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Your Health By Sharon Levy Protecting Yourself From Unsafe Plastics IN 1988, Patricia Hunt was conducting a routine experiment in her lab at Case Western Reserve University when she ran into an unforeseen complication. All of a sudden, the geneticist noticed that 40 percent of the eggs of mice in her control groupthe group she was not experimenting onhad defects in chromosome behavior, the kind of defects that can lead to genetic errors like Down syndrome in humans, and that normally occur in just 1 to 2 percent of all mouse eggs. Ultimately, Hunt and her colleagues traced the problem back to the plastic cages the mice inhabited. Just before the spike in egg abnormalities, they discovered, a lab technician had accidentally washed the cages with a harsh detergent that caused the plastic to begin breaking down. Follow-up experiments confirmed that Bisphenol A (BPA)a chemical building block of the plastichad powerfully affected the mice. After replacing the cages, the scientists reproduced the jump in abnormal eggs by keeping mice in deliberately damaged new cages and by giving mice in intact cages low doses of BPA by mouth. Yet four years later, it’s still easy to walk into a store and buy a plastic baby bottle or food container made with BPA, just one of a long list of industrial chemicals that can mimic the effects of sex hormones. Over the past decade, evidence has been building that a variety of pesticides, plastics and solvents containing these chemicals can alter normal development in both wild and domestic animals. Examples of such endocrine-disrupting effects include male frogs that developed both male and female reproductive organs after exposure to the pesticide atrazine and alligators that grew up with stunted penises or had low hatching success after a DDT spill in Lake Apopka, Florida. The bedrock of a multibillion-dollar industry, BPA forms the polycarbonate plastic used in some toddlers’ sippy cups, food can linings, dental sealants and sports water bottles as well as food containers and baby bottles. Recent studies show that BPA leaches from intact polycarbonate products, though not as fast as it does from worn or damaged plastic. Concerns about BPA ignited in 1997, when reproductive biologist Fred vom Saal of the University of MissouriColumbia (UMC) discovered that pregnant mice exposed to low doses of the chemical gave birth to male pups that developed enlarged prostates. Since then, more than 40 studies have reported low-dose effects of BPA on creatures ranging from insect larvae to fish, frogs, snails, mice and rats. These include accelerated puberty and growth of breast tissue, decreased sperm counts and changes in gender and behavior. “The evidence for low-dose effects of BPA on wildlife is extremely strong,” says Wade Welshons of UMC’s College of Veterinary Medicine. He adds that recent studies in pregnant women and in umbilical cord blood from newborns show that BPA is present in the human populationand at levels higher than those found to cause developmental changes in animals. A few large-scale studieslargely funded by the plastics industryhave failed to reproduce the effects found by vom Saal and his colleagues. Welshons, however, cites technical problems with the research that could account for this failure, including the use of feed contaminated with estrogens that would have obscured the effects of BPA. Findings of low-dose effects from BPA are controversial not just because they could damage the plastics industry, but because they also call into doubt long-held beliefs about measuring risk from any kind of chemical exposure. Generations of toxicologists have been taught that “the dose makes the poison” that the impact of a chemical will be strongest at high doses and will decrease in proportion to a decrease in dose. Below some threshold level, there should be no biological effects at all. But according to Welshons, such assumptions are wrong when it comes to chemicals that imitate hormones, because the endocrine system is designed to respond to small, subtle changes in hormone concentrationsfar below doses used in traditional toxicity testing. Industry scientists note that researchers still have not proven that BPA affects humans, and they question whether the results of mouse studies are relevant. Welshons and Hunt find that argument odd, given that BPA was developed in the 1930s as a synthetic estrogen for people. After a rival drug, diethylstilbestrol (DES), proved to be a stronger estrogen mimic, BPA was shelved until an inventive chemist realized it could be used to form a plastic polymer. “Nobody should be surprised,” says Hunt, “that a chemical designed as a synthetic estrogen can disrupt the endocrine system.” When DES given to pregnant women from 1938 to 1971 caused cancer and other serious health effects in their children, lab studies of the drug showed parallel effects in mice. “The mouse has proven to be a tremendously accurate model for the human effects of DES, the best-studied endocrine disrupter,” says Welshons. Indeed, scientists have found that human eggs are even more prone to genetic errors than are mouse eggs. Hunt is now studying male mice that were exposed to BPA in the womb or soon after birth. Her preliminary results suggest that the chemical causes genetic mistakes in the formation of sperm, just as it does in eggs. “If I could accomplish one thing from these studies,” concludes Hunt, “I’d like to get all those baby bottles and sippy cups made of polycarbonate off the market.” California writer Sharon Levy is a regular contributor to National Wildlife.
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Copyright 2004 National Wildlife Federation. All rights reserved. The above article may not be republished or redistributed, in whole or in part, without prior written consent of National Wildlife Federation. |
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