Fetal lung and placental methylation is associated with in utero nicotine exposure

One potential mechanism of IUS effects could be alterations in DNA methylation, which may have life-long implications. The goal of this study was to examine the association between DNA methylation and nicotine exposure in fetal lung and placental tissue in early development; nicotine exposure in this analysis represents a likely surrogate for in-utero smoke.

We performed an epigenome-wide analysis of DNA methylation in fetal lung tissue (n = 85, 41 smoke exposed (48%), 44 controls) and the corresponding placental tissue samples (n = 80, 39 smoke exposed (49%), 41 controls) using the Illumina HumanMethylation450 BeadChip array. Differential methylation analyses were conducted to evaluate the variation associated with nicotine exposure. The most significant CpG sites in the fetal lung analysis mapped to the PKP3 ( P = 2.94 × 10 −03 ), ANKRD33B ( P = 3.12 × 10 −03 ), CNTD2 ( P = 4.9 × 10 −03 ) and DPP10 ( P = 5.43 × 10 −03 ) genes.