BackgroundThere is a need to identify sensitive biomarkers of early tobacco‐related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis.Methods and ResultsWe studied 14 103 participants without clinical cardiovascular disease in ELSA‐Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross‐sectional associations between smoking parameters and inflammation (high‐sensitivity C‐reactive protein [hsCRP]) and measures of subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, and coronary artery calcium [CAC]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hsCRP (β=0.24, 0.19–0.29 mg/L; P<0.001) and carotid intima–media thickness (β=0.03, 0.02–0.04 mm; P<0.001) and odds of ankle‐brachial index ≤1.0 (odds ratio: 2.52; 95% confidence interval, 2.06–3.08; P<0.001) and CAC >0 (odds ratio: 1.83; 95% confidence interval, 1.46–2.30; P<0.001). Among former and current smokers, pack‐years of smoking (burden) were significantly associated with hsCRP (P<0.001 and P=0.006, respectively) and CAC (P<0.001 and P=0.002, respectively). Among former smokers, hsCRP and carotid intima–media thickness levels and odds of ankle‐brachial index ≤1.0 and CAC >0 were lower with increasing time since quitting (P<0.01). Among current smokers, number of cigarettes per day (intensity) was positively associated with hsCRP (P<0.001) and CAC >0 (P=0.03) after adjusting for duration of smoking.ConclusionsStrong associations were observed between smoking status, burden, and intensity with inflammation (hsCRP) and subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, CAC). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products.

BackgroundFew 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 ResultsWe 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.ConclusionsDespite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.

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