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A Precautionary Approach to Reducing American Exposure to Endocrine Disrupting Chemicals

Policy Date: 11/9/2010
Policy Number: 20104

There is clear evidence that exogenous hormones—those originating outside the body—can interfere with our own hormone function1 Endocrine disrupting chemicals (EDCs) are broadly defined as chemical compounds that can interfere with hormone action. Well-known examples include estrogen, classified by the International Agency for Research on Cancer as a Group 1 human carcinogen,2 and diethylstilbestrol or DES (the first synthetic hormone), which the US Food and Drug Administration (FDA) banned in 1971 for use in pregnant women after scientific studies showed higher cancer risks in their daughters.3–5
The Endocrine Society—the premier professional organization for basic and clinical endocrine research and the treatment of endocrine disorders—published its first scientific statement in June 2009, summarizing voluminous science on the EDCs.6 EDCs identified included a heterogeneous list of synthetic and natural compounds also categorizable as pharmaceuticals (e.g., estrogen, DES), pesticides (methoxychlor, chlorpyrifos, dichlorodiphenyltrichloroethane or DDT), fungicides (vinclozolin), plastic monomers (bisphenol A or BPA), plasticizer additives (phthalates), polychlorinated biphenyls, polybrominated biphenyls, and dioxins.

Exposure to EDCs
Sources of human exposure to EDCs are diverse and, therefore, difficult to characterize in their entirety. Known or strongly suspected EDCs include, for example, not only lawn, garden, and agricultural pesticides but also chemicals found in commercial toys and other household and commercial products, as well as chemical ingredients in food packaging. In addition, overall exposure to EDCs involves only a part of widespread persistent exposure to a broader mix of indoor and outdoor chemicals and contaminants. Many such industrial chemicals leach into soil or groundwater and often enter the food chain, accumulating in humans and other animals higher in the food chain. People exposed to EDCs, therefore, consist not only of those working directly with industrial chemicals and with pesticides and fungicides but also the rest of the population that drinks the water, breathes the air, ingests food, contacts the soil, or uses products contaminated with these same chemicals.
In terms of cumulative EDC exposure at the individual level, the human body integrates exposure to diverse but potentially synergistic EDCs across these different sources of exposure. The National Exposure Reports of the Centers for Disease Control and Prevention (CDC) confirm that there is widespread exposure to chemical mixtures across the population, including multiple EDCs.7 Exposure begins in utero; CDC biomonitoring data indicate that several dozen industrial chemicals, including some EDCs, are routinely found in amniotic fluid.8 This finding, combined with the importance of hormones to fetal and child development, indicates the increased vulnerability of developing fetuses and infants stemming from exposure to endocrine disrupting chemicals.

EDC Toxicity
In terms of toxicity, the Endocrine Society’s June 2009 scientific statement reads in part, “Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs (endocrine disrupting chemicals) as a significant concern to public health.”6 In particular, the Endocrine Society stated that,

• Because of the shared properties of the chemicals and the similarities of the receptors and enzymes involved in the synthesis, release, and degradation of hormones, no endocrine system is immune to endocrine disrupting chemicals.
• Effects of endocrine disrupting chemicals may be transmitted to further generations through germ line epigenetic modifications or from continued exposure of offspring to the environmental insult.
• The evidence for adverse reproductive outcomes (infertility, cancers, malformations) from exposure to endocrine disrupting chemicals is strong, and there is mounting evidence for effects on other endocrine systems, including thyroid, neuroendocrine, obesity and metabolism, and insulin and glucose homeostasis.9p4

Today, many hormone-related chronic diseases are common or on the rise, including breast and prostate cancer,10–13 thyroid disease,14–16 obesity and diabetes,11,17–21 endometriosis,21 uterine fibroids,22and infertility.23,24 Although these chronic conditions are multifactorial, the Endocrine Society statement reviews extensive literature associating exposure to individual EDCs with these same diseases.
Congress formally recognized EDCs as a public health concern in 1996 when it passed the Food Quality Protection Act (FQPA) and amendments to the Safe Drinking Water Act. Thirteen years later, in 2009, the US Environmental Protection Agency (EPA) issued its first test orders for screening of dozens of high-priority pesticides for endocrine disrupting effects. However, there is no comprehensive, coordinated approach to regulating EDCs in the United States. In other words, while independent testing of some isolated few chemicals may already have shown them to have endocrine-disrupting activity, such hazard or safety testing has never been performed for the balance of the tens of thousands of EPA-registered compounds in use and in the environment today. Thus, policies must be developed to consistently and comprehensively examine all chemicals for potential EDC activity.

The Precautionary Principle
Besides the lack of safety testing, it is the nature of science that some uncertainty around specific scientific issues pertaining to individual EDCs will persist. Conventional toxicological testing of environmental chemicals, for example, is based on presumptions about high-level exposures being predictive of effects at lower levels of exposure. The robust science around EDCs generally calls that toxicological precept into question. The Endocrine Society’s 2009 position statement therefore is grounded in the Precautionary Principle: “When conclusive evidence is lacking, but sound scientific studies indicate a strong possibility for adverse health effects, it is the responsibility of the federal government to develop policies that protect people from the risk of exposure, or at the very least inform them of [the risk to public health].”25p3
Similarly, the American Public Health Association (APHA) has longstanding support for the science-based application of the Precautionary Principle, which “encourages precautionary action to prevent potential harm to fetuses, infants, and children [from the continued manufacture and use of substances], even if some cause and effect relationships have not been established with scientific certainty.”26 For example, 2009 APHA policy urges the withdrawal of intentional economic uses of exogenous hormones from food production.27 By contrast, the proposed policy would address regulation of commercial EDCs used intentionally for applications that often can unintentionally come to contaminate food and water.
The APHA also is concerned that the public may be placed at risk because critical information about potential health effects of endocrine disrupting chemicals to which Americans are exposed is being overlooked in the development of federal guidelines and regulations. Reflecting a broad consensus among the entire medical community that more needs to be done to protect the public from potential health risks of exposure to EDCs and, more specifically reflecting the findings and recommendations of The Endocrine Society’s June 2009 peer-reviewed Scientific Statement on EDCs,6 APHA therefore adopts the following resolution, largely derived from that originated by the Endocrine Society and later endorsed by the American Medical Association.28
APHA urges—
• Support for the Endocrine Society and the American Medical Association in proclaiming that more needs to be done to protect the public from potential health risks of exposure to EDCs.
• That given the magnitude and urgency of the public health threat and the recognition that collectively EDCs likely will have common or overlapping effects on the endocrine system, steps should therefore be taken by federal agencies with regulatory oversight for various individual EDCs to coordinate and find synergies among themselves to coordinate and find synergy among federal agencies with regulatory oversight over various individual EDCs.
• Health professionals and scientists with expertise in various aspects of the toxicity, exposure, and environmental fate of EDCs, throughout the lifecycle of their manufacture, use, distribution, and disposal be consulted and be active participants in the development of public policies to regulate and restrict EDCs. These may consist of, for example, endocrinologists, toxicologists, occupational/environmental medicine specialists, epidemiologists, and policymakers.
• That these public policies further should be based on data that comprehensively include both low-level and high-level exposures.

1. Colborn T, Dumanoski D, Myers JP. Our Stolen Future. 1st ed. New York, NY: Dutton, Penguin Books; 1996.
2. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Combined estrogen-progestogen contraceptives and combined estrogen-progestogen menopausal therapy. IARC Monogr Eval Carcinog Risks Hum. 2007;91:1–528. Available at: http://monographs.iarc.fr/ENG/Monographs/vol91/index.php. Accessed June 16, 2010.
3. Swan SH. Intrauterine exposure to diethylstilbestrol: long-term effects in humans. APMIS. 2000; 108:(12):793–804.
4. EXTOXNET; a project of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Available at: http://extoxnet.orst.edu/faqs/pesticide/endocrine.htm. Updated January 1998. Accessed June 16, 2010.
5. Reigart R, Cummins S. Limit hormone-disrupting chemical exposure. AAP News. 1996;12:17.
6. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, et al. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endoc Rev. 2009;30:(4):293. Available at: www.endo-society.org/journals/scientificstatements. Accessed June 10, 2010.
7. Centers for Disease Control and Prevention. National Report on Human Exposure to Environmental Chemicals. Updated April 16, 2010. Available at: www.cdc.gov/exposurereport/. Accessed June 10, 2010.
8. Barr DB, Bishop A, Needham LL. Concentrations of xenobiotic chemicals in the maternal-fetal unit. Reprod Toxicol. 2007;23:260–266.
9. Diamanti-Kandarakis E, Bourguignon J-P, Giudice LC, et al. Endocrine Disrupting Chemicals: An Endocrine Society Scientific Statement. Chevy Chase, Md: The Endocrine Society; 2009. Available at: www.endo-society.org/journals/scientificstatements/upload/edc_scientific_statement.pdf. Accessed February 1, 2011.
10. Grandjean P, Bellinger D, Berman A, et al. The Faroes statement: human health effects of developmental exposure to chemicals in our environment. Basic Clin Pharmacol Toxicol. 2008;102:73–75. Available at: http://deepblue.lib.umich.edu/bitstream/2027.42/74573/1/j.1742-7843.2007.00114.x.pdf. Accessed February 2, 2011.
11. Cowin PA, Foster P, Pedersen J, Hedwards S, McPherson SJ, Risbridger GP. Early onset endocrine disruptor induced prostatitis in the rat. Environ Health Perspect. 2008;116:923–929.
12. Gray LE, Wilson VS, Stoker TS, et al. Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals. Int J Androl.2006;29:96–104.
13. vom Saal FS, Belcher SM, Guillette LJ, et al. Chapel Hill Bisphenol A Expert Panel consensus statement: integration of mechanisms, effects in animals and potential impact to human health at current exposure levels. Reprod Toxicol. 2007;24:131–138.
14. Meeker JD, Calafat AM, Hauser R. Di(2-ethylhexyl) phthalate metabolites may alter thyroid hormone levels in men. Environ Health Perspect. 2007;115:(7):1029–1034.
15. Crofton KE, Craft ES, Hedge JM, et al. Thyroid hormone disrupting chemicals: evidence for dose-dependent additivity or synergism. Environ Health Perspect. 2005;113:(11):1549–1554.
16. Davey JC, Nomikos AP, Wungjiranirun M, et al. Arsenic as an endocrine disruptor: arsenic disrupts retinoic acid receptor-and thyroid hormone receptor-mediated gene regulation and thyroid hormone-mediated amphibian tail metamorphosis. Environ Health Perspect. 2008;116:(2):165–172.
17. Ruhlen RL, Howdeshell KL, Mao J, et al. Low phytoestrogen levels in feed increase fetal serum estradiol resulting in the “fetal estrogenization syndrome” and obesity in CD-1 mice. Environ Health Perspect. 2008;116:322–328.
18. Smink A, Ribas-Fito N, Torrent M, Mendez MA, Grimalt JO, Sunyer J. Exposure to hexachlorobenzene during pregnancy increases the risk of overweight in children aged 6 years. Acta Pediactrica. 2008;97:(10):1465–1469.
19. Hugo ER, Brandebourg TD, Woo JG, Loftus J, Alexander JW, Ben-Jonathan N. Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environ Health Perspect. 2008;116:1642–1647.
20. Lang IA, Galloway TS, Scarlett A, et al. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA. 2008;300:(11):1303–1310.
21. Rier S, Foster WG. Environmental dioxins and endometriosis. Toxicol Sci. 2002;70:161–170.
22. Newbold RR, Jefferson WR, Banks EP. Long-term adverse effects of neonatal exposure to bisphenol A on the murine female reproductive tract. Reprod Toxicol. 2007;24:253–258.
23. Hauser R, Meeker JD, Duty S, Silva MJ, Calafat AM. Altered semen quality in relation to urinary concentrations of phthalate monoester and oxidative metabolites. Epidemiology. 2006;17:682–691.
24. Swan SH, Kruse RL, Fan L, et al., and the Study for the Future of Families Research Group. Semen quality in relation to biomarkers of pesticide exposure. Environ Health Perspect. 2003;111:1478–1484.
25. The Endocrine Society. Endocrine Disrupting Chemicals: Position Statement. Chevy Chase, Md: The Endocrine Society; 2009. Available at: www.endo-society.org/advocacy/policy/upload/Endocrine-disrupting-chemicals-position-statement.pdf. Accessed February 1, 2011.
26. American Public Health Association. APHA policy statement 2000-11: The Precautionary Principle and Children’s health. Washington, DC: American Public Health Association; 2000. Available at: www.apha.org/advocacy/policy/policysearch/default.htm?id=216. Accessed December February 2, 2011.
27. American Public Health Association. APHA policy statement 2009-8. Opposition to the use of hormone growth promoters in beef and dairy cattle production. Washington, DC: American Public Health Association; 2009. Available at: www.apha.org/advocacy/policy/policysearch/default.htm?id=1379. Accessed February 17, 2010.
28. The Endocrine Society. AMA adopts endocrine society resolution calling for new policies to decrease public exposure to endocrine-disrupting chemicals. Press Release, dated November 10, 2009. Available at: www.endo-society.org/media/press/2008/AMAAdoptsSocietyResolution.cfm. Accessed June 10, 2010.