Diabetes, Cardiac Disease, and Pollution Vulnerability

颗粒物空气污染与心血管疾病的死亡和发病率有关，但这些联系背后的机制并不是愚蠢的。患有糖尿病或既往存在的冠状动脉疾病会增加与颗粒物相关的心脏病发病风险。糖尿病患者的风险可能会增加，因为空气污染干扰了与糖尿病相同的途径？炎症、血管/内皮和自主神经功能。在波士顿的一项重复测量的前瞻性研究中，包括45名患有2型糖尿病的非吸烟者和45名冠心病患者，每隔一周观察一次，总共观察5次(450次重复测量) 我们假设：(L)血管和内皮功能(例如，基础动脉内径、内皮依赖性血管反应性)；肺和全身炎症，以及自主神经功能(例如，心率变异性)受到颗粒性空气污染的不利影响；(2)血管和内皮功能(例如，基础动脉直径、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以下水平的变化而变化：(A)以黑碳为指标的交通相关颗粒物水平，以及(B)以SO4为指标的长距离交通颗粒物水平。污染暴露将通过中央站点进行估计 (例如，连续PM2.5、黑碳；24小时综合SO4)、个人(即连续PM2.5、24小时综合PM2.5、黑碳(颗粒反射率)和SO4)和社区一级的衡量标准。观察指标包括肱动脉内径、内皮依赖性血流介导的扩张、增大指数、呼出的NO(肺部炎症的标志物)、全身炎症/内皮细胞活化的标志物(WBC、纤维蛋白原、C反应蛋白、IL-6、TNF-a；sICAM-1、sVCAM-1、ET-1)和心率变异性。这项研究将为环境污染与过度心脏风险相关的机制提供更多的见解，并可能为如何制定预防策略来降低这种风险提供线索。

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.