fukunaga K, Tsubura A, Nishiyama T. Evaluation of the estrogenic activities of some pesticides and their combinations using MtT/Se cell proliferation assay. Int. J. Hyg. Environ. Health. 2006;209:413-421.

    Not in our library10.1016/j.ijheh.2006.04.004

  116. 116.

    Soto AM, Chung KL, Sonnenschein C. The pesticides endosulfan; toxaphene; and dieldrin have estrogenic effects on human estrogen-sensitive cells. Environ. Health Perspect. 1994;102:380-383.

    Not in our library10.1289/ehp.94102380

  117. 117.

    Rawlings NC, Cook SJ, Waldbillig D. Effects of the pesticides carbofuran; chlorpyrifos; dimethoate; lindane; triallate; trifluralin; 2;4-D; and pentachlorophenol on the metabolic endocrine and reproductive endocrine system in ewes. J. Toxicol. Environ. Health A. 1998;54:21-36.

    Not in our library10.1080/009841098159006

  118. 118.

    Mahjoubi-Samet A, Hamadi F, Soussia L, Fadhel G, Zeghal N. Dimethoate effects on thyroid function in suckling rats. Ann. Endocrinol. 2005;66:96-104.

    Not in our library10.1016/s0003-4266(05)81705-6

  119. 119.

    Hurst MRR, Sheahan DA. The potential for estrogenic effects of pesticides in headwater streams in the UK. Sci. Total Environ. 2003;301:87-96.

    Not in our library10.1016/s0048-9697(02)00288-7

  120. 120.

    Grunfeld HT, Bonefeld-Jorgensen EC. Effect of in vitro estrogenic pesticides on human estrogen receptor alpha and beta mRNA levels. Toxicol. Lett. 2004;151:467-480.

    Not in our library10.1016/j.toxlet.2004.03.021

  121. 121.

    Tamura H, Yoshikawa H, Gaido KW, Ross SM, DeLisle RK, Welsh WJ, Richard AM. Interaction of organophosphate pesticides and related compounds with the androgen receptor. Environ. Health Perspect. 2003;111:545-552.

    Not in our library10.1289/ehp.5671

  122. 122.

    Verslycke T. Testosterone and energy metabolism in the estuarine mysid Neomysis integer (Crustacea, Mysidacea) following exposure to endocrine disruptors. Environ. Toxicol. Chem. 2004;23:1289-1296.

    Not in our library10.1897/03-338

  123. 123.

    Garey J, Wolff MS. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Biochem. Biophys. Res. Commun. 1998;251:855-859.

    Not in our library10.1006/bbrc.1998.9569

  124. 124.

    Eil CC, Nisula BC. The binding properties of pyrethroids to human skin fibroblast androgen receptors and to sex hormone binding globulin. J. Steroid Biochem. 1990;35:409-414.

    Not in our library10.1016/0022-4731(90)90248-q

  125. 125.

    Chen HY, Liu R, He J, Song L, Bian Q, Xu L, Zhou J, Xiao H, Dai G, Chang HC, Wang X. Effects of fenvalerate on progesterone production in cultured rat granulosa cells. Reprod. Toxicol. 2005;20:195-202.

    Not in our library10.1016/j.reprotox.2005.01.013

  126. 126.
    Differential Effects of Glyphosate and Roundup on Human Placental Cells and Aromatase · 2005
    No notice
  127. 127.

    Ralph JJ, Orgebin-Crist MC, Lareyre JJ, Nelson CC. Disruption of androgen regulation in the prostate by the environmental contaminant hexachlorobenzene. Environ. Health Perspect. 2003;111:461-466.

    Not in our library10.1289/ehp.5919

  128. 128.

    Verreault J, Skaare JU, Jenssen BM, Gabrielsen GW. Effects of organochlorine contaminants on thyroid hormone levels in Arctic breeding glaucous gulls; Larus hyperboreus. Environ. Health Perspect. 2004;112:532-537.

    Not in our library10.1289/ehp.6756

  129. 129.

    Beard AB, Rawlings NC. Thyroid function and effects on reproduction in ewes exposed to the organochlorine pesticides lindane or pentachlorophenol (PCP) from conception. J. Toxicol. Environ. Health A. 1999;58:509-530.

    Not in our library10.1080/009841099157124

  130. 130.

    Oduma JA, Wango EO, Oduor-Okelo D, Makawiti DW, Odongo H. In vivo and In vitro effects of graded doses of the pesticide heptachlor on female sex steroid production in rats. Comp. Biochem. Physiol. C Pharmacol. Toxicol. Endocrinol. 1995;111:191-196.

    Not in our library10.1016/0742-8413(95)00029-n

  131. 131.

    Fang H, Tong W, Branham WS, Moland CL, Dial SL, Hong H, Xie Q, Perkins R, Owens W, Sheehan DM. Study of 202 natural; synthetic; and environmental chemicals for binding to the androgen receptor. Chem. Res. Toxicol. 2003;16:1338-1358.

    Not in our library10.1021/tx030011g

  132. 132.
    Endocrine Disruptors and the Thyroid Gland—A Combined in Vitro and in Vivo Analysis of Potential New Biomarkers · 2007
    No notice
  133. 133.

    Ishihara A, Nishiyama N, Sugiyama S, Yamauchi K. The effect of endocrine disrupting chemicals on thyroid hormone binding to Japanese quail transthyretin and thyroid hormone receptor. Gen. Comp. Endocrinol. 2003;134:36-43.

    Not in our library10.1016/s0016-6480(03)00197-7

  134. 134.

    Porter W, Green SM, Debbink NL, Carlson I. Groundwater pesticides, interactive effects of low concentrations of carbamates aldicarb and methomyl and the triazine metribuzin on thyroxine and somatotropin levels in white rats. J. Toxicol. Environ. Health. 1993;40:15-34.

    Not in our library10.1080/15287399309531773

  135. 135.
    Measurement of pesticides and other toxicants in amniotic fluid as a potential biomarker of prenatal exposure: a validation study. · 2003
    No notice
  136. 136.

    Sonnenschein C, Soto AM. An updated review of environmental estrogen and androgen mimics and antagonists. J. Steroid Biochem. Mol. Biol. 1998;65:143-150.

    Not in our library10.1016/s0960-0760(98)00027-2

  137. 137.

    Vinggaard AM, Hass U, Dalgaard M, Andersen HR, Bonefeld-Jørgensen E, Christiansen S, Laier P, Poulsen ME. Prochloraz, an imidazole fungicide with multiple mechanisms of action. Int. J. Androl. 2006;29:186-192.

    Not in our library10.1111/j.1365-2605.2005.00604.x

  138. 138.

    Salazar KD, Schafer R, Barnett JB, Miller MR. Evidence for a novel endocrine disruptor, the pesticide propanil requires the ovaries and steroid synthesis to enhance humoral immunity. Toxicol. Sci. 2006;93:62-74.

    Not in our library10.1093/toxsci/kfl038

  139. 139.

    Kim SS, Kwack SJ, Lee RD, Lim KJ, Rhee GS, Seok JH, Kim BH, Won YH, Lee GS, Jeung EB, et al. Assessment of estrogenic and androgenic activities of tetramethrin in vitro and in vivo assays. J. Toxicol. Environ. Health A. 2005;68:2277-2289.

    Not in our library10.1080/15287390500182453

  140. 140.

    Nicolau GG. Circadian rhythms of RNA; DNA and protein in the rat thyroid; adrenal and testis in chronic pesticide exposure. III. Effects of the insecticides (dichlorvos and trichlorphon). Physiologie. 1983;20:93-101.

    Not in our library

  141. 141.

    Falck F, Ricci A, Wolff MS, Godbold J, Deckers P. Pesticides and polichlorinated biphenyl residues in human breast lipids and their relation to breast cancer. Arch. Environ. Health. 1992;47:143-146.

    Not in our library

  142. 142.

    Davis DL, Bradlow HL, Wolff M, Woodruff T, Hoel DG, Anton-Culver H. Hypothesis, xenoestrogens as preventable causes of breast cancer. Environ. Health Perspect. 1993;101:372-377.

    Not in our library10.1289/ehp.93101372

  143. 143.

    Parron T, Alarcon R, Requena MDM, Hernandez A. Increased breast cancer risk in women with environmental exposure to pesticides. Toxicol. Lett. 2010;196:S180.

    Not in our library

  144. 144.

    Dewailly E, Nantel A, Weber JP, Meyer F. High levels of PCBs in breast of Inuit women from arctic Quebec. Bull. Environ. Contam. Toxicol. 1989;4:641-646.

    Not in our library10.1007/bf01701981

  145. 145.

    Krieger N, Wolff MS, Hiatt RA, Rivera M, Vogelman J, Orentreich N. Breast cancer and serum organochlorines, a prospective study among white; black; and Asian women. J. Natl. Cancer Inst. 1994;86:589-599.

    Not in our library10.1093/jnci/86.8.589

  146. 146.

    Cohn BA. Developmental and environmental origins of breast cancer: DDT as a case study. Reprod. Toxicol. 2011;31:302-311.

    Not in our library10.1016/j.reprotox.2010.10.004

  147. 147.

    Meeker JD. Exposure to environmental endocrine disrupting compounds and men’s health. Maturitas. 2010;66:236-241.

    Not in our library10.1016/j.maturitas.2010.03.001

  148. 148.

    Alavanja MC, Samanic C, Dosemeci M, Lubin J, Tarone R, Lynch CF, Knott C, Thomas K, Hoppin JA, Barker J, Coble J, Sandler DP, Blair A. Use of agricultural pesticides and prostate cancer risk in the Agricultural Health Study cohort. Am. J. Epidemiol. 2003;157:800-814.

    Not in our library10.1093/aje/kwg040

  149. 149.

    Prins GS. Endocrine disruptors and prostate cancer risk. Endocr. Relat. Cancer. 2008;15:649-656.

    Not in our library10.1677/erc-08-0043

  150. 150.

    Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, Zoeller RT, Gore AC. Endocrine-disrupting chemicals; An Endocrine Society scientific statement. Endocr. Rev. 2009;30:293-342.

    Not in our library10.1210/er.2009-0002

  151. 151.

    Settimi L, Masina A, Andrion A, Axelson O. Prostate cancer and exposure to pesticides in agricultural settings. Int. J. Cancer. 2003;104:458-461.

    Not in our library10.1002/ijc.10955

  152. 152.

    Alavanja MC, Sandler DP, Lynch CF, Knott C, Lubin JH, Tarone R, Thomas K, Dosemeci M, Barker J, Hoppin JA, et al. Cancer incidence in the agricultural health study. Scand. J. Work Environ. Health. 2005;31:39-45.

    Not in our library

  153. 153.

    Dich J, Wiklund K. Prostate cancer in pesticide applicators in Swedish agriculture. Prostate. 1998;34:100-112.

    Not in our library10.1002/(sici)1097-0045(19980201)34:2<100::aid-pros4>3.0.co;2-o

  154. 154.

    Ndong JR, Blanchet P, Multigner L. Pesticides et cancer de la prostate: données épidémiologiques. Bull. Cancer. 2009;96:171-180.

    Not in our library10.1684/bdc.2008.0812

  155. 155.

    Multigner L, Ndong JR, Giusti A, Romana M, Delacroix-Maillard H, Cordier S, Jégou B, Thome JP, Blanchet P. Chlordecone exposure and risk of prostate cancer. J. Clin. Oncol. 2010;28:3457-3462.

    Not in our library10.1200/jco.2009.27.2153

  156. 156.

    European Commission. Monitoring of Pesticide Residues in Products of Plant Origin in the European Union, Norway, Iceland and Liechtenstein. 2007.

    Not in our library

  157. 157.

    Iñigo-Nuñez S, Herreros MA, Encinas T, Gonzalez-Bulnes A. Estimated daily intake of pesticides and xenoestrogenic exposure by fruit consumption in the female population from a Mediterranean country (Spain). Food Control. 2010;21:471-477.

    Not in our library

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