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Wildlife/human effects

The past to the present

Wildlife effects

Uncertain human effects

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Many widely-used synthetic chemicals and natural plant compounds can alter or interfere with the endocrine system. These foreign substances have been associated with health and reproductive problems in wildlife and laboratory animals. Some believe these environmental compounds can affect human health, development and reproduction in similar ways, although this has not yet been scientifically proven.

These substances can affect the endocrine system in many ways. For example, some compounds, referred to as environmental estrogens, can mimic or act like estrogens, the hormones that control female characteristics. Many can block or cancel out hormone actions and are called anti-estrogens or anti-androgens (the male hormones). Other compounds can both mimic and block hormones. Still others, known as environmental disrupters or modulators, can alter how natural hormones and their protein receptors are made, are broken down and perform. And to complicate matters even more, many chemicals have distinct effects in different species and organs and at different developmental stages.

The idea that human-made chemicals have adverse health effects, including endocrine disruption, is not entirely new. In fact, a 1938 study found that certain synthetic chemicals could mimic estrogens (1). And, more than 30 years ago, Rachel Carson's book Silent Spring described how some synthetic chemicals were collecting in and contaminating water, soil, wildlife and even humans. These chemicals, she warned, were causing severe health problems (egg shell thinning, cancer, die offs) in wildlife, especially in species at the top of the food chain that eat other contaminated animals and accumulate the most chemicals.

It was Rachel Carson that alerted the world to the adverse health effects from pollutants. And it has been the decades of scientific research since her warnings that has helped scientists begin to understand the processes of how these substances affect health. The research has:

• helped identify and restrict use of the most harmful chemicals,

• started to decipher how these substances can interfere with hormones and lead to health problems, and

• broadened the definition of toxic chemical exposure, measured mainly by their ability to cause cancer, to include reproductive and developmental health problems.

In response to this research, some of the most dangerous chemicals, such as DDT and PCBs, have been banned in the U.S. and Europe. Chemical manufacturers continue to replace the more persistent chemicals with shorter-lived ones that won't accumulate in soil, wildlife or our bodies.

1. Many different kinds of synthetic chemicals are found all over the world because they are widely used, do not easily breakdown and are carried to other places by air, water and animals. The chemicals, or sometimes their more harmful breakdown products, are found in soil, water, plants and animals everywhere from the South Pole to the North Pole.

2. Animals, including humans, can and do accumulate some of these chemicals in their fat and often pass them along to offspring and predators.

3. At high doses, some of these chemicals can affect an animal's endocrine system, especially during critical developmental stages. Studies of laboratory animals, cell cultures, wildlife and human's accidentally exposed show that these chemicals may in some cases cause reproductive and developmental problems. For instance:

   • Male fish living near municipal sewage outlets in England had both male and female sex characteristics and their livers produced vitellogenin, a female egg-yolk protein not normally found in males (2). The fish living close to the sewage outlet had severe abnormalities while the fish living farther downstream had less severe symptoms. Several different chemicals, especially the alkylphenols, the breakdown products of chemicals found in detergents and plastics, are suspected of causing the feminizing effects.

     

   • Alligators living in Florida's Lake Apopka were exposed to the estrogenic pollutants dicofol, DDT and its metabolites, DDD, DDE and chloro-DDT, when a nearby chemical plant had an extensive spill in 1980. Ten years later, researchers trying to find out why alligator populations were dropping in the Lake, found higher than normal mortality among eggs and newborn alligators. They also found that adolescent females had severe ovarian abnormalities and had blood estrogen levels two times higher than normal. The male juvenile alligators were feminized, that is, they had smaller than normal penises, had abnormal testes and had higher estrogen levels and lower testosterone levels in their blood than normal males of the same age. The researchers concluded that chemicals from the spill not only killed developing eggs outright but also altered the embryo's endocrine system (hormone levels and sexual development), which severely limited the alligator's ability to reproduce (3a, b).
     

   • Daughters of mothers who took the synthetic estrogen DES (diethylstilbestrol) during pregnancy to prevent miscarriage have higher rates of reproductive problems, reproductive cancer (vagina, cervix) and malformed reproductive organs (uterus, cervix) (4). Sons may also face higher rates of malformed or small penises, undescended testicles and abnormal sperm (5). However, a recent study found no evidence of reduced fertility in DES sons (6).

     DES is not only a potent estrogen, similar in strength to the natural estrogen estradiol, but it also has the unique ability to concentrate in target tissues, such as the reproductive tracts of birds, reptiles and other animals, during development and cause abnormalities. This drug serves as an example of what potent estrogenic compounds can do and may illustrate the health effects that other environmental estrogens can produce.

   • Considerable controversy surrounds a study that found that sperm counts in men were falling worldwide, that rates of testicular cancer were increasing and that environmental estrogens may be responsible for these trends (7). Other studies do not support all of these findings and suggest that lower fertility and high cancer rates may only occur in certain human populations. (8)

4. Fetuses and embryos, whose growth and development are highly controlled by the endocrine system, seem especially vulnerable to exposure, as detailed in the previous examples (9). Mothers can pass contaminants to their offspring prenatally in eggs (amphibians, reptiles, birds) or the womb (mammals) and after birth by breastfeeding newborns. So, even though adult animals exposed to contaminants may not show any ill effects, their offspring may have lifelong health and reproductive abnormalities including reduced fertility, altered sexual behavior, lowered immunity and even cancer.

   Studies looking at mammals, reptiles, birds and fish, as well as laboratory studies using rodents, primates and cultured cells, have linked exposure of a developing embryo to environmental contaminants with many permanent health effects in the adult. These effects include:

• abnormal blood hormone levels;
• reduced fertility;
• altered sexual behavior
• modified immune system
• masculinization of females;
• feminization of males
  (reduced testes and penis size);
• undescended testicles;
• cancers of the female and male reproductive tract;
• malformed Fallopian tubes, uterus and cervix
• altered bone density and structure.

Although no one knows exactly how or to what extent environmental estrogens affect human health, there is considerable concern because the endocrine system is so important to our well-being. The reproductive hormones, such as estrogens, regulate the growth, reproduction, metabolism and even immunity that guide physical development, maintain reproductive cycles and ensure balance of normal body systems.

Because many of these synthetic chemicals are suspected of acting like natural estrogens, the most likely health problems would be related to sexual development, reproduction, and breast and reproductive cancers. In females, estrogens, mainly the hormone estradiol, foster development of female characteristics (breasts, no facial hair, behavior), protect bone strength and the cardiovascular system, regulate liver metabolism, influence ovarian and menstrual cycles, stimulate uterine growth and maintain pregnancies. In males, estrogens play a secondary role to androgens, mainly the hormone testosterone, which defines male characteristics and aids sperm production. But, when the ratio of estrogen to testosterone is increased, feminization can occur.

Given all of this, human health effects associated with exposure to environmental estrogens are mostly unknown and highly controversial. Aside from the drug DES, environmental estrogens have never been proven to cause human health problems, so we can only speculate on possible human health effects documented from animal studies:

For women:

Breast and reproductive organ tissue cancers, fibrocystic disease of the breast, polycystic ovarian syndrome, endometriosis, uterine fibroids and pelvic inflammatory diseases. These may be influenced by developmental or chronic lifetime exposure to estrogen mimics.

For men:

Poor semen quality (low sperm counts, low ejaculate volume, high number of abnormal sperm, low number of motile sperm), testicular cancer, malformed reproductive tissue (undescended testes, small penis size), prostate disease and other recognized abnormalities of male reproductive tissues.

As with any potential health risk, many factors such as length of exposure, dose, age and individual differences will influence the kinds and severity of health problems experienced. That is, one person may experience many problems while another may experience none.

We still don't know much about how environmental estrogens affect health in humans and other animals. More research is needed to learn what we don't know. For instance, we don't know:

1. How many synthetic chemicals act like natural hormones? Certain chemicals have been identified as environmental estrogens through laboratory assays, but with virtually thousands of synthetic chemicals already introduced into the environment and many new ones developed yearly, most remain untested. There is a great need for rapid and reliable testing systems.

2. What levels of exposure over what time frames will cause adverse effects? No one is even sure how much exposure each of us faces on a daily or lifetime basis. There is a need for biomarkers to evaluate human exposure.

3. What is the effect of exposure to multiple chemicals? In other words, how do pollutants react with each other outside and inside the body? Does exposure to a range of chemicals at a low dose have the same or greater effects as exposure to one chemical at a high dose? Do chemical's in a mixture cancel out each other's effects? Are the effects additive or synergistic (greater than additive)? Recent research suggests synergistic effects (10) but more information is needed.

4. Are they sequential? For example, does exposure to one chemical predispose, or make an animal more sensitive to, subsequent chemicals? In the case of diethylstilbestrol (DES), the drug predisposes animals to an altered response to endogenous estrogens that may contribute to the development of cancer.

1. Dodds, E.C. and W. Lawson. 1938. Molecular structure in relation to oestrogenic activity. Compounds without a phenantrene nucleus. Proceedings of the Royal Society of London (Series B), 118:222-232.

2. Jobling J.S. and J.P. Sumpter. 1993. Detergent component in sewage effluent are weakly oestrogenic to fish: An invitro study using rainbow trout (Oncorynchus mykiss) hepatocyctes. Aquatic Toxicoloyg. 27:361-72.

3. a. Guillette, L.H. Jr. 1995. Endocrine disrupting environmental contaminants and developmental abnormalities in embryos. Human and Ecological Risk Assessment 1(2):25-36.

   b. Guillette, L.H. Jr., T.S. Gross, G.R. Masson, J.M. Matter, H.F. Percival and A.R. Woodward. 1994. Developmental abnormalitiies of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environmental Health Perspectives 102(8):680-688.

4. Nollar, K.L., P.C. O'Brien, T. Colton, R. Kaufman and L.J. Melton. 1990. Medical and surgical diseases associated with in utero exposure to diethylstilbesterol. ed. K.L. Nollar. Clinical Practice of Gynocology. New York: Elsevier Science Publishing Co. Inc., pp 1-7.

5. Gill, W.B., G.F.B. Schumacher and M. Bibbo. 1976. Structural and functional abnormalities in the sex organs of male offspring of mothers treated with diethylstilbestrol (DES). Journal of Reproductive Medicine, 16:147-153.

6. Raloff, J. 1995. DES sons face no fertility problems. Science News 147:324.

7. Sharpe, R.M. and Shakkebaek. 1993. Are oestrogens involved in falling sperm counts and disorders of the male reproductive tract? Lancet 341:1392-1395.

8. Fisch, H. and Goluboff. 1996. Geographic variations in sperm counts: A potential cause of bias in studies of semen quality. Fertility and Sterility 65:1044-1046.

9. Bern, H. 1992. The fragile fetus. In: Chemically-induced Alterations in Sexual and Functional Development: The Wildife/Human Connection, pp. 9-15. Eds T. Colborn and C. Clement. Vol 21. Princeton. NJ:Princeton Scientific Publishing Co.

10. Bergeron, J.M., D. Crews and J.A. McLachlan. 1994. PCBs as environmental estrogens: turtle sex determination as a biomarker of environmental contamination. Environmental Health Perspectives, 102:780-781.

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