ENVIRONMENTAL DETERMINANTS OF CHILDHOOD ASTHMA

儿童哮喘的环境决定因素

• 批准号: 3136895
• 负责人: Dennis R Ownby
• 金额: $ 29.55万
• 依托单位: HENRY FORD HEALTH SYSTEM
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-02-01 至 1997-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3136895
• 关键词: airborne allergen; asthma; bronchospasm; case history; child (0-11); disease /disorder proneness /risk; dust; family genetics; human ecology; human subject; immunoglobulin E; interview; longitudinal human study; middle childhood (6-11); mites; passive smoking; pathologic process; respiratory disorder diagnosis; respiratory disorder epidemiology; respiratory function; statistics /biometry; urinalysis

The objective of this proposal is to investigate the relationships between multiple variables: cord blood IgE concentration, family history, intensity of early allergen exposure, passive cigarette smoke exposure, allergic sensitivity, bronchial hyperresponsiveness, and asthma, in children 6 to 7 years of age. The cohort of children to be studied were initially selected prenatally from families enrolled in a large HMO. Previous research has been directed toward the 141 children, from the cohort of 797 children, who were born with cord blood IgE concentrations of greater than or equal to 0.56 IU/mL. These children were thought to be at higher risk for allergic disease and were followed monthly until 2 years, then every other month until 4 years of age. Those felt to be at lower risk of allergy (IgE < 0.56 IU/ml) have been followed yearly. For this proposal, we plan to use the entire cohort of 797 children. At 5 and 6 years of age the families of the children will be contacted for telephone interviews and brief telephone contacts will be made at 4.5 and 5.5 years. As soon as possible after 6 years of age all children will be invited to undergo a clinical evaluation to determine if the child has current asthma. The evaluation will include: a review of the family allergic history, a standardized medical history, physical examination, allergen skin testing, in vitro testing for total and allergen specific IgE, urine analysis for cotinine, pulmonary function testing (FVC, FEV1, PEFR, and FEF25-75%), and methacholine challenge. The information from the clinical evaluation will be combined with previously obtained data including: measurements of allergen (mites, Der f l, Der p l; cat, Fel d l; ragweed Amb a l; and grass, Lol p l) concentrations in bedroom air and dust samples, cord blood IgE concentrations, family histories, health histories, housing records, and urinary cotinine measurements to answer the following questions. 1) What is the prevalence of diagnosed and undiagnosed asthma and of bronchial hyperresponsiveness in this cohort of children? 2) What is the relationship between asthma and bronchial responsiveness in this cohort of children? 3) Do cord blood IgE concentration, intensity of allergen exposure in infancy, family allergic history, month of birth, or degree of passive cigarette smoke exposure significantly contribute to the risk of current asthma in 6 year old children? 4) Do cord blood IgE concentration, intensity of allergen exposure in infancy, family allergic history, month of birth, or degree of passive cigarette smoke exposure significantly contribute to the risk of bronchial hyperresponsiveness or the risk of allergic sensitivity in children? 5) How much do urinary cotinine concentrations vary in children over a 4 year period and how well do reports of cigarette smoke exposure correlate with continine measurements? 6) To what degree do in home allergen concentrations vary over 4 years and what factors influence the degree of allergen variation? 7) To what degree do allergen measurements from longitudinally collected air and dust samples correlate? The strengths of this proposal are the importance of asthma as a cause of morbidity in children, the prospective and comprehensive nature of the study design, and the high probability that significant new information will be obtained about variables influencing the development of asthma in children.

这项建议的目的是调查 多个变量之间：脐带血IgE浓度、家族 病史、早期接触过敏原的强度、被动吸烟 暴露、过敏敏感性、支气管高反应性和 哮喘，见于6至7岁的儿童。未来的儿童群体 研究对象最初是从参加了一项 大型医保组织。之前的研究针对的是141名儿童， 来自797名出生时携带脐带血IgE的儿童 浓度大于或等于0.56IU/毫升。这些孩子 被认为有更高的过敏性疾病风险，并被跟踪 每月一次，直到2岁，然后每隔一个月，直到4岁。 那些被认为有较低过敏风险的人(IgE和lt；0.56IU/ml) 每年跟进一次。对于这项提议，我们计划使用整个队列 797名儿童。在5岁和6岁时，儿童的家庭将 联系电话采访和简短的电话联系将 按4.5年和5.5年制作。6岁以后越快越好 将邀请所有儿童接受临床评估，以 确定孩子是否患有当前哮喘。评估将包括： 回顾家族过敏史，标准化病史， 体检、变应原皮肤试验、体外试验 和过敏原特异性IgE，尿可替宁分析，肺 功能测试(FVC、FEV1、PEFR和FEF25-75%)和乙酰甲胆碱 挑战。来自临床评估的信息将被结合起来 以前获得的数据包括：过敏原的测量 (螨类，L，L；猫，L；豚草，L；草，Lol P L)在卧室空气和粉尘中的浓度，脐带血免疫球蛋白E 集中度、家族史、健康史、住房记录和 尿可替宁测量以回答以下问题。1)什么 确诊的和未确诊的哮喘以及支气管哮喘的患病率 在这群孩子中有高反应性吗？2)什么是 该队列中哮喘与支气管反应性的关系 儿童？3)脐带血IgE浓度、变应原强度 婴儿期暴露、家族过敏史、出生月份或程度 被动吸烟暴露的风险显著增加。 6岁儿童当前哮喘的风险？4)脐带血IgE 婴儿期过敏原暴露浓度、强度、家族性过敏 被动吸烟史、出生月份或程度 极大地增加了支气管高反应性或 儿童过敏的风险？5)尿量 儿童的可替宁浓度在4年内的变化以及如何变化 吸烟暴露的报告与可卡因的相关性好吗？ 测量？6)家庭过敏原浓度有多大的差异？ 4年以上，影响过敏原变异程度的因素有哪些？ 7)从纵向收集的过敏原测量到什么程度 空气和尘埃样本有关联吗？这项建议的优点是 哮喘作为儿童发病原因的重要性，前瞻性 研究设计的全面性和大概率 将获得有关变量的重要新信息 影响儿童哮喘的发展。