The gender benders: are environmental 'hormones' emasculating wildlife? - includes related articles

Science News, Jan 8, 1994 by Janet Raloff

Mother Nature. The term conjures up images of a warm, nurturing, bountiful environment. But this sobriquet is proving increasingly apt for another reason -- one that should offer anything but comfort.

New studies suggest that through polution and other environmental factors, Mother Nature is exerting a feminizing hormonal influence on the animal kingdom.

Over the past 15 years, research has unmasked a number of "environmental hormones" -- chemicals and pollutants that disrupt biological processes, often by mimicking the effects of naturally produced hormones such as the female hormone estrogen. On the ever-growing list of these agents are several restricted or banned pesticides -- including DDT (and its even more toxic metabolite, DDE), kepone, heptachlor, dieldrin, mirex, and toxophene. Some polychlorinated biphenyls (PCBs) exhibit these disruptive properties, as do certain combustin pollutions, ingredients in plastics, and breakdown products of common detergents (SN: 7/3/93, p.10).

The hormonal activity of these chemicals usually bears little relationship to their intended function. indeed, there is no way of predicting -- based on structure or function -- which compounds will exhibit a horomnal alter ego.

The fact troubles a number of scientists because such environmental hormones may be contributing to an increased risk of reproductive-system cancers in females. Moreover, prenatal exposure to hormone-like pollutions can detail the developmental processes that establish gender or ensure reproductive success.

While the health community has recently begun a host of studies to explore a possible link between estrogenic pollutants and cancers in women, few researchers have focused on the related reproductive risks such environmental hormones may pose for both sexes. That's unfortunate, says Theo Colborn, a zoologist with the World Wildlife Fund in Washington, D.C., because reproductive effects are likely to be "much more widespread."

Indeed, she notes, animal data are beginning to suggest that far smaller exposures are needed to trigger reproductive effects than to induce cancers.

And because some these reproductive changes may be subtle, they could evade detection for decades--even a lifetime--unless hunted for explicitly.

Colborn has convened a number of symposia in the past few years for researchers who study reproductively impaired wildlife populations or laboratory animals exposed to environmental hormones. Most of these scientists she says, describe the links they're finding between impaired reproduction and "hormonal" pollutants as sobering -- if not downright scary.

Indeed, she and many other environmental scientists worry that if if hormone-like contaminants can feminize male animals, these ubiquitous pollutants may also underlie troubling reproductive-system trends being witnessed in men.

Some of the earliest data on unexpected reproductive risks posed by commercial chemicals came in the early 1950s. DDT, a potent and persistent organochlorine pesticide, was shown to cause the eggshells of many birds to thin. In fact, long after the compound was banned in 1972, DDT-thinned eggshells continued to put many embryonic birds--including bald eagles -- at risk of being crushed to death.

DDT even wreaked havoc among birds resistant to eggshell thinning, such as sea gulls. Recognition of the extent of these problems, however, didn't emerge until decades after the initial reports of eggshell thinning.

Through heavily contaminated gull embryos managed to hatch, reproduction in gull colonies exposed to large amounts of DDT began to decline precipitiously in the late 1960s. Biologists observed not only that many female gulls in these communities were sharing nests with other females--the co-called lesbian gulls--but also that the young within these communities bore grossly feminized reproductive tracts. Female gulls, which should have developed mature reproductive organs only on the left side, also carried dicofol spill in 1980, there has been a 90-percent reduction in the number of juvenile alligators at the lake. And in a population of animals that can live to be 60 years old, that's not healthy, he says.

Another reluctant toxicologist, Brent Palmer of Ohio University in Athens, ahs begun studying a substance in the blood of egg-laying vertebrates that he suspects will one day prove a sensitive biomarker of exposure to estrogenic pollutants, at least in males. It's vitellogenin, the egg-yolk protein.

When stimulated by estrogen, the liver produces this protein, then dumps it into the blood. From there it circulates to the ovaries, where it is deposited in an egg. Though males cna produce vitellogenin, usually only females possess sufficient estrogen to do so.

That's good, Guillette points out, because "if you have enough estrogen in a male to turn on vitellogenin, then you probably have enough to shut off the normal functioning of the testes."

Working with the red-eared slider, America's most common turtle. Palmer has demonstrated that DDT can turn on vitellogenin production in males. But DDT doesn't elicit the same broad suite of changes that estrogen does. For instance, it fails to trigger the liver's production of two other proteins and it turns on the production of some other substances that estrogen doen't. "So even though DDT is mimicking estrogen in some ways," Palmer points out, "it's not exactly the same."