Josanna Rodriguez, MD; Rui Jiang, MD, DrPH; W. Craig Johnson, MS; Barbara A. MacKenzie; Lewis J. Smith, MD; R. Graham Barr, MD, DrPH
Note: A full list of participating MESA investigators and institutions can be found at www.mesa-nhlbi.org.
Acknowledgment: The authors thank Firas Ahmed, MD, MPH, for substantial programming assistance, in addition to the other investigators, staff, and participants of the MESA and MESA Lung Study for their valuable contributions.
Grant Support: By the National Institutes of Health (R01-HL077612, N01-HC95159 to HC95169, R01-HL075476).
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M09-1690.
Reproducible Research Statement:Study protocol (for the MESA Lung Study) and statistical code: Available from Dr. Barr (e-mail, email@example.com). Data set: Available as a limited access data set from the NHLBI (www.mesa-nhlbi.org).
Requests for Single Reprints: R. Graham Barr, MD, DrPH, Columbia University Medical Center, 630 West 168th Street, PH 9 East, Room 105, New York, NY 10032; e-mail, firstname.lastname@example.org.
Current Author Addresses: Drs. Rodriguez, Jiang, and Barr: Columbia University Medical Center, PH 9 East, Room 105, 630 West 168th Street, New York, NY 10032.
Mr. Johnson: University of Washington, Collaborative Health Studies Coordinating Center, Building 29, Suite 310, 6200 NE 74th Street, Seattle, WA 98115-8160.
Ms. MacKenzie: Robert A. Taft Labs, Centers for Disease Control and Prevention, The National Institute for Occupational Safety and Health, 4676 Columbia Parkway, Cincinnati, OH 45226.
Dr. Smith: Northwestern University, 750 North Lake Shore Drive, Room 707, Chicago, IL 60611.
Author Contributions: Conception and design: R.G. Barr.
Analysis and interpretation of the data: J. Rodriguez, B.A. MacKenzie, L.J. Smith, R.G. Barr.
Drafting of the article: J. Rodriguez, R.G. Barr.
Critical revision of the article for important intellectual content: R. Jiang, L.J. Smith, R.G. Barr.
Final approval of the article: J. Rodriguez, R. Jiang, W.C. Johnson, L.J. Smith, R.G. Barr.
Provision of study materials or patients: L.J. Smith.
Statistical expertise: W.C. Johnson, R.G. Barr.
Obtaining of funding: R.G. Barr.
Administrative, technical, or logistic support: W.C. Johnson, R.G. Barr.
Collection and assembly of data: W.C. Johnson, R.G. Barr.
Rodriguez J., Jiang R., Johnson W., MacKenzie B., Smith L., Barr R.; The Association of Pipe and Cigar Use With Cotinine Levels, Lung Function, and Airflow Obstruction: A Cross-sectional Study. Ann Intern Med. 2010;152:201-210. doi: 10.7326/0003-4819-152-4-201002160-00004
Download citation file:
Published: Ann Intern Med. 2010;152(4):201-210.
Cigarette smoking is the major cause of chronic obstructive pulmonary disease, but studies on the contribution of other smoking techniques are sparse.
To determine whether pipe and cigar smoking was associated with elevated cotinine levels, decrements in lung function, and increased odds of airflow obstruction.
Population-based sample from 6 U.S. communities.
Men and women aged 48 to 90 years without clinical cardiovascular disease at enrollment who were part of MESA (Multi-Ethnic Study of Atherosclerosis).
The MESA Lung Study measured spirometry according to American Thoracic Society guidelines and urine cotinine levels by immunoassay on a subsample of MESA. Pipe-years and cigar-years were calculated as years from self-reported age of starting to age of quitting (or to current age in current users) multiplied by pipe-bowls or cigars per day.
Of 3528 participants, 9% reported pipe smoking (median, 15 pipe-years), 11% reported cigar smoking (median, 6 cigar-years), and 52% reported cigarette smoking (median, 18 pack-years). Self-reported current pipe and cigar smokers had elevated urine cotinine levels compared with never-smokers. Pipe-years were associated with decrements in FEV1, and cigar-years were associated with decrements in the FEV1â€“FVC ratio. Participants who smoked pipes or cigars had increased odds of airflow obstruction whether they had also smoked cigarettes (odds ratio, 3.43 [95% CI, 1.75 to 6.71]; PÂ < 0.001) or not (odds ratio, 2.31 [CI, 1.04 to 5.11]; PÂ = 0.039) compared with participants with no smoking history.
Pipe and cigar smoking increased urine cotinine levels and was associated with decreased lung function and increased odds of airflow obstruction, even in participants who had never smoked cigarettes.
National Heart, Lung, and Blood Institute, National Institutes of Health.
Howard R. Gordon
February 17, 2010
The article does not separate the pipe & cigar smokers who inhale versus those that do not. Prior publications have shown different risks for lung cancer in pipe smokers who inhale compared to those who do not. Did you obtain this data?
to gain full access to the content and tools.
Learn more about subscription options.
Register Now for a free account.
Cardiology, Pulmonary/Critical Care, Coronary Risk Factors, Smoking.
Results provided by:
Copyright © 2016 American College of Physicians. All Rights Reserved.
Print ISSN: 0003-4819 | Online ISSN: 1539-3704
Conditions of Use
This PDF is available to Subscribers Only