Second-hand tobacco smoke in never smokers is a significant risk factor for coronary artery calcification

The aim of this study was to assess the relationship of the extent of subclinical atherosclerosis measured by coronary artery calcification (CAC) to the extent of second-hand tobacco smoke (SHTS) exposure in asymptomatic people who never smoked.

An association between SHTS and CAC was recently reported in a single study, but the quantitative aspects of the relationship are not known.

A cohort of 3,098 never smokers 40 to 80 years of age, enrolled in the FAMRI-IELCAP (Flight Attendant Medical Research Institute International Early Lung Cancer Action Program) screening program, completed a SHTS questionnaire, and had a low-dose nongated computed tomography scan. The questionnaire provided a quantitative score for total SHTS exposure, as well as separately as a child and as an adult at home and at work; 4 categories of exposure to SHTS were identified (minimal, low, moderate, and high exposure). CAC was graded using a previously validated ordinal scale score that ranged from 0 to 12. Logistic regression analysis of the prevalence and ordered logistic regression analysis of the extent of CAC were performed to assess the independent contribution of SHTS adjusted for age, sex, diabetes, hypercholesterolemia, hypertension, and renal disease. Linear and quadratic regression analyses of CAC and SHTS were performed.

The prevalence of CAC was 24.3% (n = 754) and was significantly higher in those with more than minimal SHTS exposure compared with those with minimal SHTS exposure (26.4% vs. 18.5%, p < 0.0001). The adjusted odds ratios for CAC prevalence were 1.54 (95% confidence interval: 1.17 to 2.20) for low SHTS exposure, 1.60 (95% confidence interval: 1.21 to 2.10) for moderate exposure, and 1.93 (95% confidence interval: 1.49 to 2.51) for high exposure. The association of the extent of SHTS with the extent of CAC was confirmed by the adjusted odds ratio (p < 0.0001).

The presence and extent of CAC were associated with extent of SHTS exposure even when adjusted for other risk factors for CAC, suggesting that SHTS exposure causes CAC.