BPA, in turn, is becoming this year’s poster child for all our doubts and fears about the safety of plastic. New research highlighting the possible dangers of BPA has received tremendous media coverage. In mice, at least, BPA exposure at crucial stages of development induces observable changes (such as breast or prostate abnormalities) that last a lifetime. The research may be confusing to a layperson, yet some consensus has been reached: Last November a panel sponsored by the National Institutes of Health (NIH) determined that there was at least “some concern” about BPA’s effect on the fetal and infant brain. Around the same time, the Centers for Disease Control reported that researchers there had found BPA—the United States produces 6 billion pounds of it yearly—in 93 percent of urine samples from 2,500 Americans aged 6 to 85. Children under age 12 had the highest concentrations.
What is not known is whether infants and children under 6 are even more heavily exposed, since they have not yet been studied (for phthalates, Swan says, levels are definitely higher in children than in adults). This, at least, has been measured: Infants fed canned formula heated in a polycarbonate bottle—one source of BPA—can consume more than 20 micrograms of the chemical a day. Animal studies show effects of BPA at much lower concentrations.
To shift public understanding on this issue is staggeringly difficult, especially given that exposure to plastic is not a matter of individual lifestyle. Unlike tobacco and lead paint, plastics are so useful we can hardly manage a day without them. Biologist Frederick vom Saal of the University of Missouri likens the issue to another colossal environmental threat. “This is the global warming of biology and human health,” he says.
Last summer, a panel of 38 researchers headed by vom Saal published a report in Reproductive Toxicology warning that BPA (much like the synthetic estrogen diethylstilbestrol, or DES) is a potential chemical time bomb that may lead to multiple problems, including a higher risk of cancer, especially if exposure occurs in the womb or an infant’s early life and on an unrelenting daily basis.
Two weeks after the report came out, an NIH panel came to a different conclusion: Although public exposure to BPA could pose some risk to the brain development of babies and children, there was “negligible concern” about reproductive effects in adults. This was the first official federal report on BPA, and the chemical industry took it as good news: An August 2007 statement by the American Chemistry Council claims that “BPA is not a risk to human health at the extremely low levels to which consumers might be exposed.” Criticism of the report began even before its publication and has dogged it ever since. In January the NIH agreed to a thorough review of the report. This NIH decision came in response to claims from scientists and public health advocates that members of the panel worked for the chemical industry and cherry-picked the data in favor of industry-funded studies, which did not test low-dose exposure to BPA. A new panel has been convened, and its findings are expected in June.
Chemicals like BPA pose a challenge for conventional toxicology, vom Saal says. To determine what level of a toxin is safe, researchers take a dose that has no observed toxicological effect in an animal and divide it by 10 once (to account for the differences between species) and then again (to account for variations among humans’ ability to handle toxins); for pesticides, the dose is then divided by 10 a third time (to allow for the extraordinary sensitivity of babies and children). Although this is somewhat arbitrary, it generally gives enough room to provide protection. The first studies of BPA toxicity in the 1980s tested rats at high levels of exposure (50 milligrams of BPA per kilogram of body weight per day). Lower levels were not tested; BPA was deemed safe.
But the modus operandi of hormone-mimicking chemicals is different from that of typical toxins. In fact, they are not toxins in the strict sense of the word because they behave like ordinary hormonal signals. “It turns out we are, to a very intriguing degree, programmed by phenomenally small amounts of hormones in terms of our behavior, our core physiology, our neuroendocrine system, and our ability to metabolize drugs,” vom Saal says. “The brain along with the reproductive system and every other cell in your body is exquisitely sensitive to exceedingly small changes in estrogen and other sex hormones, and the fact that the environment is full of chemicals that can activate estrogen receptors means this phenomenally sensitive system is being perturbed constantly by environmental factors.”
At key stages of development, a seemingly infinitesimal dose of an estrogenic chemical such as BPA or phthalates may be life-altering. This is most evident in fetuses. When BPA hits cell receptors, it is as powerful as estradiol, the most potent estrogen in humans. “Our cells are built to take a single molecular-binding event,” vom Saal says, “and turn that into a huge, highly amplified outcome. We’ve studied doses of BPA between 2 and 20 micrograms per kilogram of body weight—the lowest dose ever tested before was 2,500 times higher—and it scrambles the male reproductive system in mice.”
In other research, by reproductive biologist Patricia Hunt of Washington State University, female mice exposed to low amounts of BPA in the womb—amounts deemed “environmentally relevant”—had high levels of genetic errors in the eggs they produced. Worse still, the genetic errors in those eggs led to chromosome abnormalities in 40 percent of the next generation’s eggs. That is 20 times the incidence of such abnormalities in unexposed mice. How might this relate to human risk? According to commentators reviewing Hunt’s work in PLoS Genetics, the answers will be hard to tease out: Nearly one in five human pregnancies ends in miscarriage, half of which are due to chromosomal abnormalities. Abnormalities in a woman’s eggs increase as she ages, and more women are having children at a later age. “A proper study of this problem,” they wrote, “would require assessing the woman’s level of chemical exposure now and maintaining those data for two to three decades,” tracking the abnormalities in her children and grandchildren.
Another troubling animal study comes from Randy Jirtle, a Duke University geneticist, who found that BPA permanently reprogrammed a gene in pups of mice fed BPA-laced food. Jirtle is well known for his work on mice that carry the agouti gene, which is highly vulnerable to environmental influences. In this study, he exposed lean, brown-furred female mice to 50 milligrams of BPA per kilogram of body weight daily, and the next generation was transformed: More of them were fat, with blond fur. “If I were a pregnant woman, I would try hard to avoid exposure to BPA,” Jirtle says.