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

描述（由申请人提供）：拟议研究的主要目的是研究生活在纽约市三个低收入少数族裔社区（哈莱姆中部、华盛顿高地和南布朗克斯）的儿童样本中，早期暴露于常见城市污染物对神经行为发育和哮喘的影响。采用分子流行病学方法，在连续时间点进行监测、生物标志物和临床评估，我们将扩展我们对非洲裔美国人和拉丁裔城市母亲和儿童的研究，以便跟踪整个队列，直到儿童11岁，以评估暴露对儿童健康和发育结果的长期影响。受关注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）。第一个特定目标（神经发育）建立在我们之前的研究结果的基础上，并提出评估早期接触（多环芳烃和CPF）与长期神经发育之间的关系，以评估神经毒性影响在学龄期的持久性，识别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之上。我们将在5岁、7岁和9岁时重复免疫球蛋白（lg）E的评估，并获得肺功能和气道炎症的测量结果，以及5至7岁之间哮喘的医生诊断。我们还将评估5岁前超重与儿童时期IgE、气道炎症和哮喘发展之间的关系。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，包括其他有毒接触和人口因素。通过使用多学科方法来了解给城市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.