Occupational Exposure to PM2.5 and Cardiovascular Disease(CVD)

摘要 拟议的项目是对PA-13-302的回应。这项建议的目的是扩大我们在 职业接触颗粒物对健康的影响。我们将延长对IHD事件的跟进时间 活动队列超过5年(总共20年)，并跟踪受试者在终止雇佣后，联系 这群人声称医疗保险并导致特定的死亡。 目标1：根据工作级别的暴露制定PM和选定化学品的工作暴露矩阵(JEM) 而不是不同的暴露组(DEG)，根据呼吸器的使用进行调整。目标2：审查联合行动的影响 接触化学物质和身体应激源--噪音和高温--以及工作压力，作为独立风险 IHD发病的因素，以及作为IHD的潜在混杂因素、中间体和效果修饰物 铝冶炼厂所有在职工人PM2.5暴露对心血管的影响 设施。目标3：探索植物水平、群落和早期生命对社会和环境的贡献 心血管疾病的发病特点。目标4：评估两者之间的关联 PM2.5(以及粗颗粒物PM2.5-PM10)的累积暴露和纵向下降 在肺功能方面。目标5：检查累积暴露于PM2.5、化学品 以及慢性阻塞性肺病和心血管疾病死亡率，考虑到健康状况(积极工作时的风险评分)和新的 从链接的联邦医疗保险索赔文件中获得的65岁后(离职后)的健康状况信息。 总而言之，美国铝业研究的继续与集合的调查团队一起提供了一个 无与伦比的机会来解决一系列关键的经验和方法论问题 高不可攀。除了更好地了解PM暴露的哪些方面有助于急性和 IHD、COPD和加速肺功能下降的慢性风险，我们可以了解PM是如何与 最普遍的工作场所共同暴露以及个人、工厂和社会层面的贡献 通过应用测量科学和流行病学中最先进的方法来确定决定因素。

ABSTRACT The proposed project is responsive to PA-13-302. The objective of this proposal is to extend our work on the health effects of occupational exposures to particulate matter. We will extend follow-up of incident IHD in the active cohort for 5 more years (total of 20 years) and follow subjects past termination of employment, linking the cohort to Medicare claims and cause specific mortality. Aim 1: Develop job-exposure matrices (JEMs) for PM and selected chemicals based on job-level exposures rather than distinct exposure groups (DEGs), adjusting for respirator use. Aim 2: Examine the impact of co- exposure to chemicals and physical stressors—noise and heat—as well as job stress, as independent risk factors for IHD incidence, and as potential confounders, intermediates and effect modifiers of the cardiovascular effects of PM2.5 exposure among all active workers in aluminum smelters and fabrication facilities. Aim 3: Explore the contribution of plant level, community and early life social and environmental characteristics to the incidence of cardiovascular disease. Aim 4: Estimate the associations between cumulative exposure to PM2.5 (as well as the coarse particle fraction PM2.5 - PM10) and longitudinal decline in pulmonary function. Aim 5: Examine the relationships between cumulative exposure to PM2.5, chemicals and COPD and CVD mortality, taking account of health status (risk score while actively employed) and new information on health status after age 65 (after leaving work) derived from linked Medicare claims files. Viewed altogether, continuation of the Alcoa study with the assembled team of investigators provides an unparalleled opportunity to address a host of critical empiric and methodologic issues previously unapproachable. In addition to understanding better what aspects of PM exposure contribute to acute and chronic risk of IHD, COPD and accelerated pulmonary function decline, we can learn how PM interacts with the most ubiquitous of workplace co-exposures as well as the contributions of personal, plant level and social determinants by applying state-of-the-art methods in measurement science and epidemiology.