Phthalate studies show similarly dramatic effects. When pregnant rats are exposed to high doses of phthalates, their male offspring are born with deformed genitalia. In 2005 Shanna Swan published the first study that looked for evidence of an obvious effect among boys. In 134 boys aged 2 months to 30 months, she found that sons whose mothers had higher levels of certain phthalates in their urine had a shorter distance between the anus and the penis. These boys were also likelier to have smaller penises and incompletely descended testicles. About one-quarter of American women have the higher phthalate levels she found in her study. This was particularly evident among women working in poorly ventilated nail salons, where one especially harmful phthalate, DBP, is released.
Chemicals leaching out of plastics may reshape not only your children but your children’s children.
In a recent study, Swan found that “we could predict the anogenital distance in babies just by knowing which phthalates a mother was exposed to and how much.” Those with the highest exposure to phthalates gave birth to boys with the shortest anogenital distance.
Phthalate exposure does not come just from moms. A new study gives evidence that infants and toddlers exposed to lotions, shampoos, and powders with phthalates may have up to four times as much of it in their urine as those whose parents do not use the products. The study, just published in Pediatrics by Sheela Sathyanarayana of the University of Washington, looked at 163 children between the ages of 2 months and 28 months between the years 2000 and 2005. The results were alarming, not least because manufacturers are not required to list phthalates as ingredients on labels.
So what are the long-term consequences of exposure to plastics? Teasing out the answers is difficult, in part because early exposure can have effects observed only much later in life. One of the scientists at work on the problem is Danish researcher Niels Skakkebaek of Copenhagen University Hospital, who has been documenting reproductive problems in men for more than two decades. His research in the 1970s showed links between testicular cancer in adults and abnormalities in genital development. He suspected that clues to the disorder lay in early life, when the reproductive organs are still developing. An especially crucial time is around 3 months or earlier, when boy babies experience a surge of testosterone. To see if phthalate exposure might influence this developmental period, Skakkebaek and his colleagues investigated how the amount of phthalates in breast milk correlated with a baby’s hormonal profile. In a study of 65 infants published in 2006, they discovered that the higher the level of phthalates, the greater the evidence of anti-androgenic hormonal activity.
Whatever the impact of plastics exposure, the effects are not easy to isolate. There are no babies rendered obviously deformed, as with thalidomide. There are no children robbed of mental agility, as with lead exposure. There is no clear-cut evidence of lung cancer, as with tobacco. As Swan admits: “The baby boys in our study were not freaks. They did not look abnormal. We’re talking about small changes you won’t find unless you look carefully.”
“Nobody knows what to do with the information,” says Tufts University environmentalist Sheldon Krimsky, author of Hormonal Chaos: The Scientific and Social Origins of the Environmental Endocrine Hypothesis. “This is a highly contested arena with no standards for consensus. And because, for instance, BPA is not put into food but leaches into food from containers, it doesn’t qualify for the Delaney clause, which mandates that if an additive causes cancer in any amount in two species, we can’t put it in the food supply.”
Back in the 1940s when plastics were being developed, no one suspected that chemicals leaching out of these marvelous materials could have insidious biological effects. What industrial chemists did know was that by tinkering with a highly reactive molecule called a phenol they were able to devise countless synthetic chemicals for use in new materials. Only through subsequent studies has it been shown that the estrogen receptor has a particular affinity for a characteristic molecular component of phenols. “I’d say 99.9 percent of what turn out to be chemical estrogens have a phenolic hydroxyl group on the molecule, and any of those can bind to the estrogen receptor, ” says Wade Welshons, a University of Missouri cell biologist and endocrinologist who has spent his career studying estrogen. Moreover, “almost everything that binds to the estrogen receptor turns it on in some way. I’ve run across only two chemicals that fully antagonize, or switch off, the receptor.”
Despite this new insight, regulation of synthetic estrogens as a class seems far off. BPA alone is “worth at least a million dollars every hour,” Welshons says. “And that figure is conservative. I’m surprised the chemical industry hasn’t tried to blow up our labs.”
In 1989 little was known about synthetic chemicals in everyday plastics and how they mimicked estrogens. Ana Soto, professor of cellular biology at Tufts University School of Medicine, and her colleagues were studying the effects of estrogen on a breast cancer cell line. “Suddenly all the cancer cells were proliferating maximally, whether they were being grown in a medium with estrogen or not,” Soto recalls. “We thought that somebody must have opened a bottle of the female hormone estradiol in the wrong place. We scrubbed the whole room, we bought new batches of everything, and the cells kept proliferating. So we began one by one to replace and substitute our equipment, and we finally found the contamination in tubes storing a component of the medium. The tube manufacturer had changed its formula, with the best intention of rendering the tubes more impact resistant. They said the new chemical was a trade secret. So we analyzed it ourselves, and it turned out to be nonylphenol. We injected the chemical into rats and demonstrated that it makes the epithelial lining of the uterus proliferate—a sign of its being an estrogen.” Nonylphenol is also a component in some detergents and other products, and its presence in British streams has been linked to the feminization of fish.
In 1998 another synthetic estrogen leached from animal cages and bottles in a different lab—this was the now-infamous BPA. Patricia Hunt (then working at Case Western Reserve University) was studying the endocrine environment of the aging ovary in mice. Suddenly, as in Soto’s lab, “our control data went nuts,” Hunt says. “We saw chromosomal abnormalities that would lead to pregnancy loss and birth defects. It turned out that all of our cages and water bottles were contaminated by the BPA in the polycarbonate plastic, which was being sterilized at high temperatures. We set about proving this contamination was coming from the water bottles and cages.” They published that work in 2003. In 2007 Hunt and her colleagues published a paper in PLoS Genetics demonstrating that BPA exposure in utero disrupts the earliest stages of egg development. The fetuses of pregnant mice exposed to low doses of BPA, Hunt says, had “gross aberrations. We were stunned to see the effects of this estrogenic substance.”
