School Inner-City Asthma Intervention Study

学校内城区哮喘干预研究

• 批准号: 8992349
• 负责人: WANDA PHIPATANAKUL
• 金额: $ 168.54万
• 依托单位: BOSTON CHILDREN'S HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-01-07 至 2019-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8992349
• 关键词: Accounting; Affect; Age; Air; Allergens; American; Americas; Asthma; Boston; Cells; Child; Childhood; Chronic Disease; Clinical; Clinical Trials; Communities; Disadvantaged; Disease; Effectiveness; Engineering; Environment; Environmental Exposure; Epigenetic Process; Exposure to; Funding; Gene Expression; Gene Expression Alteration; Genes; Goals; Health; Home environment; Hour; Individual; Intervention; Intervention Studies; Learning; Link; Lung; Measures; Mediation; Methylation; Molds; Molecular; Molecular Profiling; Morbidity - disease rate; Mus; National Institute of Allergy and Infectious Disease; Nose; Occupations; Outcome; Pathway interactions; Pharmaceutical Preparations; Phenotype; Prevention; Public Health; Research Infrastructure; Respiratory physiology; Risk Factors; Role; School-Age Population; Schools; Source; Specific qualifier value; Students; Symptoms; Testing; Time; Toxicant exposure; United States; Wheezing; air filter; airway inflammation; asthmatic; base; cost; educational atmosphere; elementary school; environmental intervention; epigenome; health care service utilization; high efficiency particulate air filter; improved; inner city; intervention effect; mouse allergen; novel; particle; particulate pollutant; pollutant; primary outcome; programs; secondary outcome

 DESCRIPTION (provided by applicant): Asthma is the most common chronic disease of childhood in the United States, causes significant morbidity, particularly in the inner-city, and accounts for billions of dollars in health care utilization, despite aggressive measures to identif remediable causes. Home environments are established sources of exposure that exacerbate symptoms and home-based interventions are proven effective. Prior to the inception of the School Inner-City Asthma Study (SICAS-1), no American study had comprehensively evaluated the relationship between urban exposures in school, classroom, and home environments and asthma morbidity. Nearly all elementary school children spend 7 to 12 hours a day in school, and most of that time is spent in one classroom. From SICAS-1, we learned that student classroom-specific mouse allergen, mold, and particulate pollutant exposure is associated with worsening symptoms. We also demonstrated our ability to reduce these exposures in a busy, school setting. Our proposal builds upon our established, successful school-based infrastructure to determine whether a school/classroom intervention will efficiently and effectively improve asthma morbidity by reducing these exposures. Our goal is to determine the efficacy of school/classroom based environmental intervention in reducing asthma morbidity in urban schoolchildren. Our central hypothesis is that reducing classroom/school exposure to mouse allergen, mold, and particulate pollutants will decrease asthma morbidity in students with asthma. We plan to test this hypothesis in an intervention study of 300 elementary students with asthma from multiple classrooms in 40 Boston inner-city elementary schools. Our clinical trial aims are to determine the effectiveness of a school/classroom based environmental intervention (school integrated pest management and classroom air purifying filter units within these schools) to reduce asthma morbidity. Our mechanistic aim is to test the hypothesis that effects of school/classroom- based environmental interventions on symptoms/other measures of asthma control occur through changes in gene methylation or expression in pathways (and secondarily, in genes) relevant to airway function and asthma. This will expand our understanding of asthma immunopathogenesis and create opportunities to identify potential novel targets for asthma therapy. Within pathways or networks of genes we will (a) determine how our interventions influence changes in nasal airway cell methylation or gene expression; (b) evaluate how our intervention-associated changes in methylation and gene expression influence asthma outcomes; and (c) estimate through mediation analysis how much of the intervention effects on asthma symptoms occurs through methylation/gene expression changes. This study is an unprecedented, high impact opportunity to test whether we can efficiently benefit a community of children in the school environment as opposed to individuals in single homes. It also adds a novel mechanistic application on health outcomes. It efficiently tackles a critical public health problem that affects a growing proportion of disadvantaged, urban U.S. children.

 描述（由申请人提供）：哮喘是美国最常见的儿童慢性疾病，导致高发病率，尤其是在内城区，尽管采取了积极措施来查明可补救的原因，但其医疗保健费用却高达数十亿美元家庭环境是加剧症状的既定暴露源，在学校内城哮喘研究 (SICAS-1) 启动之前，美国还没有研究全面评估过这种关系。学校、教室和家庭环境中的城市暴露与哮喘发病率之间的关系 几乎所有小学生每天在学校度过 7 至 12 个小时，其中大部分时间是在一间教室里度过的。教室特定的小鼠过敏原、霉菌和颗粒污染物的暴露与症状恶化有关。我们还证明了我们在繁忙的学校环境中减少这些暴露的能力。学校/课堂干预将通过减少这些暴露来有效地改善哮喘发病率。我们的目标是确定基于学校/课堂的环境干预在降低城市学童哮喘发病率方面的功效。我们的中心假设是减少课堂/学校与小鼠的接触。过敏原、霉菌和颗粒污染物将降低患有哮喘的学生的哮喘发病率。我们计划通过对来自 40 所波士顿市中心小学的 300 名患有哮喘的小学生进行的干预研究来检验这一假设。试验的目的是确定基于学校/教室的环境干预措施（学校综合害虫管理和教室空气净化过滤装置）对降低哮喘发病率的有效性。我们的机制目标是检验学校/教室的影响的假设。基于症状的环境干预/哮喘控制的其他措施是通过基因甲基化或与气道功能和哮喘相关的途径（其次是基因）表达的变化而发生的，这将扩大我们对哮喘免疫发病机制的理解，并创造机会识别潜在的新型药物。哮喘治疗的目标。在通路网络或基因中，我们将（a）我们的干预措施如何影响鼻气道细胞甲基化或基因表达的变化；（b）评估与我们的干预相关的甲基化和基因表达的变化如何影响哮喘结果；以及（c）通过中介进行评估；分析对哮喘症状的干预作用有多少是通过甲基化/基因表达变化产生的。这项研究是一个前所未有的、具有高影响力的机会，可以测试我们是否能够有效地使学校环境中的儿童社区而不是单亲家庭中的个人受益。它还增加了一种新颖的机械应用它有效地解决了影响越来越多的美国城市弱势儿童的关键公共卫生问题。