Research

Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study

BMJ 2006; 332 doi: 10.1136/bmj.38779.584028.55 (Published 4 May 2006)
Cite this as: BMJ 2006;332:1064

This article has a correction

Please see: Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study

  1. Thomas K Houston, assistant professor of medicine (thouston{at}uab.edu)15,
  2. Sharina D Person, associate professor of medicine5,
  3. Mark J Pletcher, assistant professor of medicine2,
  4. Kiang Liu, professor of medicine3,
  5. Carlos Iribarren, research scientist4,
  6. Catarina I Kiefe, professor of medicine15
  1. 1 Deep South Center on Effectiveness Research, Birmingham Veterans Affairs Medical Center, Birmingham, AL, USA
  2. 2 University of California, San Francisco, CA, USA
  3. 3 Northwestern University, Evanston, IL, USA
  4. 4 Kaiser Permanente, Oakland, CA
  5. 5 University of Alabama at Birmingham, Birmingham, AL
  1. Correspondence to: T K Houston, Division of General Internal Medicine, University of Alabama at Birmingham, 510 20th Street South, FOT 720, Birmingham, AL 35294, USA
  • Accepted 23 February 2006

Abstract

Objective To assess whether active and passive smokers are more likely than non-smokers to develop clinically relevant glucose intolerance or diabetes.

Design Coronary artery risk development in young adults (CARDIA) is a prospective cohort study begun in 1985-6 with 15 years of follow-up.

Setting Participants recruited from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California, USA.

Participants Black and white men and women aged 18-30 years with no glucose intolerance at baseline, including 1386 current smokers, 621 previous smokers, 1452 never smokers with reported exposure to secondhand smoke (validated by serum cotinine concentrations 1-15 ng/ml), and 1113 never smokers with no exposure to secondhand smoke.

Main outcome measure Time to development of glucose intolerance (glucose ≥ 100 mg/dl or taking antidiabetic drugs) during 15 years of follow-up.

Results Median age at baseline was 25, 55% of participants were women, and 50% were African-American. During follow-up, 16.7% of participants developed glucose intolerance. A graded association existed between smoking exposure and the development of glucose intolerance. The 15 year incidence of glucose intolerance was highest among smokers (21.8%), followed by never smokers with passive smoke exposure (17.2%), and then previous smokers (14.4%); it was lowest for never smokers with no passive smoke exposure (11.5%). Current smokers (hazard ratio 1.65, 95% confidence interval 1.27 to 2.13) and never smokers with passive smoke exposure (1.35, 1.06 to 1.71) remained at higher risk than never smokers without passive smoke exposure after adjustment for multiple baseline sociodemographic, biological, and behavioural factors, but risk in previous smokers was similar to that in never smokers without passive smoke exposure.

Conclusion These findings support a role of both active and passive smoking in the development of glucose intolerance in young adulthood.

Footnotes

  • Contributors TKH originated the research questions, designed the study, and drafted initial and subsequent versions of the paper. SDP oversaw the analyses and reviewed and contributed to drafts. MJP reviewed and contributed to drafts and contributed content expertise. KL reviewed and contributed to drafts and contributed statistical expertise. CI reviewed and contributed to drafts. CIK reviewed and contributed to all drafts and contributed to the analytic plan. TKH and CIK are the guarantors.

  • Funding Work on this manuscript was supported (or partially supported) by contracts to the University of Alabama at Birmingham, Coordinating Center, N01-HC-95095; University of Alabama at Birmingham, Field Center, N01-HC-48047; University of Minnesota, Field Center, N01-HC48048; Northwestern University, Field Center, N01-HC-48049; Kaiser Foundation Research Institute, N01-HC-48050; University of California, Irvine, Echocardiography Reading Center, N01-HC-45134; and Harbor-UCLA Research Education Institute, Computed Tomography Reading Center, N01-HC-05187 from the National Heart, Lung and Blood Institute.

  • Competing interests None declared.

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