ENVIRONMENTAL DETERMINANTS OF CHILDHOOD ASTHMA

儿童哮喘的环境决定因素

• 批准号: 2062477
• 负责人: Dennis R Ownby
• 金额: $ 29.9万
• 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/2062477
• 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.

本提案的目的是调查 多个变量之间：脐带血IgE浓度，家庭 病史、早期过敏原暴露强度、被动吸烟 暴露、过敏敏感性、支气管高反应性，以及 哮喘，6至7岁的儿童。 这群孩子将成为 研究对象最初是从参加一个 大型健康维护组织 先前的研究针对的是141名儿童， 来自797名出生时就患有脐带血IgE的儿童队列 浓度大于或等于0.56 IU/mL。 这些孩子 被认为是过敏性疾病的高风险人群， 每月一次，直到2岁，然后每隔一个月，直到4岁。 那些感觉过敏风险较低（IgE < 0.56 IU/ml）的人已经被 每年跟踪。 对于这个建议，我们计划使用整个队列的 797个孩子。 在5岁和6岁时，儿童的家庭将 电话采访和简短的电话联系将 4.5和5.5年。 6岁以后尽快 所有儿童将被邀请接受临床评估， 确定孩子是否患有哮喘。 评价将包括： 家族过敏史的回顾，标准化的病史， 体格检查、过敏原皮肤试验、体外试验 和过敏原特异性IgE，尿液分析可替宁，肺 功能测试（FVC、FEV 1、PEFR和FEF 25 -75%）和乙酰甲胆碱 挑战. 将合并临床评价的信息 先前获得的数据包括：过敏原的测量 （螨，Der f l，Der p l;猫，Fel d l;豚草，Amb a l;和草，Lol p l）卧室空气和灰尘样品中的浓度，脐带血IgE 浓度，家族史，健康史，住房记录，以及 尿可替宁测量，以回答以下问题。 1)什么 已确诊和未确诊的哮喘和支气管哮喘的患病率 高反应性的儿童吗 2)是什么 本队列中哮喘与支气管反应性的关系 孩子们吗 3)脐血IgE浓度、过敏原强度 婴儿期暴露、家族过敏史、出生月份或程度 被动吸烟暴露显著增加了 6岁儿童哮喘的发病率 4)脐带血IgE 浓度，婴儿期过敏原暴露强度，家庭过敏 病史、出生月份或被动吸烟暴露程度 显著增加支气管高反应性的风险，或 儿童过敏的风险？ 5)小便多少钱 可替宁浓度在儿童中变化超过4年， 香烟烟雾暴露的报告与continine有很好的关联 测量？ 6)在家中过敏原浓度变化到什么程度 4年以上，哪些因素影响过敏原的变化程度？ 7)从纵向收集的过敏原测量结果 空气和灰尘样本有关联吗 这项建议的优点是， 哮喘作为儿童发病原因的重要性， 研究设计的综合性和高概率 将获得有关变量的重要新信息 影响儿童哮喘的发展。