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BMJ 2004;329:918 (16 October), doi:10.1136/bmj.329.7471.918-b
| The first 150 words of the full text of this article appear below. |
EDITORWhincup 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 smoking3 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
Ruoling Chen, honorary senior lecturer
Department of Epidemiology and Public Health, University College London, London WC1E 6BT Ruoling.Chen@Westminster-pct.nhs.uk
Hugh Tunstall-Pedoe, professor of cardiovascular epidemiology, Roger Tavendale, biochemist
Cardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Ninewells Hospital, Dundee DD1 9SY
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