BACKGROUND. Although widely used in epidemiological studies, self-report has been shown to underestimate the prevalence of cigarette smoking in some populations. METHODS. In the CARDIA study, self-report of cigarette smoking was validated against a biochemical marker of nicotine uptake, serum cotinine. RESULTS. The prevalence of smoking was slightly lower when defined by self-report (30.9%) than when defined by cotinine levels equal to or greater than 14 ng/mL (32.2%, P less than .05). The misclassification rate (proportion of reported nonsmokers with cotinine levels of at least 14 ng/mL) was 4.2% and was significantly higher among subjects who were Black, had a high school education or less, or were reported former smokers. Possible reasons for misclassification include reporting error, environmental tobacco smoke, and an inappropriate cutoff point for delineation of smoking status. Using self-report as the gold standard, the cotinine cutoff points that maximized sensitivity and specificity were 14, 9, and 15 ng/mL for all, White, and Black subjects, respectively. The misclassification rate remained significantly higher in Black than in White subjects using these race-specific criteria. CONCLUSIONS. Misclassification of cigarette smoking by self-report was low in these young adults; however, within certain race/education groups, self-report may underestimate smoking prevalence by up to 4%.

Cotinine was measured in the serum of nearly all 5,115 18-30 year old, Black and White, men and women participating in the Coronary Artery Risk Development in (Young) Adults Study, 30 percent of whom reported current cigarette smoking. Ninety-five percent of the reported smokers had serum cotinine levels indicative of smoking (>13 ng/ml). The median cotinine level was higher in Black than White smokers (221 ng/ml versus 170 ng/ml; 95 percent CI for difference: 34, 65) in spite of the fact that estimated daily nicotine exposure and serum thiocyanate were higher in Whites. The differ- IntroductionCotinine, a major metabolite of nicotine, is currently considered the best indicator of tobacco smoke exposure.' It is specific for nicotine, has a long half-life (15-40 hours), and its level is thought to be directly proportional to the quantity of absorbed nicotine.2 The quantity of nicotine absorbed by smokers is quite variable, being dependent upon its concentration in the smoke, the individual's smoking pattern, and the smoke pH.3 Less is known regarding characteristics which influence the circulating levels of nicotine and cotinine or their maintenance in body fluids.!6 Such information may assist in the study of nicotine addiction and illnesses attributable to the toxic effects of this drug. This paper will assess the differences in cotinine levels in a biracial group of young adults who, as determined by self-report, are cigarette smokers. Possible behavioral and metabolic differences which might account for this observation are evaluated.

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We conducted a randomized controlled trial to determine whether a home-based intervention program could reduce infant passive smoking and lower respiratory illness. The intervention consisted of four nurse home visits during the first 6 months of life, designed to assist families to reduce the infant's exposure to tobacco smoke. Among the 121 infants of smoking mothers who completed the study, there was a significant difference in trend over the year between the intervention and the control groups in the amount of exposure to tobacco smoke; infants in the intervention group were exposed to 5.9 fewer cigarettes per day at 12 months. There was no group difference in infant urine cotinine excretion. The prevalence of persistent lower respiratory symptoms was lower among intervention-group infants of smoking mothers whose head of household had no education beyond high school: intervention group, 14.6%; and controls, 34.0%.

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The interpretation and interpretability of epidemiologic studies of environmental tobacco smoke (ETS) depend largely on the validity of self-reported exposure. To investigate to what extent questionnaires can indicate exposure levels to ETS, an international study was conducted in 13 centers located in 10 countries, and 1,369 nonsmoking women were interviewed. The present paper describes the results of the analysis of self-reported recent exposure to ETS from any source in relation to urinary concentrations of cotinine. Of the total, 19.7 percent of the subjects had nondetectable cotinine levels, the median value was 6 ng/mg, and the cut-point of the highest decile was 24 ng/mg. The proportion of subjects misreporting their active smoking habit was estimated at between 1.9 and 3.4 percent, depending on whether cut-points of 50 or 100 ng/mg creatinine were used. Large and statistically significant differences were observed between centers, with the lowest values in Honolulu, Shanghai, and Chandigarh, and the highest in Trieste, Los Angeles, and Athens. Mean cotinine/creatinine levels showed a clear linear increase from the group of women not exposed either at home or at work, to the group of those exposed both at home and at work. Values were significantly higher for women exposed to ETS from the husband but not at work, than for those exposed at work but not from the husband. The results of linear regression analysis indicated that duration of exposure and number of cigarettes to which the subject reported being exposed were strongly related to urinary cotinine. ETS exposure from the husband was best measured by the number of cigarettes, while exposure at work was more strongly related to duration of exposure. After adjustment of number of cigarettes for volume of indoor places, a similar increase in cotinine (5 ng/mg) was predicted by the exposure to 7.2 cigarettes/8 h/40 m3 from the husband and 17.9 cigarettes/8 h/40 m3 at work. The results indicate that, when appropriately questioned, nonsmoking women can provide a reasonably accurate description of ETS exposure. Assessment of individual exposure to ETS should focus on daily duration and volume of indoor places where exposure occurred.

We examined the extent of correlation between home air nicotine levels and urine cotinine/creatinine ratios (CCR) in 27 children who attended a research day care program where they were not exposed to environmental tobacco smoke (ETS) during the daytime hours. Average concentrations of nicotine in home air were determined by active air sampling during the evening and night hours on 2 consecutive days. Urine samples for cotinine and creatinine determinations were collected before, during, and after the two sampling periods. In addition, four sequential weekly urine samples for CCR were obtained from study children to determine the extent to which single determinations of CCR were representative for individual children. Fifteen children resided in homes with smokers, and 12 did not. Urine CCR consistently distinguished most exposed and unexposed children. However, three exposed children had urine CCRs that clustered routinely around the criterion CCR (30 ng/mg cotinine-creatinine) that best distinguished exposed and unexposed children. In children exposed to ETS in the home, there was a significant correlation between average home air nicotine levels and the average logarithm of urine CCR the two mornings after the home air monitoring periods (r = 0.68; p = 0.006). In study children, urine CCRs were remarkably stable over the 1-month observation period. Rank correlation coefficients for sequential weekly determinations of CCR were consistently greater than r = 0.88; p less than 0.0001.