Racial differences in the relationship between number of cigarettes smoked and nicotine and carcinogen exposure

Abstract

Introduction: Black smokers are reported to have higher lung cancer rates and greater tobacco dependence at lower levels of cigarette consumption compared to non-Hispanic White smokers. We studied the relationship between cigarettes per day (CPD) and biomarkers of nicotine and carcinogen exposure in Black and White smokers.

Methods: In 128 Black and White smokers, we measured plasma nicotine and its main proximate metabolite cotinine, urine nicotine equivalents, 4-(methylnitrosamino)-1-(3)pyridyl-1-butanol (NNAL), and polycyclic aromatic hydrocarbon (PAH) metabolites.

Results: The dose-response between CPD and nicotine equivalents, and NNAL and PAH was flat for Black but positive for White smokers (Race × CPD interaction, all ps < .05). Regression estimates for the Race × CPD interactions were 0.042 (95% CI 0.013-0.070), 0.054 (0.023-0.086), and 0.028 (0.004-0.052) for urine nicotine equivalents, NNAL, and PAHs, respectively. In contrast there was a strong correlation between nicotine equivalents and NNAL and PAH independent of race. Nicotine and carcinogen exposure per individual cigarette was inversely related to CPD. This inverse correlation was stronger in Black compared to White smokers and stronger in menthol compared to regular cigarette smokers (not mutually adjusted).

Conclusions: Our data indicate that Blacks on average smoke cigarettes differently than White smokers such that CPD predicts smoke intake more poorly in Black than in White smokers.

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 for all three biomarkers (p < .05). NNAL = 4-(methylnitrosamino)-1-(3)pyridyl-1-butanol.

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. NNAL = 4-(methylnitrosamino)-1-(3)pyridyl-1-butanol; PAH = polycyclic aromatic hydrocarbon.

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 White smokers (b); and between CPD, plasma cotinine, urine total NNAL, and urine total PAH metabolites in African American (c) and White smokers (d). *p < .05; **p < .01.