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      International Journal of COPD (submit here)

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      Active smoking among asthmatic youth—How concerned we need to be

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          Abstract

          There is no doubt that tobacco smoking, whether active or passive, has a harmful effect on health of all individuals. Children are particularly vulnerable to environmental tobacco smoke (ETS), and if exposed have higher incidence of lower respiratory tract illnesses in their early years (Cook and Strachan 1999). Furthermore, it has been suggested that the high levels of ETS exposure during childhood may increase the risk of chronic obstructive respiratory disease in adulthood. ETS exposure and asthma development Numerous studies have demonstrated that children of tobacco smoking mothers have higher risk of developing asthma (Martinez et al 1992). Maternal smoking of more than 10 cigarettes a day is associated with higher incidence of asthma, earlier onset of asthma symptoms, and an increased risk of using asthma medication compared with the children of nonsmoking mothers (Weitzman et al 1990). Other data suggest that maternal smoking prenatally and during the child’s first year of life is a significant risk factor for the development of wheeze in infancy, but not wheezing starting after the first year of life (Murray et al 2004). In utero tobacco smoke exposure may be more important than the post-natal exposure. Children born to mothers who have smoked in their pregnancies are more likely to have doctor-diagnosed asthma and current asthma requiring medication use (Gilliland et al 2001). This is an important public health issue, as the US national survey has shown that 16.5% of pregnant women smoke while expecting their babies (Ringel and Evans 2001). However, since the majority of mothers who smoke during pregnancy continue to smoke for the next few years (and children in the first years of life generally spend the majority of their time in the mother’s care), it is often difficult to distinguish what effects occur from in utero exposure and what effects are secondary to post-natal ETS exposure. The few studies that managed to carry out analyses which excluded the effect of postnatal ETS exposure showed a significant association between smoking during the pregnancy and recurrent wheezing (Lannero et al 2006). ETS exposure and asthma severity Children with established asthma who are exposed to environmental tobacco smoke have more frequent acute exacerbations and poorer lung function (Oldigs et al 1991; Chilmonczyk et al 1993). There appears to be a dose-response relationship, with children both of whose parents smoke suffering more than those where the mother alone smokes, with less respiratory symptoms in those children from families with no ETS exposure (Murray and Morrison 1993). Active smoking and asthma in adolescence Adolescence is the period when the majority of smokers start smoking. Active smoking during the childhood and adolescence seriously affects respiratory health by causing decreased lung growth, poorer lung function, increased sputum production, airway obstruction, cough, and shortness of breath (Tyc and Throckmorton-Belzer 2006). A recent study conducted among teenagers has demonstrated that regular smoking in healthy nonallergic adolescents increases the risk of subsequent development of asthma (Gilliland et al 2006). Active tobacco smoking induces lower airway inflammation, and has been associated with diminished response to inhaled and systemic steroids in asthmatic patients. Active smoking among adolescent asthmatics contributes to the frequency and severity of their asthma symptoms. This was confirmed in a study by Mallol and colleagues (2007) in this issue, which presented the data on smoking habits of asthmatic adolescents in Chile. A further alarming finding of the study was the high prevalence of adolescent female smokers. This appears to mirror the findings from many other countries, in which, even after massive media campaigns, cigarette smoking remains popular amongst teenagers, and particularly young women. Why do adolescent asthmatics smoke? Despite having a chronic respiratory disease, asthmatic adolescents do not restrain themselves from smoking, but have equally high smoking rates as their peers, which raises the question of the possible factors that may predispose them to this form of addictive behavior (Zimlichman et al 2004; Jones et al 2006). Studies have indicated that adolescents who are nonadherent to their asthma treatment are more risk-taking and rebellious, therefore more prone to undertake health-compromising behaviours (Tyc and Throckmorton-Belzer 2006). Factors like exposure to smoking at home and having friends who smoke are likely to trigger smoking behavior in asthmatic adolescents. Children with chronic illness like asthma may also have both disease and treatment-related higher psychosocial distress. School absenteeism and separation from peers due to asthma morbidity may also contribute to smoking behavior by using smoking as a vehicle for reconnecting with their peers. However, these factors can change depending on age, sex, race, and socioeconomic status (Tyc and Throckmorton-Belzer 2006). How to reduce smoking among adolescents? This topic has been the subject of a recent review article summarizing the current state of the art (Tonnesen 2002). There has been a huge number of high quality interventional studies conducted among teenagers using different school-based programs targeting smoking behaviour (Thomas and Perera 2006). Although the majority of such trials have shown some benefit on the prevention of active smoking in the short term, there is controversy about longevity of these effects. A study with the longest duration of intervention (lasting 8 years) failed to demonstrate sustained effect of specific intervention (Thomas and Perera 2006). Recently, governments and public health authorities have been trying to develop new policies which would reduce smoking. One of them has been an increase in cigarette taxes which proved to be effective among women of higher educational level (Ringel and Evans 2001). Media advertisements have great influence on smoking behavior among young adults. Successful public health campaigns to persuade governments of the need for legislation to end the tobacco advertising campaigns in media resulted in legislations banning all tobacco advertising in the UK (Tobacco Advertising and Promotion Act 2003) and many other developed countries. As a result of an EU Directive, there is a partial ban on tobacco advertising also exists throughout the EU. However, developing countries largely lack such policies, and as a consequence, tobacco companies continue to market their products. In this era of globalization, the legislations to end the tobacco advertising needs to become global, and having smoke-free schools should be our common goal.

          Most cited references18

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          Effects of maternal smoking during pregnancy and environmental tobacco smoke on asthma and wheezing in children.

          The effects of maternal smoking during pregnancy and childhood environmental tobacco smoke (ETS) exposure on asthma and wheezing were investigated in 5,762 school-aged children residing in 12 Southern California communities. Responses to a self- administered questionnaire completed by parents of 4th, 7th, and 10th grade students were used to ascertain children with wheezing or physician-diagnosed asthma. Lifetime household exposures to tobacco smoke were assessed using responses about past and current smoking histories of household members and any history of maternal smoking during pregnancy. Logistic regression models were fitted to cross-sectional data to estimate the effects of in utero exposure to maternal smoking and previous and current ETS exposure on the prevalence of wheezing and physician-diagnosed asthma. In utero exposure to maternal smoking without subsequent postnatal ETS exposure was associated with increased prevalence of physician-diagnosed asthma (OR, 1.8; 95% CI, 1.1 to 2.9), asthma with current symptoms (OR, 2.3; 95% CI, 1.3 to 4.0), asthma requiring medication use in the previous 12 mo (OR, 2.1; 95% CI, 1.2 to 3.6), lifetime history of wheezing (OR, 1.8; 95% CI, 1.2 to 2.6), current wheezing with colds (OR, 2.1; 95% CI, 1.3 to 3.4) and without colds (OR, 2.5; 95% CI, 1.4 to 4.4), persistent wheezing (OR, 3.1; 95% CI, 1.6 to 6.1), wheezing with exercise (OR, 2.4; 95% CI; 1.3 to 4.3), attacks of wheezing causing shortness of breath (OR, 2.4; 95% CI, 1.3 to 4.4) or awakening at night in the previous 12 mo (OR, 3.2; 95% CI, 1.7 to 5.8), and wheezing requiring medication (OR, 2.1; 95% CI, 1.2 to 3.7) or emergency room visits during the previous year (OR, 3.4; 95% CI, 1.4 to 7.8). In contrast, current and previous ETS exposure was not associated with asthma prevalence, but was consistently associated with subcategories of wheezing. Current ETS exposure was associated with lifetime wheezing (OR, 1.3; 95% CI, 1.1 to 1.5), current wheezing with colds (OR, 1.6; 95% CI, 1.3 to 2.0) and without colds (OR, 1.5; 95% CI, 1.1 to 1.9), wheezing with exercise (OR, 1.7; 95% CI, 1.3 to 2.2), attacks of wheezing causing shortness of breath (OR, 1.6; 95% CI, 1.2 to 2.1) or awakening at night (OR, 1.5; 95% CI, 1.1 to 2.0), and wheezing requiring medication (OR, 1.4; 95% CI, 1.1 to 1.8) or emergency room visits within the previous year (OR, 1.9; 95% CI, 1.2 to 3.0). The effects of current ETS exposure on subcategories of wheezing were most pronounced among children exposed to two or more smokers and remained significant after adjusting for maternal smoking during pregnancy. We conclude that maternal smoking during pregnancy increases the occurrence of physician-diagnosed asthma and wheezing during childhood. In contrast, current ETS exposure is associated with wheezing, but not physician-diagnosed asthma. Taken together, our findings support the hypothesis that ETS operates as a cofactor with other insults such as intercurrent infections as a trigger of wheezing attacks, rather than as a factor that induces asthma, whereas in utero exposure acts to increase physician-diagnosed asthma
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            Health effects of passive smoking-10: Summary of effects of parental smoking on the respiratory health of children and implications for research.

            Two recent reviews have assessed the effect of parental smoking on respiratory disease in children. The results of the systematic quantitative review published as a series in Thorax are summarised and brought up to date by considering papers appearing on Embase or Medline up to June 1998. The findings are compared with those of the review published recently by the Californian Environmental Protection Agency (EPA). Areas requiring further research are identified. Overall there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent smoking, the odds usually being higher in pre-school than in school aged children. For sudden infant death syndrome the odds ratio for maternal smoking is about 2. Significant effects from paternal smoking suggest a role for postnatal exposure to environmental tobacco smoke. Recent publications do not lead us to alter the conclusions of our earlier reviews. While essentially narrative rather than systematic and quantitative, the findings of the Californian EPA review are broadly similar. In addition they have reviewed studies of the effects of environmental tobacco smoke on children with cystic fibrosis and conclude from the limited evidence that there is a strong case for a relationship between parental smoking and admissions to hospital. They also review data from adults of the effects of acute exposure to environmental tobacco smoke under laboratory conditions which suggest acute effects on spirometric parameters rather than on bronchial hyperresponsiveness. It seems likely that such effects are also present in children. Substantial benefits to children would arise if parents stopped smoking after birth, even if the mother smoked during pregnancy. Policies need to be developed which reduce smoking amongst parents and protect infants and young children from exposure to environmental tobacco smoke. The weight of evidence is such that new prevalence studies are no longer justified. What are needed are studies which allow comparison of the effects of critical periods of exposure to cigarette smoke, particularly in utero, early infancy, and later childhood. Where longitudinal studies are carried out they should be analysed to look at the way in which changes in exposure are related to changes in outcome. Better still would be studies demonstrating reversibility of adverse effects, especially in asthmatic subjects or children with cystic fibrosis.
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              Association between exposure to environmental tobacco smoke and exacerbations of asthma in children.

              Exposure to environmental tobacco smoke, as reported by parents, has been linked to diminished pulmonary function and more frequent exacerbations of asthma in children with the disease. Further insight into this association might be gained by using urine cotinine levels to measure actual exposure. We measured urine cotinine levels in 199 children with asthma; 145 also underwent pulmonary-function studies. A parent answered questions about each child's exposure to environmental tobacco smoke. Acute exacerbations of asthma during the preceding year were documented through blinded review of medical records. Possible confounding factors were accounted for by the use of multivariate analysis and by comparisons of serum theophylline levels in exposed and unexposed children. The median urine cotinine levels were 5.6 ng per milliliter in the 116 children reported not to have been exposed to tobacco smoke, 13.1 ng per milliliter in the 53 children exposed to cigarette smoking by the mother or other persons, and 55.8 ng per milliliter in the 30 children exposed to cigarette smoking by the mother and other persons. Acute exacerbations of asthma increased with exposure, whether such exposure was reported by a parent or identified on the basis of the cotinine level; the relative risks for the highest as compared with the lowest exposure category were 1.8 (95 percent confidence interval, 1.4 to 2.2) for reported exposure and 1.7 (95 percent confidence interval, 1.4 to 2.1) for exposure indicated by cotinine levels. The forced expiratory volume in one second (FEV1), the forced expiratory flow between 25 and 75 percent of vital capacity, and the ratio of FEV1 to forced vital capacity also decreased with increases in both measures of exposure. Measurement of urine cotinine levels provides further evidence of an association between exposure to environmental tobacco smoke and pulmonary morbidity in children with asthma. These data emphasize the need for systematic, persistent efforts to stop the exposure of children with asthma to environmental tobacco smoke.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                March 2007
                March 2007
                : 2
                : 1
                : 3-4
                Affiliations
                Academic Division of Medicine and Surgery South, University of Manchester, Wythenshawe Hospital, North West Lung Centre, UK
                Article
                copd-2-1b
                2692109
                18044059
                d409d1d2-c0db-4d9b-a2fb-9807ef740285
                © 2007 Dove Medical Press Limited. All rights reserved
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                Respiratory medicine
                Respiratory medicine

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