Uptake of environmental tobacco smoke.
This chapter has reviewed evidence of the uptake of smoke constituents by nonsmokers through exposure to environmental tobacco smoke. Although carbon monoxide absorption reflects an acute exposure, nicotine and its metabolite cotinine are the best markers currently available. Nicotine is found in measurable concentrations in the saliva and urine of most urban nonsmokers, and is present in higher concentrations in those with some recent exposure. But the short half-life of nicotine in the body means that it is best suited to quantifying exposure over a period of a few hours only. Cotinine, which has a half-life of about one day, has been shown to be a valid and sensitive marker of current daily-life exposure to environmental tobacco smoke. Estimating the magnitude of the passive smoking dose is difficult, and it is of doubtful validity to extrapolate from the uptake of one marker to that of another. Over a period when one cigarette-equivalent of carbon monoxide is absorbed, the dose of nicotine appears to be only between one-tenth and one-third of a cigarette-equivalent. Measures of tar deposition are not available, but nicotine is probably a better guide than carbon monoxide to the size of the tar dose. It seems unlikely that nonsmokers could absorb more than one or two mg of nicotine in a day, even if they spend the majority of their waking hours in heavily smoke-polluted atmospheres. Comparison of cotinine concentrations in urban nonsmokers and active smokers suggests that average nonsmokers may receive a dose of about 0.2 mg of nicotine per day. This is a preliminary estimate which depends on a number of assumptions and will be subject to revision as data accumulate on more representative samples. Finally, the confirmation that dose-response relationships exist between cotinine concentrations and self-reported passive smoking validates questionnaire measures of the degree of environmental smoke exposure. Epidemiological studies which suggest that passive smoking carries a risk to health thereby gain increased credibility. But future progress in understanding will be best assured if epidemiological methods and biological monitoring of exposure markers are combined in the same studies.
Jarvis
M J
MJ
Addiction Research Unit, Institute of Psychiatry, Denmark Hill, London, UK.
D002248:Carbon Monoxide / Q000097:blood; D003367:Cotinine / Q000493:pharmacokinetics; D004781:Environmental Exposure; D006801:Humans; D009538:Nicotine / Q000493:pharmacokinetics*; D013861:Thiocyanates / Q000493:pharmacokinetics; D014028:Tobacco Smoke Pollution
D013861:Thiocyanates; D014028:Tobacco Smoke Pollution; D009538:Nicotine; D002248:Carbon Monoxide; D003367:Cotinine