Comparison of Serum Cotinine Concentration within and across Smokers of Menthol and Nonmenthol Cigarette Brands among Non-Hispanic Black and Non-Hispanic White U.S. Adult Smokers, 2001–2006

Caraballo, Ralph S.; Holiday, David; Stellman, Steven D.; Mowery, Paul; Giovino, Gary A.; Muscat, Joshua E.; Eriksen, Michael P.; Bernert, John T.; Richter, Patricia; Kozlowski, Lynn T.

doi:10.1158/1055-9965.epi-10-1330

Cited by 34 publications

(29 citation statements)

References 27 publications

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“…These smoothing properties support the hypothesis that menthol cigarette smoking may result in larger puffs, deeper inhalation, or longer retention time in the lung, thereby producing more adverse effects compared with non-menthol cigarette smoking (Hoffman, 2011; Lawrence et al, 2011; Besaratinia and Tommasi, 2015). However, results from studies on the smoking topography and blood biomarkers of smoke exposure in animals (Gaworski et al, 1997; Ha et al, 2015) and smokers (Heck, 2009, 2010; Caraballo et al, 2011; Hoffman, 2011; Lawrence et al, 2011) are inconclusive to support this hypothesis. Results from a clinical investigation have suggested that menthol cigarette smokers may exhibit more severe lung inflammation than non-menthol cigarette smokers in patients with COPD (Park et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory Effects of Menthol vs. Non-menthol Cigarette Smoke Extract on Human Lung Epithelial Cells: A Double-Hit on TRPM8 by Reactive Oxygen Species and Menthol

Lin

Liu

et al. 2017

Front. Physiol.

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Clinical studies suggest that smokers with chronic obstructive pulmonary disease who use menthol cigarettes may display more severe lung inflammation than those who smoke non-menthol cigarette. However, the mechanisms for this difference remain unclear. Menthol is a ligand of transient receptor potential melastatin-8 (TRPM8), a Ca2+-permeant channel sensitive to reactive oxygen species (ROS). We previously reported that exposure of human bronchial epithelial cells (HBECs) to non-menthol cigarette smoke extract (Non-M-CSE) triggers a cascade of inflammatory signaling leading to IL-8 induction. In this study, we used this in vitro model to compare the inflammatory effects of menthol cigarette smoke extract (M-CSE) and Non-M-CSE and delineate the mechanisms underlying the differences in their impacts. Compared with Non-M-CSE, M-CSE initially increased a similar level of extracellular ROS, suggesting the equivalent oxidant potency. However, M-CSE subsequently produced more remarkable elevations in intracellular Ca2+, activation of the mitogen-activated protein kinases (MAPKs)/nuclear factor-κB (NF-κB) signaling, and IL-8 induction. The extracellular ROS responses to both CSE types were totally inhibited by N-acetyl-cysteine (NAC; a ROS scavenger). The intracellular Ca2+ responses to both CSE types were also totally prevented by NAC, AMTB (a TRPM8 antagonist), or EGTA (an extracellular Ca2+ chelator). The activation of the MAPK/NF-κB signaling and induction of IL-8 to both CSE types were suppressed to similar levels by NAC, AMTB, or EGTA. These results suggest that, in addition to ROS generated by both CSE types, the menthol in M-CSE may act as another stimulus to further activate TRPM8 and induce the observed responses. We also found that menthol combined with Non-M-CSE induced greater responses of intracellular Ca2+ and IL-8 compared with Non-M-CSE alone. Moreover, we confirmed the essential role of TRPM8 in these responses to Non-M-CSE or M-CSE and the difference in these responses between the both CSE types using HBECs with TRPM8 knockdown and TRPM8 knockout, and using HEK293 cells transfected with hTRPM8. Thus, compared with exposure to Non-M-CSE, exposure to M-CSE induced greater TRPM8-mediated inflammatory responses in HBECs. These augmented effects may be due to a double-hit on lung epithelial TRPM8 by ROS generated from CSE and the menthol in M-CSE.

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Section: Discussionmentioning

confidence: 99%

Inflammatory Effects of Menthol vs. Non-menthol Cigarette Smoke Extract on Human Lung Epithelial Cells: A Double-Hit on TRPM8 by Reactive Oxygen Species and Menthol

Lin

Liu

et al. 2017

Front. Physiol.

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“…Cotinine is the primary proximate metabolite of nicotine (22, 23). NNAL is a metabolite of the TSNA 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which has been identified as a known human carcinogen by the International Agency on Research on Cancer (24, 25).…”

Section: Methodsmentioning

confidence: 99%

Nicotine and Toxicant Exposure among U.S. Smokeless Tobacco Users: Results from 1999 to 2012 National Health and Nutrition Examination Survey Data

Rostron

Chang

Bemmel

et al. 2015

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background It has been suggested that smokeless tobacco users have high levels of exposure to nicotine and some toxic substances as measured by biomarker concentrations, but studies with nationally representative data have been limited. Methods We analyzed biomarkers of tobacco exposure for 23,684 adult participants from the National Health and Nutrition and Examination Survey (NHANES) from 1999-2012. The biomarkers analyzed were serum cotinine, urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), blood lead, blood cadmium, blood mercury, urinary arsenic, and urinary N-acetyl-S-(2-cyanoethyl)-L-cysteine (CYMA). We calculated geometric mean concentrations for each biomarker by tobacco use category (exclusive smokeless tobacco use, exclusive cigarette smoking, dual cigarette and smokeless tobacco use, and non-cigarette and smokeless tobacco use) and geometric mean ratios adjusting for demographic factors. Results Exclusive smokeless tobacco users had higher geometric mean concentrations of cotinine (178.9 ng/mL, 95% CI = 145.5, 220.0) and NNAL (583.0 pg/mg creatinine, 95% CI = 445.2, 763.5) than exclusive cigarette smokers, (130.6 ng/mL, 95% CI = 122.3, 139.6 and 217.6 pg/mg creatinine, 95% CI = 193.0, 245.2, respectively). Smokeless tobacco users also had higher concentrations of blood lead compared with non-tobacco users (adjusted geometric mean ratio = 1.30, 95% CI = 1.21, 1.38). Differences in concentrations of cadmium, mercury, and CYMA between smokeless tobacco users and non-tobacco users were not observed. Based on limited sample sizes, NNAL concentrations for smokeless tobacco users appear to have declined from 2007-2008 (geometric mean = 1013.7 pg/mg creatinine, 95% CI = 738.9, 1390.8) to 2011-2012 (geometric mean = 325.7 pg/mg creatinine, 95% CI = 159.6, 664.9). Conclusions Smokeless tobacco users have higher observed levels of exposure to nicotine and carcinogenic tobacco-specific nitrosamines, as measured by cotinine and NNAL biomarker concentrations, than cigarette smokers. Impact High levels of exposure to known harmful constituents for smokeless tobacco users is a cause of concern for individual and public health.

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“…11–13 While previous research in Whites indicates that faster nicotine metabolizers smoke more cigarettes per day, it remains unclear if this relationship occurs in African Americans as well. 5–7 African Americans smoke fewer cigarettes per day but tend to smoke those cigarettes more intensely than Whites and as a consequence take in more nicotine per cigarette.…”

Section: Introductionmentioning

confidence: 99%

Racial differences in the relationship between rate of nicotine metabolism and nicotine intake from cigarette smoking

Ross

Gubner

Tyndale

et al. 2016

Pharmacology Biochemistry and Behavior

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Rate of nicotine metabolism has been identified as an important factor influencing nicotine intake and can be estimated using the nicotine metabolite ratio (NMR), a validated biomarker of CYP2A6 enzyme activity. Individuals who metabolize nicotine faster (higher NMR) may alter their smoking behavior to titrate their nicotine intake in order to maintain similar levels of nicotine in the body compared to slower nicotine metabolizers. There are known racial differences in the rate of nicotine metabolism with African Americans on average having a slower rate of nicotine metabolism compared to Whites. The goal of this study was to determine if there are racial differences in the relationship between rate of nicotine metabolism and measures of nicotine intake assessed using multiple biomarkers of nicotine and tobacco smoke exposure. Using secondary analyses of the screening data collected in a recently completed clinical trial, treatment-seeking African American and White daily smokers (10 or more cigarettes per day) were grouped into NMR quartiles so that the races could be compared at the same NMR, even though the distribution of NMR within race differed. The results indicated that rate of nicotine metabolism is a more important factor influencing nicotine intake in White smokers. Specifically, Whites were more likely to titrate their nicotine intake based on the rate at which they metabolize nicotine. However, this relationship was not found in African Americans. Overall there was a greater step down, linear type relationship between NMR groups and cotinine or cotinine/cigarette in African Americans, which is consistent with the idea that differences in blood cotinine levels between the African American NMR groups were primarily due to differences in CYP2A6 enzyme activity without titration of nicotine intake among faster nicotine metabolizers.

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Comparison of Serum Cotinine Concentration within and across Smokers of Menthol and Nonmenthol Cigarette Brands among Non-Hispanic Black and Non-Hispanic White U.S. Adult Smokers, 2001–2006

Cited by 34 publications

References 27 publications

Inflammatory Effects of Menthol vs. Non-menthol Cigarette Smoke Extract on Human Lung Epithelial Cells: A Double-Hit on TRPM8 by Reactive Oxygen Species and Menthol

Inflammatory Effects of Menthol vs. Non-menthol Cigarette Smoke Extract on Human Lung Epithelial Cells: A Double-Hit on TRPM8 by Reactive Oxygen Species and Menthol

Nicotine and Toxicant Exposure among U.S. Smokeless Tobacco Users: Results from 1999 to 2012 National Health and Nutrition Examination Survey Data

Racial differences in the relationship between rate of nicotine metabolism and nicotine intake from cigarette smoking

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