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

Abstract

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.