Maternal environmental exposure to bisphenols and epigenome-wide DNA methylation in infant cord blood. Issue 1 (23rd December 2020)

• Record Type: Journal Article
• Authors: McCabe, Carolyn F; Padmanabhan, Vasantha; Dolinoy, Dana C; Domino, Steven E; Jones, Tamara R; Bakulski, Kelly M; Goodrich, Jaclyn M
• Editors: Skinner, Mike
• Is Part Of: Environmental epigenetics. Volume 6:Issue 1(2020)
• Publication Date: 2020-12-23
• Subjects: environmental epigenomics -- prenatal exposure -- DNA methylation; Epigenetics -- Periodicals; 572.86505
• DOI: 10.1093/eep/dvaa021
• Languages: English
• ISSNs: 2058-5888

Abstract

Abstract: Maternal prenatal exposures, including bisphenol A (BPA), are associated with offspring's risk of disease later in life. Alterations in DNA methylation may be a mechanism through which altered prenatal conditions (e.g. maternal exposure to environmental toxicants) elicit this disease risk. In the Michigan Mother and Infant Pairs Cohort, maternal first-trimester urinary BPA, bisphenol F, and bisphenol S concentrations were tested for association with DNA methylation patterns in infant umbilical cord blood leukocytes ( N = 69). We used the Illumina Infinium MethylationEPIC BeadChip to quantitatively evaluate DNA methylation across the epigenome; 822 020 probes passed pre-processing and quality checks. Single-site DNA methylation and bisphenol models were adjusted for infant sex, estimated cell-type proportions (determined using cell-type estimation algorithm), and batch as covariates. Thirty-eight CpG sites [false discovery rate (FDR) <0.05] were significantly associated with maternal BPA exposure. Increasing BPA concentrations were associated with lower DNA methylation at 87% of significant sites. BPA exposure associated DNA methylation sites were enriched for 38 pathways significant at FDR <0.05. The pathway or gene-set with the greatest odds of enrichment for differential methylation (FDR <0.05) was type I interferon receptor binding. This study provides a novel understanding of fetal response to maternal bisphenol exposure through epigenetic change.