Abstract
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.
Highlights
Polybrominated diphenyl ethers (PBDEs), known as endocrine disrupting compounds, affecting the endocrine, immune, reproductive and nervous systems [1]
PBDE47 shows the most abundance among PBDEs congers in Boston Birth Cohort (BBC)
In the BBC cohort, a total of 247 maternal blood samples had available data for blood PBDEs level, which showed a wide range of variability (Table 1)
Summary
Polybrominated diphenyl ethers (PBDEs), known as endocrine disrupting compounds, affecting the endocrine, immune, reproductive and nervous systems [1]. Epigenetics mechanisms (DNA methylation, histone modifications and microRNAs) act singularly or conjointly to regulate gene expression without altering DNA sequences in response to environmental exposures. They produce an array of unique phenotypes that control cell differentiation and organ development. It suggests exposure to PBDE47 may affect cell and tissue functions by regulating gene expression through DNA methylation. Our findings may provide the insight to understand the adverse effects of maternal PBDEs exposure on human health through novel epigenetic mechanisms, affecting immunity and inflammation and resulting in higher susceptibility of immune diseases like food allergy, asthma, or other metabolic symptoms [33, 34]
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