期刊
ATHEROSCLEROSIS
卷 201, 期 1, 页码 217-224出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2007.12.058
关键词
Smoking; Inflammation; Cardiovascular disease; Epidemiology
资金
- National Heart, Lung, and Blood Institute's Framingham Heart [N01-HC 25195, RO1 HL076784, RO1 HL064753, RO1 AG028321]
- Flight Attendants Medical Research Institute's Young Clinical Scientist Award
Aims: We sought to investigate the hypothesis that smoking is accompanied by systemic inflammation. Methods and results: We examined the relation of smoking to 11 systemic inflammatory markers in Framingham Study participants (n = 2944) mean age 60 years, 55% women, 12% ethnic minorities) examined from 1998-2001. The cohort was divided into never (n = 1149), former (n = 1424), and current smokers with last cigarette >6 h (n = 134) or <= 6 h (n = 237) prior to phlebotomy. In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p < 0.0045 to account for multiple testing) for every inflammatory 9 C marker tested, except for serum CD40 ligand (CD40L), myeloperoxidase (MPO) and tumor necrosis factor receptor-2 (TNFR2). With multivariable-adjustment, pair-wise comparisons with never smokers revealed that former smokers had significantly lower concentrations of plasma CD40L (p < 0.0001) and higher concentrations of (CRP) C-reactive protein (p = 0.002). Conclusions: As opposed to never smokers, those with acute cigarette smoke exposure (<= 6h) had significantly higher concentrations of all markers p < 0.0001) except serum CD40L, MPO, and TNFR2; plasma CD40L were significantly lower. Compared with never smokers, cigarette snickers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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