Association between tobacco smoke exposure and levels of C-reactive protein in the Oslo II Study
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It is well known that tobacco smoke exposure is related to the risk of developing cardiovascular diseases and events. One mechanism could be that tobacco smoke acts on the cardiovascular system by altering the autonomic function and/or inducing inflammatory responses. We used data from 3 744 men aged 67–77 years from the city of Oslo that participated in the health screening for the Oslo II Health Study in 2000, to explore associations between C-reactive protein and environmental exposures including exposure to tobacco smoke products. Levels of C-reactive protein were higher in current smokers (2.05 mg/l, IQR, 1.11–4.17 mg/l), compared to former-smokers (1.58 mg/l, IQR, 0.83–3.03 mg/l) and non-smokers (1.26 mg/l, IQR, 0.65–2.40 mg/l). The risk of elevated C-reactive protein increased with both numbers of current cigarettes smoked per day and numbers of pack-years of smoking, when other factors were adjusted for (P < 0.001). We found a positive dose–response relationship between amount of current cigarette smoking and elevated C-reactive protein levels. These findings support the idea that the induction or exacerbation of inflammation could be a mechanism by which smoking promotes atherosclerotic cardiovascular diseases.
KeywordsC-reactive protein Tobacco smoke exposure Pack-years of smoking Environmental exposure Cardiovascular disease Cross-sectional study
tobacco smoke exposure
pack-years of smoking
The data collection was conducted in coordination with and prior to the Oslo Health Study 2000–2001 in collaboration with the Norwegian Institute of Public Health, the City of Oslo and Ullevål University Hospital in Oslo. This research was supported by grants from the University of Oslo and the Norwegian Public Roads Administration. We also wish to thank Lars Lundby for valuable help with the data collection, and Anne Johanne Søgaard for valuable help.
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