Secondhand Smoke Exposure and Subclinical Cardiovascular Disease: The Multi‐Ethnic Study of Atherosclerosis

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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 (2016)
  • Publisher: John Wiley and Sons Inc.
  • Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, volume 5, issue 12 (eissn: 2047-9980)
  • Related identifiers: pmc: PMC5210438, doi: 10.1161/JAHA.115.002965
  • Subject: atherosclerosis | ankle‐brachial index | Cardiovascular Disease | Risk Factors | coronary artery calcium | peripheral artery disease | Lifestyle | Epidemiology | inflammation | smoking | Primary Prevention | Original Research | carotid intima‐media thickness | secondhand smoke

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.