AIM To review evidence relating passive smoking to heart disease risk in never smokers. METHODS Epidemiological studies were identified providing estimates of relative risk(RR) of ischaemic heart disease and 95%CI for never smokers for various indices of exposure to environmental tobacco smoke(ETS). "Never smokers" could include those with a minimal smoking experience. The database set up included the RRs and other study details. Unadjusted and confounderadjusted RRs were entered, derived where necessary using standard methods. The fixed-effect and randomeffects meta-analyses conducted for each exposure index included tests for heterogeneity and publication bias. For the main index(ever smoking by the spouse or nearest equivalent, and preferring adjusted to unadjusted data), analyses investigated variation in the RR by sex, continent, period of publication, number of cases, study design, extent of confounder adjustment, availability of dose-response results and biomarkerdata, use of proxy respondents, definitions of exposure and of never smoker, and aspects of disease definition. Sensitivity analyses were also run, preferring current to ever smoking, or unadjusted to adjusted estimates, or excluding certain studies.RESULTS Fifty-eight studies were identified, 20 in North America, 19 in Europe, 11 in Asia, seven in other countries, and one in 52 countries. Twenty-six were prospective, 22 case-control and 10 cross-sectional. Thirteen included 100 cases or fewer, and 11 more than 1000. For the main index, 75 heterogeneous(P 0.05) association was found for workplace exposure(RR = 1.08, 95%CI: 0.99-1.19), childhood exposure(1.12, 0.95-1.31), and biomarker based exposure indices(1.15, 0.94-1.40). However, there was a significant association with total exposure(1.23, 1.12-1.35). Some significant positive dose-response trends were also seen for these exposure indices, particularly total exposure, with no significant negative trends seen. The evidence suffers from various weaknesses and biases. Publication bias may explain the large RR(1.66, 1.30-2.11) for the main exposure index for smaller studies(1-99 cases), while recall bias may explain the higher RRs seen in casecontrol and cross-sectional than in prospective studies. Some bias may also derive from including occasional smokers among the "never smokers", and from misreporting smoking status. Errors in determining ETS exposure, and failing to update exposure data in long term prospective studies, also contribute to the uncertainty. The tendency for RRs to increase as more factors are adjusted for,argues against the association being due to uncontrolled confounding.CONCLUSION The increased risk and dose-response for various exposure indices suggests ETS slightly increases heart disease risk. However heterogeneity, study limitations and possible biases preclude definitive conclusions.
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