2 years; 42% were women. Tanespimycin 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. Table 1. Demographic Comparisons by Sex and Race (25%�C75% quartile) Biomarkers of Exposure Table 2 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. Table 2. Cigarette Smoking and Biomarkers of Cigarette Smoke Exposure (M and 95% CI) Relationship Between CPD and Nicotine and Carcinogen Exposure Figure 1 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�C20 CPD, but because of the variability, the shape of the curve is not significantly different from zero. Brefeldin_A 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 (Table 3). Significant CPD �� Race interactions were observed for nicotine equivalents, NNAL, and total PAHs (all ps < .025).