Background and aims
Modern tobacco regulatory science requires an understanding of which
biomarkers of cardiovascular injury are most sensitive to cigarette smoking
exposure.
Methods
We studied self-reported current smokers from the Multi-Ethnic Study
of Atherosclerosis. Smoking intensity was defined by number of
cigarettes/day and urinary cotinine levels. Subclinical cardiovascular
injury was assessed using markers of inflammation [high-sensitivity
C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6),
tumor necrosis factor alpha (TNF-α)], thrombosis
(fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT),
endothelial damage (albumin: creatinine ratio), and vascular function
[aortic & carotid distensibility, flow-mediated dilation
(FMD)]. Biomarkers were modeled as absolute and percent change using
multivariable-adjusted linear regression models adjusted for cardiovascular
risk factors and smoking duration.
Results
Among 843 current smokers, mean age was 58 (9) years, 53%
were men, 39% were African American, mean number of cigarettes per
day was 13 (10), and median smoking duration was 39 (15) years. Cigarette
count was significantly associated with higher hsCRP, IL-6 and fibrinogen
(β coefficients: 0.013, 0.011, 0.60 respectively), while
In-transformed cotinine was associated with the same biomarkers (β
coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with
aortic distensibility (β coefficient: −0.13). There was a
limited association between smoking intensity and homocysteine, D-dimer, and
albumin:creatinine ratio in partially adjusted models only, while there was
no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT
in any model. In percent change analyses, relationships were strongest with
hsCRP.
Conclusions
Smoking intensity was associated with early biomarkers of CVD,
particularly, markers of systemic inflammation. Of these, hsCRP may be the
most sensitive.