Prenatal exposure to cadmium and cotinine and CpG island DNA methylation in mother–infant pairs

Abstract

A precise biological mechanism by which cadmium acts as a developmental toxicant is unknown but is suggested to include an epigenetic basis. In prior work, we analyzed CpG island methylation levels within gene promoters (n = 16,421) in leukocytes collected from mothers and their infants from a pregnancy cohort in Durham County, North Carolina. The CpG methylation levels were examined in relationship to prenatal exposure to cadmium and/or cotinine to identify genes and pathways influenced by in utero exposure. In the present article, we provide an enhanced description of the data collection and processing to facilitate cross-study comparisons. Data are available within the Gene Expression Omnibus database (GSE67976)