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Occup Environ Med 61:790-792 doi:10.1136/oem.2003.009167
  • Short report

Environmental tobacco smoke and prevalent coronary heart disease among never smokers in the Scottish MONICA surveys

  1. R Chen,
  2. R Tavendale,
  3. H Tunstall-Pedoe
  1. Cardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK
  1. Correspondence to:
 Dr R Chen
 Department of Epidemiology and Public Health, UCL, 1–19 Torrington Place, London WC1E 6BT, UK; ruoling.chenwestminster-pct.nhs.uk
  • Accepted 24 March 2004

Although many studies have shown that environmental tobacco smoke (ETS) or passive smoking increases the risk of coronary heart disease (CHD),1–6 there is still scepticism. This may be due to the small magnitude of the effect (about 25–35% increase5,6), inadequate adjustment for confounding variables, and misclassification of passive smoking. To estimate exposure, the majority of previous studies used only self report, without any biochemical markers, which could result in misclassification errors arising both from respondent and investigator biases. We analysed data from the Scottish MONICA surveys to see whether prevalent coronary heart disease is independently associated with passive smoking measured by self report, serum cotinine, and their combination.

SUBJECTS AND METHODS

Risk factor surveys were conducted for the Scottish MONICA Project in North Glasgow in 1986, 1989, 1992, and 1995.7 Subjects were randomly recruited from general practitioner lists after stratification into 10 year age and sex groups. A total of 1262 aged 25–64 participated in the first, 1397 in the second, 1958 (including 442 aged 65–74) in the third, and 1836 in the fourth, with response rates of 63.5%, 59.0%, 65.5%, and 65.7% respectively. Participants completed a personal health record that incorporated questions on sociodemographic and health status including details of active and passive smoking, the Rose chest pain questionnaire, and a food frequency questionnaire.3,8 Clinic examinations included electrocardiogram (ECG) and blood sampling for cotinine7 and other biochemical analyses.

Main messages

  • There was a weaker relation of CHD to serum cotinine than to self reported ETS; but when cotinine was detected, a dose-response relation was observed.

  • The combination of self reported ETS and serum cotinine showed a clearer gradient of prevalent CHD with exposure.

  • The association of CHD with ETS was independent of other cardiovascular confounders.

  • The increased risk of CHD for those in full …