BMJ  2004;329:918 (16 October), doi:10.1136/bmj.329.7471.918-b

Letter

Best estimates of coronary risk of passive smoking are needed

EDITOR—Whincup et al show passive inhalation of environmental tobacco smoke to be an unexpectedly strong risk factor for coronary heart disease, when assessed using serum cotinine concentrations, in contrast to Enstrom and Kabat, who did not.^{1 2} They emphasise the need for further prospective studies using biomarkers.

We measured serum cotinine concentration and other biomarkers of smoking at baseline in our Scottish heart health study and Scottish MONICA surveys and recently reported cardiovascular mortality in never smokers, finding excess risk with passive smoking^{3 4}; preliminary work has now been extended to include morbidity and mortality at 16 years.

Using biomarkers and questionnaire results we found discrepancies between self-reported exposure and serum cotinine concentration in passive smoking.³ Cotinine results are affected by individual differences in nicotine metabolism and by time delays from exposure. Because of this we have found a combination score of grades of self-reported exposure and of cotinine valuable.^{4 5}

Campaigners against tobacco tend to talk-up positive results on passive smoking and to discount weak or negative ones as "flawed" for non-scientific reasons. To obtain the best overall estimates of risks of exposure to smoke without bias is important. Nicotine itself is unlikely to be responsible for the risk of passive smoking, but cotinine is a useful biomarker of a recently common, now disappearing, form of smoke exposure. Banishing the traditional clouds of tobacco smoke forever may be dear to the hearts of many of us for social as well as medical reasons, but were any exposure to smoke from combustion of vegetable matter, however caused, to be labelled dangerous this might have severe long term occupational and economic consequences. It is important for that reason to get the best estimates of risk that we can.

Department of Epidemiology and Public Health, University College London, London WC1E 6BT Ruoling.Chen{at}Westminster-pct.nhs.uk

Cardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Ninewells Hospital, Dundee DD1 9SY

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Competing interests: None declared.

References

1. Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Feyerabend C, Bryant A, et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ 2004;329: 200-5. (24 July.)[Abstract/Free Full Text]
2. Enstrom JE, Kabat GC. Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98. BMJ 2003;326: 1057-67.[Abstract/Free Full Text]
3. Tunstall-Pedoe H, Brown CA, Woodward M, Tavendale R. Passive smoking by self-report and serum cotinine and the prevalence of respiratory and coronary heart disease in the Scottish heart health study. J Epidemiol Community Health 1995;49: 139-43.[Abstract]
4. Chen R, Tavendale R, Tunstall-Pedoe H. Passive smoking measured by self report, serum cotinine and their combination and 14-year cardiovascular mortality among never smokers in the Scottish Heart Health Study. Circulation 2003;108: IV 751. (Abstract.)
5. Chen R, Tavendale R, Tunstall-Pedoe H. Measurement of passive smoking in adults: self-reported questionnaire or serum cotinine? J Cancer Epidemiol Prev 2002;7: 85-95.[Medline]

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

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