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Environ Epigenet. 2016 Mar;2(1). pii: dvv013. Epub 2016 Feb 10.

In utero exposures to environmental organic pollutants disrupt epigenetic marks linked to fetoplacental development.

Author information

1
Departments of Preventive Medicine, Pediatrics, Oncological Sciences, Obstetrics, Gynecology and Reproductive Sciences, Icahn School of Medicine at Mount Sinai, New York, NY.
2
School of Public Health, University of Illinois at Chicago, Chicago, IL.
3
Departments of Obs/Gyn, and Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY.
4
Department of Obs/Gyn, Baylor School of Medicine, Houston, TX.
5
Department of Genetics and Genomic Sciences and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York City, NY.
6
Carolina Population Center, University of North Carolina, Chapel Hill, NC.
7
Department of Pediatrics and Obs/Gyn, University of Utah, Salt Lake City, UT.
8
Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD.
9
Division of Pediatric and Maternal Health, US Food and Drug Administration, Silver Spring, MD, USA.

Abstract

While the developing fetus is largely shielded from the external environment through the protective barrier provided by the placenta, it is increasingly appreciated that environmental agents are able to cross and even accumulate in this vital organ for fetal development. To examine the potential influence of environmental pollutants on the placenta, we assessed the relationship between polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE) and several epigenetic marks linked to fetoplacental development. We measured IGF2/H19 imprint control region methylation, IGF2 and H19 expression, IGF2 loss of imprinting (LOI) and global DNA methylation levels in placenta (n = 116) collected in a formative research project of the National Children's Study to explore the relationship between these epigenetic marks and the selected organic environmental pollutants. A positive association was observed between global DNA methylation and total PBDE levels (P <0.01) and between H19 expression and total PCB levels (P = 0.04). These findings suggest that differences in specific epigenetic marks linked to fetoplacental development occur in association with some, but not all, measured environmental exposures.

KEYWORDS:

DDE; H19; IGF2; PBDE; PCB; environmental organic pollutants; global DNA methylation

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