Demographics and Smoking History
Demographic, smoking, and alcohol consumption data for the subjects compared by race and sex are presented in . The average age of the subjects was 38.2 years; 42% were women. The subjects smoked an average of 17.2 CPD. On average, Black smokers were significantly older and had a higher BMI and fewer years of education. On average, Blacks smoked one fewer CPD than Whites, but this difference was not significant. Despite reporting during telephone screening that they smoked 10 or more CPD on average over the past year, 25% of Blacks and 16% of Whites smoked on average 10 or fewer CPD in the 3 days preceding the blood and urine sample. Blacks and Whites began smoking at similar ages on average, but Blacks had smoked for significantly longer (because they were older). The prevalence of menthol cigarette smoking and the average machine-determined nicotine and tar yields of cigarettes (ISO method) smoked were significantly higher in Blacks. The score and the time to first cigarette in the morning (another measure of dependence and also a component of the FTND) was similar between races.
Demographic Comparisons by Sex and Race (25%–75% quartile)
Biomarkers of Exposure
presents data on mean values for CPD, expired-air CO, plasma nicotine and metabolites, and urine nicotine metabolites, NNAL, and PAHs, comparing Blacks and Whites, men and women, and menthol versus non-menthol cigarette smokers. The time from the last cigarette to blood sampling was significantly longer (by 27 min on average) in Blacks versus Whites and tended to be longer (25 min on average) in menthol versus regular cigarette smokers. Plasma cotinine/CPD was significantly higher in Blacks versus Whites. Plasma nicotine levels were significantly higher in regular compared to menthol cigarette smokers. Urine nicotine equivalents, total NNAL, 2-naphthol, and total PAH metabolites were significantly lower in Black compared to White smokers. Urine nicotine equivalents, 2-naphthol, and total PAHs were significantly higher in women compared to men and in regular compared to menthol cigarette smokers.
Cigarette Smoking and Biomarkers of Cigarette Smoke Exposure (M and 95% CI)
Relationship Between CPD and Nicotine and Carcinogen Exposure
shows the relationship between CPD and urine nicotine equivalents, urine NNAL, and urine PAH metabolites in Blacks and Whites. In Whites, exposure to nicotine, NNAL, and PAHs increased with increasing CPD, but for Blacks, the CPD versus biomarker curves were generally flat. In Blacks, urine nicotine equivalents and NNAL were on average lower at less than 20 CPD compared to 11–20 CPD, but because of the variability, the shape of the curve is not significantly different from zero. Multivariate regression analyses revealed significant positive associations between CPD and urine nicotine equivalents, NNAL, and PAHs in Whites (all p < .002), but no significant associations for Blacks (). Significant CPD × Race interactions were observed for nicotine equivalents, NNAL, and total PAHs (all ps < .025). Thus, the slopes of the curves were significantly different for Black compared to White smokers. Significant interactions were also observed between race and CPD when CPD was assessed categorically (data not shown). There was not a significant effect for CPD or an interaction between CPD and race for expired-air CO.
Figure 1. Relationship between cigarettes per day (CPD) and urine nicotine equivalents (a), CPD and urine total NNAL (b), and CPD and urine total PAH metabolites (c), comparing African American(AA) and White (W) smokers. The Race × CPD interaction was significant (more ...)
Multiple Linear Regression Models of Predictors of Urine Nicotine Equivalents, Expired-Air Carbon Monoxide, Urine Total NNAL, and Urine Total PAH Metabolitesa
Relationship Between Nicotine Intake and Carcinogen Exposure
shows the relationship between urine nicotine equivalents and urine NNAL and urine PAH metabolites in Black and White smokers. In contrast to the racial difference observed in the CPD versus exposure curves, a positive relationship between urine nicotine equivalents and both carcinogen biomarker levels and expired-air CO (data for CO not shown) was seen both in Blacks and Whites. In multivariate analysis, urine nicotine equivalents were the strongest predictors of urine NNAL, PAH, and expired-air CO (all ps < .001). Multivariate regression analysis found no significant Urine Nicotine Equivalent × Race interaction between nicotine equivalents and urinary NNAL or expired-air CO, but there is a significant interaction for urine PAH metabolites (p = .012).
Figure 2. Relationship between urine nicotine equivalents (by quartlile) and urine total NNAL (a) and urine total PAH metabolites (b), comparing African American (AA) and White (W) smokers. The Nicotine Equivalent × Race interactions were not significant. (more ...)
Relationship Between CPD and Nicotine and Carcinogen Exposure per Individual Cigarette
Exposure to nicotine and carcinogens per individual cigarette increased as CPD decreased. There was a significant negative correlation between urine nicotine equivalents/CPD, NNAL/CPD, and total PAHs/CPD versus the number of CPD among all subjects. This was particularly marked at the very lowest level of cigarette consumption, where exposure per individual cigarette was very high. In general, the inverse correlations were stronger for Black compared to White smokers. Correlations with CPD were as follows: versus urine nicotine equivalents/CPD, Black r = −.54 (p < .01), White r = −.30 (p < .05); versus NNAL/CPD, Black r = −.48 (p < .01), White r = −.09 (ns); and versus PAHs/CPD, Black r = −.47 (p < .01), White r = −.34 (p < .05). The inverse correlations were similarly stronger for menthol compared to regular cigarette smokers. Correlations with CPD were as follows: versus urine nicotine equivalents/CPD, menthol r = −.54 (p < .01), regular r = −.42 (p < .01); versus NNAL/CPD, menthol r = −.46 (p < .01), regular r = −.16 (ns); and versus PAHs/CPD, menthol r = −.45 (p < .01), regular r = −.36 (p < .01).
Cross-Correlations Among CPD and Biomarkers of Exposure by Race
presents the correlation coefficients between CPD, urine nicotine equivalents, plasma cotinine, urine NNAL, and urine total PAHs for Black and for White smokers. Compared to White smokers, the correlations were weaker for Blacks for CPD versus nicotine equivalents (r = .031 vs. .258 in Black vs. White, respectively), plasma cotinine (r = .103 vs. .376), urine NNAL (r = .099 vs. .273), and urine PAHs (r = .153 vs. .216). In contrast, the correlations between nicotine equivalents or plasma cotinine and other biomarkers of exposure were generally strong and were similar in magnitude for both races. For urine nicotine equivalents, the correlations in Blacks versus Whites were as follows: urine NNAL, r = .570 versus .580; and urine PAHs, r = .719 versus 0.783. For plasma cotinine, the correlations were as follows: urine NNAL, r = .452 versus .629; and urine PAHs, r = .556 versus .496.
Figure 3. Pearson correlation coefficients between cigarettes per day (CPD), urine nicotine equivalents, urine total 4-(methylnitrosamino)-1-(3)pyridyl-1-butanol (NNAL), and urine total polycyclic aromatic hydrocarbon (PAH) metabolites in African American (a) and (more ...)