Age Modifies the Association Between Smoking and Carotid Artery Plaque: A Cross-Sectional Study in Non-Diabetic...

To examine whether age modifies the cross-sectional association between current smoking and carotid artery plaque (CAP) in non-diabetic adults.

This retrospective cross-sectional study included 9088 non-diabetic adults undergoing health examinations at the Second Hospital of Hebei Medical University. CAP was assessed via ultrasonography. Smoking was classified as current smoker versus non-smoker (including former smokers). Multivariable logistic regression evaluated the interaction between current smoking and age group (<45 vs ≥45 years). Sensitivity analyses included age-stratified models, a continuous age-by-smoking interaction model, additional adjustment for drinking status, and a male-only analysis. Restricted cubic spline (RCS) analysis characterized the non-linear association between age and CAP.

CAP was detected in 1086 (11.95%) participants. A significant age-group-by-smoking interaction was observed (interaction OR = 0.342, 95% CI: 0.223-0.522; P < 0.001), indicating that the relative smoking-CAP association was weaker among adults aged ≥45 years. Current smoking was associated with CAP among adults aged <45 years in both the interaction model (OR = 2.104, 95% CI: 1.465-3.022; P < 0.001) and the age-stratified model (OR = 1.754, 95% CI: 1.179-2.610; P = 0.006), whereas the association was attenuated among adults aged ≥45 years. Continuous age-by-smoking and male-only sensitivity analyses showed consistent age-dependent patterns. The continuous RCS model confirmed a significant non-linear relationship (P < 0.001), visually demonstrating that the risk curves for smokers and non-smokers diverged most widely in early adulthood (<45 years) and converged at older ages. Male-only analysis yielded a consistent pattern.

Current smoking was associated with prevalent CAP predominantly among adults aged <45 years, and the relative association weakened at older ages. These findings support age-aware interpretation of smoking-related carotid atherosclerosis but should be considered hypothesis-generating because of the cross-sectional design and lack of cumulative smoking exposure data.