ArticleTobacco induced diseases2026
Association of serum cotinine with phenotypic age acceleration and oxidative stress markers in US adults: A cross-sectional study.
Article in Tobacco induced diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Association of smoking behaviors with GOLD biological age acceleration and potential mediation: Evidence from NHANES 1999-2023.Tobacco induced diseases · 2026Article
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5 authors.
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Abstract
introductionTobacco exposure is a plausible accelerator of biological aging, yet population-level evidence and mechanisms remain insufficiently defined. We examined the association between serum cotinine and phenotypic age acceleration (PhenoAgeAccel), and assessed whether oxidative-stress biomarkers were related to the serum cotinine-PhenoAgeAccel association.
methodsWe conducted a cross-sectional, survey-weighted analysis of n=19744 adults from NHANES 2011-2018. PhenoAgeAccel was computed as the residual from regressing PhenoAge on chronological age. Multivariable linear regressions related serum cotinine to PhenoAgeAccel across hierarchical adjustment models. Restricted cubic splines assessed non-linearity. Mediation analysis was conducted to quantify the extent to which oxidative-stress biomarkers contribute to this association.
resultsHigher serum cotinine was associated with accelerated biological aging: each doubling of serum cotinine corresponded to a 0.22-year increase in PhenoAgeAccel (β=0.22; 95% CI: 0.16-0.29). Mediation analyses indicated that γ-glutamyl transferase (GGT) and uric acid (UA) statistically accounted for 9.5% of the association between serum cotinine and PhenoAgeAccel (p<0.001). Interactions were observed for sex and PIR, with stronger associations among women and participants with lower socioeconomic status. There was no evidence of non-linearity in the relationships of the serum cotinine with GGT, PhenoAgeAccel, or UA.
conclusionsIn this nationally representative cross-sectional study of US adults, higher serum cotinine levels were associated with greater phenotypic age acceleration. Oxidative-stress biomarkers were related to the observed association, although causal inferences cannot be drawn.
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