Time to First Cigarette Predicts Cessation Outcomes in Adolescent Smokers

Mercincavage, Melissa; Branstetter, Steven A.; Muscat, Joshua E.; Horn, Kimberly

doi:10.1093/ntr/ntt087

Cited by 34 publications

(17 citation statements)

References 35 publications

(55 reference statements)

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“…In a large sample European Americans seeking treatment for smoking cessation (the U. Wisconsin Transdisciplinary Tobacco Use Research Center smoking cessation trials (McCarthy et al, ; Piper et al, ; Piper et al, )), a significant association was found between FMO3 genotype and scores reported for the Fagerström Test of Nicotine Dependence (FTND), the most widely used instrument for measuring nicotine dependence. Among the questionnaire items from the FTND, ‘time to first cigarette’ and ‘cigarettes per day’ are the two strongest predictors of smoking cessation (Baker et al, ; Mercincavage, Branstetter, Muscat, & Horn, ; Rohsenow, Martin, Tidey, Monti, & Colby, ). Importantly, the association between FMO3 genotype and FTND score was driven entirely by the time to first cigarette, and unlike CYP2A6 , FMO3 genotype was not significantly associated with overall cigarette consumption among dependent smokers.…”

Section: Discussionmentioning

confidence: 99%

Strain‐specific altered nicotine metabolism in 3,3′‐diindolylmethane (DIM) exposed mice

Bloom

Upadhyaya

Kharasch

2019

Biopharm & Drug Disp

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Two indole compounds, indole‐3‐carbinol (I3C) and its acid condensation product, 3,3′‐diindolymethane (DIM), have been shown to suppress the expression of flavin‐containing monooxygenases (FMO) and to induce some hepatic cytochrome P450s (CYPs) in rats. In liver microsomes prepared from rats fed I3C or DIM, FMO‐mediated nicotine N‐oxygenation was decreased, whereas CYP‐mediated nicotine metabolism to nicotine iminium and subsequently to cotinine was unchanged. Therefore, it was hypothesized that in mice DIM would also suppress nicotine N‐oxygenation without affecting CYP‐mediated nicotine metabolism. Liver microsomes were produced from male and female C57BL/6 J and CD1 mice fed 2500 parts per million (ppm) DIM for 14 days. In liver microsomes from DIM‐fed mice, FMO‐mediated nicotine N‐oxygenation did not differ from the controls, but CYP‐mediated nicotine metabolism was significantly increased, with results varying by sex and strain. To confirm the effects of DIM in vivo, control and DIM‐fed CD1 male mice were injected subcutaneously with nicotine, and the plasma concentrations of nicotine, cotinine and nicotine‐N‐oxide were measured over 30 minutes. The DIM‐fed mice showed greater cotinine concentrations compared with the controls 10 minutes following injection. It is concluded that the effects of DIM on nicotine metabolism in vitro and in vivo differ between mice and rats and between mouse strains, and that DIM is an effective inducer of CYP‐mediated nicotine metabolism in commonly studied mouse strains.

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Section: Discussionmentioning

confidence: 99%

Strain‐specific altered nicotine metabolism in 3,3′‐diindolylmethane (DIM) exposed mice

Bloom

Upadhyaya

Kharasch

2019

Biopharm & Drug Disp

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“…1 = within 5 minutes; 2 = 6-30 minutes; 3 = from more than 30 minutes to 1 hour; and 4 = more than 1 hour) that has been adopted by later nicotine dependence questionnaires, including the Fagerström Test for Nicotine Dependence (FTND; [11]). Since Kozlowski and colleagues' initial work on TTFC, a number of studies have confirmed that TTFC may be the single best predictor of nicotine dependence; an earlier time to first cigarette is closely associated with poor smoking outcomes such as increased levels of tobacco exposure biomarkers, increased tolerance and decreased likelihood of quitting during and an inability to maintain abstinence following a quit attempt [16][17][18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Time to first cigarette predicts 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in adolescent regular and intermittent smokers, National Health and Nutrition and Examination Survey (NHANES) 2007-10

2014

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Background and aims The time to first cigarette (TTFC) of the day is an indicator of nicotine intake in adults and adolescents. However, the relation between TTFC and biological markers of nicotine addiction and health risk in youths has not been well described. The current study examined whether an earlier TTFC predicts higher levels of a tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridal)-1 (NNAL), in regular and intermittent adolescent smokers and if this relation is mediated by nicotine intake (measured by cotinine) or cigarettes per day (CPD). Design A cross-sectional analysis of a nationally representative subsample of adolescents. Setting A general community sample from the 2007–2008 and 2009–2010 National Health and Nutrition and Examination Survey. Participants 215 adolescents in the United States between the ages of 12 and 19 who reported smoking at least once in the 5 days prior to data collection. Measurements The primary outcome measure was urinary levels of NNAL. Findings In both regular and intermittent smokers, earlier TTFC was dose-dependently associated with higher levels of NNAL (p < 0.03 in both cases). TTFC had an indirect effect on NNAL, mediated by nicotine intake (cotinine) in both regular (β = −.08, SE = .03, 95% CI [−.15, −.04]), and intermittent (β = −.02, SE = .01, 95% CI [−.05, −.002]) smokers. CPD was not found to be an important mediator of the relation between TTFC and NNAL. Conclusions Time between waking and the first cigarette of the day is correlated in daily and non-daily adolescent smokers with overall nicotine and therefore carcinogen intake.

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“…(ITT) sample, participants were considered to have experienced failure to quit if they reported continuing smoking or were not available for followup at 3-months post baseline. Conservatively, analysis assumed that unavailable participants continued to smoke, accounting for 27% of the treatment failure sample 34,36 . The study uniquely applied 'treatment failure', unlike the majority of tobacco cessation studies that commonly focus on quit rates 9,[37][38][39] .…”

Section: Data Sourcesmentioning

confidence: 99%

“…pack-years). TTFC has been shown to be highly related to: nicotine dependence, exposure to nicotine and carcinogens in both adolescent daily and non-daily smokers, and cessation outcomes among adolescents 36,[52][53][54] (Table 1).…”

Section: Predictor Variablesmentioning

confidence: 99%

School-level disadvantage and failed cessation treatment among adolescent smokers

Horn¹,

Ali²,

Gray³

et al. 2018

Tob. Prev. Cessation

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INTRODUCTION While understanding factors that lead to successful adolescent smoking cessation outcomes is necessary, it is also prudent to determine factors and conditions that contribute to failure to quit smoking. The present study posits that adolescents' proximal environments, such as schools, may influence cessation treatment outcomes. METHODS Using aggregated and geographically-referenced data from multi-year school-based cessation trials with 14-19 year olds seeking cessation in 5 States of the USA, the present study developed and applied a tobacco-specific socio-spatial model inclusive of Hierarchical Linear Modeling. Specifically, this novel approach spatially joined individual data files (n=8855) with measures of school (n=807) and county socio-economic factors. Once linked multi-level analyses explored the extent to which cessation treatment failure was explained by the interplay of individual, school and county-level factors. Treatment was deemed as failing to meet its primary goals if participants continued to smoke cigarettes, measured 3-months post baseline. RESULTS Ten per cent of the variation in cessation treatment failure was attributable to school-level variables. Adolescent smokers were more likely to experience failure to quit in: a) school districts with large percentages of the population having less than high-school education, and b) schools with a higher ratio of students to teachers. The strength of the relationship between cessation self-efficacy and treatment success was further weakened among adolescents attending schools with higher percentages of students eligible for free or reduced lunch programs. CONCLUSIONS Findings implicate school-level socio-economic disadvantage as a significant factor inhibiting cessation, regardless of adolescent self-efficacy to quit smoking. Understanding the interplay of proximal school environments and individual-level factors may provide insights to educators, policy makers and practitioners into the complexities that inhibit or strengthen an adolescent's smoking cessation treatment experience. INTRODUCTIONOne in four US high-school students currently use some form of tobacco, with 9.3 % of these tobacco users reporting smoking combustible cigarettes in the past 30 days in 20151 . The onset of smoking before the age of 18 years hastens nicotine dependence, elevating risks for detrimental and lasting effects on the developing brain and sustained tobacco use 2 . Although the percentage of US adolescents reporting combustible cigarette use is at a historic low 1 , with all products combined (e.g. cigars, e-cigarettes, smokeless tobacco), the overall tobacco use prevalence remains unchanged over the past two decades [1][2][3][4][5] . Even though over half of current

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Time to First Cigarette Predicts Cessation Outcomes in Adolescent Smokers

Cited by 34 publications

References 35 publications

Strain‐specific altered nicotine metabolism in 3,3′‐diindolylmethane (DIM) exposed mice

Strain‐specific altered nicotine metabolism in 3,3′‐diindolylmethane (DIM) exposed mice

Time to first cigarette predicts 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in adolescent regular and intermittent smokers, National Health and Nutrition and Examination Survey (NHANES) 2007-10

School-level disadvantage and failed cessation treatment among adolescent smokers

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