Endocrine Disruptors



The term endocrine disruptor was first used in July 1991 by scientists during a meeting held at the Wingspread Conference Center in Racine, Wisconsin. As a result of this conference, the impact of these endocrine disruptors on the endocrine system was studied intensively. The endocrine system is a network of glands and hormones that regulates many of the body's functions, such as growth, development, behavior, and maturation.

The endocrine glands include the pituitary, thyroid, adrenal, thymus, pancreas, and the male and female gonads (testes and ovaries). These glands secrete regulated amounts of hormones into the bloodstream, where they act as chemical messengers as they are carried throughout the body to control and regulate many of the body's functions. The hormones bind to specific cell sites called receptors. By binding to the receptors, the hormones trigger various responses in the tissues that contain the receptors.

These hormones are highly sensitive to chemical disruptions, especially when an organism is moving from its stage of a fertilized egg to being a fully developed baby. As cells begin to grow and differentiate in the early stage of life, important changes to hormones and proteins occur. Consequently, any type of disruption to this development, such as with a chemical disruptor, can produce damage in a developing fetus. A disruption in endocrine function during the prenatal period can produce immediate birth defects, or the effects may become evident later in adult life or in a subsequent generation. Adverse effects that might be a result of endocrine disruption include the development of cancers, reproductive and developmental effects, neurological effects (effects on behavior, learning and memory, sensory function, and psychomotor development), and immunological effects (immunosuppression, with resulting disease susceptibility).

Risk factors

One of the most highly publicized incidents of an endocrine disruptor being introduced into wildlife occurred in the middle part of the twentieth century when bald eagles consumed prey that contained high levels of dichlorodiphenyldichloroethylene (DDE), which results from the breakdown of the pesticide DDT. The endocrine system of the bald eagles was degraded when the pesticide bound to their estrogen receptor. This resulted in thinner eggshells for the female birds because less calcium was allowed to deposit onto the shells during formation. Thinner shells resulted in the eggs cracking easier, which caused a significant decline in their population. However, when DDT was banned in the 1970s, the population of bald eagles began to recover.

Another highly publicized example of endocrine disruption occurred in humans between 1948 and 1971 in Australia, Europe, and the United States. During this period, a synthetic type of estrogen called diethylstilbestrol (DES) was given to women in order to minimize the risk of miscarriage during pregnancy. However, it was eventually determined that when DES is given during the first five months of pregnancy, it can alter the development of the reproductive system of fetuses. Some daughters born to these mothers had irregular menstruation; infertility; miscarriages; abnormalities in their vagina, cervix, or uterus; and other reproduction problems. Some sons of these mothers had testicular abnormalities. The Food and Drug Administration subsequently withdrew DES from the U.S. market.


Based on changing patterns within childhood diseases and disorders, scientists are researching the effects that endocrine disruptors have on the developmental stage of children. Some of the diseases and disorders being studied are asthma, atopy, attention deficit hyperactivity disorder, autism, cancer, diabetes (type I and type II), hay fever, hearing problems, intrauterine growth restriction, learning disabilities, obesity, prematurity, and testicular dysgenesis syndrome. For instance, scientists are already suggesting various chemicals and substances to avoid during the development of the fetus and early in childhood, such as tobacco; dioxin and dioxin-like compounds; particulate air pollution, polychlorinated biphenyls, lead and methyl mercury.

Causes and symptoms

A variety of chemicals, including some pesticides, have been shown in laboratory animal studies to result in endocrine disruption. However, except for the cases of endocrine disruption caused by chemical exposures in the workplace and by the use of DES, causal relationships between exposure and adverse health effects in humans have not yet been firmly established.

There is more evidence that the endocrine systems of fish and wildlife have been affected by chemical contamination in their habitats. Groups of animals that have been affected by endocrine disruption include snails, oysters, fish, alligators and other reptiles, and birds, including gulls and eagles. Whether effects on individuals of a particular species have an impact on populations of that organism is difficult to prove. Scientists also do not know if endocrine disruption is confined to specific areas or is more widespread. In addition, proving that a specific chemical causes a particular endocrine effect is difficult, as animals are exposed to a variety of chemicals and nonchemical stressors. However, some persistent organic chemicals such as DDT, PCBs, dioxin, and some pesticides have been shown to act as endocrine disruptors in the environment. Adverse effects that may be caused by endocrine disrupting mechanisms include abnormal thyroid function and development in fish and birds; decreased fertility in shellfish, fish, birds, and mammals; decreased hatching success in fish, birds, and reptiles; demasculinization and feminization of fish, birds, reptiles, and mammals; defeminization and masculinization of gastropods, fish, and birds; and alteration of immune and behavioral function in birds and mammals. Many potential endocrine disrupting chemicals are persistent and bioaccumulate in fatty tissues of organisms and increase in concentration as they move up through the food web. Because of this persistence and mobility, they can accumulate and harm organisms far from their original source.

Public health role and response

Many laws have been enacted in the United States to help control endocrine disruptors. They include the Clean Air Act; the Clean Water Act; the Federal Insecticide, Fungicide, and Rodenticide Act; the Food, Drug and Cosmetic Act; the Safe Drinking Water Act; and the Toxic Substances Control Act.

A predisposition toward allergic reactions.
A pesticide with the formal name dichlorodiphenyltrichloroethane and the chemical formula C14H9Cl5, where C stands for carbon, H for hydrogen, and Cl for chlorine.
A steroid hormone produced primarily in the ovaries that is used for the development of female sexual characteristics.
An unborn vertebrate in which all structural features of the associated adult are recognizable.
Any chemical secreted by the endocrine gland or some types of nerve cells, which regulates the function of a specific tissue or organ.
Polychlorinated biphenyls (PCBs)—
Any compound derived from biphenyl and containing chlorine (Cl), which is considered a hazardous environmental pollutant.
Before birth.

Further, the Congress passed the Food Quality Protection Act and the Safe Drinking Water Act Amendments in 1996, in part to help screen chemicals affecting humans. Then, in 1998, due to the number of endocrine disruptors that have the potential to cause health problems in humans and wildlife, the U.S. Environmental Protection Administration (EPA) instituted the Endocrine Disruptor Screening Program. The program would set a priority for over 85,000 commercial chemicals with respect to screening and testing. The first group of chemicals to be screened was announced in April 2009. Eventually, a more comprehensive list of potentially adverse chemicals will be included in the list. The EPA will use a two-tiered system for the screening and testing process. In the first stage (tier 1), chemicals will be screened and tested for their “potential to interact with the endocrine system.” In the second stage (tier 2), the EPA will determine “the endocrine-related effects caused by each chemical and obtain information about effects at various doses.”




In order to eliminate pollutants from humans and wildlife it is generally agreed that policies need to be enacted to phase out the production of such commercial chemicals and eventually to eliminate their use. In addition, policies are also needed that require the labeling of foods, along with awareness programs that inform the public of the possibility of problems from endocrine disruptors. For instance, current mass media campaigns have made pregnant women and nursing mothers aware that some seafood contains high levels of mercury, which is harmful to fetuses and babies. Thus, they are cautioned against consuming such foods. It is also recommended that certain foods be inspected and certified when harm to the public is possible. As an example, meats could be certified for the presence of persistent organic pollutants (POPs), which are organic compounds sometimes used in pesticides that can accumulate in animal tissues and be passed on to human consumers.

See also Bisphenol A .



Camacho, Pauline M., Hossein Gharib, and Glen W. Sizemore. Evidence-based Endocrinology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2012.

Gardner, David G., and Dolores Shoback, eds. Greenspan's Basic & Clinical Endocrinology. New York: McGrawHill Medical, 2011.

Kovacs, William J., and Sergio R. Ojeda, eds. Textbook of Endocrine Physiology. Oxford: Oxford University Press, 2012.


Environmental Protection Agency. “Endocrine Disruptor Screening Program (EDSP).” http://epa.gov/endo/ (accessed September 11, 2012).

National Institute of Health. “Endocrine Diseases (General).” http://health.nih.gov/topic/EndocrineDiseasesGeneral (accessed September 11, 2012).

School of Public Health, University of Minnesota. “Environmental Estrogen Endocrine Disruptors.” http://enhs.umn.edu/current/5200/estrogen/history.html (accessed September 11, 2012).


American Medical Association, 515 N State St., Chicago, IL, 60654, (800) 621-8335, http://www.ama-assn.org .

Environmental Protection Agency, 1200 Pennsylvania Ave. NW, Ariel Rios Bldg., Washington, DC, 20460, (202) 272-0167, http://www.epa.gov/ .

Judith L. Sims
Revised by William A. Atkins, BB, BS, MBA

  This information is not a tool for self-diagnosis or a substitute for professional care.