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      Smoking: it’s still a big problem in children with asthma Translated title: Tabagismo: ainda é um grande problema em crianças com asma,

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      Jornal de pediatria

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          Abstract

          See paper by Jordão et al. in pages x-y. Smoking is an independent risk factor for the development of asthma symptoms, 1 loss of lung function, 2 and asthma exacerbations. 3 The mechanisms of smoking-related lung disease can include increased small-airway inflammation with neutrophils and macrophages, airway hyper-responsiveness, and airflow obstruction. 4,5 Additionally, patients with asthma who smoke have a reduced response to inhaled corticosteroids. 6 The effect of smoking on asthmatic lungs also appears to increase the development of features of chronic obstructive pulmonary disease (COPD), and there is an increasing body of knowledge about an asthma-COPD overlap syndrome. Most adults who smoke regularly started the habit as adolescents. The Global Initiative for Asthma (GINA) guidelines stresses the critical importance of identifying modifiable risk factors for exacerbations, such as smoking. 7 It also asks healthcare providers to encourage smokers to quit at every visit and provide access to counseling and resources. Tobacco use worldwide peaked in the 1980s and is now decreasing. While the highest rates of smoking are currently in developed countries; the prevalence of smoking is actually decreasing in developed countries and increasing in developing countries. Globally, over 24 million children aged 13–15 years smoke cigarettes. 8 In Brazil, a concentrated effort to control tobacco use has led to a decrease in smoking rates. However, the 2009 Global Youth Tobacco Survey in São Paulo estimated that nearly 30% among adolescents aged 13–15 years use tobacco products. 8 In this issue, Jordão et al. 9 aimed to study the associations between degrees of active smoking, smoke exposure, and reported asthma in 66,394 adolescents (age 12–17 years) in Brazil through a multicenter, national, school based questionnaire study. Data were collected between March and December of 2013 and 2014. They defined smoking exposure as: “experimentation,” for those who have smoked cigarettes at least once in their lives; “current smoking,” for those who have smoked cigarettes on at least one day in the past 30 days; “regular smoking,” for those who have smoked cigarettes for at least seven consecutive days in the past 30 days; and “passive smoking,” for those who had at least one smoker in the household. Current asthma was characterized as the presence of at least one wheezing crisis attack in the last 12 months, a similar definition to that used in the International Study of Asthma and Allergies in Childhood (ISAAC). 10 Severe asthma was defined as the presence of at least one wheezing crisis attack in the last 12 months. The prevalences of smoking exposure were 18%, 25%, 12%, and 28% for experimentation, current smoking, regular smoking, and passive smoke exposure, respectively. The prevalence of current asthma was 13.2% and severe asthma was 2.4%. The association between smoking and asthma was significant and consistent among all regions of Brazil, despite climate and cultural differences. All smoking exposure types increased the odds of current asthma even after adjustment for gender, age, ethnicity, and school type. The odds of smoking exposure were higher in severe asthmatics. There was also a dose-response relationship between the number of smokers in the household and odds of reported current asthma; i.e., the prevalence of current asthma significantly increased between households with 0, 1, and 2–3 smokers. Other epidemiologic studies have found high rates of smoking in adolescents with asthma; in fact, rates are consistently equal or higher than those observed in adolescents without asthma. 11 Since smoking leads to the development of asthma symptoms, there may be an inherent selection bias. However, it is also plausible that psychosocial factors stemming from having asthma may attract some adolescents to smoking. A risk-taking behavior may be reaction to chronic illness, and peer pressure leads these individuals to attempt to enhance their self-image and fit in with their peers. 12 The current study also reinforces that there may be no safe level of exposure to tobacco smoke, whether active or passive. Passive smoking or environmental tobacco smoke consists of the direct inhalation of tobacco smoke (second- hand smoke) as well as exposure to tobacco residue left behind after smoking (third-hand smoke). Although active smoking and secondhand smoking have been well recognized to increase the risk of exacerbations, there is increasing evidence that third-hand smoking is also associated with increased lower respiratory symptoms. 13 The dose-response relationship between smokers in the home and asthma observed in this study emphasize that some smoke exposure is bad, but more smoke exposure is worse. Smoking not only impacts lung health through direct effects on lung function and airway remodeling, but it is also linked to an increase in the risk of respiratory tract infections. Smoke exposure has been found to increase susceptibility to pathogens by impairing macrophage function, decrease microbial clearance, and cause exaggerated pro- inflammatory responses to infection. 14 Thus, smoking poses a real threat to both impairment (daily symptoms) as well as risk (exacerbations) domains. However, despite the high prevalence of smoking among adolescents with asthma and the major risks to acute and long-term health, healthcare providers frequently fall short of inquiring and counseling about smoking. Healthcare providers are generally taught to confidentially screen and counsel adolescents on risky behavior, including smoking. The good news is that adolescents with asthma are more likely to be screened and advised not to smoke by a health professional than those who do not have asthma. 13,15 Unfortunately, specialists-who are specifically trained to treat uncontrolled asthma -are less likely to counsel adolescents on smoking than primary care practitioners. 16 This is an area specialists need to improve. Asking parents to step out of the room for a confidential encounter is not standard practice in many subspecialty clinics, however, is important not only to elicit a smoking history but also to help adolescents with the transition of care from childhood through adolescence into adulthood. Moreover, addressing smoking in the context of asthma symptoms and exacerbations may give patients additional incentives to quit. To enhance screening, healthcare providers might consider discussing with the families about assessing tobacco smoke exposure. Cotinine is a stable metabolite of nicotine and has been widely used as a diagnostic test for tobacco use and compliance with smoking cessation. In asthma, cotinine levels have been shown to correlate with passive smoke exposure. 17 Serum and salivary cotinine levels were found to be more reliable than reported tobacco exposure for hospital readmission. 18 Cotinine levels have not been specifically used to evaluate adolescent smoking behaviors, but it may have a role in identifying environmental exposures in those with poorly controlled asthma. Additionally, there is a lack of studies about interventions to prevent and stop smoking in adolescents with asthma. Adolescents are less likely to be driven by addiction to nicotine than adults, although they are particularly vulnerable; nicotine dependence can develop after less than 100 cigarettes. 11 A helpful screening test can be to ask how long a teen can wait after waking up to have their first cigarette-less than an hour indicates nicotine dependence. 19 Evidence in adolescents has supported the use of similar approaches to those used in adults. Physician advice increases quit rates and has been associated with healthier attitudes about smoking in adolescents. 20 Pharmacotherapy for smoking cessation has not been well studied in adolescents with asthma, and is only generally recommended for selected individuals. Policy-based measures such as comprehensive smoke-free legislation have been extremely effective in communities, reducing the rate of asthma admissions. 21 Further development of evidence-based interventions is needed, but all adolescents with asthma need to hear from their healthcare providers that smoking will worsen their condition and that there is a risk of permanent lung damage. Furthermore, healthcare providers can help these patients to quit smoking. Smoke exposure continues to be a significant modifiable risk factor in adolescents with asthma. Screening and counseling rates for smoking cessation are inadequate and should be conducted by all healthcare providers who manage adolescents with asthma. More work needs to be done on the prevention and treatment of smoking in adolescents with asthma, who are at increased risk for use, nicotine dependence, and poor asthma control. Even brief interventions have been beneficial; nonetheless, further studies in behavioral counseling, biomarkers, mechanisms of disease, and policy measures will guide additional strategies.

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          Most cited references20

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          International Study of Asthma and Allergies in Childhood (ISAAC): rationale and methods.

          The aetiology of asthma and allergic disease remains poorly understood, despite considerable research. The International Study of Asthma and Allergies in Childhood (ISAAC), was founded to maximize the value of epidemiological research into asthma and allergic disease, by establishing a standardized methodology and facilitating international collaboration. Its specific aims are: 1) to describe the prevalence and severity of asthma, rhinitis and eczema in children living in different centres, and to make comparisons within and between countries; 2) to obtain baseline measures for assessment of future trends in the prevalence and severity of these diseases; and 3) to provide a framework for further aetiological research into genetic, lifestyle, environmental, and medical care factors affecting these diseases. The ISAAC design comprises three phases. Phase 1 uses core questionnaires designed to assess the prevalence and severity of asthma and allergic disease in defined populations. Phase 2 will investigate possible aetiological factors, particularly those suggested by the findings of Phase 1. Phase 3 will be a repetition of Phase 1 to assess trends in prevalence.
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            Influence of cigarette smoking on inhaled corticosteroid treatment in mild asthma.

            Although inhaled corticosteroids have an established role in the treatment of asthma, studies have tended to concentrate on non-smokers and little is known about the possible effect of cigarette smoking on the efficacy of treatment with inhaled steroids in asthma. A study was undertaken to investigate the effect of active cigarette smoking on responses to treatment with inhaled corticosteroids in patients with mild asthma. The effect of treatment with inhaled fluticasone propionate (1000 microg daily) or placebo for 3 weeks was studied in a double blind, prospective, randomised, placebo controlled study of 38 steroid naïve adult asthmatic patients (21 non-smokers). Efficacy was assessed using morning and evening peak expiratory flow (PEF) readings, spirometric parameters, bronchial hyperreactivity, and sputum eosinophil counts. Comparison was made between responses to treatment in non-smoking and smoking asthmatic patients. There was a significantly greater increase in mean morning PEF in non-smokers than in smokers following inhaled fluticasone (27 l/min v -5 l/min). Non-smokers had a statistically significant increase in mean morning PEF (27 l/min), mean forced expiratory volume in 1 second (0.17 l), and geometric mean PC20 (2.6 doubling doses), and a significant decrease in the proportion of sputum eosinophils (-1.75%) after fluticasone compared with placebo. No significant changes were observed in the smoking asthmatic patients for any of these parameters. Active cigarette smoking impairs the efficacy of short term inhaled corticosteroid treatment in mild asthma. This finding has important implications for the management of patients with mild asthma who smoke.
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              Risk factors associated with persistent airflow limitation in severe or difficult-to-treat asthma: insights from the TENOR study.

              The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens study is among the largest to assess persistent airflow limitation and the first to evaluate a wide range of potential risk factors in high-risk patients with severe or difficult-to-treat asthma. A better understanding is needed regarding factors associated with persistent airway obstruction; this study was performed to determine demographic and clinical characteristics associated with persistent airflow limitation. Data from adult patients (>or= 18 years old) with severe or difficult-to-treat asthma were evaluated. Patients with COPD, obesity with a restrictive respiratory pattern, or a >or= 30 pack-year history of smoking were excluded. Patients with persistent airflow limitation (postbronchodilator FEV1/FVC ratio
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                Author and article information

                Journal
                2985188R
                5134
                J Pediatr (Rio J)
                J Pediatr (Rio J)
                Jornal de pediatria
                0021-7557
                1678-4782
                14 May 2019
                24 December 2018
                Sep-Oct 2019
                24 October 2019
                : 95
                : 5
                : 506-508
                Affiliations
                Duke University, School of Medicine, Division of Allergy, Immunology and Pulmonary Medicine, Durham, United States
                Author notes
                [* ]Corresponding author. jason.lang@ 123456duke.edu (J.E. Lang).
                Author information
                http://orcid.org/0000-0001-9115-5312
                http://orcid.org/0000-0001-8847-5817
                Article
                NIHMS1022090
                10.1016/j.jped.2018.12.005
                6812481
                30590013
                c221b5f7-3e7e-48a5-a1bc-98a93fa205af

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

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