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Environ Health Perspect. 2017 Aug 29;125(8):087022. doi: 10.1289/EHP1467.

Prenatal Exposure to Mercury: Associations with Global DNA Methylation and Hydroxymethylation in Cord Blood and in Childhood.

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Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute , Boston, Massachusetts, USA.
Department of Public Health and Primary Care, Katholieke Universiteit Leuven , Leuven, Belgium.
IDEWE , External Service for Prevention and Protection at Work, Heverlee, Belgium.
Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University , New York, New York, USA.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital , Boston, Massachusetts, USA.
Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai , New York, New York, USA.
Diabetes Unit, Massachusetts General Hospital , Boston, Massachusetts, USA.
Environmental Influences on Child Health Outcomes (ECHO) Program, Office of the Director, National Institutes of Health , Department of Health and Human Services, Bethesda, Maryland, USA.



Mercury is a global pollutant, and prenatal exposure is associated with adverse health effects. To date, no studies have evaluated the association between prenatal mercury exposure and DNA hydroxymethylation, an epigenetic modification important for tissue differentiation and embryonic development.


We sought to evaluate the association between prenatal mercury exposure and offspring global DNA methylation and hydroxymethylation at birth and test for persistence of the association in childhood.


Within Project Viva, a U.S. prebirth cohort, we examined associations of maternal second trimester red blood cell mercury (RBC-Hg) concentrations with global 5-hydroxymethylcytosine (%-5hmC) and 5-methylcytosine (%-5mC) DNA content in blood collected at birth (n=306), early childhood (n=68; 2.9 to 4.9 y), and midchildhood (n=260; 6.7 to 10.5 y).


Median prenatal RBC-Hg concentration was 3.23μg/g [interquartile range (IQR)=3.29]. At birth, median cord blood %-5mC, %-5hmC, and their ratio were 4.95%, 0.22%, and 24.37, respectively. The mean adjusted difference [95% confidence interval (CI)] of blood %-5hmC for a doubling in prenatal RBC-Hg concentration was -0.013% (-0.029, 0.002), -0.031% (-0.056, -0.006), and 0.005% (-0.007, 0.018) at birth, early, and midchildhood, respectively. The corresponding relative adjusted change in the genomic ratio of %-5mC to %-5hmC for a doubling in prenatal RBC-Hg concentration was 4.70% (0.04, 9.58), 22.42% (7.73, 39.11), and 0.73% (-4.18, 5.88) at birth, early, and midchildhood, respectively. No associations were present between prenatal maternal RBC-Hg and %-5mC at any time point.


Prenatal mercury exposure was associated with lower %-5hmC genomic content and a corresponding increase in the ratio of %-5mC to %-5hmC in cord blood. This association was persistent in early but not midchildhood blood. Our results demonstrate the potential malleability of epigenetic modifications associated with mercury exposure in utero.

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