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

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.

Abbreviation
Sci Rep
Publication Date
2017-03-21
Volume
7
Issue
1
Page Numbers
288
Pubmed ID
28325913
Medium
Electronic
Full Title
Persistent DNA methylation changes associated with prenatal mercury exposure and cognitive performance during childhood.
Authors
Cardenas A, Rifas-Shiman SL, Agha G, Hivert MF, Litonjua AA, DeMeo DL, Lin X, Amarasiriwardena CJ, Oken E, Gillman MW, Baccarelli AA