Health Effects of Early-Life Exposure to Urban Pollutants in Minority Children

描述(申请人提供)：拟议研究的主要目标是研究早期接触常见城市污染物对居住在纽约市三个低收入少数族裔社区(中央哈莱姆区、华盛顿高地和南布朗克斯区)的儿童神经行为发育和哮喘的影响。使用分子流行病学方法，在连续的时间点上进行监测、生物标记物和临床评估，我们将扩大我们对非洲裔美国人和拉丁裔城市母亲和儿童的研究，以便跟踪队列直到11岁儿童，以评估暴露于环境中对儿童健康和发育结果的长期影响。令人关切的暴露包括空气中的多环芳烃(PAHs)和有机磷农药，如毒死蜱(CPF)。第一个具体目标(神经发育)建立在我们之前的研究结果的基础上，并建议评估早期暴露(PAHs和CPF)与长期神经发育之间的关系，以评估神经毒性影响在学年中的持久性，确定可能随着时间的推移而出现的影响，并更深入地研究行为领域，以更好地理解在学龄前几年观察到的行为问题的重要性。第二个目标(哮喘)也建立在我们之前关于哮喘危险因素的发现的基础上。我们将在5岁、7岁和9岁时重复免疫球蛋白(LG)E的评估，并在5到7岁之间获得肺功能和呼吸道炎症的测量，以及医生对哮喘的诊断。我们还将评估在生命的前5年超重与儿童时期的IgE、呼吸道炎症和哮喘的发展之间的关系。这项研究将考虑已知的疾病决定因素和潜在混杂因素的影响，包括其他毒性暴露和人口统计因素。通过使用多学科方法来理解给市中心儿童带来如此沉重负担的发育障碍和哮喘的复杂发病机制，我们预计拟议的研究将对预防具有重要意义。

DESCRIPTION (provided by applicant): The major objective of the proposed research is to study the impact of early-life exposures to common urban pollutants on neurobehavioral development and asthma in a sample of children living in three low-income, minority communities of New York City (Central Harlem, Washington Heights and the South Bronx). Using a molecular epidemiologic approach with monitoring, biomarkers, and clinical assessments at serial time points, we will extend our study of African-American and Latina urban mothers and children in order to follow the cohort through child age 11 years to assess the longer-term impact of exposures on child health and developmental outcomes. The exposures of concern include airborne polycyclic aromatic hydrocarbons (PAHs) and orgnaophosphate pesticides such as chlorpyrifos (CPF). The first Specific Aim (Neurodevelopmental) builds on our prior findings and proposes to evaluate relationships between early exposures (PAHs and CPF) and longer-term neurodevelopment, in order to assess the persistence of neurotoxic effects into the school years, identify effects that may emerge over time, and delve more deeply into the behavioral domains to better understand the significance of behavior problems observed in the preschool years. The second aim (Asthma) also builds on our previous findings with respect to risk factors for asthma. We will repeat the assessment of immunoglobulin (lg)E at ages 5, 7, and 9 and obtain measures of lung function and airway inflammation, and a physician-diagnosis of asthma between ages 5 and 7 years. We will also assess the association between becoming overweight in the first 5 years of life and the development of IgE, airway inflammation, and asthma in childhood. The research will consider the effect of known determinants of disease and potential confounders, including other toxic exposures and demographic factors. By using a multidisciplinary approach to understand the complex pathogenesis of developmental disorders and asthma that impose such a heavy burden on inner-city children, we anticipate that the proposed research will have important implications for prevention.