Modified effect of active or passive smoking on the association between age and abdominal aortic calcification: a nationally representative cross-sectional study

Objective The deleterious effects of smoking on atherosclerosis were well known; however, the interaction among ageing, smoking and atherosclerosis remains unclear. This study tested the hypothesis that the association between age and vascular calci?cation, a critical mark of atherosclerosis, was modified by smoking. Design Cross-sectional study. Setting A nationally representative sample, the National Health and Nutrition Examination Surveys 2013-2014. Participants This study included 3140 adults aged 40-80 years with eligible data for abdominal aortic calcification (AAC). Active and passive smoking exposure was identified through self-reports and tobacco metabolites (serum cotinine and urinary 4-methylnitrosamino-3-pyridyl-1-butanol). Primary outcome measures AAC score was determined using dual-energy X-ray absorptiometry (DXA) scans. OR was estimated using the logistic regression method to assess the association between age and the presence of severe or subclinical AAC stratified by smoking exposure. The survey-weighted Wald test was used to evaluate potential interactions. Results AAC was positively associated with age in the general population. After adjustment for age, sex, race/ethnicity and other cardiovascular risk factors, age was significantly associated with the odds of severe AAC (OR for each 5-year increase in age: 1.66, 95% CI 1.48 to 1.87, p<0.001). As expected, the association between age and vascular calcification was especially stronger in smokers than in never smokers (p value for interaction <= 0.014). According to spline fitting, the progression of vascular calcification was significantly increased after 45 years in smokers compared with that after 60 years in never smokers. Quitting smoking may compromise the deleteriousness of the vascellum especially in younger adults. However, the difference in age-related calcification among never smokers with or without secondhand smoke exposure was minor, regardless of the definition by self-report, serum cotinine, or urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol. Conclusions Smoking significantly accelerated the progression of age-related subclinical atherosclerosis. Early smoking cessation should be encouraged among young smokers. The effect of passive smoking exposure on arteriosclerosis should be assessed further.