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

PM2.5 职业接触与心血管疾病 (CVD)

• 批准号: 9176958
• 负责人: MARK RICHARD CULLEN
• 金额: $ 58.39万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-09-01 至 2020-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9176958
• 关键词: Occupational; Exposure; PM2.5; Cardiovascular; Disease

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.

抽象的 拟议的项目对PA-13-302有反应。该提议的目的是扩展我们的工作 职业暴露于特定问题的健康影响。我们将扩展事件IHD的随访 活跃队列多5年（总计20年），并遵循上班终止的受试者，链接 Medicare主张的队列并引起特定的死亡率。 AIM 1：根据工作水平的暴露开发PM和选定化学物质的工作曝光矩阵（JEMS） 而不是不同的暴露组（DEG），调整呼吸器的使用。目标2：检查共同的影响 暴露于化学物质和身体压力源（液压和热量）以及工作压力，作为独立风险 IHD事件的因素，以及作为潜在的混杂因素，中间体和效应修饰符 PM2.5在铝冶炼厂和制造中所有活跃工人暴露的心血管效应 设施。目标3：探索植物水平，社区和早期生活的贡献 心血管疾病事件的特征。目标4：估计 累积暴露于PM2.5（以及粗粒子分数PM2.5 -PM10）和纵向下降 在肺功能中。目标5：检查累积暴露于PM2.5，化学物质之间的关系 以及COPD和CVD死亡率，考虑到健康状况（积极就业的风险评分）和新的 从链接的Medicare索赔文件中得出的65岁以后的健康状况的信息。 完全查看，与集会的调查员团队一起进行了铝业研究的延续 以前无与伦比解决许多关键经验和方法论问题 无法接近。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下降，我们可以了解PM如何与 工作场所共同曝光以及个人，植物层面和社会的贡献，大多数无处不在 通过在测量科学和流行病学中应用最先进的方法来决定因素。