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

• Published in: PloS one Vol. 10; no. 9; p. e0138815
• Main Authors: Dao, Tyna, Hong, Xiumei, Wang, Xiaobin, Tang, Wan-Yee
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 25.09.2015; Public Library of Science (PLoS)
• Subjects: Adult; Adults; Bioaccumulation; Biological effects; Blood; Children; Cohort Effect; Cord blood; CpG islands; CpG Islands - drug effects; Deoxyribonucleic acid; DNA; DNA methylation; DNA Methylation - drug effects; Endocrine disruptors; Epigenesis, Genetic - drug effects; Epigenetics; Ethers; Exposure; Female; Fetal Blood - chemistry; Fetal Blood - drug effects; Fetuses; Flame retardants; Gene expression; Halogenated Diphenyl Ethers - adverse effects; Halogenated Diphenyl Ethers - blood; Health risks; Humans; Immune response; Immunology; Infant, Newborn; Inflammation; Intrauterine exposure; Male; Maternal Exposure; Nucleotide sequence; Offspring; Persistent organic pollutants; Pollutants; Polybrominated diphenyl ethers; Pregnancy; Pregnancy Outcome; Retardants; Tumor Necrosis Factor-alpha - blood; Tumor Necrosis Factor-alpha - genetics; Tumor necrosis factor-TNF; Tumor necrosis factor-α; United States > US; Maryland; Baltimore Maryland
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0138815

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 (TNFα). We measured the maternal blood PBDE levels and cord blood TNFα promoter methylation levels on 46 paired samples of maternal and cord blood from the Boston Birth Cohort (BBC). We showed that decreased cord blood TNFα 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 TNFα methylation associated with an increase in TNFα 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.