by Dikshya Bastakoty
Dioxin has been linked to diminished fertility and an increased risk of preterm birth in both male and female mice exposed in utero to this common environmental contaminant.
In 2011, Kaylon Bruner-Tran, Ph.D., Kevin Osteen, Ph.D., and colleagues reported increased risk of preterm birth in mating partners of exposed male mice even though the female mice were not exposed to dioxin.
In a paper published last month by PLOS ONE, they found that the increased risk of preterm birth was passed down two generations, although the third generation was not directly exposed to the toxicant.
Since the placenta is largely derived from the male (the sperm), the researchers examined the testicular environment in which the sperm developed. Males destined to have partners delivering preterm had excessive testicular inflammation, which negatively affected sperm development.
If these findings hold true in humans, intervention designed to reduce preconception testicular inflammation may be a valuable tool to reduce the overall incidence of preterm birth, the researchers concluded.
This research was supported by a grant from the National Institute for Environmental Health Sciences (ES014942) and by Vanderbilt University School of Medicine.
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