Poverty and InequalitySexual and Reproductive HealthFamily, Maternal & Child HealthMethodology

Aberrant 5'-CpG Methylation of Cord Blood TNFalpha Associated with Maternal Exposure to Polybrominated Diphenyl Ethers

TitleAberrant 5'-CpG Methylation of Cord Blood TNFalpha Associated with Maternal Exposure to Polybrominated Diphenyl Ethers
Publication TypeJournal Article
Year of Publication2015
AuthorsDao, T, Hong, X, Wang, X, Tang, WY
JournalPLoS One
ISBN Number1932-6203
Accession Number26406892

Growing evidence suggests that maternal exposures to endocrine disrupting chemicals during pregnancy may lead to poor pregnancy outcomes and increased fetal susceptibility to adult diseases. Polybrominated diphenyl ethers (PBDEs), which are ubiquitously used flame-retardants, could leach into the environment; and become persistent organic pollutants via bioaccumulation. In the United States, blood PBDE levels in adults range from 30-100 ng/g- lipid but the alarming health concern revolves around children who have reported blood PBDE levels 3 to 9-fold higher than adults. PBDEs disrupt endocrine, immune, reproductive and nervous systems. However, the mechanism underlying its adverse health effect is not fully understood. Epigenetics is a possible biological mechanism underlying maternal exposure-child health outcomes by regulating gene expression without changes in the DNA sequence. We sought to examine the relationship between maternal exposure to environmental PBDEs and promoter methylation of a proinflammatory gene, tumor necrosis factor alpha (TNFalpha). We measured the maternal blood PBDE levels and cord blood TNFalpha promoter methylation levels on 46 paired samples of maternal and cord blood from the Boston Birth Cohort (BBC). We showed that decreased cord blood TNFalpha methylation associated with high maternal PBDE47 exposure. CpG site-specific methylation showed significantly hypomethylation in the girl whose mother has a high blood PBDE47 level. Consistently, decreased TNFalpha methylation associated with an increase in TNFalpha protein level in cord blood. In conclusion, our finding provided evidence that in utero exposure to PBDEs may epigenetically reprogram the offspring's immunological response through promoter methylation of a proinflammatory gene.