2011-08-012024-05-13https://scholars.lib.ntu.edu.tw/handle/123456789/648479摘要：背景：氣喘盛行率的急遽上升，尤其是學齡孩童的氣喘盛行率上升更明顯，如此不但造成社會成本與醫療成本的增加，更是對國家未來主人翁健康的危害。國內對於孩童氣喘的環境危險因子調查研究並不多，尤其是菸害方面猶有許多空間仍待努力。另外，IL-4、IL-4Rα、IL-13、IL-13Rα、FcεRⅠ-β、TNF-α 及LT-α 基因，是否會彼此相互影響細胞激素濃度及孩童氣喘的發生，證據仍十分缺乏，並且過去幾乎完全沒有研究顯示，環境介入模式是否會對於孩童肺功能與血清細胞激素表現造成影響。因此進行大規模流的行病學研究，不僅可探討基因-環境、基因-基因對氣喘發生與肺功能之交互作用，更可提供菸害防制策略施行下，孩童氣喘等異位性疾病的變化，相信將對訂定預防政策，降低社會與醫療成本，增進孩童健康是有很大的幫助。目的：將探討菸害及早期環境因子與孩童氣喘及肺功能的相關性，亦將同時探討細胞激素基因及其功能表現，對於孩童氣喘及肺功能的影響。並以環境介入追蹤模式探討不同菸害及氣喘組別，對於孩童肺功能、血清細胞激素表現的影響，及氣喘新個案的發生情形。方法：本計畫建立於「台灣孩童健康研究」基礎世代上，往前利用病例對照研究，往後進行環境介入追蹤模式研究，進行學童健康、菸害及早期環境暴露等資料之收集，肺功能檢查，以及血清中total IgE 與specific IgE 的檢測工作，並利用先前收集之口腔黏膜樣本進行基因易感性分析，探討菸害及早期環境因子與易感性基因對於氣喘及肺功能變化的交互作用，並追蹤各地區學童的新發生氣喘個案，探討環境介入對於孩童肺功能、血清細胞激素表現的影響。結果：我們嘗試利用三年的時間，達成以下研究目的：1. 接續先前的研究，收集孩童氣喘與對照組，探討環境菸害及早期環境因子（如飼養寵物、家中蟑螂出沒及潮濕狀態、是否早產、母乳哺育期長短、母親懷孕時飲食等等）與孩童氣喘及肺功能的相關性。2. 分析IL-4、IL-13、TNF-α、ECP及EOS濃度之相互關係，以及對於氣喘、IgE及肺功能影響程度。3. 探討IL-4、IL-4Rα、IL-13、IL-13Rα、FcεRⅠ-β、TNF-α及LT-α等細胞激素基因對於細胞激素、孩童氣喘是否扮演重要遺傳角色。4. 探討細胞激素基因是否與環境菸害等環境因子在孩童氣喘的發生及肺功能下降上有交互作用關係。5. 以環境介入追蹤模式探討不同環境菸害及氣喘組別，對於孩童肺功能、血清細胞激素表現的影響。6. 在環境介入追蹤模式下，探討早期環境因子與主動吸菸對於孩童新發生氣喘(incidence rate)之關係。7. 探討細胞激素基因與各種環境因子對於孩童新發生氣喘(incidence rate)之關係。<br> Abstract: Background: Rapid increase in asthma prevalence, especially in schoolchildren, caused notonly medical cost increase but also substantial health hazard. In Taiwan, few studies haveinvestigated the roles of environmental risk factors on childhood asthma, especially in ETS(environmental tobacco smoke) and active smoking. There is no substantial evidenceindicating that IL-4, IL-4Rα, IL-13, IL-13Rα, FcεRⅠ-β, TNF-α and LT-α genes wouldinfluence cytokines to childhood asthma in epidemiological studies. There is also no relatedliterature concerning effects of environmental interventions on pulmonary function indices,cytokines and asthma in childhood. Therefore, a large-scale epidemiologic study could tell usthat gene-environment and gene-gene interactions on childhood asthma and pulmonaryfunction. We could also measure the effectiveness of tobacco control, and provide a newrationale for smoking prevention interventions.Objectives: To determine whether ETS, active smoking and early life exposures areassociated with the asthma and pulmonary function in childhood. We would like to explorethe roles of cytokine related genes and how do they express on childhood asthma? Underenvironmental interventions, we also want to clarify the associations between ETS or activesmoking and pulmonary function, cytokines and new-onset asthma.Methods: We plan to continue our previous work, Taiwan Children’s Health Study (TCHS),and conduct a case-control study and a prospective cohort study. We will performquestionnaire survey, pulmonary function tests, and serum samples for cytokines levels, totalIgE and specific IgE. Interactive effects between environmental factors, genetic susceptibility,and asthma/pulmonary function will be assessed. Telephone interview will also be applied tomonitor incident rates of childhood asthma in different communities.Results: By this three-year study, we would achieve the following research aims:1. To understand whether ETS and early life exposures are associated with theasthma/pulmonary function in childhood.2. To explore the roles of cytokines, such as IL-4, IL-13, TNF-α, ECP, and EOS wouldinfluence IgE and asthma/pulmonary function in childhood.3. To explore the roles of cytokine genes, such as IL-4, IL-4Rα, IL-13, IL-13Rα, FcεRⅠ-β,TNF-α, and LT-α would interfere cytokines and asthma/pulmonary function in childhood.4. To understand whether there are gene-environment intervention between cytokine genesand ETS on asthma/pulmonary function in childhood.5. Under environmental interventions, to examine the associations between ETS and activesmoking and changes of pulmonary function and cytokines between different groups.6. Under environmental interventions, to explore whether the early life exposures and activesmoking are associated with new-onset asthma in childhood.7. To understand whether there are significant interactive effects between cytokine geneticpolymorphisms, environmental factors on incident asthma in childhood?