Smoking heaviness associated with CVD risk-associated inflammatory markers

Longitudinal Impact of Smoking and Smoking Cessation on Inflammatory Markers of Cardiovascular Disease Risk

Literature - King CC, Arterioscler Thromb Vasc Biol, 2017

King CC, Piper ME, Gepner AD, et al.
Arterioscler Thromb Vasc Biol 2017;37:published online ahead of print


Tobacco smoking increases the CVD risk by activating inflammatory pathways, lipid oxidation, hypercoagulability, and vascular dysfunction [1,2]. There are data showing that smokers have higher levels of CVD risk-associated inflammatory markers, however, the effects of smoking cessation on such inflammatory markers have not been evaluated [3,4].

In this study, the cross-sectional and longitudinal relationships between smoking burden, smoking cessation and six inflammatory markers were assessed, in a large cohort of smokers.
The inflammatory markers, which are predictive of CVD events, included: c-reactive protein (CRP), D-dimer, fibrinogen, urinary F2 isoprostane:creatinine [F2:Cr] ratio, myeloperoxidase, and WBC count. These were compared with smoking heaviness markers exhaled carbon monoxide (CO), cigarettes per day, and packyears.

Main results

  • Smokers were on average 49.6 years old, smoked 16.8 cigarettes/day, and had a smoking burden of 27.3 pack-years with CO levels of 14.4 ppm.
  • The mean BMI was 29.4 kg/m2, 18% of participants were on lipid-lowering therapy and 8.7% of participants were receiving antidiabetic medications.  
  • There were strong, independent associations between smoking heaviness markers and the F2:Cr ratio, WBC counts, and myeloperoxidase.
  • There were no statistically significant associations between CRP, D-dimers, and fibrinogen levels and any smoking heaviness marker.
  • Out of the 888 participants who made an aided quit attempt and completed the year 1 assessments, 344 (29.7%) participants had biochemically confirmed 7-day point-prevalence abstinence at 1 year.
  • Eventual abstainers smoked fewer cigarettes/day (t=2.95; P=0.003) and had lower CO levels (t=4.17; P<0.001) at baseline compared with continuing smokers.
  • Abstainers gained more weight compared with continued smokers (4.0 kg vs. 0.4 kg; P<0.001) and had greater increases in homeostasis model of insulin resistance scores (15.4 U versus 7.2 U; P=0.02).
  • There were statistically significant correlations between changes in CO with changes in urinary F2:Cr ratio (P=0.002) and WBC counts (P<0.001), but no significant correlations with the other inflammatory biomarkers after 1 year.


In a large cohort, smoking heaviness was independently associated with urinary F2:Cr ratio, myeloperoxidase and WBC count, which are three inflammatory markers related to CVD risk. However, no association was observed with CRP, fibrinogen or D-dimer. In addition, cessation reduced urinary F2:Cr ratios and WBC counts. As F2:CR ratio and myeloperoxidase reflect oxidative stress, these results suggest that oxidant stress may mediate increased inflammation and CVD risk in smokers.

Find this article online at Aterioscler Thromb Vasc Biol


1. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43:1731–1737.
2. Yasue H, Hirai N, Mizuno Y, et al. Low-grade inflammation, thrombogenicity, and atherogenic lipid profile in cigarette smokers. Circ J. 2006;70:8–13.
3. Asthana A, Johnson HM, Piper ME, et al. Effects of smoking intensity and cessation on inflammatory markers in a large cohort of active smokers. Am Heart J. 2010;160:458–463.
4. Aldaham S, Foote JA, Chow HH, et al. Smoking status effect on inflammatory markers in a randomized trial of current and former heavy smokers. Int J Inflam. 2015;2015:439396. 

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