<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lozano M</submitter><funding>Intramural NIH HHS</funding><funding>NICHD NIH HHS</funding><funding>European Research Council</funding><funding>NIEHS NIH HHS</funding><funding>Medical Research Council</funding><funding>NHLBI NIH HHS</funding><funding>NINR NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>Wellcome Trust</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>112093</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10879652</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>204(Pt B)</volume><pubmed_abstract>Mercury (Hg) is a ubiquitous heavy metal that originates from both natural and anthropogenic sources and is transformed in the environment to its most toxicant form, methylmercury (MeHg). Recent studies suggest that MeHg exposure can alter epigenetic modifications during embryogenesis. In this study, we examined associations between prenatal MeHg exposure and levels of cord blood DNA methylation (DNAm) by meta-analysis in up to seven independent studies (n = 1462) as well as persistence of those relationships in blood from 7 to 8 year-old children (n = 794). In cord blood, we found limited evidence of differential DNAm at cg24184221 in MED31 (β = 2.28 × 10&lt;sup>-4&lt;/sup>, p-value = 5.87 × 10&lt;sup>-5&lt;/sup>) in relation to prenatal MeHg exposure. In child blood, we identified differential DNAm </pubmed_abstract><journal>Environmental research</journal><pubmed_title>DNA methylation changes associated with prenatal mercury exposure: A meta-analysis of prospective cohort studies from PACE consortium.</pubmed_title><pmcid>PMC10879652</pmcid><funding_grant_id>MC_UU_12013_2</funding_grant_id><funding_grant_id>G9815508</funding_grant_id><funding_grant_id>N01ES75558</funding_grant_id><funding_grant_id>MC_UU_12013_1</funding_grant_id><funding_grant_id>WT088806</funding_grant_id><funding_grant_id>R01 HL111108</funding_grant_id><funding_grant_id>MC_UU_00011/1</funding_grant_id><funding_grant_id>BB/I025263/1</funding_grant_id><funding_grant_id>R01 ES025531</funding_grant_id><funding_grant_id>268479</funding_grant_id><funding_grant_id>R01 NR013945</funding_grant_id><funding_grant_id>102215/2/13/2</funding_grant_id><funding_grant_id>U01 NS047537</funding_grant_id><funding_grant_id>217065/Z/19/Z</funding_grant_id><funding_grant_id>102215</funding_grant_id><funding_grant_id>R37 HD034568</funding_grant_id><funding_grant_id>MC_UU_12013_8</funding_grant_id><funding_grant_id>MC_PC_15018</funding_grant_id><funding_grant_id>MC_UU_12013_5</funding_grant_id><funding_grant_id>Z01 ES049019</funding_grant_id><funding_grant_id>MC_PC_19009</funding_grant_id><funding_grant_id>BB/I025751/1</funding_grant_id><funding_grant_id>MC_UU_00011/5</funding_grant_id><pubmed_authors>Rifas-Shiman S</pubmed_authors><pubmed_authors>Huel G</pubmed_authors><pubmed_authors>Pesce G</pubmed_authors><pubmed_authors>Relton C</pubmed_authors><pubmed_authors>Kishi R</pubmed_authors><pubmed_authors>Vafeiadi M</pubmed_authors><pubmed_authors>Vrijheid M</pubmed_authors><pubmed_authors>Kim WJ</pubmed_authors><pubmed_authors>Ikeda-Araki A</pubmed_authors><pubmed_authors>Bakulski KM</pubmed_authors><pubmed_authors>Ballester F</pubmed_authors><pubmed_authors>Gutzkow KB</pubmed_authors><pubmed_authors>Won S</pubmed_authors><pubmed_authors>Fallin MD</pubmed_authors><pubmed_authors>Lozano M</pubmed_authors><pubmed_authors>Broberg K</pubmed_authors><pubmed_authors>Annesi-Maesano I</pubmed_authors><pubmed_authors>Llop S</pubmed_authors><pubmed_authors>Park J</pubmed_authors><pubmed_authors>Yousefi P</pubmed_authors><pubmed_authors>Oken E</pubmed_authors><pubmed_authors>Hivert MF</pubmed_authors><pubmed_authors>Dou JF</pubmed_authors><pubmed_authors>Rahman M</pubmed_authors><pubmed_authors>Soler-Blasco R</pubmed_authors><pubmed_authors>Miyashita C</pubmed_authors><pubmed_authors>Haug LS</pubmed_authors><pubmed_authors>Bustamante M</pubmed_authors></additional><is_claimable>false</is_claimable><name>DNA methylation changes associated with prenatal mercury exposure: A meta-analysis of prospective cohort studies from PACE consortium.</name><description>Mercury (Hg) is a ubiquitous heavy metal that originates from both natural and anthropogenic sources and is transformed in the environment to its most toxicant form, methylmercury (MeHg). Recent studies suggest that MeHg exposure can alter epigenetic modifications during embryogenesis. In this study, we examined associations between prenatal MeHg exposure and levels of cord blood DNA methylation (DNAm) by meta-analysis in up to seven independent studies (n = 1462) as well as persistence of those relationships in blood from 7 to 8 year-old children (n = 794). In cord blood, we found limited evidence of differential DNAm at cg24184221 in MED31 (β = 2.28 × 10&lt;sup>-4&lt;/sup>, p-value = 5.87 × 10&lt;sup>-5&lt;/sup>) in relation to prenatal MeHg exposure. In child blood, we identified differential DNAm </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-26T08:06:46.07Z</modification><creation>2025-04-06T12:32:29.354Z</creation></dates><accession>S-EPMC10879652</accession><cross_references><pubmed>34562483</pubmed><doi>10.1016/j.envres.2021.112093</doi></cross_references></HashMap>