Persistent DNA methylation changes associated with prenatal mercury exposure and cognitive performance during childhood

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Persistent DNA methylation changes associated with prenatal mercury exposure and cognitive performance during childhood

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Title: Persistent DNA methylation changes associated with prenatal mercury exposure and cognitive performance during childhood
Author: Cardenas, Andres; Rifas-Shiman, Sheryl L.; Agha, Golareh; Hivert, Marie-France; Litonjua, Augusto A.; DeMeo, Dawn L.; Lin, Xihong; Amarasiriwardena, Chitra J.; Oken, Emily; Gillman, Matthew W.; Baccarelli, Andrea A.

Note: Order does not necessarily reflect citation order of authors.

Citation: Cardenas, A., S. L. Rifas-Shiman, G. Agha, M. Hivert, A. A. Litonjua, D. L. DeMeo, X. Lin, et al. 2017. “Persistent DNA methylation changes associated with prenatal mercury exposure and cognitive performance during childhood.” Scientific Reports 7 (1): 288. doi:10.1038/s41598-017-00384-5. http://dx.doi.org/10.1038/s41598-017-00384-5.
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Abstract: Prenatal exposure to mercury, a known neurotoxic metal, is associated with lower cognitive performance during childhood. Disruption of fetal epigenetic programming could explain mercury’s neurodevelopmental effects. We screened for epigenome-wide methylation differences associated with maternal prenatal blood mercury levels in 321 cord blood DNA samples and examined the persistence of these alterations during early (n = 75; 2.9–4.9 years) and mid-childhood (n = 291; 6.7–10.5 years). Among males, prenatal mercury levels were associated with lower regional cord blood DNA methylation at the Paraoxonase 1 gene (PON1) that persisted in early childhood and was attenuated in mid-childhood blood. Cord blood methylation at the PON1 locus predicted lower cognitive test scores measured during early childhood. Methylation at the PON1 locus was associated with PON1 expression in an independent set of cord blood samples. The observed persistent epigenetic disruption of the PON1 gene may modulate mercury toxicity in humans and might serve as a biomarker of exposure and disease susceptibility.
Published Version: doi:10.1038/s41598-017-00384-5
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428306/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:33029964
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