The Association of Secondhand Tobacco Smoke and CT Angiography-Verified Coronary Atherosclerosis

Objectives The aim of this study was to assess the relationship of the extent of atherosclerosis on coronary computed tomographic angiography to the extent of secondhand tobacco smoke (SHTS) exposure in asymptomatic never smokers. Background A dose-related association between SHTS and coronary artery calcium has been reported, but the total extent of atherosclerosis has not been investigated. Methods A total of 268 never smokers, ages 40 to 80 years, completed a questionnaire assessing risk factors and extent of lifetime SHTS exposure, providing a total SHTS exposure score. Ordinal coronary artery calcium scores were derived from low-dose nongated computed tomographic scans, followed by computed tomographic angiography. Analyses of the prevalence, extent, and plaque characteristics of atherosclerosis were performed, and the independent contribution of SHTS, adjusted for other documented risk factors, was determined. Results Coronary atherosclerosis was noted in 48% and was more frequent with low to moderate and high versus minimal SHTS exposure (48% and 69% vs. 25%; p < 0.0001). Adjusted odds ratios for any atherosclerosis were 2.1 (95% confidence interval: 1.0 to 4.4; p = 0.05) for low to moderate and 3.5 (95% confidence interval: 1.4 to 8.5; p = 0.01) for high exposure versus minimal SHTS exposure and were not significant for standard risk factors of diabetes (p = 0.56), hyperlipidemia (p = 0.11), hypertension (p = 0.65), and renal disease (p = 0.24). With increasing SHTS exposure, the percentage of major vessel (14%, 41%, and 45%; p = 0.0013) with any plaque or stenosis increased, as did the number with 5 or more involved segments (0%, 39%, and 61%; p = 0.0001). Also the average number of involved segments increased (0.82, 1.98, and 3.49; p < 0.0001), with calcified plaques alone (0.25, 0.77, and 1.52; p < 0.0001), with calcified and partially calcified plaques (0.28, 0.82, and 1.58; p < 0.001), but not with noncalcified plaques alone (p = 0.11). Conclusions The presence and extent of atherosclerosis were associated with the extent of SHTS exposure even when adjusted for other risk factors, further demonstrating the causal relationship of SHTS exposure and coronary disease.