Air pollution exposure and COPD in the Framingham Heart Study

描述(申请人提供)：空气污染已被发现会引发慢性阻塞性肺疾病(COPD)的恶化和死亡，但尚不清楚美国的慢性室外空气污染是否会导致COPD的发展。在美国，每四名COPD患者中就有一人从未吸烟，但除了吸烟之外，对暴露在COPD发病机制中的作用知之甚少。很少有研究能够重复测量肺活量并检查多次暴露，包括细颗粒物的成分，以了解哪些暴露对肺功能最有害。该项目的目的是确定暴露于周围污染物(来自交通、发电厂和工业过程)对患有和不患有COPD的受试者的肺功能的急性影响；其次，使用最先进的暴露评估工具，确定长期暴露于空气污染是否会增加临床或亚临床COPD的风险。我们将在弗雷明翰心脏研究的后代和第三代队列的7,000多名受试者中调查这些问题，从1995年到现在，我们一直在使用重复的肺活量测定、近3,000名受试者的定量胸部CT和我们小组最近开发的详细的地理编码暴露评估数据进行跟踪。我们假设，短期暴露于空气污染物(细颗粒物、黑碳、臭氧、氮氧化物、硫酸盐和金属)的高度将通过肺活量测定和经吸烟调整后的DLCO来损害肺功能。我们进一步假设，长期接触细颗粒物(使用卫星模型)、黑碳(使用区域时空模型)和交通(使用住宅到主要道路的距离和住宅周围的交通密度)将与(1)肺活量测量中的气流阻塞增加和(2)定量CT测量的低密度区(肺气肿的测量)和壁面厚度(呼吸道疾病的测量)的增加相关。作为研究培训计划的一部分，首席调查员将完成 公共卫生硕士，专注于定量方法，以掌握完成这项工作所需的流行病学和生物统计学技能。这项研究项目将在流行病学和空气污染健康影响研究方面的知名调查员的指导下进行，并听取环境阻塞性肺病和CT定量分析专家的建议。

DESCRIPTION (provided by applicant): Air pollution has been found to trigger chronic obstructive pulmonary disease (COPD) exacerbations and deaths, but it is unknown whether chronic outdoor air pollution in the U.S. contributes to the development of COPD. One in four patients in the U.S. with COPD has never smoked, yet little is known about the role of exposures other than smoking in COPD pathogenesis. Few studies have been able to measure spirometry repeatedly and examine multiple exposures, including constituents of fine particulate matter, to understand which exposures are most harmful to lung function. The purpose of this project is to identify the acute effects of exposure to ambient pollutants (from traffic, power plants and industrial processes) on lung function in subjects with and without COPD and secondly to determine, using state-of-the art exposure assessment tools, if chronic exposures to air pollution increase risk of developing clinical or subclinical COPD. We will investigate these questions in the more than 7,000 subjects of the Framingham Heart Study's Offspring and Third Generation cohorts, who have been followed from 1995 to the present with repeated spirometry, a quantitative chest CT in a subset of nearly 3,000 subjects, and detailed geocoded exposure assessment data recently developed by our group. We hypothesize that elevations in short-term exposure to air pollutants (fine particulate matter, black carbon, ozone, nitrogen oxides, sulfates and metals) will impair lung function by spirometry and DLCO after adjustment for smoking. We further hypothesize that long-term exposure to fine particulate matter (using a satellite model), black carbon (using a regional tempero-spatial model) and traffic (using distance from residence to major roadway and traffic density around residence) will be associated with (1) increased airflow obstruction on spirometry and (2) increased percentage of low attenuation area (a measure of emphysema) and wall area thickness (a measure of airways disease) measured by quantitative CT. As part of the research training program, the principle investigator will complete a Master of Public Health with a concentration in Quantitative Methods in order to master the needed skills in epidemiology and biostatistics to complete this work. This research project will be performed under the guidance of a well-established investigator in epidemiology and air pollution health effects research and with advice from experts in environmental obstructive lung disease and quantitative CT analysis.