Menthol Cigarette Smokers Research Articles

Menthol cigarette use and pain reporting among African American adults seeking treatment for smoking cessation.

Nicotine has acute pain-relieving properties, and tobacco smokers often report using cigarettes to cope with pain. The proportion of smokers using menthol cigarettes has increased in recent years, and there is reason to suspect that menthol may enhance the analgesic effects of nicotine. Up to 90% of African American smokers report using menthol cigarettes, and African Americans tend to report more severe pain and greater difficulty quitting. Yet no known research has examined the relationship between menthol cigarette use and pain reporting. Thus, the goal of the current study was to test associations between menthol (vs. nonmenthol) cigarette use and pain among a sample of African American smokers. Current daily cigarette smokers (N = 115; 70% male; Mage = 47.05; MCPD = 15.2) were recruited to participate in a smoking cessation study. These data were collected at the baseline session. Daily menthol (vs. nonmenthol) cigarette use was associated with lower current pain intensity, lower average and worst pain over the past 3 months, and less pain-related physical impairment over the past 3 months. This study demonstrates that menthol (vs. nonmenthol) cigarette use is associated with less pain and pain-related functional interference among African American smokers seeking tobacco cessation treatment. Future research is needed to examine the potential acute analgesic effects of menthol versus nonmenthol cigarette use, examine temporal covariation between menthol cigarette use and pain reporting, and test whether pain-relevant processes contribute to the maintenance of menthol cigarette smoking among those with and without chronic pain. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Racial/ethnic differences in daily, nondaily, and menthol cigarette use and smoking quit ratios in the United States: 2002 to 2016

In the United States (US), racial/ethnic groups differ in cigarette smoking behaviors. We examined changes in cigarette prevalence and quit ratios over 15 years by racial/ethnic group (Non-Hispanic (NH) White, NH Black, Hispanic, NH Other). Data were drawn from the 2002–2016 National Survey on Drug Use and Health (NSDUH) public use data files and analyzed in 2018. Linear time trends of the prevalence of daily, nondaily, and menthol cigarette use and quit ratios (i.e., proportion of former smokers among lifetime smokers) were assessed using logistic regression models. 19.35% of NH White persons were daily smokers in 2016; this prevalence was significantly higher than all other groups (NH Black 10.99%, Hispanic 6.81%, NH Other 9.10%). Menthol use was significantly more common among NH Black individuals than all other groups in every year from 2002 to 2016 (2016: NH Black 23.38%, NH White 14.52%, Hispanic 10.49%, NH Other 8.97%). From 2002 to 2016, daily and nondaily smoking decreased significantly among all groups. The rate of decline of nondaily smoking was more rapid among Hispanic than NH White individuals while the rate of menthol smoking decline was more rapid among NH White than among Hispanic individuals. The quit ratio did not change significantly from 2002 to 2016 among NH Black individuals (31% to 35%) in contrast to a significant increase among NH White (2002, 45%; 2016, 50%) and Hispanic (2002, 33%; 2016, 41%) individuals. Further progress in tobacco control for vulnerable groups may need to include innovative strategies to address these concerning trends.

Circulating Inflammation Proteins Associated With Lung Cancer in African Americans

IntroductionLung cancer incidence is higher among African Americans (AAs) compared with European Americans (EAs) in the United States. We and others have previously shown a relationship between immune and inflammation proteins with lung cancer in EAs. Our aim was to investigate the etiologic relationship between inflammation and lung cancer in AAs. MethodsWe adopted a two-stage, independent study design (discovery cases, n = 316; control cases, n = 509) (validation cases, n = 399; control cases, n = 400 controls) and measured 30 inflammation proteins in blood using Meso Scale Discovery V- PLEX multiplex assays. ResultsWe identified and validated 10 proteins associated with lung cancer in AAS, some that were common between EAs and AAs (C-reactive proteins [OR: 2.90; 95% confidence interval (CI): 1.99–4.22], interferon γ [OR: 1.55; 95% CI: 1.10–2.19], interleukin 6 [OR: 6.28; 95% CI: 4.10–9.63], interleukin 8 [OR: 2.76; 95% CI: 1.92–3.98]) and some that are only observed among AAs (interleukin 10 [OR: 1.69; 95% CI: 1.20–2.38], interleukin 15 [OR: 2.83; 95% CI: 1.96–4.07], interferon gamma-induced protein 10 [OR: 1.54; 95% CI: 1.09–2.18], monocyte chemotactic protein-4 [OR: 0.54; 95% CI: 0.38–0.76], macrophage inflammatory protein-1 alpha [OR: 1.57; 95% CI: 1.12–2.21], and tumor necrosis factor β [OR: 0.52; 95% CI: 0.37–0.74]). We did not find evidence that either menthol cigarette smoking or global genetic ancestry drove these population differences. ConclusionsOur results highlight a distinct inflammation profile associated with lung cancer in AAs compared with EAs. These data provide new insight into the etiology of lung cancer in AAs. Further work is needed to understand what drives this relationship with lung cancer and whether these proteins have utility in the setting of early diagnosis.

Menthol Inhibits UGT2B10‐catalyzed Detoxification of the Potent Tobacco‐carcinogen, NNAL

Menthol may be added to tobacco products as either naturally occurring L‐menthol or synthesized racemic DL‐menthol and is excreted as a menthol glucuronide (MG). The most potent tobacco carcinogen is 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK). NNK is extensively metabolized to enantiomers [(R) or (S)] of the equally carcinogenic chiral 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanol (NNAL). Both (R)‐ and (S)‐NNAL have been shown to be carcinogenic. Detoxification of (R)‐ and (S)‐NNAL through glucuronidation on NNAL's pyridine ring nitrogen (NNAL‐N‐gluc) is primarily mediated by UGT2B10. Menthol has been shown to inhibit NNAL‐N‐gluc formation in human liver microsomes (HLM). The goal of the present study was to elucidate the impact of menthol on NNAL‐N‐gluc formation in vivo. In vitro inhibition assays using HLM or microsomes from UGT2B10 over‐expressing HEK293 cells were performed with racemic (R/S)‐NNAL as substrate with each menthol enantiomer added separately as inhibitor. In vivo data were gathered from analysis of MG, NNAL, and NNAL metabolites from 50 menthol smokers and 50 non‐menthol smokers. Samples were obtained from the Southern Community Cohort Study. Both L‐ and D‐menthol enantiomers were inhibitors of UGT2B10 in vitro with IC50 values of 236 and 202 μM, respectively. In vivo D‐MG levels, when present, were far below the levels of L‐MG observed in smokers of both menthol or non‐menthol cigarettes, with D‐MG comprising an average of 1.3% of total MG. Urinary L‐MG was detectable in 98 subjects and levels were not significantly different between menthol and non‐menthol smokers (p=0.50). When stratified by tertiles of urinary MG levels, NNAL‐N‐gluc levels were highest in smokers with the lowest MG levels, with NNAL‐N‐gluc levels inversely associated with MG levels in smokers (p<0.05). These data suggest that menthol inhibits a major detoxification pathway of the tobacco carcinogen, NNK. The relatively high levels of urinary menthol in smokers of both menthol and non‐menthol cigarettes raise the possibility that menthol branding may not be the best approach to studying the impact of menthol as a tobacco additive.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Experimental Tobacco Marketplace in Regulating Flavored Tobacco Products in Menthol Cigarette Smokers

Experimental Tobacco Marketplace in Regulating Flavored Tobacco Products in Menthol Cigarette Smokers

Menthol Smoking Patterns and Smoking Perceptions Among Youth: Findings From the Population Assessment of Tobacco and Health Study

Youth may be attracted to menthol cigarettes because they are perceived as less harmful and harsh to smoke relative to non-menthol cigarettes. This study examined demographic factors and menthol cigarette smoking patterns as correlates of youth harm perceptions of cigarette smoking and ease of smoking menthol versus non-menthol cigarettes. Data were from the Wave 1 (2013-2014) youth sample of the Population Assessment of Tobacco and Health Study. Weighted multivariable logistic regression models were used to examine correlations between demographic factors and menthol cigarette smoking patterns (menthol initiation, past 30-day menthol cigarette smoking, and menthol cigarette brand preference), with harm perceptions of cigarette smoking and ease of smoking a menthol cigarette. Nearly half of ever cigarette smoking youth (43%) first used a menthol cigarette; 21% reported past 30-day menthol cigarette smoking; and 42% of past 30-day smokers providing brand information used a menthol cigarette as their preferred brand. In bivariate analyses, initiation with a menthol cigarette and menthol brand preference (versus non-menthol) were correlated with black race, older age at initiation, and past 30-day menthol cigarette smoking. In adjusted models, past 30-day menthol cigarette smoking and menthol cigarette brand preference, but not menthol initiation, were correlated with the perception that menthol cigarettes are easier to smoke. Youth who smoke menthol cigarettes perceive them as easier to smoke, even after adjusting for other factors. Age of initiation and black race emerged as correlates of menthol cigarette initiation, brand preference, and cigarette harm perceptions, and may inform future prevention campaigns.

An African-specific haplotype in MRGPRX4 is associated with menthol cigarette smoking.

In the U.S., more than 80% of African-American smokers use mentholated cigarettes, compared to less than 30% of Caucasian smokers. The reasons for these differences are not well understood. To determine if genetic variation contributes to mentholated cigarette smoking, we performed an exome-wide association analysis in a multiethnic population-based sample from Dallas, TX (N = 561). Findings were replicated in an independent cohort of African Americans from Washington, DC (N = 741). We identified a haplotype of MRGPRX4 (composed of rs7102322[G], encoding N245S, and rs61733596[G], T43T), that was associated with a 5-to-8 fold increase in the odds of menthol cigarette smoking. The variants are present solely in persons of African ancestry. Functional studies indicated that the variant G protein-coupled receptor encoded by MRGPRX4 displays reduced agonism in both arrestin-based and G protein-based assays, and alteration of agonism by menthol. These data indicate that genetic variation in MRGPRX4 contributes to inter-individual and inter-ethnic differences in the preference for mentholated cigarettes, and that the existence of genetic factors predisposing vulnerable populations to mentholated cigarette smoking can inform tobacco control and public health policies.

Reduction in Exposure to Selected Harmful and Potentially Harmful Constituents Approaching Those Observed Upon Smoking Abstinence in Smokers Switching to the Menthol Tobacco Heating System 2.2 for 3 Months (Part 1).

IntroductionThe Tobacco Heating System (THS) is a “heat-not-burn” tobacco product designed to generate significantly lower levels of harmful and potentially harmful constituents (HPHCs) and present lower risk of harm than cigarettes. This study assessed the exposure reduction to selected HPHCs in smokers switching to menthol Tobacco Heating System (mTHS) 2.2 compared with smokers continuing smoking menthol cigarettes (mCCs) and smoking abstinence (SA) for 5 days in a confined setting, followed by an 86-day ambulatory period.MethodsA total of 160 healthy adult US smokers participated in this randomized, three-arm parallel group, controlled clinical study. Biomarkers of exposure to 16 HPHCs were measured in blood and 24-hour urine. Safety was monitored throughout the study. Information was also gathered on product evaluation, product use, subjective effects, and clinical risk markers (co-publication Part 2).ResultsNicotine uptake was comparable in both exposure groups (mTHS:mCC ratio of 96% on day 90). On day 5, biomarker of exposure levels to other HPHCs were reduced by 51%–96% in the mTHS group compared with the mCC group, and these reductions were sustained for most biomarkers of exposure over ambulatory period. After 90 days of use, the level of satisfaction with mTHS and suppression of urge to smoke were comparable to mCC.ConclusionSwitching from mCCs to mTHS significantly reduced the exposure to HPHCs to levels approaching those observed in subjects who abstained from smoking for the duration of the study.ImplicationsThis study compared the impact of switching to mTHS on biomarkers of exposure, relative to continued smoking or SA.Clinical SignificanceSwitching to mTHS 2.2 led to significant reductions of exposure (total NNAL, total NNN, COHb, MHBMA, 3-HPMA, S-PMA, Total 1-OHP, 4-ABP, 1-NA, 2-NA, o-tol, CEMA, HEMA, HMPMA, and B[a]P) after 5 days in confinement, which were maintained throughout the subsequent ambulatory period of 86 days. The reductions were similar to those observed upon SA.Moderate compliance in the mTHS group during the ambulatory period was indicative of dual use of mTHS and mCC.mTHS provides an acceptable alternative to mCC for adult smokers.Trial RegistrationNCT01989156 (ClinicalTrials.gov).

Menthol Binds to Extracellular and Transmembrane Domains of the Human A4β2 Nicotinic Receptor

Menthol, a small organic compound, has long been used for its flavor as well as its local anesthetic and counterirritant properties. In the US, the 2009 Family Smoking Prevention and Tobacco Control Act by the Congress banned all additives to cigarettes with the exception of menthol. However, an abundance of scientific and clinical research characterize menthol as a non-inert molecule in the body. Smoking menthol cigarettes has been correlated with lower quitting rates and higher relapse rates and it has been shown that all cigarettes, even if labeled as nonmenthol, contain menthol. Unfortunately, at the molecular level not much is known about menthol's interaction with its sites of action, most prominently nicotinic acetylcholine receptors (nAChRs) in the brain. The published X-ray crystal structure of the human α;4β;2 nicotinic receptor - the most abundant nAChR in the human brain - provided an unprecedented opportunity for us to perform molecular dynamics simulations to investigate the interaction between menthol and a heteropentameric nAChR. In this study, we first used free energy perturbation calculations as well as flooding simulations to calculate menthol's water-membrane partition coefficient. The results from the flooding simulations were used to determine the penetration depth as well as the preferred orientation of menthol molecules in a POPC lipid bilayer. Umbrella sampling simulations were performed to derive the free energy profile of menthol across a POPC lipid bilayer. After concluding that menthol molecules partition in mammalian membranes in large numbers we performed flooding simulations in the presence of the human α;4β;2 nicotinic receptor. We demonstrate that menthol molecules bind to both the extracellular and transmembrane domains of the protein with larger numbers of menthol molecules binding to the transmembrane domain of the protein after partitioning into the membrane.

Chronic Menthol Does Not Change Stoichiometry or Functional Plasma Membrane Levels of Mouse α3β4-Containing Nicotinic Acetylcholine Receptors

Heteromeric α3β4 nicotinic acetylcholine (ACh) receptors (nAChRs) are pentameric ligand-gated cation channels that include at least two α3 and two β4 subunits. They have functions in peripheral tissue and peripheral and central nervous systems. We examined the effects of chronic treatment with menthol, a major flavor additive in tobacco cigarettes and electronic nicotine delivery systems, on mouse α3β4 nAChRs transiently transfected into neuroblastoma-2a cells. Chronic menthol treatment at 500 nM, near the estimated menthol concentration in the brain following cigarette smoking, altered neither the [ACh]-response relationship nor Zn2+ sensitivity of ACh-evoked currents, suggesting that menthol does not change α3β4 nAChR subunit stoichiometry. Chronic menthol treatment failed to change the current density (peak current amplitude/cell capacitance) of 100 μM ACh-evoked currents. Chronic menthol treatment accelerated desensitization of 100 and 200 μM ACh-evoked currents. Chronic nicotine treatment (250 μM) decreased ACh-induced currents, and we found no additional effect of including chronic menthol. These data contrast with previously reported, marked effects of chronic menthol on β2* nAChRs studied in the same expression system. Mechanistically, the data support the emerging interpretation that both chronic menthol and chronic nicotine act on nAChRs in the early exocytotic pathway, and that this pathway does not present a rate-limiting step to the export of α3β4 nAChRs; these nAChRs include endoplasmic reticulum (ER) export motifs but not ER retention motifs. Previous reports show that smoking mentholated cigarettes enhances tobacco addiction; but our results show that this effect is unlikely to arise via menthol actions on α3β4 nAChRs.

An African-specific haplotype in MRGPRX4 is associated with menthol cigarette smoking

An African-specific haplotype in MRGPRX4 is associated with menthol cigarette smoking

Menthol Cigarette Smoke Induces More Severe Lung Inflammation Than Non-menthol Cigarette Smoke Does in Mice With Subchronic Exposure – Role of TRPM8

In smokers with chronic obstructive pulmonary disease, more severe lung inflammation is associated with menthol cigarette smoking compared to non-menthol cigarette smoking. However, the mechanisms remain unclear. Menthol is an activator of transient receptor potential melastatin-8 (TRPM8), which is also sensitive to reactive oxygen species (ROS). Our recent in vitro study demonstrated that the extracts of menthol cigarette smoke (M-CS) can induce greater ROS-sensitive, TRPM8-mediated, mitogen-activated protein kinase (MAPK)-dependent inflammatory responses in lung epithelial cells than the extracts of non-menthol cigarette smoke (Non-M-CS) can. In this study, we tested the hypothesis that M-CS can induce more severe lung inflammation than Non-M-CS can via the additional action of menthol in M-CS on epithelial and lung TRPM8 in mice. Compared with Non-M-CS exposure, subchronic M-CS exposure for 7 days up-regulated the epithelial and lung expression of TRPM8, induced more vigorous activation of epithelial and lung MAPKs, and caused more severe lung inflammation. The MAPK activation was evidenced by the increased expression of phosphor-extracellular signal-regulated and phosphor-c-Jun N-terminal kinases. The lung inflammation was evidenced by pathohistological findings and increases in several inflammatory indices. Moreover, treatment with a TRPM8 antagonist (N-(3-aminopropyl)-2-{[(3-methylphenyl)methyl]oxy}-N-(2-thienylmethyl)benzamide; AMTB) greatly suppressed the MAPK activation and lung inflammation induced by Non-M-CS and M-CS, and the residual responses to these two types of CS did not differ. Conversely, the levels of biomarkers of acute CS exposure (20 min), including carboxyhemoglobin and cotinine (a nicotine metabolite) in blood plasma, and superoxide and hydrogen peroxide (two major types of ROS) in bronchoalveolar lavage fluid, did not show significant differences in the mice with Non-M-CS and M-CS exposure. We concluded that M-CS could induce greater TRPM8-mediated activation of MAPKs and lung inflammation than Non-M-CS could in mice with subchronic exposure. The augmented inflammatory effects of M-CS are unlikely due to a larger total amount of CS inhaled, but may be caused by an additional stimulation of epithelial and lung TRPM8 by menthol in M-CS. A common stimulant (presumably ROS) generated by both CS types may also stimulate TRPM8, activate MAPKs, and induce lung inflammation because treatment with AMTB could reduce these responses to Non-M-CS.

Characterising smokers of menthol and flavoured cigarettes, their attitudes towards tobacco regulation, and the anticipated impact of the Tobacco Products Directive on their smoking and quitting behaviours: The EUREST-PLUS ITC Europe Surveys.

INTRODUCTIONLittle research exists on the sociodemographic characteristics of menthol and flavoured cigarette (MFC) smokers in Europe. This study assessed the proportion of MFC smokers in Europe, their sociodemographic characteristics, and their attitudes towards tobacco control measures.METHODSCross-sectional data were collected in 2016 among 10760 adult current smokers from 8 European countries (ITC Europe Project and EUREST-PLUS). Smokers of menthol, other flavoured, unflavoured tobacco, or no usual brand were compared on sociodemographic characteristics, attitudes towards a range of tobacco control measures (e.g. ban on flavouring), and on intentions regarding their smoking behaviour following the ban on flavoured tobacco. Data were analysed in SPSS Complex Samples Package using univariate analyses.RESULTSAmong the respondents, 7.4% smoked menthol cigarettes and 2.9% other flavoured tobacco, but large differences existed between countries (e.g. 0.4% smokers smoked menthol cigarettes in Spain vs 12.4% in England). Compared to other groups, menthol cigarette smokers were younger, more likely to be female, better educated, had higher household income, and smoked fewer cigarettes (all p<0.001). A quarter of menthol smokers supported a ban on additives, compared with almost half of all other smokers (p<0.001). In case of a ban on flavourings, around a fifth of all MFC smokers intended to switch to another brand, and a third to reduce the amount they smoked or to quit smoking, but there was no consistent pattern across MFC smokers among the countries.CONCLUSIONSThe ban on flavourings introduced by the EU Tobacco Products Directive (extended to 2020 for menthols) will affect one in ten smokers in the countries surveyed, which provides an opportunity for targeting these groups with cessation programmes. However, smokers of menthol and flavoured cigarettes in the different European countries are a heterogeneous group and may need different approaches.

Menthol Cigarettes, Tobacco Dependence, and Smoking Persistence: The Need to Examine Enhanced Cognitive Functioning as a Neuropsychological Mechanism.

Despite the overall decline in the prevalence of cigarette use in the United States, menthol cigarette use among smokers is rising, and evidence shows that it may lead to more detrimental effects on public health than regular cigarette use. One of the mechanisms by which nicotine sustains tobacco use and dependence is due to its cognitive enhancing properties, and basic science literature suggests that menthol may also enhance nicotine's acute effect on cognition. The purpose of this review is to suggest that the cognitive enhancing effects of menthol may be a potentially important neuropsychological mechanism that has yet to be examined. In this narrative review, we provide an overview of basic science studies examining neurobiological and cognitive effects of menthol and menthol cigarette smoking. We also review studies examining menthol essential oils among humans that indicate menthol alone has acute cognitive enhancing properties. Finally, we present factors influencing the rising prevalence of menthol cigarette use among smokers and the importance of this gap in the literature to improve public health and smoking cessation treatment. Despite the compelling evidence for menthol's acute cognitive enhancing and reinforcing effects, this mechanism for sustaining tobacco dependence and cigarette use has yet to be examined and validated among humans. On the basis of the basic science evidence for menthol's neurobiological effects on nicotinic receptors and neurotransmitters, perhaps clarifying menthol's effect on cognitive performance can help to elucidate the complicated literature examining menthol and tobacco dependence. Menthol cigarette use has continued to be a topic of debate among researchers and policy makers, because of its implications for understanding menthol's contribution to nicotine dependence and smoking persistence, as well as its continued use as a prevalent flavoring in tobacco and nicotine products in the United States and internationally. As international tobacco regulation policies have begun to target menthol cigarettes, research studies need to examine how flavoring additives, specifically menthol, may acutely influence neurobiological and cognitive functioning as a potential mechanism of sustained smoking behavior to develop more effective treatments.

Co-occurring vulnerabilities and menthol use in U.S. young adult cigarette smokers: Findings from Wave 1 of the PATH Study, 2013–2014

This study incorporates intersectionality theory to address potential effects of age on other documented risk factors for current smoking and menthol cigarette use in young adults aged 18–34 using Wave 1 of the Population Assessment of Tobacco and Health (PATH) Study (2013–2014). We explored known correlates of current cigarette and menthol cigarette smoking and interaction analyses by age group (18–24 vs. 25–34), accounting for survey weighting. Use of non-cigarette tobacco products and e-cigarettes was characterized among current cigarette smokers. Young adults experience multiple vulnerabilities to smoking beyond age and some of these known risk factors for smoking place those aged 18–24 at different risk of cigarette smoking compared to their 25–34 year old counterparts. These include lower odds of cigarette smoking by age for sex (female; AOR = 0.62 in those aged 18–24 vs. 0.72 in those aged 25–34) and Hispanic ethnicity (vs. White; AOR = 0.77 vs. 0.45), and higher odds of smoking among past 30-day alcohol users aged 18–24 vs. 25–34 (AOR = 1.62 vs. 1.32). Correlations between lower education and smoking were nearly two-fold higher in 25–34 than 18–24 year olds. Having any medical comorbidity had opposite effects on current smoking by age (18–24 positive correlation, AOR = 1.17; 25–34 negative correlation, AOR = 0.84). Lower education was correlated with menthol cigarette use among young adult smokers. This study suggests that higher smoking prevalence among young adults is associated with the intersection of multiple vulnerabilities to smoking.

Metadata Correction: Mobile Phone Ownership Is Not a Serious Barrier to Participation in Studies: Descriptive Study

[This corrects the article DOI: 10.2196/mhealth.8123.].

Abstract P102: Menthol Cigarette Use and Subclinical Cardiovascular Disease in African Americans in the Jackson Heart Study

Background: African Americans smoke menthol cigarettes at higher rates than other races and have a disproportionate burden of cardiovascular disease (CVD). Whereas smoking is a well described risk factor for CVD, it is unclear if menthol cigarettes are associated with more or less risk. Therefore, our aim was to evaluate the association between menthol cigarette use and subclinical atherosclerosis in the Jackson Heart Study (JHS). Methods: JHS participants (n=5,301) were classified by self-reported smoking status as current, past (smoked ≥400 cigarettes/life), or never smokers at Visit 1 (V1, 2000-2004). Menthol cigarette use data were captured at Visit 3 (V3, 2009-2013). We used multivariable logistic and robust linear regression models to examine the associations between cigarette type and measures of subclinical atherosclerosis [carotid intimal medial thickness (CIMT, Visit 1) and coronary artery calcium (CAC) or aorto-iliac calcium (AIC) by computed tomography (Visit 2, V2, 2005-2008)] to estimate β-coefficients (adjusted differences) comparing menthol to non-menthol (reference group) smoking. Results: There were 401 current smokers with available data on cigarette preference including 326 menthol (81%) and 75 non-menthol (19%) smokers at V3. Menthol cigarette preference in current smokers was not associated with significant differences in measures of subclinical atherosclerosis: CIMT (β -0.003, 95% CI -0.053, 0.046, p=0.90); CAC (β -0.20, 95% CI -1.09, 0.69, p=0.66) or AIC (β -0.32, 95% CI -1.23, 0.59, p=0.48). Conclusion: Our study provides no evidence for an association of menthol cigarette use with subclinical atherosclerosis in African Americans. These findings warrant replication by studies that address the limitations of this study, including the assumption that menthol smokers in V3 were long-term menthol smokers before V1 and V2, potential selection by exclusions of deaths related to smoking and CVD among participants at V3 and lack of longitudinal data on outcomes after the collection of menthol use data at V3.

Mobile Phone Ownership Is Not a Serious Barrier to Participation in Studies: Descriptive Study.

BackgroundRather than providing participants with study-specific data collection devices, their personal mobile phones are increasingly being used as a means for collecting geolocation and ecological momentary assessment (EMA) data in public health research.ObjectiveThe purpose of this study was to (1) describe the sociodemographic characteristics of respondents to an online survey screener assessing eligibility to participate in a mixed methods study collecting geolocation and EMA data via the participants’ personal mobile phones, and (2) examine how eligibility criteria requiring mobile phone ownership and an unlimited text messaging plan affected participant inclusion.MethodsAdult (≥18 years) daily smokers were recruited via public advertisements, free weekly newspapers, printed flyers, and word of mouth. An online survey screener was used as the initial method of determining eligibility for study participation. The survey screened for twenty-eight inclusion criteria grouped into three categories, which included (1) cell phone use, (2) tobacco use, and (3) additional criteriaResultsA total of 1003 individuals completed the online screener. Respondents were predominantly African American (605/1003, 60.3%) (60.4%), male (514/1003, 51.3%), and had a median age of 35 years (IQR 26-50). Nearly 50% (496/1003, 49.5%) were unemployed. Most smoked menthol cigarettes (699/1003, 69.7%), and had a median smoking history of 11 years (IQR 5-21). The majority owned a mobile phone (739/1003, 73.7%), could install apps (86.8%), used their mobile phone daily (89.5%), and had an unlimited text messaging plan (871/1003, 86.8%). Of those who completed the online screener, 302 were eligible to participate in the study; 163 were eligible after rescreening, and 117 were enrolled in the study. Compared to employed individuals, a significantly greater proportion of those who were unemployed were ineligible for the study based on mobile phone inclusion criteria (P<.001); yet, 46.4% (333/717) of the individuals who were unemployed met all mobile phone inclusion criteria.ConclusionsInclusion criteria requiring participants to use their personal mobile phones for data collection was not a major barrier to study participation for most respondents who completed the online screener, including those who were unemployed.Trial RegistrationClinicalTrials.gov NCT02261363; https://clinicaltrials.gov/ct2/show/NCT02261363 (Archived by WebCite at http://www.webcitation.org/6wOmDluSt)

Menthol cigarette smoking among individuals in treatment for substance use disorders

There are higher rates of menthol cigarette smoking within certain population subgroups. Limited research has examined menthol use among individuals in treatment for substance use disorders (SUD), a population with a high prevalence of cigarette smoking, poor smoking cessation outcomes, and high tobacco disease burden. Survey data were collected from 863 smokers sampled from 24 SUD treatment programs affiliated with the NIDA Clinical Trials Network (CTN) in the United States. Prevalence of menthol cigarette smoking was examined for the sample. Bivariate and multivariate analyses were used to examine demographic and tobacco use characteristics associated with menthol cigarette smoking. Overall, the prevalence of menthol smoking among individuals in SUD treatment was 53.3%. Smoking menthol versus non-menthol cigarettes was associated with being female (AOR=1.61, p=0.003), African American (AOR=7.89, p<0.001), Hispanic/Latino (AOR=3.39, p<0.001), and lower odds of having a college degree (AOR=0.49, p=0.015). Controlling for demographic factors, menthol smokers were more likely to report marijuana (AOR=3.33, p<0.007) as their primary drug compared to alcohol. Lastly, menthol smokers were more likely to report interest in getting help for quitting smoking (AOR=1.53, p=0.01), although they were not more likely to report making a past year quit attempt. In conclusion, use of menthol cigarettes was higher among smokers in SUD treatment than in general population smokers. Regulatory policies targeting the manufacture, marketing, or sale of menthol cigarettes may benefit vulnerable populations, including smokers in SUD treatment.

Accuracy of the Smoking Questionnaire

Summary The smoking questionnaire (SQ), a multidimensional questionnaire covering the major dimensions of cigarette smoking, was developed to address the heterogeneity in the assessment of smoking exposure. It consists of eight questions and can be completed within a few minutes. Test-retest reliability of the SQ and concurrent validity with the Behavior Risk Factor Surveillance System (BRFSS) 2011 questionnaire were examined in a clinical study conducted in adult US current menthol cigarette smokers. The SQ and the BRFSS were self-administrated twice before and after randomization with a 6-day interval. The inter-temporal analyses included current smokers aged 22 to 66 years who completed the SQ at both timepoints. The percent agreement of items and 95% confidence intervals were calculated for the comparisons between the two timepoints and between the SQ and the BRFSS questionnaire. To evaluate the feasibility of the SQ and to capture subjects’ opinions about the SQ, a meta-questionnaire was administrated. High test-retest reliability levels (percent agreement of &gt; 70 to 100% between the two timepoints) were found for SQ smoking behavior items, in particular for items related to current smoking status, 100-cigarettes lifetime, regular smoking, age of initiation and preferred brand. Moderate (55% agreement) to high test-retest reliability (84% agreement) was found for daily consumption of manufactured cigarettes. The comparison between the SQ and the BRFSS 2011 showed a high concurrent validity (98 to 100% agreement). The SQ was completed on average in 3 to 4 min and was assessed as easy to use. The findings demonstrate that the SQ is reliable in smokers and a practical tool to assess smoking exposure in clinical studies.