Abstract
The impact of childhood exposure to parental smoking on epigenetic age acceleration (EAA) in later life has not been thoroughly investigated. This study investigates the relationship while considering genetic susceptibility to smoking. We analyzed data from 3102 participants in the Health and Retirement Study (HRS) who also participated in the 2016 Venous Blood Study and the 2015–2017 Life History Mail Survey. Self-reported measures included childhood parental smoking exposure and smoking status in late adulthood. We utilized five epigenetic clocks—HorvathAA, HannumAA, GrimAA, PhenoAA, and DunedinAA—and assessed genetic susceptibility with a polygenic risk score (PRS) for smoking initiation, categorized into tertiles. We regressed the clocks against chronological age to derive EAA residuals. Associations between childhood exposure and EAA were examined in the overall sample and by PRS tertiles, stratified by race. The model controlled for age, sex, education, smoking, alcohol consumption, body mass index, and CESD scores. Significant associations were found between childhood exposure to parental smoking and the EAA measured by GrimAA (β = 0.98; p < 0.001) and DunedinAA (β = 0.01; p = 0.002) among White participants, with stronger effects in those with a high PRS. Similar patterns were observed in Black participants, highlighting the importance of preventing secondhand smoke exposure in children.
Published Version
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