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

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 37; no. 2; pp. 374 - 379
• Main Authors: King, Cecile C, Piper, Megan E, Gepner, Adam D, Fiore, Michael C, Baker, Timothy B, Stein, James H
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.02.2017
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers - blood; Biomarkers - urine; Cardiovascular Diseases - blood; Cardiovascular Diseases - etiology; Cardiovascular Diseases - prevention & control; Cardiovascular Diseases - urine; Comparative Effectiveness Research; Creatinine - urine; F2-Isoprostanes - urine; Female; Humans; Inflammation - blood; Inflammation - etiology; Inflammation - prevention & control; Inflammation - urine; Inflammation Mediators - blood; Inflammation Mediators - urine; Leukocyte Count; Longitudinal Studies; Male; Middle Aged; Oxidative Stress; Peroxidase - blood; Protective Factors; Randomized Controlled Trials as Topic; Risk Assessment; Risk Factors; Risk Reduction Behavior; Smoking - adverse effects; Smoking - blood; Smoking - urine; Smoking Cessation - methods; Smoking Prevention; Time Factors; Young Adult; carbon monoxide; cardiovascular diseases; inflammation; oxidative stress; smoking
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/ATVBAHA.116.308728

OBJECTIVE—To evaluate longitudinal changes in 6 inflammatory markers that predict cardiovascular disease events among smokers making a quit attempt and to characterize their cross-sectional associations between smoking and smoking heaviness. APPROACH AND RESULTS—In a longitudinal cohort study of contemporary smokers (n=1652), we evaluated (1) independent associations of smoking heaviness markers (exhaled carbon monoxide, cigarettes/d, pack-years) with inflammatory markers (C-reactive protein, D-dimer, fibrinogen, urinary F2 isoprostane:creatinine [F2:Cr] ratio, white blood cell [WBC] count, myeloperoxidase) and (2) the effects of smoking cessation and continued smoking on these inflammatory markers after 1 year, among the 888 smokers who made an aided quit attempt as part of a randomized comparative effectiveness trial or standard care. There were strong, independent associations between smoking heaviness markers and the F2:Cr ratio, WBC, and myeloperoxidase (all Padj<0.001), but not high-sensitivity C-reactive protein, D-dimer, or fibrinogen. Participants were mean (SD) 49.6 years old (11.6), 54% women, 34% non-white, and smoked 16.8 cigarettes/d (8.5) for 27.3 pack-years (18.6). After 1 year, the 344 successful abstainers gained more weight (4.0 [6.0] versus 0.4 [5.7] pounds; P<0.001) and had larger increases in insulin resistance scores (P=0.02) than continuing smokers. Despite these increases, abstainers had significant decreases in F2:Cr ratio (P<0.001) and WBC counts (P<0.001). Changes in other markers were not related to quitting. CONCLUSIONS—Smoking heaviness is associated with increased F2:Cr ratio, myeloperoxidase, and WBC counts. Cessation improves the F2:Cr ratio and WBC counts independent of weight change, suggesting reduced inflammation related to less oxidant stress.