Relation of smoking status to a panel of inflammatory markers: The Framingham offspring

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 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 (≤6 h) 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 smokers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state.