Treatment of Tobacco Smoking: A Review.

IMPORTANCE: More deaths in the US are attributed to cigarette smoking each year than to any other preventable cause. Approximately 34 million people and an estimated 14% of adults in the US smoke cigarettes. If they stopped smoking, they could reduce their risk of tobacco-related morbidity and mortality and potentially gain up to 10 years of life. OBSERVATIONS: Tobacco smoking is a chronic disorder maintained by physical nicotine dependence and learned behaviors. Approximately 70% of people who smoke cigarettes want to quit smoking. However, individuals who attempt to quit smoking make an average of approximately 6 quit attempts before achieving long-term abstinence. Both behavioral counseling and pharmacotherapy while using nicotine replacement therapy (NRT) products, varenicline, or bupropion are effective treatments when used individually, but they are most effective when combined. In a meta-analysis including 19 488 people who smoked cigarettes, the combination of medication and behavioral counseling was associated with a quit rate of 15.2% over 6 months compared with a quit rate of 8.6% with brief advice or usual care. The EAGLES trial, a randomized double-blind clinical trial of 8144 people who smoked, directly compared the efficacy and safety of varenicline, bupropion, nicotine patch, and placebo and found a significantly higher 6-month quit rate for varenicline (21.8%) than for bupropion (16.2%) and the nicotine patch (15.7%). Each therapy was more effective than placebo (9.4%). Combining a nicotine patch with other NRT products is more effective than use of a single NRT product. Combining drugs with different mechanisms of action, such as varenicline and NRT, has increased quit rates in some studies compared with use of a single product. Brief or intensive behavioral support can be delivered effectively in person or by telephone, text messages, or the internet. The combination of a clinician's brief advice to quit and assistance to obtain tobacco cessation treatment is effective when routinely administered to tobacco users in virtually all health care settings. CONCLUSIONS AND RELEVANCE: Approximately 34 million people in the US smoke cigarettes and could potentially gain up to a decade of life expectancy by stopping smoking. First-line therapy should include both pharmacotherapy and behavioral support, with varenicline or combination NRT as preferred initial interventions.

Factors affecting brain structure in smoking-related diseases: Chronic Obstructive Pulmonary Disease (COPD) and coronary artery disease.

BACKGROUND: Changes in brain structure and cognitive decline occur in Chronic Obstructive Pulmonary Disease (COPD). They also occur with smoking and coronary artery disease (CAD), but it is unclear whether a common mechanism is responsible. METHODS: Brain MRI markers of brain structure were tested for association with disease markers in other organs. Where possible, principal component analysis (PCA) was used to group markers within organ systems into composite markers. Univariate relationships between brain structure and the disease markers were explored using hierarchical regression and then entered into multivariable regression models. RESULTS: 100 participants were studied (53 COPD, 47 CAD). PCA identified two brain components: brain tissue volumes and white matter microstructure, and six components from other organ systems: respiratory function, plasma lipids, blood pressure, glucose dysregulation, retinal vessel calibre and retinal vessel tortuosity. Several markers could not be grouped into components and were analysed as single variables, these included brain white matter hyperintense lesion (WMH) volume. Multivariable regression models showed that less well organised white matter microstructure was associated with lower respiratory function (p = 0.028); WMH volume was associated with higher blood pressure (p = 0.036) and higher C-Reactive Protein (p = 0.011) and lower brain tissue volume was associated with lower cerebral blood flow (p<0.001) and higher blood pressure (p = 0.001). Smoking history was not an independent correlate of any brain marker. CONCLUSIONS: Measures of brain structure were associated with a range of markers of disease, some of which appeared to be common to both COPD and CAD. No single common pathway was identified, but the findings suggest that brain changes associated with smoking-related diseases may be due to vascular, respiratory, and inflammatory changes.

Abnormal resting-state EEG power and impaired inhibition control in young smokers.

Exposure to nicotine during adolescence may cause neurophysiological changes and increase the risks of developing nicotine dependence; it can even lead to lifelong smoking. The intake of nicotine may also lead to abnormal patterns of oscillatory brain activity and inhibition control deficits. However, little is known about the specific relationship between oscillatory brain activity during the resting state and inhibition control capacity in young smokers. In the present study, we acquired resting-state electroencephalography (EEG) data from thirty-four young smokers and 39 age-matched non-smoking controls. Inhibition control performance was measured by a Go/NoGo task. Compared with non-smoking controls, we detected reduced low-frequency delta band activity in the frontal, central and posterior cortices of young smokers. Furthermore, young smokers committed more errors in response to infrequent NoGo trials. Notably, we demonstrated that delta absolute power in the frontal region was negatively correlated with NoGo errors and that alpha power in the central region was positively correlated with NoGo errors in non-smoking controls but not in young smokers. These findings may suggest that these inhibitory control processes were associated with alterations in oscillatory brain activity during the resting state. Our findings suggest that alterations of power spectra in delta bands may act as a useful biomarker of inhibitory control performance and provide a scientific basis for the diagnosis and treatment of nicotine addiction in adolescents.

Prevalence of nevi, atypical nevi, and lentigines in relation to tobacco smoking.

BACKGROUND: Melanocytic nevi have a complex evolution influenced by several endogenous and exogenous factors and are known risk factors for malignant melanoma. Interestingly, tobacco use seems to be inversely associated with melanoma risk. However, the association between tobacco use and nevi and lentigines has not yet been evaluated. METHODS: We investigated the prevalence of nevi, atypical nevi, and lentigines in relation to tobacco smoking in a cohort of 59 smokers and 60 age- and sex-matched nonsmokers, using a questionnaire and performing a total body skin examination by experts. RESULTS: No significant differences were detected between smokers and nonsmokers in the numbers of nevi, atypical nevi, and lentigines in sun-exposed areas (p = 0.966, 0.326, and 0.241, respectively) and in non-sun-exposed areas (p = 0.095, 0.351, and 0.546, respectively). CONCLUSION: Our results revealed no significant differences in the prevalence of nevi, atypical nevi, and lentigines between smokers and nonsmokers in sun-exposed and non-sun-exposed areas.

Neurometabolic alterations in the nucleus accumbens of smokers assessed with 1 H magnetic resonance spectroscopy: The role of glutamate and neuroinflammation.

Tobacco use is one of the leading causes of premature death and morbidity worldwide. For smokers trying to quit, relapse rates are high, even after prolonged periods of abstinence. Recent findings in animal models highlight the role of alterations in glutamatergic projections from the prefrontal cortex onto the nucleus accumbens (NAc) in relapse vulnerability. Moreover, inflammatory responses in the NAc have been reported during withdrawal. A novel proton magnetic resonance spectroscopy (1 H-MRS) protocol was applied in humans to measure molar concentrations for glutamate, its sum with glutamine (Glx), and myoinositol plus glycine (mI + Gly) in the NAc (19 smokers, 20 matched controls). Smokers were measured at baseline and during withdrawal and satiation. No difference between groups or smoking states was found for glutamate or Glx, but, in smokers, stronger craving and more severe nicotine dependence were associated with lower baseline glutamate and Glx levels, respectively. Interestingly, mI + Gly concentrations were higher during withdrawal than baseline and correlated negatively with nicotine dependence severity and pack years of smoking. The lack of glutamatergic changes between groups and smoking states may imply that glutamate homeostasis is not significantly altered in smokers or that changes are too small for detection by 1 H-MRS. Moreover, the observed increase in mI + Gly may imply that neuroinflammatory processes occur in the NAc during nicotine withdrawal. These findings shed light on neurobiological relapse mechanisms in smokers and may provide the opportunity to develop more effective treatment options targeting the glutamate and neuroinflammation system.

Declining trend of smoking and smokeless tobacco in India: A decomposition analysis.

There has been a relative reduction of tobacco consumption between Global Adult Tobacco Survey-India (GATS-India) 2009-10 and GATS-India 2016-17. However, in terms of absolute numbers, India still has the highest number of tobacco consumers. Therefore, this paper aims to examine the socioeconomic correlates and delineate the factors contributing to a change in smoking and smokeless tobacco use from GATS (2009-10) to GATS (2016-17) in India. We used multivariable binary logistic regressions to examine the demographic and socioeconomic correlates of smoking and smokeless tobacco use for both the rounds of the survey. Further decomposition analysis has been applied to examine the specific contribution of factors in the decline of tobacco consumption over a period from 2009 to 2016. Results indicated that the propensity component was primarily responsible for major tobacco consumption decline (smoking- 41%, smokeless tobacco use- 81%). Most of the decrease in propensity to smoke has been explained by residential type and occupation of the respondent. Age of the respondent contribute significantly in reducing the prevalence of smokeless tobacco consumption during the seven-year period, regardless of change in the composition of population. To achieve the National Health Policy, 2017 aim of reducing tobacco use up to 15% by 2020 and up to 30% by 2025, targeted policies and interventions addressing the inequalities identified in this study, must be developed and implemented.

COVID-19 y tabaco / COVID-19 and Tobacco

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COVID-19 y tabaquismo: revisión sistemática y metaanálisis de la evidencia / COVID-19 and Smoking: A Systematic Review and Meta-Analysis of the Evidence

OBJETIVO: El objetivo del estudio ha sido responder a las siguientes preguntas: ¿se asocia el consumo de tabaco en pacientes con COVID-19 con una progresión negativa y desenlace adverso de la enfermedad? y, ¿se asocia el consumo de tabaco, actual y pasado a una mayor posibilidad de desarrollar COVID-19? MATERIAL Y MÉTODOS: Se realizó una revisión sistemática (RS) y metaanálisis (MA) de trabajos publicados previamente. La estrategia de búsqueda incluyó todos los descriptores conocidos sobre COVID-19 y tabaco, y se realizó en diferentes bases de datos. Se utilizaron modelos estadísticos adecuados para abordar el tamaño del efecto en un MA: modelo de efectos aleatorios y de efectos fijos. RESULTADOS: Fueron identificados 34 artículos en la RS de los cuales fueron incluidos 19 en el MA. Ser fumador o exfumador se mostró como un factor de riesgo para una peor progresión de la infección por COVID-19 (OR 1,96, IC del 95%, 1,36-2,83) y una mayor probabilidad de presentar una condición más crítica de la infección (OR 1,79, IC del 95%, 1,19-2,70). Como limitaciones del MA encontramos que la mayoría de los estudios analizados eran observacionales con un sesgo de publicación limitado y con 2 estudios discrepantes con el resto, aunque tras retirarlos del MA se mantenía el tabaco como un factor de riesgo de peor evolución. CONCLUSIÓN: El tabaquismo actual y pasado produce una forma clínica más grave de la COVID-19 y lleva con mayor frecuencia a estos pacientes a ingresar en Cuidados Intensivos, sean intubados y mueran

OBJECTIVE: The aim of this study was to determine if tobacco use in patients with Covid-19 is associated with a negative disease course and adverse outcome, and if smoking, current and past, is associated with a greater possibility of developing COVID-19. MATERIAL AND METHODS: A systematic review (SR) and meta-analysis (MA) of previously published works were performed. The search strategy included all known descriptors for Covid-19 and tobacco and was conducted in different databases. Appropriate statistical models were used to address the effect size in meta-analysis, namely random effects and fixed effects model. RESULTS: Thirty-four articles were identified in the SR of which 19 were included in the MA. Being a smoker or former smoker was shown to be a risk factor for worse progression of Covid-19 infection (OR 1.96, 95% CI, 1.36 - 2.83) and a greater probability of presenting a more critical condition (OR 1.79 95% CI, 1.19 - 2.70). As limitations of the MA, we found that most of the studies analyzed were observational with limited publication bias. Two studies that disagreed with the rest were included, although after withdrawing them from the MA, smoking was maintained as a risk factor for worse progress. CONCLUSION: Current and past smoking produces a more serious clinical form of Covid-19 and more frequently leads to intensive care admission, intubation, and death

The changes in pulmonary functions in occupational divers: smoking, diving experience, occupational group effects.

BACKGROUND: Diving challenges the respiratory system because of the pressure changes, breathing gases, and cardiovascular effects. We aimed to analyse the long term effect of occupational diving on pulmonary functions in terms of diving experience (year), smoking history, and occupational groups (commercial divers and SCUBA instructors). MATERIALS AND METHODS: We retrospectively analysed respiratory system examination results of the experienced occupational divers who were admitted to the Undersea and Hyperbaric Medicine Department for periodic medical examination between January 1, 2013 and February 28, 2019. RESULTS: Sixty-four divers applied to our department. Candidate divers were not included in our study. The mean diving experience (year) was 13.6 ± 7.3. None of the divers complained of pulmonary symptoms. Pulmonary auscultation and chest radiography were normal in all cases. In divers with 20 years or more experience, the FEV1/FVC ratio and FEF25-75(%) was significantly lower (p < 0.001, p < 0.05, respectively). In addition, there was a statistically significant negative correlation between FEV1/FVC ratio and FEF25-75(%) and diving experience (year) (p < 0.05, r = -0.444, p < 0.05, r = -0.300, respectively). As the diving experience increase per 1 year, the FEF25-75(%) value decreases by 1.04% according to linear regression analyses. However, smoking and occupational groups did not show any significant influence on pulmonary function test parameters. CONCLUSIONS: Occupational diving seems to create clinically asymptomatic pulmonary function test changes related to small airway obstruction after long years of exposure.

Smoking cessation and related factors in middle-aged and older Chinese adults: Evidence from a longitudinal study.

OBJECTIVES: There are more than 300 million smokers in China. This study aimed to evaluate the rate of smoking cessation, smoking relapse and related factors in middle-aged and older smokers in China. METHODS: We performed a secondary analysis of data from China Health and Retirement Longitudinal Study (CHARLS) that recruited a nationally representative sample of adults aged 45 and older. Participants were 3708 smokers in 2011 who completed two waves of follow-up interviews in 2013 and 2015. Self-reported quit and relapse rates at follow-ups were estimated. Multiple logistic regressions were conducted to identify factors associated with smoking cessation and relapse. RESULTS: The overall quit rate was 8.5% (95% CI 7.7% - 9.5%) at the 2-year follow-up in 2013, and 16.6% (95% CI 15.5% - 17.9%) at the 4-year follow up. Smoking cessation in 2013 was associated with not living in the northeast region (p = 0.003), fewer cigarettes smoked daily (p <0.001), and longer time to the first cigarette in the morning (p<0.001). Smoking cessation in 2015 was associated with older age (p = 0.049), smoking initiation at age ≥20 years (p<0.001), longer time to the first cigarette in the morning (p<0.001), and self-perceived poor health (p<0.001). Of the 317 participants who stopped smoking in 2013, 13.3% (95% CI 9.9% - 17.5%) relapsed by 2015. Smoking relapse was associated with younger age (p = 0.025), shorter time to the first cigarette in the morning (p = 0.003), and self-perception of not poor health (p = 0.018). CONCLUSION: The overall quit rate was 8.5% at the 2-year follow up, and 16.6% at the 4-year follow up in the middle-aged and older smokers, but 13% of quitters returned to smoking in two years. Successful smoking cessation was associated with older age, lower nicotine dependence, and self-perceived poor health.

Implications of Tobacco Smoking and Alcohol Consumption on Ectopic Fat Deposition in Individuals After Pancreatitis.

OBJECTIVES: Tobacco smoking and alcohol consumption are established risk factors for pancreatitis. This study investigated the associations between tobacco smoking/alcohol consumption in people after an attack of pancreatitis and intrapancreatic fat deposition (IPFD), intrahepatic fat deposition (IHFD), and skeletal muscle (SMFD) fat deposition. METHODS: In this cross-sectional study, magnetic resonance imaging was used to quantify IPFD, IHFD, and SMFD by 2 independent raters. A validated questionnaire was used to determine tobacco smoking and alcohol consumption. RESULTS: A total of 119 individuals after an attack of pancreatitis were included. Average tobacco smoking contributed most to variance in IPFD (R = 6.5%) and least to variance in SMFD (R = 0.4%). Average alcohol consumption contributed most to variance in variance in IPFD (R = 2.8%) and least to IHFD (R = 1.1%). Packs/day contributed more than years of smoking to variance in IPFD (R = 4.9 and 0.2%, correspondingly), whereas years of drinking contributed more than average daily alcohol consumption (R = 3.9 and 3.2%, correspondingly). CONCLUSIONS: Tobacco smoking and alcohol consumption contributed more to variance in IPFD than IHFD and SMFD. Smoking contributed more than drinking to variance in IPFD. The daily amount of tobacco smoked appeared to be more important than years of smoking for IPFD.

Cigarette Smoking Cessation Temporarily Enhances the Release of Phosphorylated-HSP27 from Human Platelets.

Objective Cigarette smoking is a risk factor for arteriopathy, including acute coronary syndrome, stroke and peripheral vascular disease. Thus, cessation is strongly recommended in order to reduce these risks. We recently demonstrated that smoking cessation causes temporary hyper-aggregability of human platelets. We previously showed that heat shock protein 27 (HSP27) is released from human platelets stimulated by collagen, accompanied by its phosphorylation. Accumulating evidence indicates potent roles of extracellular HSP27 as a modulator of inflammation. In the present study, using the stored samples obtained in the previous study, we investigated the effect of cigarette smoking cessation on the release of phosphorylated-HSP27 from collagen-activated human platelets (n=15 patients). Methods We enrolled patients who visited smoking cessation outpatient services between January 2012 and November 2014. Platelet-rich plasma, chronologically obtained before and after the cessation, was stimulated by collagen using a PA-200 aggregometer in the previous study. The levels of phosphorylated-HSP27 released from platelets were determined by an enzyme-linked immunosorbent assay. The phosphorylation of HSP27 in platelets was evaluated by a Western blot analysis. Results Cessation of cigarette smoking significantly upregulated the levels of collagen-stimulated release of phosphorylated-HSP27 at four and eight weeks after quitting smoking compared to before cessation. However, there was no significant difference between the levels before cessation and those at 12 weeks after cessation. The levels of phosphorylated-HSP27 stimulated by collagen in the platelets at four weeks after smoking cessation were remarkably enhanced compared to before cessation. Conclusion Cigarette smoking cessation temporarily enhances the collagen-stimulated release of phosphorylated-HSP27 from human platelets in the short term.

COPD Positive Screening with Spirometry Increases Motivation to Quit Tobacco Smoking in an Addiction Treatment Center.

Providing an on-site immediate diagnosis of Chronic Obstructive Pulmonary Disease (COPD) and lung age in tobacco smokers could be a motivational tool for smoking cessation. Our aim was to investigate the effects of an abnormal spirometry results on motivational change and subsequent smoking cessation. We conducted a retrospective analysis of smoking status after 3 months of tobacco counseling. Patients were recruited in an addiction outpatient center. Spirometry results were obtained with a portable device during the first visit. The sample was thus divided in 3 groups: COPD, subthreshold-group (no COPD but abnormal lung age) and normal spirometry. Among the three groups, we compared the immediate motivation change, difference in Q-MAT motivation scale score after minus before spirometry (Kruskal-Wallis test) and the smoking status after 3 months (Fisher test). We included 48 patients (37 males, median age 44 years, median cigarette-per-day 20). Spirometry results divided the sample in COPD (N = 13), subthreshold (N = 11) and normal group (N = 24). Mean Q-MAT score change after spirometry was different between groups (p = 0.019), greater in COPD (4.62 ± 3.38) than normal group (1.46 ± 3.11), and lower in patient with a co-occuring hazardous alcohol use (p = 7.6 × 10-3). Three-months smoking status was different between spirometry results groups (p = 0.0021). COPD (5/13, 38.5%) and subthreshold patients (6/10, 60.0%) had stopped more frequently than patients from the normal-group (2/22, 9.1%). The effect of immediate spirometry results on motivation to quit varies according to the screened pulmonary damages and hazardous alcohol use. It could be a useful tool in addiction treatment centers.

Active Tobacco Smoking Impairs Cardiac Systolic Function.

Tobacco smoking is a well-established risk factor for cardiovascular disease, but its direct effect on myocardial structure and function remains unclear. This study investigated the effects of smoking using a nested matched case-control study design. 5,668 participants of the UK Biobank study who underwent cardiovascular magnetic resonance imaging were screened for inclusion. 102 smokers (56 males) with a median age of 56 years were matched to non-smokers based on sex, age, and body surface area. Manual post-processing and feature tracking analyses were performed to determine left ventricular (LV) and right ventricular (RV) structure and function measures. Linear regression analyses were performed to determine the effect of tobacco smoking on imaging measures. Tobacco smoking was associated with increased LV and RV end-systolic volume (4.98 ± 2.08 mL, 5.19 ± 2.62 mL, P = 0.018, 0.049 respectively), reduced LV and RV ejection fraction (ß: -2.21 ± 0.82%, -2.06 ± 0.87%, P = 0.007, 0.019 respectively), and reduced absolute measures of LV peak global longitudinal, radial, and circumferential strain (ß: 0.86 ± 0.30%, -2.52 ± 0.99%, 1.05 ± 0.32%, P = 0.004, 0.011, 0.001 respectively). Effect sizes were larger in daily smokers compared to occasional smokers. In a general Caucasian population without known clinical cardiovascular disease, active tobacco smoking was dose dependently associated with impaired cardiac systolic function.

Tobacco and electronic cigarettes adversely impact ECG indexes of ventricular repolarization: implication for sudden death risk.

Tobacco cigarette smoking is associated with increased sudden death risk, perhaps through adverse effects on ventricular repolarization. The effect of electronic (e-)cigarettes on ventricular repolarization is unknown. The objective of the study was to test the hypothesis that tobacco cigarettes and e-cigarettes have similar adverse effects on electrocardiogram (ECG) indexes of ventricular repolarization and these effects are attributable to nicotine. ECG recordings were obtained in 37 chronic tobacco cigarette smokers, 43 chronic e-cigarette users, and 65 nonusers. Primary outcomes, Tpeak to Tend (Tp-e), Tp-e/QT ratio, and Tp-e/QTc ratio, were measured in tobacco cigarette smokers pre-/post-straw control and smoking one tobacco cigarette and in e-cigarette users and nonusers pre-/post-straw control and using an e-cigarette with and without nicotine (different days). Mean values of the primary outcomes were not different among the three groups at baseline. In chronic tobacco cigarette smokers, all primary outcomes, including the Tp-e (12.9 ± 5.0% vs. 1.5 ± 5%, P = 0.017), Tp-e/QT (14.9 ± 5.0% vs. 0.7 ± 5.1%, P = 0.004), and Tp-e/QTc (11.9 ± 5.0% vs. 2.1 ± 5.1%, P = 0.036), were significantly increased pre-/post-smoking one tobacco cigarette compared with pre-/post-straw control. In chronic e-cigarette users, the Tp-e/QT (6.3 ± 1.9%, P = 0.046) was increased only pre/post using an e-cigarette with nicotine but not pre/post the other exposures. The changes relative to the changes after straw control were greater after smoking the tobacco cigarette compared with using the e-cigarette with nicotine for Tp-e (11.4 ± 4.4% vs. 1.1 ± 2.5%, P < 0.05) and Tp-e/QTc (9.8 ± 4.4% vs. -1.6 ± 2.6%, P = 0.05) but not Tp-e/QT(14.2 ± 4.5% vs. 4.2 ± 2.6%, P = 0.061) . Heart rate increased similarly after the tobacco cigarette and e-cigarette with nicotine. Baseline ECG indexes of ventricular repolarization were not different among chronic tobacco cigarette smokers, electronic cigarette users and nonusers. An adverse effect of acute tobacco cigarette smoking on ECG indexes of ventricular repolarization was confirmed. In chronic e-cigarette users, an adverse effect of using an e-cigarette with nicotine, but not without nicotine, on ECG indexes of ventricular repolarization was also observed.NEW & NOTEWORTHY Abnormal ventricular repolarization, as indicated by prolonged Tpeak-end (Tp-e), is associated with increased sudden death risk. Baseline ECG indexes of repolarization, Tp-e, Tp-e/QT, and Tp-e/QTc, were not different among tobacco cigarette (TC) smokers, electronic cigarette (EC) users, and nonsmokers at baseline, but when TC smokers smoked one TC, all parameters were prolonged. Using an electronic cigarette with nicotine, but not without nicotine, increased the Tp-e/QT. Smoking induces changes in ECG indexes of ventricular repolarization associated with increased sudden death risk.

Efectos biológicos protectores del ejercicio en modelos experimentales de tabaquismo: más allá de la cesación y la abstinencia / Protectives biological effects of exercise in animals models of tobacco smoking: beyond tobacco cessation and withdrawal

El tabaquismo es considerado una de las principales causas de morbilidad y mortalidad en la población general. En Chile la prevalencia de tabaquismo alcanza el 36,7% en hombres y 28,5% en mujeres. En este contexto, diversas estrategias farmacológicas y no farmacológicas han sido propuestas para promover la cesación de su consumo, así como para contrarrestar las comorbilidades asociadas al tabaquismo prolongado. Entre ellas, el ejercicio físico ha sido tradicionalmente considerado, por su impacto en la promoción de la cesación del hábito tabáquico, así como también por sus efectos en la reducción de las manifestaciones clínicas del síndrome de abstinencia post cesación. No obstante, estudios realizados en modelos animales durante los últimos 10 años han proporcionado datos contundentes para sustentar la hipótesis de que la práctica regular de ejercicio físico sería también efectiva para prevenir o modular el estrés oxidativo y la respuesta inflamatoria inducida por el tabaco, previniendo el deterioro orgánico de los sistemas fisiológicos expuestos. Esta revisión tiene por objetivo discutir la evidencia publicada respecto a los efectos biológicos inducidos por ejercicio físico y su impacto en la reversión de los mecanismos fisiopatológicos que subyacen a las comorbilidades asociadas al hábito tabáquico, focalizando el análisis en los mecanismos de estrés oxidativo y respuesta inflamatoria del sistema respiratorio y cardiovascular.

Smoking is considered one of the main causes of morbidity and mortality in the general population. In Chile, the prevalence of smoking reaches 36.7% in men and 28.5% in women. In this context, several pharmacological and non-pharmacological strategies have been proposed to promote the cessation of their use, as well as to counteract the comorbidities associated with prolonged smoking. Among them, physical exercise has been traditionally considered, due to its impact on the promotion of cessation of smoking, as well as its effects in reducing the clinical manifestations of withdrawal syndrome. However, studies conducted in animal models during the last 10 years have provided strong data to support the hypothesis that regular practice of physical exercise would also be effective in preventing or modulating oxidative stress and the inflammatory response induced by tobacco, preventing the organic deterioration of exposed physiological systems. The objective of this review is to discuss the published evidence regarding the biological effects induced by physical exercise and its impact on the reversion of the pathophysiological mechanisms underlying the comorbidities associated with smoking, focusing the analysis on the mechanisms of oxidative stress and inflammatory response of the respiratory and cardiovascular system.

Phenotypic comparison between smoking and non-smoking chronic obstructive pulmonary disease.

BACKGROUND: Although COPD among non-smokers (NS-COPD) is common, little is known about this phenotype. We compared NS-COPD subjects with smoking COPD (S-COPD) patients in a rural Indian population using a variety of clinical, physiological, radiological, sputum cellular and blood biomarkers. METHODS: Two hundred ninety subjects (118 healthy, 79 S-COPD, 93 NS-COPD) performed pre- and post-bronchodilator spirometry and were followed for 2 years to study the annual rate of decline in lung function. Body plethysmography, impulse oscillometry, inspiratory-expiratory HRCT, induced sputum cellular profile and blood biomarkers were compared between 49 healthy, 45 S-COPD and 55 NS-COPD subjects using standardized methods. Spirometric response to oral corticosteroids was measured in 30 female NS-COPD patients. RESULTS: Compared to all male S-COPD subjects, 47% of NS-COPD subjects were female, were younger by 3.2 years, had greater body mass index, a slower rate of decline in lung function (80 vs 130 mL/year), more small airways obstruction measured by impulse oscillometry (p < 0.001), significantly less emphysema (29% vs 11%) on CT scans, lower values in lung diffusion parameters, significantly less neutrophils in induced sputum (p < 0.05) and tended to have more sputum eosinophils. Hemoglobin and red cell volume were higher and serum insulin lower in S-COPD compared to NS-COPD. Spirometric indices, symptoms and quality of life were similar between S-COPD and NS-COPD. There was no improvement in spirometry in NS-COPD patients after 2 weeks of an oral corticosteroid. CONCLUSIONS: Compared to S-COPD, NS-COPD is seen in younger subjects with equal male-female predominance, is predominantly a small-airway disease phenotype with less emphysema, preserved lung diffusion and a slower rate of decline in lung function.

Habitual cigarette smoking attenuates shear-mediated dilation in the brachial artery but not in the carotid artery in young adults.

In the present study, we hypothesized that habitual cigarette smoking attenuates endothelial function in the cerebral circulation as well as that of the peripheral circulation in young adults. To test this hypothesis, we measured cerebrovascular and peripheral flow-mediated dilation (FMD) in young smokers and nonsmokers in the present study. Ten healthy nonsmokers and 10 smokers participated in the study. We measured blood velocity and diameter in the brachial artery and internal carotid artery (ICA) using Doppler ultrasound. We identified shear-mediated dilation in the brachial artery and ICA by the percentage change in peak diameter during hyperemia stimulation (reactive hyperemia and hypercapnia). We measured the baseline diameter and the shear rate area under the curve from the onset of hyperemia to peak dilation in the brachial artery and ICA, finding the measurements of the smokers and those of the nonsmokers did not differ (p > .05). In contrast to brachial FMD (5.07 ± 1.79% vs. 7.92 ± 3.01%; smokers vs. nonsmokers, p = .019), FMD in the ICA was not attenuated in the smokers compared with that of the nonsmokers (5.46 ± 2.32% vs. 4.57 ± 2.70%; p = .442). These findings indicate that in young healthy smokers, cerebral endothelial function was preserved, and the response of cerebral endothelial function to smoking was different from that of peripheral vasculature.

Association of Tobacco Smoking with Physical Fitness of Military Males in Taiwan: The CHIEF Study.

Tobacco smoking has been found associated with lower cardiorespiratory fitness in white and black males; however, few studies have not been conducted to clarify such relationship in Asian males. We performed a cross-sectional study to investigate the association between tobacco smoking status and physical fitness in 3,669 military males, averaged 29.4 years of age, from the cardiorespiratory fitness and hospitalization events in armed forces (CHIEF) study in Taiwan during 2014. There were 1,376 current smokers, and the others were noncurrent smokers. The effective sample size estimated was 1,230 participants, as the margin of error was ±3% at the 99% confidence level. Physical fitness was evaluated by time for a 3000-meter run test (aerobic fitness) and repetitive numbers of 2-minute sit-ups and 2-minute push-ups (anaerobic fitness) where all procedures were standardized by using computerized scoring systems. A multiple linear analysis adjusting for age, service specialty, body mass index, heart rate, alcohol intake, and training frequency was used to determine the relationship. As compared with noncurrent smoking, current smoking was inversely correlated with longer time for a 3000-meter run (ß = 15.66 (95% confidence intervals (CI): 10.62, 20.70)) and fewer repetitive numbers of 2-minute sit-ups and 2-minute push-ups (ß = -1.53 (95% CI: -2.08, -0.97) and -1.31 (95% CI: -2.12, -0.50), respectively). Our finding reconfirms the concept that tobacco smoking might reduce both aerobic and anaerobic fitness among young Asian males.