CLEVELAND Researchers have found disturbing new evidence suggesting that environmental exposure to a ubiquitous substance may cause chromosomally abnormal pregnancies. They have learned that low levels of a compound used in the manufacture of common plastic food and beverage containers and baby bottles interfere with cell division in the eggs of female mice. The disruption of cell division can result in an abnormal number of chromosomes in the eggs, a condition known as aneuploidy, which is the leading cause of mental retardation and birth defects in humans. Down syndrome is an example of a disorder caused by the addition of an extra chromosome.
Patricia Hunt, Ph.D., lead author of the study appearing in the April issue of the journal Current Biology, is concerned because the compound, called Bisphenol A (BPA), which shows hormone-like properties and mimics the effects of naturally produced estrogens, produces a significant increase in genetic abnormalities at extremely low levels.
Our studies provide the first direct evidence that environmental exposure to BPA acts to disrupt the maturation of the egg and demonstrate a dose-related increase in abnormalities, says Hunt, an associate professor of genetics at the Case Western Reserve University School of Medicine and an expert in the causes of genetic abnormalities in egg cells. In addition, they show that, at least in the mouse, exposure to very low doses of BPA within the human exposure range produces detectable effects.
These studies raise important questions about the potential impact on human reproduction of BPA and other man-made substances that mimic the actions of hormones, she says.
Hunts laboratory began studying the effects of BPA after control (or normal) mice in research projects began showing genetic abnormalities. In mice, the rate of these abnormalities usually is low. The defects were traced to plastic cages and plastic water bottles that had been inadvertently
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Contact: George Stamatis
gxs18@po.cwru.edu
216-368-3635
Case Western Reserve University
31-Mar-2003
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