摘要：Objectives. We sought to determine the effects of exposure to environmental tobacco smoke (ETS) and childhood cigarette smoking on asthma symptoms among middle school children in North Carolina. Methods. During 1999–2000, information was collected from a survey completed by the children. Outcomes of asthma symptom reporting were regressed on tobacco smoke exposures. Results. Children who currently smoked or reported any exposure to ETS were at increased risk of reporting active asthma symptoms. Exposure to ETS and childhood cigarette smoking was responsible for 15% of the asthma cases observed in the study population and $1.34 million in excess medical expenditures. Conclusions. Even at low levels of exposure, childhood cigarette smoking and ETS are independently associated with asthmatic symptoms. Asthma is the most common chronic childhood illness. The incidence of asthma among 4- to 15-year-olds increased 74% between 1980 and 1994. 1 Similar increases have been reported worldwide with no clear causal link, despite extensive research. Current theories suggest that increased exposure to asthma risk factors may be responsible for a substantial amount of the increase in asthma prevalence rates. 2 Some important, established risk factors include tobacco smoke, dust mite and cockroach allergens, pet dander, and household molds. 3 Exposure to tobacco smoke is one of the strongest and most consistent risk factors in regard to development and exacerbation of asthma. 3 Of the potential sources of tobacco smoke, environmental tobacco smoke (ETS) has become a significant area of research, while cigarette smoking among school-aged children and its association with asthma symptoms have been relatively neglected. While environmental smoke exposure is a proven significant risk factor, 3– 6 there is a relative paucity of data corroborating an association between asthma symptom reporting and cigarette smoking among school-aged children. Several studies, mostly conducted among adults, have revealed no association between asthma symptoms and smoking 7, 8 ; however, there are notable exceptions. 9 In one adult study, active smoking was a dose-dependent risk factor for wheezing symptoms but was not a risk factor for physician-diagnosed asthma. 10 Conversely, the data supporting ETS as a risk factor are so strong that in 1992 the US Environmental Protection Agency concluded that ETS is causally associated with additional episodes and increased severity of symptoms among asthmatic children and that it is a risk factor for new cases of asthma in previously symptom-free children. 4 Most published studies support this association between parental smoking and childhood asthma or wheezing. 5, 11, 12 Although inconsistent and sometimes crudely measured, a dose–response effect has been reported in numerous studies. 13, 14 The ability to characterize the etiology of this disease has been limited by the lack of standardized measures designed to assess population levels of asthma and respiratory symptoms. Most survey-based population studies rely on a physician diagnosis of asthma or parental reports of wheezing. While wheezing is often used as a surrogate measure of asthma, the variable between-studies definitions of wheezing make comparisons challenging and imperfect. 15 Problems include lack of symptom recognition by parents and children and variations in physicians’ diagnostic criteria. In response to this issue, the International Study of Asthma and Allergy in Childhood (ISAAC) was developed to assess respiratory and allergy symptoms with a validated questionnaire and a descriptive video according to a standard protocol. 16 The predictive validity of the ISAAC survey in terms of clinical outcomes has been demonstrated among both adolescents and adults. 17– 19 This survey, intended for children, and its paired video demonstrating wheezing attacks have helped bring uniformity to data collection and have been used in studies published in more than 56 countries. 20 Yet, to date, few studies employing the ISAAC protocol with US children have been published. In the present study, we did not rely solely on parental reporting of asthma symptoms, as is the case in much of the literature; instead, we used validated ISAAC data provided by middle school students. Furthermore, in addition to the effects of environmental smoke exposure on asthma symptom reporting, we also estimated the effects of childhood cigarette smoking, an area of study often neglected in the literature. We examined dose–response associations between reported asthma symptoms and both secondary smoke exposure in the home and primary childhood smoking. We used impact measures to estimate attributable cases of active asthma due to tobacco smoke. Finally, building on previous Medicaid cost estimates for asthma services rendered in the state of North Carolina, 21 we estimated statewide medical costs of tobacco in the age group under study.
