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 Derived from numerous synthetic and natural sources, substances that interfere with normal estrogenic activity in the body have been linked to various reproductive abnormalities and cancers.
 hat do Barbie dolls, food wrap, and spermicides have in common? And what do they have to do with low sperm counts, precocious puberty, and breast cancer? "Everything," say those who support the notion that hormone mimics are disrupting everything from fish gender to human fertility. "Nothing," counter others who regard the connection as trumped up, alarmist chemophobia. The controversy swirls around the significance of a number of substances that behave like estrogens and appear to be practically everywhere--from plastic toys to topical sunscreens.
Estrogens are a group of hormones produced in both the female ovaries and male testes, with larger amounts made in females than in males. They are particularly influential during puberty, menstruation, and pregnancy, but they also help regulate the growth of bones, skin, and other organs and tissues. Over the past 10 years, many synthetic compounds and plant products present in the environment have been found to affect hormonal functions in various ways. Those that have estrogenic activity have been labeled as environmental estrogens, ecoestrogens, estrogen mimics, or xenoestrogens (xenos means foreign). Some arise as artifacts during the manufacture of plastics and other synthetic materials. Others are metabolites (breakdown products) generated from pesticides or steroid hormones used to stimulate growth in livestock. Ecoestrogens that are produced naturally by plants are called phytoestrogens (phyton means plant). Many of these estrogen mimics bind to estrogen receptors (within specialized cells) with roughly the same affinity as estrogen itself, setting up the potential to wreak havoc on reproductive anatomy and physiology. They have therefore been labeled as disruptors of endocrine function. BIZARRE CHANGES IN REPRODUCTIVE SYSTEMS  eightened concern about estrogen-mimicking substances arose when several nonmammalian vertebrates began to exhibit bizarre changes in reproductive anatomy and fertility. Evidence that something was amiss came serendipitously in 1994, from observations by reproductive physiologist Louis Guillette of the University of Florida. In the process of studying the decline of alligator populations at Lake Apopka, Florida, Guillette and coworkers noticed that many male alligators had smaller penises than normal. In addition, females superovulated, with multiple nuclei in some of the surplus ova. Closer scrutiny linked these findings to a massive spill of DDT (dichloro-diphenyl-trichloroethane) into Lake Apopka in 1980. Guillette concluded that the declining alligator population was related to the effects of DDT exposure on the animals' reproductive systems.
Although DDT was banned for use in the United States in the early 1970s, it continues to be manufactured in this country and marketed abroad, where it is sprayed on produce that is then sold in U.S. stores. The principal metabolite derived from DDT is
Ecoestrogens are further concentrated in animals higher up in the food chain. In the Great Lakes region, birds including male herring gulls, terns, and bald eagles exhibit hermaphroditic changes after feeding on contaminated fish. Increased embryo mortality among these avians has also been observed. In addition, evidence from Florida links sterility in male and female panthers to their predation on animals exposed to pesticides with estrogenic activity. The harmful effects of DDT have also been observed in rodents. Female rodents treated with high concentrations of DDT become predisposed to mammary tumors, while males tend to develop testicular cancer. These observations raise the question of whether pharmacological (that is, low) doses of substances with estrogenic activity translate into physiological effects. Usually they do not, but chronic exposure may be enough to trigger such effects. DANGERS TO HUMANS  f xenoestrogens cause such dramatic reproductive effects in vertebrates, including mammals, what might be the consequences for humans? Nearly a decade ago, Frederick vom Saal, a developmental biologist at the University of Missouri–Columbia, cautioned that mammalian reproductive mechanisms are similar enough to warrant concern about the effects of hormone disruptors on humans.
A 1993 article in Lancet looked at decreasing sperm counts in men in the United States and 20 other countries and correlated these decreases with the growing concentration of environmental estrogens. The authors--Niels Skakkenbaek, a Danish reproductive endocrinologist, and Richard Sharpe, of the British Medical Research Council Reproductive Biology Unit in Scotland--performed a meta-analysis of 61 sperm-count studies published between 1938 and 1990 to make their connection. "Nonbelievers" state that this interpretation is contrived. Others suggest alternative explanations. For instance, the negative effects on sperm counts could have resulted from simultaneous increases in the incidence of venereal diseases. Besides, there are known differences in steroid hormone metabolism between lower vertebrates (including nonprimate mammals) and primates, so one cannot always extrapolate from the former group to the latter. Even so, the incidence of testicular cancer, which typically affects young men in their 20s and 30s, has increased worldwide. Between 1979 and 1991, over 1,100 new cases were reported in England and Wales--a 55 percent increase over previous rates. In Denmark, the rate of testicular cancer increased by 300 percent from 1945 to 1990. Intrauterine exposure to xenoestrogens during testicular development is thought to be the cause. Supporting evidence comes from Michigan, where accidental contamination of cattle feed with PCBs in 1973 resulted in high concentrations in the breast milk of women who consumed tainted beef. Their sons exhibited defective genitalia. Furthermore, observers in England
Perhaps one of the most disturbing current trends is the alarming increase in breast cancer incidence. Fifty years ago, the risk rate was 1 woman in 20; today it is 1 in 8. Numerous studies have implicated xenoestrogens as the responsible agents. For instance, high concentrations of pesticides, especially DDT, have been found in the breast tissue of breast cancer patients on Long Island. In addition, it has long been known that under certain conditions, estrogen from any source can be tumor promoting, and that most breast cancer cell types have estrogen receptors.
f that were not enough, the growing number of estrogen mimics in the environment has been linked to early puberty in girls. The normal, average age of onset is between 12 and 13. A recent study of 17,000 girls in the United States indicated that 7 percent of white and 27 percent of black girls exhibited physical signs of puberty by age seven. For 10-year-old girls, the percentages increased to 68 and 95, respectively. Studies from the United Kingdom, Canada, and New Zealand have shown similar changes in the age of puberty onset.
It is difficult, however, to elucidate the exact mechanisms that underlie these trends toward precocious puberty. One explanation, which applies especially to cases in the United States, points to the increasing number of children who are overweight or obese as a result of high-calorie diets and lack of regular exercise. Physiologically, an enhanced amount of body fat implies reproductive readiness and signals the onset of puberty in both boys and girls. For girls, more body fat ensures that there is enough stored energy to support pregnancy and lactation. Young women with low percentages of body fat caused by heavy exercise, sports, or eating disorders usually do not experience the onset of menses until their body composition reflects adequate fat mass. Many who study the phenomenon of premature puberty attribute it to environmental estrogens in plastics
Another study from Puerto Rico revealed higher concentrations of phthalate--a xenoestrogen present in certain plastics--in girls who showed signs of early puberty, compared with controls. It may be that excess body fat and exposure to estrogenic substances operate in concert to hasten puberty. Body fat is one site of endogenous estrogen synthesis. Exposure to environmental estrogens may add just enough exogenous hormone to exert the synergistic effect necessary to bring on puberty, much like the last drop of water that causes the bucket to overflow. Although most xenoestrogens produce detrimental effects, at least one subgroup--the phytoestrogens--includes substances that can have beneficial effects. Phytoestrogens are generally weaker than natural estrogens. They are found in various foods, such as flax seeds, soybeans and other legumes, some herbs, and many fruits and vegetables. Some studies suggest that soy products may offer protection against certain cancers, including breast, prostate, uterus, and colon cancers. On the other hand, high doses of certain phytoestrogens--such as coumestrol (in sunflower seeds and alfalfa sprouts)--have been found to adversely affect the fertility and reproductive cycles of animals. Unlike artificially produced xenoestrogens, phytoestrogens are generally not stored in the body but are readily metabolized and excreted. Their health effects should be evaluated on a case-by-case basis, considering such factors as the individual's age, medical and family history, and potential interactions with medications or supplements.
t has been estimated that perhaps 100,000 synthetic chemicals are registered for commercial use in the world today and 1,000 new ones are formulated every year. While many are toxic and carcinogenic, little is known about the chronic effects of the majority of them. And there is growing concern about their potential hormone-disrupting effects. The problem of exposure is complicated by numerous carrier routes, including air, food, water, and consumer products.
Consider certain synthetics that turn up in familiar places, including food and consumer goods. Such seemingly inert products as plastic soda and water bottles, baby bottles, food wrap, Styrofoam, many toys, cosmetics, sunscreens, and even spermicides either contain or break down to yield xenoestrogens. In addition, environmental estrogens are among the byproducts created by such processes as the incineration of biological materials or industrial waste and chlorine bleaching of paper products. In April 1999, Consumers Union confirmed information previously reported by the Food and Drug Administration regarding 95 percent of baby bottles sold in the United States. The bottles, made of a hard plastic known as polycarbonate, leach out the synthetic estrogen named bisphenol-A, especially when heated or scratched. Studies verifying the estrogenic activity of bisphenol-A were published in Nature in the 1930s, but it did not arouse much concern then. A 1993 report published in Endocrinology showed that bisphenol-A produced estrogenic effects in a culture of human breast cancer cells. Additional studies published by vom Saal in 1997 and '98 have shown that bisphenol-A stimulates precocious puberty and obesity in mice. Others have detected leaching of bisphenol-A from polycarbonate products such as plastic tableware, water cooler jugs, and the inside coatings of certain cans (used for some canned foods) and bottle tops. Autoclaving in the canning process causes bisphenol-A to migrate into the liquid in cans. Spokespersons from polycarbonate manufacturers have stated that they cannot replicate vom Saal's results, but he counters that industry researchers have not done the experiments correctly. DEHA (di-[2-ethylhexyl] adipate) is a liquid plasticizer added to some plastic food wraps made of polyvinyl chloride (PVC). Scientific studies have shown that the fat-soluble DEHA can migrate into foods, especially luncheon meats, cheese, and other products with a high fat content. For a 45-pound child eating cheese wrapped in such plastic, the limit of safe intake is 1.5 ounces by European standards or 2.5 ounces by Environmental Protection Agency criteria. Studies conducted by Consumers Union indicate that DEHA leaching from commercial plastic wraps is eight times higher than European directives allow. Fortunately, alternative wraps--such as Handi-WrapTM and Glad?Cling Wrap--are made of polyethylene; chemicals in them do not appear to leach into foods. Barbie dolls manufactured in the 1950s and '60s are made of PVC containing a stabilizer that degrades to a sticky, estrogen-mimicking residue and accumulates on the dolls' bodies. This phenomenon was noted by Danish museum officials in August 2000. Yvonne Shashoua, an expert in materials preservation at the National Museum of Denmark, warns that young children who play with older Barbie and Ken dolls expose themselves to this estrogenic chemical, and she suggests enclosing the dolls with xenoestrogen-free plastic wrap. Storing the dolls in a cool, dark place also helps prevent the harmful stabilizer from oozing out. Who would have thought that these models of glamour would become health hazards? Another consumer nightmare is a group of chemical plasticizers known as phthalates. They have been associated with various problems, including testicular depletion of zinc, a necessary nutrient for spermatogenesis. Zinc deficiency results in sperm death and consequent infertility. Many products that previously contained phthalates have been reformulated to eliminate them, but phthalates continue to be present in vinyl flooring, medical tubing and bags, adhesives, infants' toys, and ink used to print on food wrap made of plastic and cardboard. They have been detected in fat-soluble foods such as infant formula, cheese, margarine, and chips. Some environmental estrogens can be found in unusual places, such as contraceptive products containing the spermicide nonoxynol-9. This chemical degrades to nonylphenol, a xenoestrogen shown to stimulate breast cancer cells. Nonylphenol and other alkylphenols have been detected in human umbilical cords, plastic test tubes, and industrial detergents. Various substances added to lotions (including sunscreens) and cosmetics serve as preservatives. Some of them, members of a chemical family called parabens, were shown to be estrogen mimics by a study at Brunel University in the United Kingdom. The researchers warned that "the safety of these chemicals should be reassessed with particular attention being paid to .... levels of systemic exposure to humans." Officials of the European Cosmetic Toiletry and Perfumery Association dismissed the Brunel study as "irrelevant," on the grounds that parabens do not enter the systemic circulation. But they ignored the possibility of transdermal introduction. Additional questions have been raised about the safety--in terms of xenoestrogen content--of recycled materials, especially plastics and paper. Because it is unlikely that a moratorium on chemical synthesis will occur anytime soon, such questions will continue to surface until the public is satisfied that regulatory agencies are doing all they can to minimize exposure. Fortunately, organizations such as the National Institutes of Health, the National Academy of Sciences, the Environmental Protection Agency, the Centers for Disease Control, many universities, and other institutions are involved in efforts to monitor and minimize the effects of environmental estrogens on wildlife and humans. 
On the Internet EPA, Endocrine Disruptors Research Initiative www.epa.gov/endocrine/gedri/ Tulane and Xavier Universities, Environmental Estrogens and Other Hormones www.som.tulane.edu/ecme/eehome/ World Wildlife Fund, Toxic Chemicals, Endocrine Disruptors www.worldwildlife.org/toxics/progareas/ed/index.htm Michele L. Trankina is professor of biological sciences at St. Mary's University and adjunct associate professor of physiology at the University of Texas Health Science Center, both in San Antonio. Her previous article for T |
