The Problem with Plastics
Male Babies Less Male
One focus of Zoeller’s research is how thyroid hormone controls what are called cell fate specifications. “Undifferentiated cells in the fetal brain have to make decisions about what they want to be when they grow up. Thyroid hormone helps them make the right choice,” says Zoeller. “But interfere with the thyroid signal and cells start to make the wrong decision. That’s irrevocable.”
In animal studies with rats, Zoeller has shown that low levels of BPA are quite capable of disrupting fetal brain development, a situation that could lead to “a mosaic of effects,” which he’s currently attempting to document. And he’s hardly alone in demonstrating BPA’s ability to interfere with hormone signaling in animal experiments.
Yale School of Medicine reproductive biologist Hugh Taylor studies what are known as HOX genes, particularly a suite of them essential for normal uterine development and fertility. In an ongoing series of investigations, Taylor has exposed pregnant mice and their fetuses to DES and BPA and gotten similar results: females whose reproductive systems will not function correctly when they reach adulthood. “There’s a crucial, vulnerable time period during development,” says Taylor. “These endocrine disruptors change the fine tuning of the entire program, and then the effects are locked in for life.”
Phthalates seem to work in a similar manner, except they target the male set of hormones known as androgens. “The default developmental plan is actually female,” says Shanna Swan, an epidemiolo-gist at the University of Rochester School of Medicine and Dentistry. “The movement toward becoming male is controlled by testosterone during what we call the fetal programming window. Phthalates, like DEHP, can compromise the whole cascade toward masculinization.”
In “Environmental Phthalate Exposure in Relation to Reproductive Outcomes and Other Health Endpoints in Humans,” a paper published last year in Environmental Research, Swan showed that male babies born to mothers with relatively high concentrations of several phthalates in urine samples were, in fact, less male, according to a measure long used to gauge sexual dimorphism in rodents but only recently used for humans. This standard is called the anogenital distance, and it turns out that the distance in females is normally about half that of males. However, in Swan’s study, which builds on groundbreaking work that she and her team published in Environmental Health Perspectives in 2005 and 2006, the greater the concentration of phthalates in the mothers, the shorter the anogenital distance in their male offspring. Girls, as was predicted from rodent data, were not affected—by this measure, at least. The more phthalate-exposed boys also had narrower penises, compared to male infants whose mothers had lower levels of phthalates, and a greater propensity to have undescended testicles. It’s too early to tell whether these infants will also have, later in life, a lower sperm count, a higher incidence of testicular cancer and other hallmarks of what some researchers term “the phthalate syndrome.”
Swan admits that we can’t yet know what the long-lasting impact of exposure, if any, will be on these, or any other, boys. But she cautions against complacency. “So far, when we’ve made predictions from rodent studies, they’ve been borne out in humans,” she says. “And the prediction from rodent studies is that exposure does matter—and should affect male sperm count and fertility.”
In the mid-1980s, British epidemiologist David Barker proposed that the pattern of heart disease he was seeing in England actually had its roots in the womb. However, the problem was not simply bad genes; rather, it was the environment in which the fetus developed and the mother’s diet, in particular.
The “fetal origins of adult disease” hypothesis was initially dismissed as ridiculous, but there’s growing evidence to support it, says Soto, a Tufts University developmental biologist and one of the pioneers in studying the health effects of EDCs. “Many of the bad health trends we’re now seeing, from infertility to cancer, can be correlated with early exposure to BPA and other endocrine disruptors at levels that fetuses and infants experience every day,” says Soto.
Correlation, of course, does not imply causation—you learn that in statistics 101. But sometimes the public and their congressional representatives don’t make that distinction, especially when they see an increasing number of studies that seem to explain the pattern of many of the disturbing disease trends of the 21st century.