Physicians' Academy for Cardiovascular Education

Second-hand tobacco smoke shows a dose-response relation with coronary calcification

Literature - Yankelevitz DF, Henschke CI, Yip R et al - J Am Coll Cardiol Img. 2013. doi:10.1016/j.jcmg.2013.02.004


Second-Hand Tobacco Smoke in Never Smokers Is a Significant Risk Factor for Coronary Artery Calcification ONLINE FIRST

Yankelevitz DF, Henschke CI, Yip R et al
J Am Coll Cardiol Img. 2013. doi:10.1016/j.jcmg.2013.02.004


Background

Accumulating evidence led to the conclusion that a causal link exists between second-hand tobacco smoke (SHTS) exposure and mortality and morbidity due to coronary artery disease (CAD) [1]. Recently, an association was demonstrated between SHTS and subclinical atherosclerosis, as evidenced by coronary artery calcification (CAC) [2]. CAC scores were higher in SHTS-exposed individuals than in non-exposed individuals, even after correction for common CV risk factors. CAC measurement by CT scan is increasingly common in CAD risk evaluation.

This study addresses the prevalence and extent of subclinical atherosclerosis, in relation to SHTS exposure, by performing low-dose non-gated CT in 3098 asymptomatic people who had never smoked. Based on a background questionnaire SHTS exposure was assessed (permission status, duration and daily intensity) before age 18 as a child and after age 18 as an adult at home and at work. A total SHTS score was calculated based on these different exposures.

 

Main results

  • Prevalence of CAC was higher in those with higher than minimal SHTS exposure, as compared to those with minimal SHTS exposure (26.4% vs. 18.5%, P=0.0001).
  • The prevalence of any CAC increased significantly with increasing SHTS exposure:  minimal: 18.5%, low: 22.1%, moderate: 22.1% and high: 35,1% (P< 0.0001).
  • When adjusted for other risk factors for CAC, odds ratios (Ors) were 1.5 for low SHTS exposure (95%CI: 1.2-2.0, P=0.002), 1.6 for moderate (95%CI: 1.2-2.1, P=0.0008), and 1.9 for high exposure (95%CI: 1.5-2.5, P<0.000).
  • The total SHTS score was a significant independent predictor of the prevalence of CAC after adjusting for other risk factors. Also childhood SHTS exposure alone, or adult home or work exposure alone were statistically significant independent predictors of CAC.

Conclusion

SHTS exposure, either in childhood or in adult life, is an independent risk factor for CAC. There is a dose-response relationship between SHTS exposure and extent of CAC. OR of SHTS exposure is as high as or higher than decade of age, diabetes, hypertension, hypercholesterolemia and renal disease. SHTS is a thus far underappreciated health issue but an avoidable risk factor. Limiting SHTS exposure is at least as beneficial as reducing well-established risk factors for coronary artery disease. Gated CT scans at low-dose radiation are a useful measure for early detection of CAC.


References

1. U.S. Department of Health and Human Services. The Health Consequences of Involuntary Exposure to
Tobacco Smoke. A Report of the Surgeon General. Atlanta, GA: U.S. Dept. of Health and Human Services,
Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2006.
2. Hirayama T. Passive smoking. N Z Med J 1990;103:54.


 

Abstract

Objectives
  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.

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

Methods
  A cohort of 3,098 never smokers 40 to 80 years of age, enrolled in the 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.

Results 
The prevalence of CAC was 24% (n = 754) and was significantly higher in those with more than minimal SHTS exposure compared with those with minimal SHTS exposure (21% vs. 19%, 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).

Conclusions
  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.
 

Share this page with your colleagues and friends: