The Joint Contribution of Childhood Exposure to Parental Smoking and Genetic Susceptibility to Smoking to Epigenetic Age Acceleration in Late Adulthood: The Health and Retirement Study

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The Joint Contribution of Childhood Exposure to Parental Smoking and Genetic Susceptibility to Smoking to Epigenetic Age Acceleration in Late Adulthood: The Health and Retirement Study
by Tingting Liu 1ORCID,Yixi Sun 2,3,Ruiyuan Zhang 4ORCID andChangwei Li 5,*
1
College of Nursing, Florida State University, Tallahassee, FL 32308, USA
2
Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, IL 60612, USA
3
Division of Nephrology, Department of Medicine, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA
4
Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA 70112, USA
5
O’Donnell School of Public Health, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
*
Author to whom correspondence should be addressed.
Future 2024, 2(4), 185-193; https://doi.org/10.3390/future2040015
Submission received: 18 October 2024 / Revised: 14 November 2024 / Accepted: 25 November 2024 / Published: 6 December 2024
(This article belongs to the Special Issue Feature Papers in Future)
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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.