Urban Diesel Exposure and Inner City Asthma
Urban Diesel Exposure and Inner City Asthma
批准号:
7472464
负责人:
RACHEL L MILLER
金额:
$62.1万
依托单位国家:
美国
项目类别:
财政年份:
2005
资助国家:
美国
项目状态:
已结题
起止时间:
2005-07-16 至 2010-06-30
关键词:
AdolescentAfrican AmericanAgeAir PollutantsAir PollutionAllergensAllergicAntigensAreaAsthmaBirthCarbonCarbon BlackChildChildhood AsthmaDataDevelopmentDiagnosisDiesel ExhaustDominicanEnvironmental ExposureEnvironmental HealthEnvironmental Tobacco SmokeExposure toGoalsHealthHome environmentHypersensitivityHypersensitivity skin testingIgEInterventionLeadLifeLungMalignant NeoplasmsMeasurementMeasuresMedical ResearchMonitorNew YorkOutcomeParticulate MatterPollenProtocols documentationRecruitment ActivityRelative (related person)ReportingRespiratory physiologyRiskSerumSymptomsT-Cell ProliferationThird Pregnancy TrimesterTrace metalUrineWeekair monitoringatopybasecohortinner citymemberpulmonary functionrespiratorytrafficking
中文摘要
描述(由申请人提供):生活在机动交通量大的地区与儿童的呼吸道症状和肺功能下降有关。根据这些流行病学调查结果和支持性实验数据,暴露于与柴油相关的空气污染可能会导致包括哮喘和过敏在内的健康问题。然而,尽管我们在认识到可能的柴油引起的哮喘或过敏症状方面取得了很大进展,但暴露于柴油相关的空气污染与幼儿特应性和哮喘发作之间的直接联系尚未得到证实。柴油暴露与其他城市暴露对呼吸系统健康的相互作用也不清楚。我们假设,暴露于北方曼哈顿和南布朗克斯的柴油排放物与5至6岁儿童的过敏原特异性致敏、肺功能下降和哮喘发作有关。我们的策略是利用一个已建立的内城出生队列,其中多种环境暴露和健康结果已经被测量,以评估是否暴露于柴油相关的空气污染独立,或与其他流行的城市环境暴露(过敏原,环境烟草烟雾[ETS]),增加特应性或哮喘发作的风险。具体而言,我们建议使用我们已建立的队列:
目标1。确定暴露于柴油相关的空气污染是否与5至6岁时过敏原特异性致敏、肺功能下降和/或哮喘的发生相关,
目标2.确定暴露于柴油相关空气污染是否与a)过敏原和/或B)ETS暴露相互作用,在5-6岁时发生过敏原特异性致敏、肺功能下降和/或哮喘。
作为哥伦比亚儿童环境健康中心的一部分,将招募居住在北方曼哈顿的300名多米尼加和非洲裔美国儿童,他们从出生起就接受前瞻性随访,年龄为5至6岁。将在家中进行为期两周的空气监测,以监测多环芳烃、黑碳、质量和痕量金属。6个月后将重复测量PM25和碳。结果包括血清IgE、抗原特异性T细胞增殖、过敏皮肤试验、肺功能和哮喘诊断。主要目标是确定柴油相关暴露是否会诱发过敏和/或哮喘的发生,并确定其相对于其他城市暴露的贡献。
英文摘要
DESCRIPTION (provided by applicant): Living in areas with high volumes of motorized traffic has been associated with respiratory symptoms and deceased lung function in children. Based on both these epidemiological findings and supporting experimental data, exposure to diesel-related air pollution has potential for health concerns that include asthma and allergy. However, despite substantial gains in our recognition of likely diesel-induced asthmatic or allergic symptoms, direct associations between exposure to diesel-related air pollution and the onset of atopy and asthma in young children have not yet been demonstrated. The interaction of diesel exposure with other urban exposures on respiratory health also is not clear. We hypothesize that exposure to diesel emissions in Northern Manhattan and the South Bronx is associated with allergen-specific sensitization, decreased lung function, and the onset of asthma in children at age 5 through 6 years. Our strategy is to take advantage of an established inner city birth cohort in which multiple environmental exposures and health outcomes already are being measured to evaluate whether exposure to diesel-related air pollution independently, or jointly with other prevalent urban environmental exposures (allergens, environmental tobacco smoke [ETS]), increase the risk for the onset of atopy or asthma. Specifically, we propose to use our established cohort to:
Aim 1. Determine whether exposure to diesel-related air pollution is associated with the onset of allergen-specific sensitization, decreased lung function and/or asthma at age 5 through 6 years, and
Aim 2. Determine whether exposure to diesel-related air pollution interacts with a) allergen, and/or b) ETS exposure, on the onset of allergen-specific sensitization, decreased lung function and/or asthma at age 5-6 years.
300 Dominican and African American children residing in Northern Manhattan that are being followed prospectively since birth as part of Columbia Center for Children's Environmental Health will be recruited at age 5 through 6 years. Two-week air monitoring at home for PAHs, black carbon, mass, and trace metals will be performed. Repeat measures of PM25 and carbon will be repeated 6 months later. Outcomes include sera IgE, antigen-specific T cell proliferation, allergy skin tests, lung function, and asthma diagnosis. The primary goals are to determine whether diesel-related exposure can induce the development of allergy and/or asthma, and to identify its contribution relative to other urban exposures.
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科研奖励(0)
会议论文
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海外基金