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Editor,—Although “passive smoking” may be intuitively harmful, the paper by Bonita and colleagues1on the risk of stroke and environmental tobacco smoke (ETS) exposure suffers from two fundamental defects. The first is the enormously disproportionate effect due to a small exposure, and the second is the lack of allowance for confounding variables, especially diet.
Serum cotinine concentrations have recently been determined at the US National Center for Environmental Health using the most sensitive method to date of high resolution gas chromatography with mass spectrometry.2 In 10 000 subjects it was shown that the mean serum cotinine concentration in ETS exposed non-smokers was 0.6 ng/ml compared to 300 ng/ml in active smokers. This represents 1/500th of the dose received by the active smoker.
It is difficult to reconcile this degree of exposure with an increased risk of stroke which is one quarter that of the active smoker. A similar disproportionate effect has been claimed for the increased risk of ischaemic heart disease and ETS exposure, but the biological plausibility and mechanisms of effect advanced to support this have been shown to lack credibility.3 4
It is well established that active smokers have other associated risk factors. They are physically less active and have lower intakes of fruit, vegetables, folate, and flavenoids,5 which are all linked to a substantial increased risk for stroke,6-8 and many of these characteristics are shared with non-smokers …