Early Environmental Hygiene and Pediatric Asthma

哮喘的患病率在世纪在大多数发达国家（如果不是全部的话）有所增加， 世界欧洲共同体呼吸健康调查和国际研究的主要结果 儿童哮喘和过敏的主要原因是哮喘的患病率在全球范围内不断增加; 在西方国家很常见;在英语国家更普遍;在发展中国家越来越多 随着西方化和城市化的发展，CDC估计，从1月到3月， 2006年，超过2200万美国人（8.0%）患有哮喘，比2005年的7.8%有所增加。而 许多研究表明，哮喘的发展有很强的遗传影响，这些变化 已经太快了，不能仅仅用遗传学来解释，人们普遍假设早期生命 暴露会影响婴儿对哮喘的易感性。 在美国，哮喘发病率和死亡率在少数民族中最高。一 减少种族差异的方法包括通过调整哮喘发病率来降低哮喘发病率 的风险因素。本提案的目的是对生命早期环境进行流行病学调查 因素，重点是宠物暴露和内毒素，可能会改变免疫发育，基于 这是一个前提，即对环境刺激的早期免疫反应的变化会影响哮喘的风险。 在过去的100年里，人类接触动物（可能是内毒素）的比例已经下降， 城市化和郊区化，尽管人类在与动物密切接触的情况下进化。 作为正在进行的研究的一部分，韦恩县健康，环境，过敏和哮喘纵向 研究（WHEALS），一个多种族的孕妇队列已被招募的前瞻性研究，他们的 孩子通过这次更新，我们将对1248名不同种族的儿童进行5 - 6岁的随访。 背景（60%黑色）。我们将使用WHEALS队列来1）评估宠物接触和家庭是否 内毒素水平影响总的和变应原特异性IgE和细胞外细胞因子（IL 4，IL 5，IL 13，IFN β，IL2，IL12， 在婴儿期（出生，6岁）的4个时间点测量受刺激的T细胞产生的TNF和IL 10）模式 月、12个月和2年）和2）这些暴露和免疫模式如何与 5 - 6岁时临床哮喘的患病率。最后，将对数据进行分析，以评估布莱克 种族在早期环境暴露与免疫学生物标志物之间的关系中发挥作用， 在考虑了其他不可改变和可改变的风险因素（包括CD14基因型、家族史）后， 病史、儿童性别、出生顺序、出生特征、社会经济地位以及其他社会、行为和 环境变量。如果与动物或内毒素接触有关的因素与哮喘风险有关， 这些因素可能有助于公共卫生干预。

The prevalence of asthma has increased over the 20th century in most, if not all, developed countries of the world. Major findings from the European Community Respiratory Health Survey and the International Study of Asthma and Allergies in Childhood were that asthma prevalence is increasing worldwide; is generally more common in Western countries; more prevalent in English-speaking countries; and increasing in developing countries as they become more Westernized or become urbanized. CDC estimated that from January to March of 2006 more than 22 million Americans (8.0%) suffered from asthma, an increase from 7.8% in 2005. While many studies have demonstrated strong inherited influences on the development of asthma, these changes have been too rapid to be explained solely by genetics, and it has been widely hypothesized that early life exposures influence an infant¿s susceptibility to asthma. In the US, asthma morbidity and mortality are highest among persons who are of minority status. One approach to reducing racial disparities involves targeting reductions in asthma incidence through modification of risk factors. The objective of this proposal is the epidemiological investigation of early life environmental factors, focusing on pet exposure and endotoxin, that may alter immunologic development, based on the premise that variations in the early immune response to environmental stimuli affects risk for asthma.The level of exposure of humans to animals (and presumably endotoxin) has declined over the last 100 years through urbanization and suburbanization, although humans have evolved with close contact with animals. As part of an ongoing study, the Wayne County Health, Environment, Allergy & Asthma Longitudinal Study (WHEALS), a multi-ethnic cohort of pregnant women has been recruited for prospective study of their children. With this renewal, we will extend follow-up to 5-6 years of age for the 1248 children of varied racial backgrounds (60% Black). We will use the WHEALS cohort to 1) evaluate whether pet contact and household endotoxin levels affect total and allergen-specific IgE and extracellular cytokine (IL4, IL5, IL13, IFN?, IL2, IL12, TNF and IL10 production by stimulated T-cells) patterns measured at 4 points in time during infancy (birth, 6 months, 12 months and 2 years) and 2) how these exposures and immunological patterns are related to the prevalence of clinical asthma at age 5-6 years. Finally, the data will be analyzed to evaluate the role that Black race plays in the relationship between early environmental exposures and immunological biomarkers and asthma, after accounting for other non-modifiable and modifiable risk factors including CD14 genotype, family history, child sex, birth order, birth characteristics, socioeconomic status, and other social, behavioral and environmental variables. If factors associated with animal or endotoxin contact are related to asthma risk, such factors would likely lend themselves to public health interventions.