By Janet Raloff
Two animal studies demonstrate that early exposure to a chemical known to leach from baby bottles, the linings of food cans, and other plastic items can trigger illness and even changes in genetic expression. A building block of polycarbonate plastics, bisphenol A (BPA) ends up in food, people, and the environment.
In one of the new studies, the pollutant permanently reprogrammed a gene in pups of mice fed BPA-laced chow.
The mice carried the Agouti gene, which is particularly vulnerable to what are called epigenetic changes. In such effects, hormones and other agents typically remove chemical units known as methyl groups from genes, or add them, interfering with the genes’ function. Epigenetically affected Agouti mice, normally lean and brown-haired, become fat and blond (SN: 6/24/06, p. 392).
Randy L. Jirtle and his colleagues at Duke University in Durham, N.C., fed female mice chow that delivered 50 milligrams of BPA daily per kilogram of body weight throughout the animals’ pregnancies and lactation periods. Blond fur and obesity in pups demonstrated Agouti reprogramming, say the researchers.
However, supplementing the mothers’ diet with methyl-donating agents such as folate blocked BPA’s epigenetic impacts, Jirtle’s team reports in the Aug. 7 Proceedings of the National Academy of Sciences.
In a second study, Retha R. Newbold’s team at the National Institute of Environmental Health Sciences (NIEHS) in Research Triangle Park, N.C., exposed newborn female mice to BPA for 5 days. Injected under the skin, doses ranged from 10 to 1,000 micrograms per kg of body weight.
Eighteen months later, the researchers examined the middle-aged animals’ reproductive tracts and found more fertility-jeopardizing impairments than in a group of untreated mice. Problems included cysts inside and outside the ovaries, development of glands at inappropriate places in the uterine lining, and polyps or other excessive-tissue growths in or on the uterine lining. Newbold’s group reports its findings online and in an upcoming Reproductive Toxicology.
The brief BPA doses delivered to the reproductive organs of affected mice “are below the levels measured in the serum of human adults today,” Newbold told Science News.
Reproductive Toxicology is also publishing five reviews of BPA studies and a consensus statement signed by 38 researchers who last fall took part in an NIEHS-sponsored expert-review conference on low-dose effects of the pollutant. Generally, the new reports and the consensus statement conclude that animals can be harmed by BPA at body burdens below those found in most adult residents of industrial nations.
Steven G. Hentges of the American Chemistry Council in Arlington, Va., finds both the Jirtle and Newbold teams’ studies of academic interest but argues that neither contributes much to the debate on human health. In one instance, says Hentges, the doses in mice were too large, and the other study was based on injected doses, which he terms irrelevant for assessing risks to people.
Frederick S. vom Saal of the University of Missouri–Columbia disagrees. He and other participants at NIEHS’ BPA-review conference concluded that injecting BPA is appropriate for modeling exposures, especially in young animals. Moreover, the Duke group’s study provides the evidence confirming researchers’ suspicions that BPA can exert epigenetic changes, says vom Saal.
