Relationship between Cigarette Smoking and Novel Risk Factors for Cardiovascular Disease in the United States

Relationship between Cigarette Smoking and Novel Risk Factors for Cardiovascular Disease in the United States

Lydia A. Bazzano, MD, PhD;
Jiang He, MD, PhD;
Paul Muntner, PhD;
Suma Vupputuri, PhD; and
Paul K. Whelton, MD, MSc

From Tulane University School of Public Health and Tropical Medicine and Tulane University School of Medicine, New Orleans, Louisiana, and the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.

Abstract

Background: Few studies have examined the relationship between cigarette smoking and novel risk factors for cardiovascular disease in a general population or have included a biochemical marker of current smoking.

Objective: To examine the relationship between cigarette smoking and serum C-reactive protein, fibrinogen, and homocysteine levels.

Design: Cross-sectional study.

Setting: The U.S. general population.

Patients: 4187 current smokers, 4791 former smokers, and 8375 never-smokers 18 years of age or older who participated in the Third National Health and Nutrition Examination Survey conducted between 1988 and 1994.

Measurements: Serum C-reactive protein levels were categorized as detectable (2.2 to 9.9 mg/L) or clinically elevated (≥ 10 mg/L), and fibrinogen and homocysteine levels were defined as elevated if in the 85th percentile or greater (11.1 µmol/L and 12.7 mmol/L, respectively).

Results: After adjustment for traditional cardiovascular disease risk factors, cigarette smoking was related to elevated levels of C-reactive protein, fibrinogen, and homocysteine. Compared with never smoking cigarettes, self-reported current cigarette smoking was associated with a C-reactive protein level in the detectable (odds ratio, 1.66 [95% CI, 1.40 to 1.97]; P < 0.001) or clinically elevated (odds ratio, 1.98 [CI, 1.57 to 2.51]; P < 0.001) ranges, with elevated levels of fibrinogen (odds ratio, 2.15 [CI, 1.65 to 2.80]; P < 0.001) and homocysteine (odds ratio, 2.10 [CI, 1.62 to 2.74]; P < 0.001). There were positive and significant dose–response relationships between measures of cigarette smoking (cigarettes per day, pack-years, and serum cotinine levels) and elevated levels of novel risk factors.

Conclusions: These findings suggest that inflammation and hyperhomocysteinemia may be important mechanisms by which smoking promotes atherosclerotic disease.

Article and Author Information

Grant Support: In part by grant RO1 HL60300 from the National Heart, Lung, and Blood Institute of the National Institutes of Health.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Jiang He, MD, PhD, Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, 1430 Tulane Avenue SL18, New Orleans, LA 70112.
Current Author Addresses: Dr. Bazzano: Department of Internal Medicine, Beth Israel Deaconess Hospital, 330 Brookline Avenue, Deaconess Building 300, Boston, MA 02215.
Drs. He, Muntner, and Whelton: Tulane University School of Public Health and Tropical Medicine, 1430 Tulane Avenue SL18, New Orleans, LA 70112.
Dr. Vupputuri: National Institute of Environmental Health Sciences, 111 Alexander Drive, Research Triangle Park, NC 27709.
Author Contributions: Conception and design: L.A. Bazzano, J. He.
Analysis and interpretation of the data: L.A. Bazzano, J. He, P. Muntner.
Drafting of the article: L.A. Bazzano, J. He.
Critical revision of the article for important intellectual content: L.A. Bazzano, J. He, P. Muntner, S. Vupputuri, P.K. Whelton.
Final approval of the article: L.A. Bazzano, J. He, P. Muntner, S. Vupputuri, P.K. Whelton.
Statistical expertise: L.A. Bazzano, J. He, P. Muntner.
Obtaining of funding: J. He.
Administrative, technical, or logistic support: J. He.