Summary
This large observational cohort study (n=276,259) examined how early-life tobacco exposure—both in utero and during childhood—associates with accelerated biological aging in adulthood, assessed through multiple ageing biomarkers. In utero exposure was associated with KDM-BA acceleration of 0.26 years and PhenoAge acceleration of 0.49 years, alongside a 5.34% decrease in telomere length. The findings suggest genetic susceptibility and lifestyle factors (diet) moderate these associations, highlighting the importance of early-life tobacco exposure reduction for healthy ageing trajectories.
UK applicability
The findings are broadly applicable to UK populations, where maternal and childhood smoking exposure remain public health concerns despite declining rates. The interactions with diet and deprivation suggest that UK-based interventions targeting smoking cessation in pregnancy and early childhood, particularly in deprived communities, could have measurable benefits for adult health trajectory and ageing-related disease prevention.
Key measures
Klemera-Doubal biological age (KDM-BA) acceleration, PhenoAge acceleration, telomere length, polygenic risk score, age of smoking initiation
Outcomes reported
The study measured associations between in utero and childhood tobacco exposure with biological age acceleration (using Klemera-Doubal biological age and PhenoAge metrics) and telomere length among 276,259 participants. It assessed joint effects of tobacco exposure and polygenic risk score on accelerated aging, and identified interactions with age, sex, deprivation, and diet.
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