|Appears in Collections:||Faculty of Health Sciences and Sport Journal Articles|
|Peer Review Status:||Refereed|
|Title:||Impact of smoking cessation and lifetime exposure on C-reactive protein|
|Author(s):||Hastie, Claire E|
|Citation:||Hastie CE, Haw S & Pell J (2008) Impact of smoking cessation and lifetime exposure on C-reactive protein, Nicotine and Tobacco Research, 10 (4), pp. 637-642.|
|Abstract:||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 never-smokers (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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