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Hostility and cigarette use: a comparison between smokers and nonsmokers in a matched sample of adolescents.

ABSTRACT: INTRODUCTION:We examined the association between hostility-a personality trait reflective of negativity and cynicism toward others-and smoking in adolescents by measuring (a) several subcomponents of hostility, and (b) facial emotion processing ability, which has been previously linked to hostility. METHODS:Participants (N = 241 aged 14-19) were 95 smokers and 95 demographically matched nonsmokers as well as 51 nonmatched smokers. All participants completed the Cook-Medley (C-M) hostility scale, which provides a general hostility score and 3 component scores (cynicism, hypersensitivity, and aggressive responding), and a facial emotion processing task. This task, designed to assess emotion recognition, requires quickly identifying the emotion of faces that gradually morph from neutral to high-intensity happy, angry, or fearful. RESULTS:Independent sample t tests indicated that matched smokers scored significantly higher in cynicism and aggressive responding than nonsmokers. Among smokers, age of smoking onset was negatively correlated with general hostility and aggressive responding. All hostility scales were positively correlated with the intensity needed to recognize happy faces. Counterintuitively, smokers required a greater intensity to recognize angry faces than nonsmokers. No other relations between hostility/smoking status and facial emotion processing were observed. CONCLUSIONS:Aspects of hostility, particularly aggressive responding, may be a risk factor for early onset smoking. Although hostile participants exhibited a deficiency in their ability to recognize happiness in facial pictures, these results did not translate to differences in smoking status. This study elucidates some of the complex interrelations between hostility, emotion processing, and adolescent smoking, which may have implications for teen smoking prevention.

SUBMITTER: Bernstein MH

PROVIDER: S-EPMC4155423 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature

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Hostility and cigarette use: a comparison between smokers and nonsmokers in a matched sample of adolescents.

Bernstein Michael H MH Colby Suzanne M SM Bidwell L Cinnamon LC Kahler Christopher W CW Leventhal Adam M AM

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco 20140401 8

<h4>Introduction</h4>We examined the association between hostility-a personality trait reflective of negativity and cynicism toward others-and smoking in adolescents by measuring (a) several subcomponents of hostility, and (b) facial emotion processing ability, which has been previously linked to hostility.<h4>Methods</h4>Participants (N = 241 aged 14-19) were 95 smokers and 95 demographically matched nonsmokers as well as 51 nonmatched smokers. All participants completed the Cook-Medley (C-M) h ...[more]

PMID: 24692670

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Project description:BackgroundNicotine-containing electronic cigarette (e-cig) use has become widespread. However, understanding the biological impact of e-cigs compared with smoking on the lung is needed. There are major gaps in knowledge for chronic effects and for an etiology to recent acute lung toxicity leading to death among vapers.MethodsWe conducted bronchoscopies in a cross-sectional study of 73 subjects (42 never-smokers, 15 e-cig users, and 16 smokers). Using bronchoalveolar lavage and brushings, we examined lung inflammation by cell counts, cytokines, genome-wide gene expression, and DNA methylation.ResultsThere were statistically significant differences among never-smokers, e-cig users, and smokers for inflammatory cell counts and cytokines (FDR q < 0.1). The e-cig users had values intermediate between smokers and never-smokers, with levels for most of the biomarkers more similar to never-smokers. For differential gene expression and DNA methylation, e-cig users also more like never-smokers; many of these genes corresponded to smoking-related pathways, including those for xenobiotic metabolism, aryl hydrocarbon receptor signaling, and oxidative stress. Differentially methylated genes were correlated with changes in gene expression, providing evidence for biological effects of the methylation associations.ConclusionsThese data indicate that e-cigs are associated with less toxicity than cigarettes for smoking-related pathways. What is unknown may be unique effects for e-cigs not measured herein, and a comparison of smokers completely switching to e-cigs compared with former smokers. Clinical trials for smokers switching to e-cigs who undergo serial bronchoscopy and larger cross-sectional studies of former smokers with and without e-cig use, and for e-cigs who relapse back to smoking, are needed.ImpactThese data can be used for product regulation and for informing tobacco users considering or using e-cigs. What is unknown may be unique effects for e-cigs not measured herein, and clinical trials with serial bronchoscopy underway can demonstrate a direct relationship for changes in lung biomarkers.

Project description:IntroductionThe severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for the COVID-19 pandemic, gains entry into the host cell when its Spike protein is cleaved by host proteases TMPRSS2 and furin, thereby markedly increasing viral affinity for its receptor, angiotensin-converting enzyme-2 (ACE2). In rodent and diseased human lungs, tobacco cigarette (TCIG) smoke increases ACE2, but the effect of electronic cigarette vaping (ECIG) is unknown. It is unknown whether nicotine (in both TCIGs and ECIGs) or non-nicotine constituents unique to TCIG smoke increase expression of key proteins in COVID-19 pathogenesis.MethodsImmune (CD45+) cells collected before the pandemic in otherwise healthy young people, including TCIG smokers (n = 9), ECIG vapers (n = 12), or nonsmokers (NS) (n = 12), were studied. Using flow cytometry, expression of key proteins in COVID-19 pathogenesis were compared among these groups.ResultsTCIG smokers and ECIG vapers had similar smoking or vaping burdens as indicated by similar plasma cotinine levels. TCIG smokers compared with NS had a significantly increased percentage of cells that were positive for ACE2 (10-fold, p < .001), TMPRSS2 (5-fold, p < .001), and ADAM17 (2.5-fold, p < .001). Additionally, the mean fluorescence intensity (MFI) consistently showed greater mean ACE2 (2.2-fold, p < .001), TMPRSS2 (1.5-fold, p < .001), furin (1.1-fold, p < .05), and ADAM17 (2-fold, p < .001) in TCIG smokers compared with NS. In ECIG vapers, furin MFI was increased (1.15-fold, p < .05) and TMPRSS2 MFI tended to be increased (1.1-fold, p = .077) compared with NS.ConclusionsThe finding that key instigators of COVID-19 infection are lower in ECIG vapers compared with TCIG smokers is intriguing and warrants additional investigation to determine if switching to ECIGs is an effective harm reduction strategy. However, the trend toward increased proteases in ECIG vapers remains concerning.Implications(1) This is the first human study to report a marked increase in proteins critical for COVID-19 infection, including ACE2, TMPRSS2, and ADAM17, in immune cells from healthy tobacco cigarette smokers without lung disease compared with e-cigarette vapers and nonsmokers. (2) These findings warrant additional investigation to determine whether switching to electronic cigarettes may be an effective harm reduction strategy in smokers addicted to nicotine who are unable or unwilling to quit. (3) The increase in proteases in electronic cigarette vapers remains concerning.

Project description:PurposeCigarette smoking is an independent risk factor for coronary heart disease and is associated with impaired postprandial metabolism. Acute exercise reduces postprandial lipemia and improves other coronary heart disease risk markers in nonsmokers. Less is known about responses in cigarette smokers.MethodsTwelve male cigarette smokers (mean ± SD; age = 23 ± 4 yr, body mass index = 24.9 ± 3.0 kg·m-2) and 12 male nonsmokers (age = 24 ± 4 yr, body mass index = 24.1 ± 2.0 kg·m-2) completed two, 2-d conditions (control and exercise) in a randomized crossover design. On day 1, participants rested for 9 h (0800-1700) in both conditions except a 60-min treadmill run (65% ± 7% peak oxygen uptake, 2.87 ± 0.54 MJ) was completed between 6.5 and 7.5 h (1430-1530) in the exercise condition. On day 2 of both conditions, participants rested and consumed two high-fat meals over 8 h (0900-1700) during which 13 venous blood samples and nine resting arterial blood pressure measurements were collected.ResultsSmokers exhibited higher postprandial triacylglycerol and C-reactive protein than nonsmokers (main effect group effect size [Cohen's d] ≥ 0.94, P ≤ 0.034). Previous day running reduced postprandial triacylglycerol, insulin, and systolic and diastolic blood pressure (main effect condition d ≥ 0.28, P ≤ 0.044) and elevated postprandial nonesterified fatty acid and C-reactive protein (main effect condition d ≥ 0.41, P ≤ 0.044). Group-condition interactions were not apparent for any outcome across the total postprandial period (0-8 h; all P ≥ 0.089), but the exercise-induced reduction in postprandial triacylglycerol in the early postprandial period (0-4 h) was greater in nonsmokers than smokers (-21%, d = 0.43, vs -5%, d = 0.16, respectively; group-condition interaction P = 0.061).ConclusionsAcute moderate-intensity running reduced postprandial triacylglycerol, insulin, and resting arterial blood pressure the day after exercise in male cigarette smokers and nonsmokers. These findings highlight the ability of acute exercise to augment the postprandial metabolic health of cigarette smokers and nonsmokers.

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Hostility and cigarette use: a comparison between smokers and nonsmokers in a matched sample of adolescents.

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Hostility and cigarette use: a comparison between smokers and nonsmokers in a matched sample of adolescents.

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