Mechanisms of Air Pollution Health Effects in Subjects with Heart Failure

有证据表明，暴露在环境空气颗粒物中会促进自主神经系统的改变 功能、全身炎症、血管内皮损伤和功能障碍。虽然在流行病学上 研究表明，65岁以上的人患与污染有关的心血管疾病的风险最大 这些机械性假说经常在年轻的健康志愿者或 具体的患者群体，而不是未经选择的社区居住的老年人。因此，我们将 进行一项前瞻性的重复测量研究，以评估颗粒性空气 在一组65岁或以上的社区老年人中，污染影响自主神经功能、炎症、血管内皮损伤和功能。具体地说，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(特定血清标记物的循环水平)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。我们将使用从中央环境监测点收集的前瞻性测量数据来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每小时细颗粒物(PM2.5)、黑碳(BC，与交通相关的污染的衡量标准)、硫酸盐(地区污染的衡量标准)、气态污染物(CO、N02、S02、臭氧)和气象数据。此外，我们将使用经过验证的时空土地使用回归模型来预测住宅短期暴露于交通污染的风险。我们假设，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利变化相关。支持这些假设的结果将表明，环境颗粒物对社区老年人的代表性人群样本具有不良影响，并为了解与污染相关的急性心血管事件的机制提供了洞察力。

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.