Diabetes, Cardiac Disease, and Pollution Vulnerability

空气颗粒物污染与心血管疾病的死亡和发病率有关，但这些关联背后的机制尚未完全了解。患有糖尿病或既存冠状动脉疾病会增加颗粒相关的心脏病发病风险。糖尿病患者的风险可能会增加，因为空气污染会扰乱与糖尿病相同的途径？炎症、血管/内皮和自主神经功能。在一项重复测量波士顿前瞻性研究中，包括45例2型糖尿病非吸烟受试者和45例冠状动脉疾病受试者，每隔一周观察一次，共5次访视（450次重复测量） 我们假设：（1）血管和内皮功能（例如，基底动脉直径，内皮依赖性血管反应性）;肺部和全身炎症，以及自主功能（例如，心率变异性）受到颗粒空气污染的不利影响;和（2）血管和内皮功能（例如，基底动脉直径、内皮依赖性血管反应性）、炎症标志物和自主神经功能将随着（a）交通相关颗粒水平（如由炭黑指示的）和（B）长程运输颗粒水平（如由SO 4指示的）的水平而变化。将通过中心站点估计污染暴露 (e.g、连续PM2.5、黑碳; 24小时综合SO 4）、个人（即，连续PM2.5; 24小时综合PMa.s、黑碳（颗粒反射率）和SO 4）以及社区水平测量。结果测量将包括肱动脉直径、内皮依赖性血流介导的扩张、增强指数、呼出的NO（肺部炎症的标志物）、全身性炎症/内皮活化的标志物（WBC、纤维蛋白原、C-反应蛋白、IL-6、TNF-α; sICAM-1、sVCAM-1、内皮素-1）和心率变异性。这项研究将提供额外的洞察机制，环境污染与过度的心脏风险，并可能提供线索，如何制定预防策略，以减少这种风险。

Particulate air pollution has been associated with cardiovascular deaths and morbidity, but the mechanisms behind those associations are not folly understood. Having diabetes or pre-existing coronary artery disease increases the particle-associated risk for cardiac morbidity. Diabetics may be at increased risk because air pollution disturbs the same pathways as diabetes ? inflammation, vascular/endothelial and autonomic function. In a repeated measures Boston prospective study including 45 non-smoking subjects with Type 2 diabetes and 45 subjects with coronary artery disease observed every other week for 5 total visits (450 repeated measures) we hypothesize that:(l) Vascular and endothelial function (e.g., basal arterial diameter, endothelium-dependent vascular reactivity); pulmonary and systemic inflammation, and autonomic function (e.g, heart rate variability) are adversely affected by particulate air pollution; and (2) Vascular and endothelial function (e.g., basal arterial diameter, endothelium-dependent vascular reactivity), inflammatory markers, and autonomic function will vary with level of (a) traffic-related particles levels, as indexed by black carbon, and (b) long-range transport particles levels, as indexed by SO4. Pollution exposure will be estimated through central site (e.g, continuous PM2.5, black carbon; 24-h integrated SO4), personal (i.e., continuous PM2.5; 24-h integrated PMa.s, black carbon (particle reflectance), and SO4), and community level measures. Outcome measures will include brachial artery diameter, endothelium-dependent flow mediated dilation, augmentation index, exhaled NO (marker of pulmonary inflammation), markers of systemic inflammation/endothelial activation (WBC, fibrinogen, C-reactive protein, IL-6, TNF-a; sICAM-1, sVCAM-1, endothelin-1), and heart rate variability. This study will provide additional insight into the mechanisms whereby ambient pollution is associated with excess cardiac risk and may provide clues as to how to develop preventive strategies to reduce this risk.