Secondhand Smoke Exposure and Subclinical Cardiovascular Disease: The Multi‐Ethnic Study of Atherosclerosis. Issue 12 (December 2016)

• Record Type: Journal Article
• Authors: Jones, Miranda R.; Magid, Hoda S.; Al‐Rifai, Mahmoud; McEvoy, John W.; Kaufman, Joel D.; Hinckley Stukovsky, Karen D.; Szklo, Moyses; Polak, Joseph; Burke, Gregory L.; Post, Wendy S.; Blaha, Michael J.; Navas‐Acien, Ana
• Is Part Of: Journal of the American Heart Association. Volume 5:Issue 12(2016)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2016-12
• Subjects: ankle‐brachial index -- atherosclerosis -- carotid intima‐media thickness -- coronary artery calcium -- inflammation -- peripheral artery disease -- secondhand smoke -- smoking; Heart -- Diseases -- Periodicals; Cardiovascular system -- Diseases -- Periodicals; Cerebrovascular disease -- Periodicals; Cardiology -- Periodicals; 616.1
• DOI: 10.1161/JAHA.115.002965
• Languages: English
• ISSNs: 2047-9980

Abstract

Abstract : Background: Few studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima‐media thickness, coronary artery calcification, and peripheral arterial disease). Methods and Results: We examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi‐Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self‐report, and urinary cotinine was measured in a representative subset (n=2893). The multi‐adjusted geometric mean ratios (95% CIs) for high‐sensitivity C‐reactive protein and interleukin‐6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02–1.26) and 1.04 (0.98–1.11), respectively. The multi‐adjusted geometric mean ratio for carotid intima‐media thickness was 1.02 (0.97–1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle‐brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09–4.04) but not with self‐reported SHS. Urinary cotinine was not associated with inflammation or carotid intima‐media thickness. Conclusions: Despite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.