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. 2024 May 3;10(18):eadl3747.
doi: 10.1126/sciadv.adl3747. Epub 2024 May 3.

Early-life exposure to tobacco, genetic susceptibility, and accelerated biological aging in adulthood

Feipeng Cui  1   2 , Linxi Tang  1   2 , Dankang Li  1   2 , Yudiyang Ma  1   2 , Jianing Wang  1   2 , Junqing Xie  3 , Binbin Su  4 , Yaohua Tian  1   2 , Xiaoying Zheng  4
Affiliations

Early-life exposure to tobacco, genetic susceptibility, and accelerated biological aging in adulthood

Feipeng Cui et al. Sci Adv. .

Abstract

Early-life tobacco exposure serves as a non-negligible risk factor for aging-related diseases. To understand the underlying mechanisms, we explored the associations of early-life tobacco exposure with accelerated biological aging and further assessed the joint effects of tobacco exposure and genetic susceptibility. Compared with those without in utero exposure, participants with in utero tobacco exposure had an increase in Klemera-Doubal biological age (KDM-BA) and PhenoAge acceleration of 0.26 and 0.49 years, respectively, but a decrease in telomere length of 5.34% among 276,259 participants. We also found significant dose-response associations between the age of smoking initiation and accelerated biological aging. Furthermore, the joint effects revealed that high-polygenic risk score participants with in utero exposure and smoking initiation in childhood had the highest accelerated biological aging. There were interactions between early-life tobacco exposure and age, sex, deprivation, and diet on KDM-BA and PhenoAge acceleration. These findings highlight the importance of reducing early-life tobacco exposure to improve healthy aging.

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Figures

Fig. 1.
Fig. 1.. The joint effects of in utero exposure to tobacco smoke and the age of smoking initiation on accelerated biological aging.
(A) The β (95% CIs) of KDM-BA acceleration with joint categories of in utero exposure to tobacco smoke and the age of smoking initiation. (B) The β (95% CIs) of PhenoAge acceleration with joint categories of in utero exposure to tobacco smoke and the age of smoking initiation. (C) The percent change (95% CIs) of telomere length with joint categories of in utero exposure to tobacco smoke and the age of smoking initiation. All models were adjusted for age at recruitment, sex, ethnicity, birthplace, and body sizes at age 10 years.
Fig. 2.
Fig. 2.. The joint effects of in utero exposure to tobacco smoke or the age of smoking initiation and genetic susceptibility on accelerated biological aging.
(A) The β (95% CIs) of KDM-BA acceleration with joint categories of in utero exposure to tobacco smoke and PRS of KDM-BA. (B) The β (95% CIs) of PhenoAge acceleration with joint categories of in utero exposure to tobacco smoke and polygenic risk scores of PhenoAge. (C) The percent change (95% CIs) of telomere length with joint categories of in utero exposure to tobacco smoke and polygenic risk scores of telomere length. (D) The β (95% CIs) of KDM-BA acceleration with joint categories of the age of smoking initiation and polygenic risk scores of KDM-BA. (E) The β (95% CIs) of PhenoAge acceleration with joint categories of the age of smoking initiation and polygenic risk scores of PhenoAge. (F) The percent change (95% CIs) of telomere length with joint categories of the age of smoking initiation and polygenic risk scores of telomere length. (A) to (C) Models were adjusted for age at recruitment, sex, ethnicity, birthplace, genotyping batch, and the first 10 genetic principal components. (D) to (F) Models were adjusted for age at recruitment, sex, ethnicity, birthplace, body sizes at age 10 years, genotyping batch, and the first 10 genetic principal components.
Fig. 3.
Fig. 3.. The joint effects of in utero exposure to tobacco smoke, the age of smoking initiation, and genetic susceptibility on accelerated biological aging.
(A) The β (95% CIs) of KDM-BA acceleration with joint categories of in utero exposure to tobacco smoke, the age of smoking initiation, and polygenic risk scores of KDM-BA. (B) The β (95% CIs) of PhenoAge acceleration with joint categories of in utero exposure to tobacco smoke, the age of smoking initiation, and polygenic risk scores of PhenoAge. (C) The percent change (95% CIs) of telomere length with joint categories of in utero exposure to tobacco smoke, the age of smoking initiation, and polygenic risk scores of telomere length. Models were adjusted for age at recruitment, sex, ethnicity, birthplace, body sizes at age 10 years, genotyping batch, and the first 10 genetic principal components.
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