AO/Dioxin Birth Defect Research: Fetal origins: How adult disease risk takes shape before you are born

A variety of pollutants appear capable of programming fetal metabolism to increase the risk of adult-onset disorders.

Michael Skinner of Washington State University and colleagues found that fetal exposure to high doses of the widely used fungicide, vinclozolin, produces lasting changes in the way genes are turned on and off in rats.

The changes reduced the fertility of male rats. They also made offspring more likely to develop tumors and kidney disease. Affected males passed the changes on to their offspring. Further studies showed that high doses of dioxin, jet fuel, and the plastic chemicals BPA and phthalate induced the same changes in fetal rodents.

Skinner said that each agent caused a distinct pattern of changes in genes turned on and off, so distinct that it might prove possible to determine whether a baby was exposed to the substance during development.

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