Abstract
Telomere shortening is an established marker of cellular aging, and can be induced by stress and environmental exposure, promoting disease. Likewise placental telomere length (TL) has been shown to physiologically shorten throughout gestation with evidence of accelerated shortening in adverse pregnancy outcomes such as PPROM, IUGR, and preeclampsia. Our objective was to assess the association of maternal urinary levels of di(2-ethylhexyl) phthalate (DEHP) metabolites with placental TL.
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