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Placental PFAS concentrations are associated with perturbations of placental DNA methylation.

Environ Pollut

January 2025

Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR; Arkansas Children's Nutrition Center, Little Rock, AR.

The placenta is crucial for fetal development, is affected by PFAS toxicity, and evidence is accumulating that gestational PFAS perturb the epigenetic activity of the placenta. Gestational PFAS exposure can adversely affect offspring, yet individual and cumulative impacts of PFAS on the placental epigenome remain underexplored. Here, we conducted an epigenome-wide association study (EWAS) to examine the relationships between placental PFAS levels and DNA methylation in a cohort of mother-infant dyads in Arkansas (N=151).

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Background: Prenatal maternal smoking, lower birthweight, and shorter breastfeeding duration have all been associated with an earlier age at menopause in daughters. We estimated the extent to which birthweight-for-gestational-age z-score and breastfeeding duration mediate the effect of prenatal maternal smoking on time to natural menopause in daughters.

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Engineered nanomaterials (ENM) are capable of crossing the placental barrier and accumulating in fetal tissue. Specifically, the ENM nano-titanium dioxide (nano-TiO), has been shown to accumulate in placental and fetal tissue, resulting in decreased birthweight in pups. Additionally, nano-TiO is an established cardiac toxicant and regulator of glucose homeostasis, and exposure in utero may lead to serious maladaptive responses in cardiac development and overall metabolism.

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