The Problem with Plastics
Guilty Until Proven Innocent
Worldwide production of BPA exceeds 6 billion pounds per year; about a billion pounds of phthalates are produced annually. These molecules are an external and, clearly, an internal fact of life, and over the past decade there’s been a rapidly increasing amount of research on the effects that plastics might be having on human health, particularly that of the unborn and infants—the most vulnerable among us. “There are at least several hundred studies that show worrisome problems,” says Wargo. “The quality of evidence about the risk of health effects is such that the EPA would not be allowed under current law to register BPA as a pesticide.” This year alone, three august scientific journals—Environmental Research; Philosophical Transactions of the Royal Society B: Biological Sciences; and Molecular and Cellular Endocrinology—devoted entire special issues to reviews of the latest EDC science. And on June 29, the Endocrine Society, the 14,000-member professional organization for basic and clinical researchers, took an unprecedented step in its nearly 100-year-old history, when it issued policy and scientific statements on EDCs that call for fundamental change in the way these chemicals are regulated. Acknowledging gaps in the understanding of EDC effects, the society nevertheless proposed that “until such time as conclusive scientific evidence exists to either prove or disprove harmful effects of substances, a precautionary approach should be taken in the formulation of EDC policy.”
In other words, says Wargo, a national plastics policy with a “first, do no harm” foundation would be prudent. “We need to get untested products out of the marketplace,” he says. Not surprisingly, Steven Hentges, the executive director of the polycarbonate/BPA global group at the American Chemistry Council, the industry’s trade organization, disagrees. Hentges characterized the research as an “enormous, confusing database” in which the only consistency is a “lack of effect” on human health. “BPA has been around for more than 50 years, but I’ve not seen anything in the science that would make us shift our views on its safety,” he says.
Regulatory agencies in this country, as well as those of the European Union, several individual European countries, Japan, Australia, New Zealand and, most recently, California, would agree with Hentges. Indeed, a statement issued in February 2008 by the FDA concluded that “the current levels of exposure to BPA through food packaging do not pose an immediate health risk to the general population, including infants and children.”
But more recently, prompted perhaps by a highly contentious investigation last year by the U.S. House of Representatives’ Energy and Commerce Committee about BPA safety and alleged industry-FDA collusion, the FDA began to backtrack.
The agency had already been stung by a September 2008 report, issued a month after the FDA had given BPA another clean bill of health, from the National Toxicology Program (NTP) that said, essentially, “Wait a minute.” Scientists at the NTP, which is part of the National Institutes of Health, reviewed the existing evidence and found that while there were “many conflicting findings” and a “number of remaining uncertainties,” there was “some concern”—the midpoint in the NTP’s five-level scale—that BPA exposure, at levels currently measured in the human population, could affect “the brain, behavior and prostate gland in fetuses, infants, and children.” (The NTP had fewer concerns, but not none, about BPA’s ability to bring about abnormal breast development, premature puberty in girls, birth defects and reproduction problems in adults.)
In October of that year, the FDA’s own science board questioned the adequacy of the parent agency’s earlier review, and last June FDA commissioner Margaret Hamburg told a House hearing on the Food Safety Enhancement Act that the agency was undertaking a new safety assessment; it is expected to be completed by the end of November.
Other governments around the world have already acted. Last year, Health Canada, that country’s health assessment organization, issued a ban, effective next year, on BPA-containing baby bottles. But in announcing the action, health minister Tony Clement termed it “precautionary” and said that “although our science tells us that exposure levels of newborns and infants are below the levels that cause effects, it is better to be safe than sorry.”
Minnesota and Connecticut, along with Chicago and Suffolk County in New York, have adopted similar bans. A number of companies, including retail giant Walmart and baby bottle manufacturers such as Avent, Playtex and Gerber, are opting to purge the molecule from products aimed at the under-3 set.
With phthalates, there’s a similar movement toward avoidance and, in some quarters, an outright ban. But again, this is based, according to published statements, more on precaution than on traditional toxicology. No one is suggesting that BPA and phthalates, at the minuscule levels in which they’re found in the human body, are either outright poisons or mutagens.
But that doesn’t mean, say scientists such as R. Thomas Zoeller, a developmental endocrinologist at the University of Massachusetts, that low-level exposures are without effect. “We have a huge potential problem here, and it’s one that our regulatory agencies are not prepared to handle,” says Zoeller. “Exposure, particularly early in life, to chemicals such as BPA and phthalates can result in a predisposition to disease and morbidity. This is, or should be, a significant cause for concern.”
As endocrine disruptors, BPA and phthalates belong to an array of molecules that either mimic or block the actions of hormones in the body. BPA is a synthetic estrogen that was first synthesized in 1891, and by the 1930s it and a close relative, diethylstilbestrol (DES), were being investigated as medications that could enhance estrogen levels and, so the theory went, help prevent miscarriages and other problems in pregnancy. DES proved the more potent of the two and was developed into a drug that was prescribed to as many as 10 million women until 1971. By then, studies had shown not only that the medication didn’t do the job, but that the daughters born to mothers who had taken DES during pregnancy were at greatly increased risk of developing clear cell adenocarcinoma, a rare form of vaginal cancer.
BPA, of course, was never designed to be deliberately ingested, but in the plastics boom that followed World War II—and well before the advent of the Clean Water Act in the 1970s—an untold amount of the material and the industrial waste products that went into manufacturing it were dumped into rivers and lakes. BPA con-tinues to enter the natural environment in sewage treatment effluent, including the BPA metabolites that we excrete, and in what leaches from landfills. Plastics dumped into the water—a garbage patch the size of Texas, much of it BPA-containing plastic junk, currently floats in the Pacific—also contribute to the environmental contamination; bacteria degrade the material into its component molecules, which can, sooner or later, enter the wildlife and human food chain.
Environmentalists started voicing concern about the impact of plastic pollution on the natural world in the early 1970s, and in 1993 biologists Theo Colborn, Frederick vom Saal and Ana Soto, synthesizing a growing body of disturbing research, first publicized the term endocrine-disrupting chemicals to describe what BPA, phthalates, pesticides (including DDT) and other industrial substances, such as dioxins and PCBs, might be doing to a wide variety of animals.
The endocrine-disrupting effects, the authors wrote in Environmental Health Perspectives in a seminal article that set the agenda for future research, “may be manifested in an entirely different way, and with permanent consequences, in the early embryo, fetus, and neonate from effects as a result of exposure only in adulthood; can change the course of development and potential of offspring, with the outcome depending on the specific developmental period(s) of exposure; and are often delayed and thus may not be fully or obviously expressed until the offspring reaches maturity or even middle age, even though critical exposure occurred during early embryonic, fetal, or neonatal life.”
The Colborn group study and a 1996 book on endocrine disruptors, Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival?—A Scientific Detective Story, by Colborn, Dianne Dumanoski and John Peterson Myers garnered headlines. Widespread concern about the possible effects of these chemicals on human health also helped build public support for the passage of the 1996 Food Quality Protection Act, legislation that mandated the creation of the EPA’s Endocrine Disruptor Screening Program. (That effort, after years of delays and false starts, is just now evaluating its first set of chemicals. Five phthalates, but neither DEHP nor BPA, will be screened in the initial group.)
But right from the beginning there was a scientific problem in the endocrine disruptor argument. BPA, as became apparent when it was initially tested for potency in the 1930s, is a weak estrogen; to have any kind of demonstrable effect, the concentrations of the stuff in the body and the environment would have had to have been many times what scientists were seeing. So, out of sight, out of mind—or so went conventional regulatory wisdom.
“The EPA limits are not safeguards at all,” says Wargo. For endocrine-disrupting chemicals answer to a different set of principles than do ordinary toxins, and as has been shown over and over in a welter of recent studies, these hormone mimics
can be most powerful at parts-per-billion, even parts-per-trillion, concentrations—infinitesimal levels well below the current regulatory radar, but levels, say scientists, that most of us now experience throughout our lives. New work has also uncovered the existence of previously unknown and exquisitely sensitive hormone receptors through which EDCs can work their mischief.
“There are many ways that chemicals at very low doses can produce slight alterations in endocrine signaling,” says endocrinologist Zoeller, “and it doesn’t take much, if you’re early in development, to cause long-term problems.”