present in cigarette smoke. Specifically, CYP1A1 converts such compounds in a way that can eventually be excreted in Phase II metabolism, a process modulated in part by other genes (Suter, et al., 2010). Suter and colleagues found that methylation at these sites was significantly lower in the placentas of babies born to mothers who smoked during pregnancy versus non-smoking controls. This downregulation of methylation was also significantly correlated with increased placental CYP1A1 expression, a finding which may have substantial potential implications for future behavior. Wilhelm-Benartzi and colleagues showed that differential methylation of repetitive elements – stretches of DNA exhibiting a large number of repeated bases – in the placenta is associated with birth weight percentile and maternal smoking during pregnancy. More specifically, they found that mean methylation levels of the repetitive element AluYb8 significantly differed by maternal tobacco use during pregnancy (Wilhelm-Benartzi et al., 2011).
