View clinical trials related to Cigarette Smoking.
Filter by:Ventilation heterogeneity is a hallmark feature of most obstructive pulmonary diseases. In particular, chronic obstructive pulmonary disease (COPD) is pathologically and physiologically characterized by small airway destruction and marked airway cellular inflammation, which result in prominent expiratory airflow limitation, air trapping, hyperinflation and abnormal gas exchange. COPD is strongly linked with the exposition to inhaled irritants, most notably tobacco smoke, and is as such a potentially preventable disease. COPD-related morbidity, mortality and social costs are high: in Canada, COPD is the main cause of hospital admission among all chronic diseases and is the fourth leading cause of death. Diagnosis of COPD requires the objective demonstration of expiratory airflow limitation using spirometry. In the right clinical context, a post-bronchodilator forced vital capacity (FVC) / forced expiratory volume in 1 second (FEV1) ratio <0.70 is considered indicative of the presence of COPD, and therefore pulmonary function testing is required to make the diagnosis. However, the natural history of COPD represents a slowly-progressive continuum: active smokers that do not meet the criteria for COPD are still at risk of developing the disease. In fact, when compared to healthy non-smokers, active smokers without overt COPD can already show some pathological and clinical features of the disease. Notably, they report increased levels of resting dyspnea, chronic cough, lower exercise capacity, exercise-induced dynamic hyperinflation and marked airway inflammatory cellular infiltration, while conserving normal pulmonary function test values. These findings highlight the negative, clinically-measurable effects of tobacco smoking on pulmonary function, but also the limitations of standard pulmonary function testing in identifying the presence of early, mild airway disease and quantifying physiological limitations in these subjects. As such, there is a need for a novel, simple and reliable method of quantifying airway disease in this population. Quantitative lung ventilation single-photon emission computed tomography (SPECT) allows an objective quantification of the regional heterogeneity of ventilation in humans. The coefficient of variation (CV) of the distribution of a radioactive tracer, inhaled during the test, allows the generation of heterogeneity maps and density curves of small elements of the lung. These variables are sensitive to the presence of COPD, asthma, air trapping and are correlated to even slight anomalies in pulmonary function testing in otherwise healthy subjects. As such, SPECT could prove useful as an early marker of airway disease in active smokers at risk of developing COPD, but its use in this context has never been formally tested. This pilot study addresses the question of whether lung SPECT could provide clinically relevant information on airway disease in active smokers without overt lung disease on pulmonary lung function testing.
The objective of this study is to determine whether treatment with random nicotine delivery via a nicotine film both before and after the target quit date will facilitate smoking cessation relative to treatment with steady state delivery or placebo. The investigators hypothesize that smoking cessation will be greater in subjects assigned to a random nicotine delivery regimen (as compared to those assigned to a steady state or placebo regimen). The nicotine film product is not part of the standard of care and is not available in non-investigational settings in the United States.
In this study, 21 non-treatment-seeking cigarette smokers were recruited to investigate the effects of acute stress on brain function and nicotine seeking/self-administration behavior.
In this study, participants will complete a behavioral economics laboratory task and validation field assessments to understand how menthol cigarette policy restrictions may affect tobacco product purchasing and use.
One population of tobacco users that is severely affected by the consequences of smoking is people living with HIV (PLWH). Between 40-84% of PLWH smoke, a percentage that has remained constant since the first studies of smoking in HIV were conducted in the 1990's. Overall, smoking related morbidity and mortality is also greatly increased among PLWH smokers. Compared with PLWH nonsmokers, PLWH who smoke have more than 5 times the risk of non-HIV-related mortality and almost 4 times the risk of all-cause mortality. Compared with the general population, incidence ratio of smoking related cancers (eg, lung, head, neck, bladder and esophageal) is more than 5 times higher. At a critical time when advances in HIV care are providing an opportunity for prolonged life, smoking is significantly impeding the health of PLWH. To produce meaningful changes in smoking, however, treatment will have to be acceptable and engaging to this population as well as feasible and sustainable to implement in a busy clinic. Novel technology-based interventions that incorporate evidence-based behavioral and pharmacologic interventions for smoking and are culturally tailored offer real solutions to these implementation barriers. Research shows that internet- or computer-delivered interventions (CDI) that are tailored and interactive can be efficacious in reducing smoking and are significantly more effective than usual care or written self-help materials. CDIs can also be readily adapted to different sociodemographic characteristics of a patient population because content is modular and menu driven. Moreover, technology-based interventions appear as effective as counselor-delivered interventions in reducing smoking. This growing body of evidence strongly suggests that these interventions offer promise in reducing smoking, the potential to reach significantly more patients, and the ability to overcome barriers of cost, implementation, and cultural nonspecificity. The goal of this pilot study is test to examine feasibility, acceptability of a computer-delivered smoking cessation intervention for PLWH, and to determine if intervention participation results in increased readiness to quit smoking and increased confidence in ability to quit smoking.
Rationale: The World Health Organization Framework Convention on Tobacco Control (WHO FCTC) aims for a regulatory strategy including the regulation of the contents of tobacco products (Article 9). Cigarette smoke includes more than 7000 chemicals which are harmful and cause tobacco-related diseases. In the future, regulation of these harmful cigarette constituents should be based on more chemical classes, as the WHO suggested. However, in order to introduce such class-based regulation, a scientific base is needed to define upper limits of allowed amounts of chemicals (groups) in cigarette smoke emissions and to ensure decreased harmful health effects due to cigarette smoking. To date, the causality between human exposure to specific cigarette smoke compounds and the harmful effects is unknown. The first step in closing the gap in knowledge between cigarette smoke exposure and developing tobacco-related diseases includes a proper determination of human exposure to cigarette smoke chemicals. This includes measuring smoking topography and inhalation. Smoking topography is how the smoker smokes the cigarette (puff volume, duration, flow etc). The goal is to link smoking behavior to smoke exposure, for 2 different cigarette brands. The participants will smoke their 'normal' brand Marlboro (experimental day 1) after which they receive the low TNCO (tar, nicotine and carbon monoxide) Marlboro Prime to smoke at home. A week later the experimental day (day 2) is repeated with this cigarette. On the last experimental day (day 3), the participants will smoke the Prime cigarette while the ventilation holes of this low-TNCO cigarette are taped. Afterwards, the personal smoking profiles of the participants, and thus their individual exposures, will be mimicked in the lab using machine smoking. The observed smoking topography and inhalation parameters together give information about the exposure to smoke toxicants. In addition, this study is also designed to measure biomarkers of exposure in body fluids of smokers, such as nicotine and the most abundant cigarette smoke chemicals and their metabolites. Objective: We want to find out whether the individual habitudinal smoking topography of a smoker smoking his usual brand, and the changes between cigarettes over the day, can be compared to that of smoking a low-TNCO or high nicotine cigarette (i.e. the Marlboro Prime and Red Sun). In addition, differences in inhalation patterns are investigated. Next to that, the exposure will be connected to the nicotine and carbon monoxide levels in blood and/or urine. Also smoke toxicants (and metabolites) in exhaled air, saliva, urine and blood of smokers are determined. Study design: This prospective observational study monitors smokers in their habitudinal smoking during the day (for 10 hr) while smoking Marlboro, Marlboro Prime and Marlboro Prime taped cigarette, while during the day bodily fluids are sampled at several time points. Study population: This population consists of 18 Caucasian, healthy, adult males, aged between 25-34 years old. Participants should be used to smoke Marlboro (red/regular) for at least 3 years with a daily average of 13 to 25 cigarettes (about a package every day). Nature and extent of the burden and risks associated with participation, benefit and group relatedness: The participating smokers smoke according to their habitudinal smoking pattern, and are therefore not increasingly exposed to the harmful health effects of cigarette smoking. The invasive part of the study is their stay for 3 days (and 1 night when wanted) in a hotel, and the sampling of blood, saliva, urine and exhaled air.
Participants will be given the opportunity to purchase ventilated, unventilated, and alternative nicotine products at different prices using an account balance based on their typical, daily nicotine product purchasing. Additionally, account balances will differ across trials.
The goal of this study is to evaluate correlations between brain reactivity (as assessed via functional magnetic resonance imaging (fMRI) following 24-h abstinence) and the amount of smoking in a specific location. The investigators will use ecological momentary assessment (EMA) to ask smokers to rate their exposure to, and smoking in, specific personal smoking environment cues (PSEs) over the course of 2 weeks before quitting smoking and 2 weeks after quitting smoking. The investigators propose to identify 48 regular cigarette smokers who will complete 8 visits (1 screening visit, 1 training visit, 1 camera turn-in visit, 1 fMRI session and 4 post-quit medication check sessions). Multiple methods will be used to test hypotheses about brain functioning during cue-reactivity (CR). The investigators will examine correlation between brain responses to smoking environments (minus non-smoking environments) and smoking cessation outcomes (i.e. days to lapse, days to relapse). Our EMA+Global Positioning System (GPS) analysis will primarily focus on locations where smokers smoke before and after quitting smoking. The investigators will evaluate whether EMA-assessed smoking intensity values are correlated with brain responses to these personal smoking environments.
This study aims to investigate the benefit of administering two differing doses of Bupropion (BUP) to smokers to assist with smoking cessation.
The central objective of this project is to obtain proof-of-concept data demonstrating the effects of propranolol (a beta-adrenergic antagonist) on neurobiological responses to personal smoking environments and behavioral responses in a laboratory smoking behavior task. Human cigarette smokers (N = 50) will take photographs of locations where they do and do not smoke cigarettes. They will then be randomly assigned to receive either propranolol (40 mg) or placebo prior to completing: A) An MRI session assessing neural responses to personal smoking/non-smoking environments, standard smoking/non-smoking environments and proximal smoking/non-smoking cues; and B) A laboratory session examining smoking behavior in response to environmental cues.