Journal
NICOTINE & TOBACCO RESEARCH
Volume 10, Issue 4, Pages 637-642Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/14622200801978722
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C-reactive protein (CRP) levels predict coronary heart disease (CHD) risk. Levels are raised among smokers, but the effect of smoking cessation is unclear. Exposure to secondhand smoke (SHS) may be a confounder. Lifetime smoking exposure may have a dose effect on CRP among smokers, but it is unclear if this persists after cessation. We analyzed cross-sectional data on 4,072 adults recruited to a Scotland-wide population health survey who did not have CHD and were not on nicotine replacement therapy. CRP fell with time from cessation but was still raised up to 5 years after adjustment for case-mix (p <.001). SHS exposure was greater among ex-smokers than neversmokers (median cotinine 0.5 ng/ml vs. 0.4 ng/ml, p <.001) but did not explain the difference. Among smokers, there was a dose relationship between pack years and CRP on both univariate, F(4,1279)=31.841, p <.001, and multivariate, F(4,1085)=3.499, p=.008, analysis. Among ex-smokers there was also a dose relationship between pack-years and CRP, F(4,751)=14.108, p <.001, which was independent of time from cessation and case-mix, F(4,466) = 3.744, p =.005. That CRP does not fall to normal levels immediately and that lifetime smoking exposure continues to impact on CRP levels post cessation suggest that CRP is not raised as a direct effect of cigarette smoke but rather via a secondary mechanism, such as tissue damage causing an inflammatory stimulus. Our results reinforce the need to encourage smoking cessation as early as possible.
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