Mechanisms of Air Pollution Health Effects in Subjects with Heart Failure

空气污染对心力衰竭患者健康影响的机制

• 批准号: 7911207
• 负责人: GREGORY A WELLENIUS
• 金额: $ 24.9万
• 依托单位: BROWN UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-29 至 2012-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7911207
• 关键词: Acute; Adverse effects; Affect; Age; Air; Air Pollution; American; Area; Autonomic nervous system; Blood Vessels; Boston; Carbon Black; Cardiovascular system; Cerebrum; Cessation of life; Clinical; Communities; Data; Elderly; Epidemiologic Studies; Event; Exposure to; Fibrinogen; Functional disorder; Health; Heart Rate; Heart failure; Hospitalization; Inflammation; Injury; Inorganic Sulfates; Intercellular adhesion molecule 1; Interleukin-6; Laboratories; Lead; Libraries; Link; Longitudinal Studies; Lung; Measurement; Measures; Modeling; Monitor; Nervous System Physiology; Ozone; Participant; Particulate; Particulate Matter; Pollution; Publishing; Risk; Sampling; Serum Markers; Site; Testing; Unspecified or Sulfate Ion Sulfates; Vascular Cell Adhesion Molecule-1; Vascular resistance; aged; ambient particle; base; burden of illness; cohort; healthy aging; healthy volunteer; heart rate variability; human old age (65+); improved; insight; land use; particle; patient population; pollutant; population based; prospective; regional pollution; trafficking; vascular inflammation; von Willebrand Factor

Evidence suggests that exposure to ambient air particles promotes altered autonomic nervous system function, systemic inflammation, and vascular endothelial injury and dysfunction. Although epidemiologic Studies suggest that people older than 65 years are at greatest risk of pollution-related cardiovascular events, these mechanistic hypotheses have frequently been evaluated in young healthy volunteers or specific patient populations, rather than in unselected community-dwelling elderly. Accordingly, we will conduct a prospective, repeated-measures study to evaluate the mechanisms by which particulate air pollution affects autonomic function, inflammation, and vascular endothelial injury and function in a cohort of community dwelling elderly aged 65 years or older. Specifically, we will link detailed environmental data with non-invasive measures of autonomic nervous system function (heart rate variability), systemic inflammation (circulating levels of specific serum markers), and endothelial function (cerebral vascular resistance and reactivity). We will assess short-term exposure to ambient air pollution using prospectively-collected measurements from a central ambient monitoring site. Available environmental data includes hourly measures of fine particulate matter (PM2.5), black carbon (BC, a measure of traffic-related pollution), sulfates (a measure of regional pollution), gaseous pollutants (CO, N02, S02, ozone), and meteorologic data. Additionally, we will use a validated spafiotemporal land-use regression model to predict short-term residential exposure to pollution specifically from traffic. We hypothesize that short-term exposure to ambient PM will be associated with adverse changes in autonomic function, inflammation, and vascular function. Results supporting these hypotheses would suggest that ambient PM has adverse effects in a representative population-based sample of community-dwelling elderly and provide insight into the mechanism of pollution-related acute cardiovascular events.

有证据表明，暴露于环境空气颗粒物会促进自主神经系统的改变。 功能、全身性炎症和血管内皮损伤和功能障碍。虽然流行病学 研究表明，65岁以上的人患污染相关心血管疾病的风险最大。 这些机制假设经常在年轻健康志愿者或 具体的患者人群，而不是在社区居住的老年人。因此，我们将 进行一项前瞻性的、重复测量的研究，以评估颗粒空气 污染影响65岁以上社区老年人的自主神经功能、炎症和血管内皮损伤和功能。具体来说，我们将把详细的环境数据与自主神经系统功能（心率变异性）、全身炎症（特定血清标志物的循环水平）和内皮功能（脑血管阻力和反应性）的非侵入性测量联系起来。我们会利用从中央环境监测站预先收集的测量数据，评估短期暴露于环境空气污染的情况。可用的环境数据包括细颗粒物（PM2.5）、黑碳（BC，交通相关污染的量度）、硫酸盐（区域污染的量度）、气态污染物（CO、N02、S02、臭氧）的每小时量度以及气象数据。此外，我们将使用一个经过验证的时空土地利用回归模型来预测短期住宅暴露于污染，特别是从交通。我们推测，短期暴露于环境PM将与自主神经功能，炎症和血管功能的不良变化。支持这些假设的结果表明，环境PM有不利影响，在一个代表性的人口为基础的样本的社区居住的老年人，并提供深入了解污染相关的急性心血管事件的机制。