Extending candidate gene studies to other populations and tissue sources, researchers assessed the impact of maternal smoking on promoter methylation at brain-derived neurotrophic factor (BDNF) in adolescent offspring whole blood samples [39], and cytochrome P450 oxidase 1A1 (CYP1A1) in placental samples [40], finding hypomethylation in each case. Murphy and colleagues [41] examined differences in methylation at two loci, the imprinted domain at 11p15.5, expressing paternal Insulin-like Growth Factor II (IGF2), and maternal H19, a noncoding RNA, in smoking exposed versus non-exposed infants, finding that infants born to smokers had increased methylation at the IGF2 differentially methylated region (DMR) as composed to those who never smoked or quit during pregnancy. Finally, given the established link between smoking and cancer, cancer-related candidate genes were studied using exhaled breath condensate in smokers and non-smokers, showing differential patterns of methylation at ras association domain family 1 isoform A (RASSF1A) related to smoking status [42].
