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Original Research: COPD |

The Association Between Alcohol Consumption and Risk of COPD Exacerbation in a Veteran Population

Courtney C. Greene, MD; Katharine A. Bradley, MD, MPH; Chris L. Bryson, MD, MS; David K. Blough, PhD; Laura E. Evans, MD, MS, FCCP; Edmonds M. Udris, MPH; David H. Au, MD, MS
Author and Funding Information

*From the Health Services Research and Development (Drs. Au, Bradley, and Bryson, and Mr. Udris), Seattle, WA; the Department of Medicine (Dr. Greene), University of Washington, Seattle, WA; the Department of Pharmacy (Dr. Blough), University of Washington, Seattle, WA; and the Department of Medicine (Dr. Evans), New York University, New York, NY.

Correspondence to: Courtney C. Greene, MD, Department of Medicine, University of Washington, Campus Box 356522, 1959 NE Pacific St, Seattle, WA 98195; e-mail: greenec@u.washington.edu


This work was supported by VA IIR #IAC 05-206-1. The VA ACQUIP was funded by VA Health Services Research and Development Service grants #SDR96-002 and IIR99-376 and the Firlands Foundation. Dr. Bryson is supported by a Department of Veterans Affairs Career Development Award (RCD00-018 and RCD03-177). Views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs. Each author declares no conflict of interest.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(4):761-767. doi:10.1378/chest.07-3081
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Background:  Alcohol has been associated with COPD-related mortality but has not yet been demonstrated to be an independent risk factor for COPD exacerbation. Our objective was to evaluate the association between alcohol consumption and the subsequent risk of COPD exacerbation.

Methods:  A prospective cohort study of general medicine outpatients seen at one of seven Veterans Affairs (VA) medical centers who returned health screening questionnaires. Three screening questionnaires, AUDIT-C (0 to 12 points), CAGE (0 to 4 points), and a single item about the frequency of drinking six or more drinks on an occasion (binge drinking), were used to classify alcohol consumption. The main outcome, COPD exacerbation, was based on primary VA discharge diagnosis (International Classification of Diseases, Ninth Revision) or outpatient diagnosis of COPD accompanied by prescriptions for either antibiotics or prednisone within 2 days.

Results:  Among the 30,503 patients followed up for a median of 3.35 years, those patients with AUDIT-C scores ≥ 6, CAGE scores ≥ 2, or who reported binge drinking at least weekly were at an increased risk of COPD exacerbation in age-adjusted analysis. Adjusted hazard ratios were 1.4 (95% confidence interval [CI], 1.1 to 1.7) for AUDIT-C score ≥ 6, 1.4 (95% CI, 1.3 to 1.5) for CAGE score ≥ 2, and 1.6 (95% CI, 1.2 to 2.2) for those who reported binge drinking daily or almost daily. However, with adjustment for measures of tobacco use, the association between alcohol consumption and increased risk of COPD exacerbation was no longer evident.

Conclusions:  Alcohol consumption, whether quantified by AUDIT-C, CAGE score, or binge drinking, was not associated with an increased risk of COPD exacerbation independent of tobacco use.

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