Issue Date: January 15, 2007
Exposure to Bisphenol A (BPA) disrupts early egg development in mouse fetuses, reports Patricia A. Hunt, a geneticist at Washington State University (PLoS Genetics, DOI: 10.1371/journal.pgen.0030005). This is the second study by Hunt showing that the monomer used to manufacture polycarbonate can cause chromosomal abnormalities in mouse eggs at exposure levels comparable with what humans receive today (C&EN, April 7, 2003, page 7).
Hunt and her colleagues exposed pregnant mice to a low dose of BPA-20 µg per kg of body weight per day-for one week and found that the process of meiosis in the fetuses' eggs was perturbed. When these fetuses reached adulthood and were fertilized, the perturbations led to an increase in chromosomally abnormal embryos, Hunt says.
A mouse fetus with chromosomal abnormalities would generally be resorbed in the womb, reducing litter size. Human fetuses with similar aberrations are usually miscarried during the first trimester, but some are born with serious defects, such as Down's syndrome, she says. Thus, when extrapolated to humans, these results suggest that "BPA exposure during pregnancy has multigenerational consequences," she concludes.
In a commentary also published in PLoS Genetics, R. Scott Hawley, an investigator at Stowers Institute for Medical Research, says Hunt's "observations provide the most convincing evidence to date that environmental exposures may affect meiotic processes in mammals." Her findings raise the possibility that BPA may perturb meiotic processes in humans, he explains.-
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