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Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement

BMJ 2004; 329 doi: https://doi.org/10.1136/bmj.38146.427188.55 (Published 22 July 2004) Cite this as: BMJ 2004;329:200
  1. Peter H Whincup (p.whincup{at}sghms.ac.uk), professor of cardiovascular epidemiology1,
  2. Julie A Gilg, research statistician1,
  3. Jonathan R Emberson, BHF junior research fellow2,
  4. Martin J Jarvis, professor of health psychology3,
  5. Colin Feyerabend, principal biochemist4,
  6. Andrew Bryant, senior analyst4,
  7. Mary Walker, research administrator2,
  8. Derek G Cook, professor of epidemiology1
  1. 1 Department of Community Health Sciences, St George's Hospital Medical School, London SW17 0RE
  2. 2 Department of Primary Care and Population Sciences, Royal Free Campus, Royal Free and University College Medical School, London NW3 2PF
  3. 3 Cancer Research UK Health Behaviour Research Unit, Department of Epidemiology and Public Health, Royal Free and University College Medical School, London WC1E 6BT
  4. 4 Medical Toxicology Unit, New Cross Hospital, London SE14 5ER
  1. Correspondence to: P H Whincup
  • Accepted 6 May 2004

Abstract

Objective To examine the associations between a biomarker of overall passive exposure to tobacco smoke (serum cotinine concentration) and risk of coronary heart disease and stroke.

Design Prospective population based study in general practice (the British regional heart study).

Participants 4729 men in 18 towns who provided baseline blood samples (for cotinine assay) and a detailed smoking history in 1978-80.

Main outcome measure Major coronary heart disease and stroke events (fatal and non-fatal) during 20 years of follow up.

Results 2105 men who said they did not smoke and who had cotinine concentrations < 14.1 ng/ml were divided into four equal sized groups on the basis of cotinine concentrations. Relative hazards (95% confidence intervals) for coronary heart disease in the second (0.8-1.4 ng/ml), third (1.5-2.7 ng/ml), and fourth (2.8-14.0 ng/ml) quarters of cotinine concentration compared with the first (≥ 0.7 ng/ml) were 1.45 (1.01 to 2.08), 1.49 (1.03 to 2.14), and 1.57 (1.08 to 2.28), respectively, after adjustment for established risk factors for coronary heart disease. Hazard ratios (for cotinine 0.8-14.0 ν ≥ 0.7 ng/ml) were particularly increased during the first (3.73, 1.32 to 10.58) and second five year follow up periods (1.95, 1.09 to 3.48) compared with later periods. There was no consistent association between cotinine concentration and risk of stroke.

Conclusion Studies based on reports of smoking in a partner alone seem to underestimate the risks of exposure to passive smoking. Further prospective studies relating biomarkers of passive smoking to risk of coronary heart disease are needed.

Footnotes

  • Contributors PHW and DGC had the idea for this paper and raised a grant with MJJ and MW to carry out the study. CF and AB provided biochemical analyses; JAG and JRE provided statistical analyses. All authors contributed to the writing of the paper. PHW is guarantor.

  • Funding The analysis of cotinine measurements was supported by a Project Grant from the BUPA Foundation. The British regional heart study is funded by the British Heart Foundation and the Department of Health.

  • Competing interests None declared.

  • Ethical approval Ethical approval was provided by the Medical Research Council and subsequently by the relevant local and multicentre research ethics committees.

  • Accepted 6 May 2004
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