Acute and Chronic Effects of Cigarette Smoking on sRAGE.
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ABSTRACT:
SUBMITTER: Biswas SK
PROVIDER: S-EPMC6423098 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC6423096 | biostudies-literature
Project description:Electronic cigarettes (ECs) and tobacco cigarettes (TCs) both release nicotine, a sympathomimetic drug. We hypothesized that baseline heart rate variability (HRV) and hemodynamics would be similar in chronic EC and TC smokers and that after acute EC use, changes in HRV and hemodynamics would be attributable to nicotine, not non-nicotine, constituents in EC aerosol. In 100 smokers, including 58 chronic EC users and 42 TC smokers, baseline HRV and hemodynamics [blood pressure (BP) and heart rate (HR)] were compared. To isolate the acute effects of nicotine vs. non-nicotine constituents in EC aerosol, we compared changes in HRV, BP, and HR in EC users after using an EC with nicotine (ECN), EC without nicotine (EC0), nicotine inhaler (NI), or sham vaping (control). Outcomes were also compared with TC smokers after smoking one TC. Baseline HRV and hemodynamics were not different in chronic EC users and TC smokers. In EC users, BP and HR, but not HRV outcomes, increased only after using the ECN, consistent with a nicotine effect on BP and HR. Similarly, in TC smokers, BP and HR but not HRV outcomes increased after smoking one TC. Despite a similar increase in nicotine, the hemodynamic increases were significantly greater after TC smokers smoked one TC compared with the increases after EC users used the ECN. In conclusion, chronic EC and TC smokers exhibit a similar pattern of baseline HRV. Acute increases in BP and HR in EC users are attributable to nicotine, not non-nicotine, constituents in EC aerosol. The greater acute pressor effects after TC compared with ECN may be attributable to non-nicotine, combusted constituents in TC smoke.NEW & NOTEWORTHY Chronic electronic cigarette (EC) users and tobacco cigarette (TC) smokers exhibit a similar level of sympathetic nerve activity as estimated by heart rate variability. Acute increases in blood pressure (BP) and heart rate in EC users are attribute to nicotine, not non-nicotine, constituents in EC aerosol. Acute TC smoking increased BP significantly more than acute EC use, despite similar increases in plasma nicotine, suggestive of additional adverse vascular effects attributable to combusted, non-nicotine constituents in TC smoke.
| S-EPMC7473924 | biostudies-literature
Project description:Introduction and aimsImpulsivity may be a risk factor that increases vulnerability to nicotine dependence. However, nicotine exposure itself may directly increase impulsivity. This is a secondary analysis of the first study in a controlled laboratory setting, which assessed the effects of nicotine administration (acute and repeated) and exposure to smoking cues on behavioural impulsivity in humans (ClinicalTrials.gov Identifier: NCT01395797).Design and methodsTwenty-seven smokers completed three tasks to assess behavioural impulsivity (the Immediate Memory Task and the Delayed Memory Task assessing response initiation, and the GoStop Task assessing response inhibition) following: (i) 4 days of cigarette smoking (nicotinised or denicotinised cigarette); (ii) acute cigarette smoking (nicotinised); and (iii) exposure to smoking-related cues.ResultsFour days of nicotinised cigarette smoking (vs. denicotinised) did not significantly increase Immediate Memory Task, Delayed Memory Task and GoStop scores. However, acute cigarette smoking increased GoStop impulsivity, but only following 4 days of smoking nicotinised cigarettes (P < 0.05). Exposure to smoking-related cues had no statistically significant effect on impulsivity.Discussion and conclusionsOur results suggest that repeated nicotine exposure may sensitise subsequent acute nicotine effects on behavioural impulsivity in heavy smokers.
| S-EPMC8088442 | biostudies-literature
Project description:BackgroundChronic smoking is the main risk factor for chronic obstructive pulmonary disease. Knowledge on the response to the initial smoke exposures might enhance the understanding of changes due to chronic smoking, since repetitive acute smoke effects may cumulate and lead to irreversible lung damage.MethodsWe investigated acute effects of smoking on inflammation in 16 healthy intermittent smokers in an open randomised cross-over study. We compared effects of smoking of two cigarettes on inflammatory markers in exhaled air, induced sputum, blood and urine at 0, 1, 3, 6, 12, 24, 48, 96 and 192 hours and outcomes without smoking. All sputum and blood parameters were log transformed and analysed using a linear mixed effect model.ResultsSignificant findings were: Smoking increased exhaled carbon monoxide between 0 and 1 hour, and induced a greater decrease in blood eosinophils and sputum lymphocytes between 0 and 3 hours compared to non-smoking. Compared to non-smoking, smoking induced a greater interleukin-8 release from stimulated blood cells between 0 and 3 hours, and a greater increase in sputum lymphocytes and neutrophils between 3 and 12 hours.ConclusionWe conclude that besides an increase in inflammation, as known from chronic smoking, there is also a suppressive effect of smoking two cigarettes on particular inflammatory parameters.
| S-EPMC554761 | biostudies-literature
Project description:The study objectives were to examine smoking abstinence and reinstatement effects on subjective experience and cognitive performance among adolescent smokers.Adolescents (aged 14-17 years, 60 daily smokers and 32 nonsmokers) participated. Participants completed baseline assessments (Session 1) and returned to the laboratory 1-3 days later to repeat assessments (Session 2); half of the smokers were randomly assigned to 15-17 hr tobacco abstinence preceding Session 2.During Session 2, abstaining smokers reported significantly greater increases in withdrawal symptoms, smoking urges, and negative affect compared with smokers who did not abstain and compared with nonsmokers. Smoking reinstatement reversed abstinence effects, returning to baseline levels for smoking urges and negative affect. Abstaining smokers showed significantly enhanced cognitive performance on two of six tasks (two-letter search compared with nonabstaining smokers; serial reaction time compared with nonsmokers); smoking reinstatement resulted in significant decrements on these two tasks relative to nonabstaining smokers.Effects of smoking abstinence and reinstatement on self-report measures are consistent with earlier research with adolescent as well as adult smokers and may help to elucidate the motivational underpinnings of smoking maintenance among adolescent smokers. Effects found on cognitive performance were contrary to hypotheses; further research is needed to understand better the role of cognitive performance effects in smoking maintenance among adolescents.
| S-EPMC2902909 | biostudies-other
Project description:ObjectiveTo determine if the declining trend in U.S. youth cigarette smoking changed after e-cigarettes were introduced, and if youth e-cigarette users would have been likely to smoke cigarettes based on psychosocial and demographic predictors of smoking.MethodsAn interrupted time series analysis was used for cross-sectional data from the 2004 to 2018 National Youth Tobacco Surveys (NYTS) to assess changes in cigarette and e-cigarette use over time. A multivariable logistic regression model used 2004-2009 NYTS data on psychosocial risk factors to predict individual-level cigarette smoking risk from 2011 to 2018. Model-predicted and actual cigarette smoking behavior were compared.ResultsThe decline in current cigarette smoking slowed in 2014 (-0.75 [95% CI: -0.81, -0.68] to -0.26 [95% CI: -0.40, -0.12] percentage points per year). The decline in ever cigarette smoking accelerated after 2012 (-1.45 [95% CI: -1.59, -1.31] to -1.71 [95% CI: -1.75, -1.66]). Ever and current combined cigarette and/or e-cigarette use declined during 2011-2013 and increased during 2013-2014 with no significant change during 2014-2018 for either variable. The psychosocial model estimated that 69.0% of current cigarette smokers and 9.3% of current e-cigarette users (who did not smoke cigarettes) would smoke cigarettes in 2018.ConclusionsThe introduction of e-cigarettes was followed by a slowing decline in current cigarette smoking, a stall in combined cigarette and e-cigarette use, and an accelerated decline in ever cigarette smoking. Traditional psychosocial risk factors for cigarette smoking suggest that e-cigarette users do not fit the traditional risk profile of cigarette smokers.
| S-EPMC7796895 | biostudies-literature
Project description:Given the lack of consensus regarding changes in temporal and probability discounting as a function of smoking abstinence in cigarette smokers, the present study comprehensively examined possible changes in these processes following a period of acute smoking abstinence consistent with elevated withdrawal symptoms and craving.Computerized temporal and probability discounting assessments were collected from cigarette smokers following normal smoking and 24-hr smoking abstinence, with the order of normal smoking and abstinence sessions counterbalanced across participants. Other conditions included commodity (money and cigarettes), sign (gains and losses), and magnitude ($50 and $1,000).Twenty four-hour smoking abstinence resulted in a reduction in expired carbon monoxide to near-zero levels and increases in withdrawal and craving. Examination of discounting parameters as a function of smoking abstinence revealed a general pattern of increase in the temporal discounting of monetary gains and losses following abstinence but not in the temporal discounting of cigarettes nor probability discounting of money or cigarettes. Pearson correlations also revealed an expected pattern of significant relationships.The present study is a comprehensive examination of temporal and probability discounting following smoking abstinence and reveals a generalized change in intertemporal decision making for monetary rewards.
| S-EPMC3337536 | biostudies-other
Project description:Increasing age and chronic cigarette smoking are independently associated with adverse effects on multiple aspects of neurocognition in those seeking treatment for alcohol use disorders. However, the potential interactive effects of age and cigarette smoking on neurocognition in early abstinent alcohol-dependent individuals (ALC) have not investigated.Cross-sectional performances of never-smoking healthy comparison participants (nvsCOM; n = 39) and 1-month-abstinent, treatment-seeking, never-smoking (nvsALC; n = 30), former-smoking (fsALC; n = 21), and actively smoking (asALC; n = 68) ALC were compared on a comprehensive neurocognitive battery. Domains of functioning evaluated were cognitive efficiency, executive functions, fine motor skills, general intelligence, learning and memory, processing speed, visuospatial functions and working memory. Participants were between 26 and 71 years of age at the time of assessment.asALC showed steeper age-related effects than nvsCOM on the domains of visuospatial learning, auditory-verbal memory, cognitive efficiency, executive functions, processing speed, and fine motor skills. In pairwise comparisons, fsALC and asALC performed more poorly than both nvsCOM and nvsALC on multiple domains; nvsCOM and nvsALC showed no significant differences. Domain scores for the ALC groups generally fell in the low-to-high-average range of functioning. A clinically significant level of impairment was apparent in only 25% of ALC participants on visuospatial learning, visuospatial memory, and fine motor skills domains. Measures of alcohol use or consumption were not significantly related to neurocognition in the ALC cohorts.The age-related findings suggest that the combination of active chronic smoking and alcohol dependence in this 1-month-abstinent ALC cohort was associated with greater than normal age-related effects in multiple domains. In general, a low level of clinically significant impairment was observed in the alcohol-dependent participants. The findings from this study, in conjunction with previous research, strongly support smoking cessation interventions for those seeking treatment for alcohol and substance use disorders.
| S-EPMC3749254 | biostudies-literature
Project description:ObjectiveWe examined if chronic cannabis smoking is associated with hepatic steatosis, insulin resistance, reduced β-cell function, or dyslipidemia in healthy individuals.Research design and methodsIn a cross-sectional, case-control study, we studied cannabis smokers (n = 30; women, 12; men, 18; 27 ± 8 years) and control subjects (n = 30) matched for age, sex, ethnicity, and BMI (27 ± 6). Abdominal fat depots and intrahepatic fat content were quantified by magnetic resonance imaging and proton magnetic resonance spectroscopy, respectively. Insulin-sensitivity indices and various aspects of β-cell function were derived from oral glucose tolerance tests (OGTT).ResultsSelf-reported cannabis use was: 9.5 (2-38) years; joints/day: 6 (3-30) [median (range)]. Carbohydrate intake and percent calories from carbohydrates, but not total energy intake, were significantly higher in cannabis smokers. There were no group differences in percent total body fat, or hepatic fat, but cannabis smokers had a higher percent abdominal visceral fat (18 ± 9 vs. 12 ± 5%; P = 0.004). Cannabis smokers had lower plasma HDL cholesterol (49 ± 14 vs. 55 ± 13 mg/dL; P = 0.02), but fasting levels of glucose, insulin, total cholesterol, LDL cholesterol, triglycerides, or free fatty acids (FFA) were not different. Adipocyte insulin resistance index and percent FFA suppression during an OGTT was lower (P < 0.05) in cannabis smokers. However, oral glucose insulin sensitivity index, measures of β-cell function, or incretin concentrations did not differ between the groups.ConclusionsChronic cannabis smoking was associated with visceral adiposity and adipose tissue insulin resistance but not with hepatic steatosis, insulin insensitivity, impaired pancreatic β-cell function, or glucose intolerance.
| S-EPMC3714514 | biostudies-literature
Project description:RationaleCigarette smoking has been demonstrated in laboratory studies to have effects on lung epithelial and endothelial function similar to those observed in acute lung injury (ALI). However, the association between active and passive cigarette smoke exposure and susceptibility to ALI has not been prospectively studied.ObjectivesWe hypothesized that both active and passive cigarette smoke exposure would be associated with increased susceptibility to ALI after severe blunt trauma.MethodsWe measured levels of cotinine, a metabolite of nicotine and validated biomarker of tobacco use, in plasma samples obtained immediately on arrival at the emergency department from 144 adult subjects after severe blunt trauma. Patients were then followed for the development of ALI.Measurements and main resultsIncreasing quartiles of plasma cotinine were associated with the development of ALI (odds ratio [OR] for developing ALI in highest cotinine quartile, 3.25; 95% confidence interval [CI], 1.22-8.68; P = 0.017 for trend across quartiles). Moderate to heavy passive smoke exposure was associated with nearly the same odds of developing ALI as active smoking (OR for moderate to heavy passive smoking compared with no exposure or low level exposure, 3.03; 95% CI, 1.15-8.04; OR for active smoking, 2.77; 95% CI, 1.28-5.99). This association persisted after adjusting for other predictors of ALI, including Injury Severity Score and alcohol abuse.ConclusionsBoth moderate to heavy passive smoking and active smoking are independently associated with the development of ALI after severe blunt trauma. This finding has important implications both for public health and for understanding the pathogenesis of ALI.
| S-EPMC3136993 | biostudies-literature