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  Because these newborns are underdeveloped, they may be especially vulnerable to the chemical's hormonal impacts. The cellular barriers to their brains and organs are more easily permeated. What's more, they don't yet have the capacity of adults or even of older children to clear the chemical from their systems, meaning it circulates for a longer time, increasing the potential for damage.

  As the CDC has pointed out, the mere presence of DEHP, or any chemical, in someone's blood or urine does not mean it is a health hazard. The big, and difficult, question is whether the small amounts to which we are all regularly exposed are sufficient to affect some people's health. We may all be a little plastic, but that doesn't mean we are all affected in the same way. Some individuals, such as NICU babies, may be at greater risk because of the amounts they take in or their stage of life. Given that researchers can't subject humans to the kinds of tests done with lab rats to pinpoint the conditions that cause adverse effects, it's not unreasonable to view ourselves as subjects of a vast, uncontrolled experiment. But we are not entirely blind as we journey through this vast plastic laboratory called modern life. Epidemiological studies—surveys of large groups of people—offer an indirect way to gather evidence. Shanna Swan, a reproductive epidemiologist at the University of Rochester School of Medicine and Dentistry, has conducted several such studies, and her findings suggest that some of us do pay a price for being a little plastic.

  In one study, she measured phthalate levels in 134 pregnant women and then later closely examined the genitalia of their baby sons. She found the sons of mothers with the highest phthalate levels had subtle but unmistakable symptoms echoing the phthalate syndrome seen in rats. They were more likely to have undescended testicles, a smaller penis, and a shorter distance between the base of the penis and the anus, the measurement that in the rat studies was considered a hallmark of decreased fetal testosterone levels. "These babies had no abnormalities that a clinician would recognize," Swan emphasized. But given the long-term effects on exposed rats, she considered even these subtle changes a worrisome collection of symptoms that could affect the boys' fertility later in life.

  Swan then decided to look at how else an antiandrogen might affect a developing fetus. The male reproductive tract isn't the only body system touched by testosterone. Like estrogen, the hormone circulates throughout the body, affecting metabolism, growth, behavior, and cognition, as well as the actions of other hormones, in both boys and girls. "The brain is the largest sex organ," Swan likes to say. "It also is developed under the influence of testosterone."

  Normally, testosterone levels in the brain surge during certain critical points of development, which is thought to play an essential role in the process of sexual differentiation. Studies have shown that when pregnant rats are exposed to drugs known to block that hormonal surge, their male offspring don't engage in the same kind of rough-and-tumble play as unexposed pups.

  Taking her cue from those findings, Swan went back to the same group of parents and children she'd studied before. The kids were now in preschool. For this study, she had the parents fill out a detailed questionnaire about how their children play. She asked them to rate how frequently their child played with toys like dolls or trucks, how often the child set up house or pretended to fight. The boys with the highest fetal exposure to the phthalates DEHP and DBP had the lowest scores on typical boy play, such as pretending to shoot a gun. They were also more likely to prefer gender-neutral play, such as working on puzzles. The girls showed no effect.

  It was the kind of finding headline writers love. "Common Chem­icals Make Boys Soft," one Australian paper declared. But Swan wasn't reporting a nifty solution to macho aggression. She was describing a subtle shift in the hard-wiring of the boys' brains so that they played in "less typically masculine" ways. It was a small effect but one with potentially profound implications, given that testosterone, estrogen, and other hormones shape the many differences in how male and female brains develop and process the world.

  Both studies need to be replicated. But having found that phthalates can affect two very different body systems, Swan asked, "Why should we assume the effects are just limited to two? My concern is we are seeing changes throughout the body wherever testosterone matters, and that's many, many places."

  Other epidemiological findings lend weight to her concerns. A variety of small studies have found an association between exposure to phthalates and obesity, early puberty, allergies, ADD, and altered thyroid function—all conditions that could plausibly be related to hormonal disruptions. Most of the studies have focused on boys. But a handful suggest that girls may also be affected by the drops in testosterone or by some as-yet-undescribed effect on their estrogen levels. Some researchers have postulated that the chemical can suppress estrogen production in females, said Swan. "We're all struggling to figure out what's going on with females. It's difficult because the female reproductive system is invisible. The males are easier because it all hangs out." Still, a small number of epidemiological studies have found correlations between phthalate levels and endometriosis, miscarriage, uterine fibroids, and premature breast development.

  DEHP's hormonal effects may not be the only problem. A 2010 study suggested that in very young infants, the chemical may interfere with the cellular systems involved in controlling inflammation, part of the body's method of fighting infection. Other studies have linked DEHP with immune system and respiratory problems and have continued to raise red flags about toxicity to the liver, especially in premature babies who are being exposed due to their treatment in NICUs. German researchers showed that babies in intensive care who received fluids from IV bags containing DEHP were more likely to develop a particular type of liver problem than those whose IV bags didn't contain the chemical.

  This all sounds like pretty strong evidence, right? And yet science rarely delivers straight slam dunks. Consider just one endpoint thought to be affected by DEHP: cells in the testes that secrete testosterone. Rat studies have repeatedly found that DEHP damages those cells. But rats are the most phthalate-sensitive of all species tested. Recent primate studies involving young marmosets have found no such effect. Does that mean primates—our closest relatives—aren't as sensitive to the chemical as rodents? Or were the marmosets past the age when they would have been vulnerable to the effects? Researchers are still debating the question. Likewise, the epidemiological findings on sperm quality have been inconsistent: some studies show correlations with phthalate levels, some don't.

  It's hard and expensive to mount the kinds of studies that can deliver clear-cut answers. For instance, Drs. Short and Luban have long wanted to do a study following babies who were heavily exposed to DEHP as a result of being on heart-lung machines. "If any population would have long-term reproductive effects, it would be those kids," said Short. "If the results came back negative, it would put all this stuff to rest." They did a small pilot study in which they found and tested eighteen teenagers who as infants had spent time in the NICU on the machines. None showed signs of any reproductive problems. But it's impossible to draw any valid conclusions from a group that small. Statistically speaking, at least two hundred and fifty kids would have to be studied to get robust results. Short and Luban estimated it would take ten million dollars to track down and test that many survivors. They wrote up a proposal to do such a study, but neither the National Institutes of Health nor private industry was willing to make the investment. "That ten-million-dollar price tag was just prohibitive," said Short.

  "But, boy, it would have been nice to have [the answers]," added Luban.

  The continuing uncertainties are one reason why expert panels that have looked at DEHP and other phthalates have come to differing conclusions and also why nearly every research paper ends with the same mantra: more and better studies are needed.

  One of the biggest gaps in research is the paucity of studies looking at the real world of chemical exposure. A person is not exposed to just a single chemical at a time; each day each
of us encounters hundreds. And that chemical bombardment begins even before birth: a study by the organization Environmental Working Group found an average of two hundred industrial chemicals and pollutants in the umbilical-cord blood of ten newborns. What's the cumulative effect? Researchers have only begun addressing that question. The early findings are cause for concern.

  Earl Gray, the EPA researcher who identified phthalate syndrome, tested mixtures of phthalates in rats. He deliberately used low doses of each, well below amounts that could produce effects individually. Yet when he exposed male rats in utero to the mixtures, as many as 50 percent were born with hypospadias or other reproductive abnormalities. In combination, the chemicals were far more potent than they were individually, suggesting that compounds that act on the same hormonal pathways have an additive effect, he said.

  Researchers say we need more of these kinds of studies, ones designed to mimic the real experience of human exposure. Swan and others want to see more research that focuses on pregnant women and children to gain a long-term picture of chemical effects rather than isolated snapshots. That's just what a recently begun study aims to do: the National Children's Study will follow a hundred thousand children across the United States from birth to the age of twenty-one in an effort to tease out environmental influences, including exposure to phthalates and bisphenol A, on health.

  So if DEHP and other phthalates haven't been proven unsafe, does that mean they are safe?

  The chemical industry, as might be expected, maintains they are. There is, after all, a $1.4 billion market in phthalates on the line. The American Chemistry Council's position, as one spokeswoman noted, is that "DEHP medical devices have been used for better than fifty years, and there hasn't been any verified evidence of harm to humans." Even in the case of neonates, the group maintains, the benefits of treatment outweigh the risks posed by exposure.

  The ACC vigilantly tracks the research, publicizing studies that show no adverse effects and picking apart each finding that suggests a problem. It criticized Swan for using "unproven methods," such as the anogenital distance measurement and the play survey, and hammered on methodological errors, which she acknowledges but insists did not affect the statistical significance of her final results. In general, the ACC draws on a standing set of criticisms to point out flaws that may be accurate but not always meaningful. Among the oft-cited complaints: the sample sizes are too small; rats are poor models for human health hazards; the doses administered in animal studies are much higher than those experienced by humans; the demonstrated health effects are not necessarily adverse. Almost invariably, when an epidemiological study reports a risk associated with phthalates, the group counters with a press release pointing out that the study shows a correlation only, not proof of a causal effect. Which is true—that's precisely what epidemiological studies do. Still, the correlations highlighted by epidemiological studies have long been the gold standard for assessing risks to public health.

  The insistent focus on the flaws of each individual study ignores—and obscures—how each may be contributing to an increasingly disturbing body of evidence. The nitpicking zeroes in on and tries to amp up the uncertainty that is always inherent in science. It's a strategy taken straight from the tobacco industry, and one that, incredibly enough, was committed to paper in 1969 by an executive at the cigarette maker Brown and Williamson: "Doubt is our product since it is the best means of competing with the 'body of fact' that exists in the mind of the general public."

  As Swan and others have pointed out, there was never a single study that "proved" smoking causes lung cancer. It took a combination of in vitro, animal, and human population studies to demonstrate the dangers of tobacco. A series of epidemiological studies pointed to the risk, prompting the surgeon general to issue his famous 1964 warning. Over the next forty-some years, researchers painstakingly pieced together, through cell and animal studies, the biological mechanisms that explained how tobacco smoke could induce tumors in the lungs. Meanwhile, the tobacco industry spent those decades denying there was any connection.

  It's unlikely science will deliver neat, definitive answers about the risks of endocrine disrupters any time soon. So do we wait for children like Amy to grow up before we discover the dangers of DEHP exposure? Do we wait to see if she develops liver problems, launches into puberty at an early age, has trouble conceiving a child? Or have we reached the point where there is enough evidence to fairly act on the side of caution? I think we have. Yet our current system for regulating chemicals makes that difficult to do.

  We have no coherent or comprehensive body of law for managing the chemicals we experience in daily life. Instead, there's a weak and uncoordinated patchwork of national and state laws. Federal regulation of chemicals is divided among various agencies, leading to fragmented and inconsistent policies. The EPA, for instance, recently announced it would take steps to limit use of phthalates, including DEHP. The FDA, however, still judges that the chemical offers more benefit than risk and has thus far ignored calls to limit its use in medical devices and require labeling of medical products that contain it. The FDA's only action to date has been a 2002 advisory recommending that hospitals not use devices containing DEHP in women pregnant with boys, in male infants, and in young teenage boys. U.S. regulators at both the FDA and the EPA have lagged behind the changing scientific understanding about chemical risks. For instance, both agencies still base their safety assessments of chemicals on studies of one chemical at a time, rather than looking at aggregate effects.

  But there is a much bigger problem: U.S. law tends to treat chemicals as safe until proven otherwise. Regulators are required to find what author Mark Schapiro called "a scientifically improbable smoking gun" before they can pull a suspect chemical off the market. Nowhere are the failings of that approach more clear than in the main federal law regulating synthetic chemicals, the Toxic Substance and Control Act. Enacted in 1976, the law gives the EPA the power to require testing of and restrict chemical substances. Yet it's had little opportunity to exercise that power. The sixty-two thousand chemicals in use when the law was passed were exempted from the testing requirements. And the law's provisions bind EPA regulators in a Catch-22: they need evidence of harm or exposure before they can require a manufacturer to provide more information about a chemical, but without the information, how do they establish evidence of harm? In the absence of that evidence, the regulators cannot act. So while twenty thousand chemicals have been introduced since 1976, the EPA has been able to require intensive reviews for only two hundred, and it has used its authority to restrict only five. The hurdles are so high, the agency could not even successfully ban asbestos, an undisputed carcinogen. "This means," wrote John Wargo, an expert on chemical policy, "that nearly all chemicals in commerce have been poorly tested to determine their environmental behavior or effects on human health."

  Are all those chemicals dangerous? It's hard to tell, but the EPA has said that at least sixteen thousand were potentially causes for concern owing to their high production volume and chemical properties. Meanwhile, European regulators have estimated that an astounding 70 percent of new chemicals have some hazardous property, ranging from carcinogenicity to flammability.

  Everyone concerned with chemical policy—the head of the EPA, environmental activists, even the American Chemistry Council—agrees the law is a poor vehicle for navigating our current chemical landscape. Yet agreeing on some alternative approach is another matter (as has been evident in debate over a reform bill winding its way through Congress as of mid-2010). A major point of contention is that American policymakers are starting to look to Europe as a model for regulating the chemical industry.

  In Europe, the burden of proof is on safety rather than danger. European regulators "act on the principle of preventing harm before it happens, even in the face of scientific uncertainty." Guided by that precautionary principle, Europeans began limiting DEHP and other phthalates while American regulators continued debating the risks. (The
EU, for instance, barred the use of DEHP in children's toys in 1999, nine years before the U.S. Congress passed similar legislation.) A new directive known as REACH (for Registration, Evaluation, and Authorization of Chemicals), adopted in 2007, requires testing of both newly introduced chemicals and those already in use, with the burden on manufacturers to demonstrate that they can be used safely. The agency charged with implementing REACH targeted DEHP as one of the first fifteen "substances of very high concern" to be regulated. In essence, European regulators are treating chemicals the way U.S. regulators treat drugs: they're presumed to be dangerous unless shown to be otherwise. American manufacturers are already selling products in European markets that have been reformulated to comply with the precautionary principle. Shouldn't American citizens demand the same on this side of the Atlantic?

  Some states have already taken the initiative. In 2008, California passed landmark safer chemicals legislation that requires the state to collect data on chemical toxicity, restrict some of the most hazardous substances, and promote research into safer substitutes. The law expands on the approach taken by Massachusetts, which since 1989 has required companies using large quantities of toxic materials to disclose that use and explore alternatives to dangerous chemicals and has promoted programs to help companies either switch to safer alternatives or use smaller quantities of the hazardous substances.

  Still, state efforts are no substitute for across-the-board federal protections. John Wargo, a professor at Yale University, argued convincingly that what we need is a national "plastics control law." Congress, he pointed out, has passed laws to regulate other health or environmental risks, such as pesticides, pharmaceuticals, and tobacco. Why not the same for plastics—materials that touch the life of every single American? He proposed a comprehensive policy that, among other things, would include tough premarket testing of chemicals used in plastics, mandatory labeling of ingredients, and strict prohibitions of chemicals and compounds that pose a threat to human health or that don't quickly degrade into harmless substances.