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Tobacco Cessation |

Genetic African Ancestry and Nicotine Metabolism FREE TO VIEW

Marilyn Foreman, MS; Hari Ravipati, MPH; Wayne Hairston, MBA; Olutola Akiode; Margaret Parker; Wonsuk Yoo; Joi Johnson; Kimberly Peterson; Eric Flenaugh
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Johns Hopkins School of Public Health, Baltimore, MD


Chest. 2014;146(4_MeetingAbstracts):964A. doi:10.1378/chest.1995106
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Abstract

SESSION TITLE: Tobacco Cessation and Prevention Posters

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PM

PURPOSE: African Americans are admixed with varying proportions of African, European, and Native American ancestry. We analyzed whether African ancestry associated with urinary NNAL (nicotine, 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol); 3-hydroxycotinine (3HC); or cotinine.

METHODS: In 151 African American smokers, nicotine dependence was measured by Fagerstrom score ≧ 7 or first cigarette ≦ 30 minutes after awakening. Nicotine metabolites were standardized with urinary creatinine or average cigarettes smoked per day (cpd). We inferred locus-specific genetic ancestry with the Local Ancestry in Admixed Populations (LAMP-LD) program. Multivariate linear regression models were constructed with nicotine metabolites as the dependent variables and percentage African ancestry, age, gender, pack-years or duration smoking as the predictor variables.

RESULTS: Individuals who smoked within 30 minutes of awakening (n = 111) did not differ by gender, education, age, smoking duration, pack-years of smoking, or lung function (p > 0.05, respectively), but currently smoked 5 additional cigarettes daily, 15 ± 8 vs. 10 ± 7 (p = 0.0002). Urinary nicotine metabolites standardized by cpd differed: cotinine/cpd (sqrt) 2.9 vs. 5.5 (p = 0.02); 3-hydroxycotine/cpd (sqrt) 5.5 vs. 10.8 (p = 0.01); NNAL/urinary creatinine/cpd (sqrt) 1.4 vs. 2.8 (p = 0.03). African ancestry percentage was similar, 0.79 ± 0.12 vs. 0.82 ± 0.07 (p = 0.06). Nicotine addicted subjects by Fagerstrom score (n = 35) were younger, 51 vs. 54 years (p = 0.04) with higher lung function; postbronchodilator FEV1 83 vs. 75 % predicted (p = 0.01); postbronchodilator FEV1/FVC 0.77 vs. 0.71 (p = 0.002). They smoked more cigarettes per day (lifetime), 22 vs. 18 cigarettes (p = 0.01) and currently, 21 vs. 12 cpd (p < 0.0001). They differed in cotinine/cpd (sqrt) 2.3 vs. 4.0 (p = 0.01) and NNAL normalized for urinary creatinine/cpd (sqrt) 0.96 vs. 2.02 (p = 0.0009) but not by African ancestry percentage (p = 0.4). African ancestry associated with cotinine and 3-hydroxycotinine levels/cpd. Controlling for age, gender, pack-years of smoking, BMI, and education, individuals with higher levels of African ancestry had lower cotinine [-8.0 (3.5), p = 0.03 and lower 3-hydroxycotinine levels [-14.6 (7.0), p = 0.04].

CONCLUSIONS: We find association between genetic ancestry and metabolites of nicotine.

CLINICAL IMPLICATIONS: Understanding mechanisms underlying nicotine addiction in African Americans may lead to improved success with smoking cessation strategies.

DISCLOSURE: The following authors have nothing to disclose: Marilyn Foreman, Hari Ravipati, Wayne Hairston, Olutola Akiode, Margaret Parker, Wonsuk Yoo, Joi Johnson, Kimberly Peterson, Eric Flenaugh

No Product/Research Disclosure Information


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