Air Pollution, Coronary Events and Atherosclerotic Progression in a Susceptible Population

易感人群中的空气污染、冠状动脉事件和动脉粥样硬化进展

• 批准号: 10454154
• 负责人: Meng Wang
• 金额: $ 29.21万
• 依托单位: STATE UNIVERSITY OF NEW YORK AT BUFFALO
• 依托单位国家: 美国
• 财政年份: 2021
• 资助国家: 美国
• 起止时间: 2021-07-21 至 2026-04-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10454154
• 关键词: 12-HETE; Address; Age; Air; Air Pollutants; Air Pollution; Algorithms; American; Angiography; Arterial Fatty Streak; Atherosclerosis; Biological; Biological Markers; Biological Process; Biometry; Blood; Blood Vessels; Caliber; Carbon Black; Cardiovascular system; Caring; Cause of Death; Cessation of life; China; Clinic Visits; Clinical Management; Clinical assessments; Coronary; Coronary Arteriosclerosis; Coronary Stenosis; Coronary heart disease; Data; Development; Disease; Disease Progression; Environmental Exposure; Environmental Risk Factor; Epidemiology; Exposure to; Fatty acid glycerol esters; Functional disorder; Health Benefit; Health Policy; Health protection; Imaging technology; Individual; Indoor Air Pollution; Inflammation; Intervention; Joints; Knowledge; Lipid Peroxidation; Lipids; Longitudinal cohort study; Measures; Mediating; Modality; Modeling; Morbidity - disease rate; Morphology; Nitrogen Oxides; Noise; Outcome; Oxidative Stress; Ozone; Participant; Particle Size; Particulate Matter; Pathway interactions; Patients; Play; Policies; Pollution; Population; Prevention; Public Health; Public Policy; Regulation; Risk; Role; Rupture; Site; Source; Stenosis; Thrombosis; Time; Toxic effect; X-Ray Computed Tomography; ambient air pollution; attenuation; calcification; cardiovascular health; clinical biomarkers; coarse particles; cohort; cooking; coronary calcium scoring; coronary event; critical period; evidence base; experience; fine particles; high risk; improved; indexing; indoor pollutant; inflammatory marker; insight; interest; mortality; multidisciplinary; novel; novel marker; novel strategies; phenotypic data; population based; public health priorities; response; solid fuel; specific biomarkers; stressor; ultrafine particle; vascular inflammation

Abstract Cardiovascular health is a global public health priority. Atherosclerosis is the most common form of coronary heart diseases (CHD) which constitutes 17.5 million deaths worldwide annually. Globally, both outdoor and indoor air pollutants are known as major contributors to the burdens of CHD. Despite population-based evidence suggesting that exposure to ambient air pollutants and use of solid fuel for cooking causes increased mortality from CHD, there is little known about the impact of air pollution on CHD morbidity and progression. For example, the extent to which exposure to air pollution accelerates atherosclerosis, initiate plaque instability to rupture and develop coronary events, and the mechanistic pathways underneath are largely unknown. A better understanding of air pollutants as potential factors to the development and progression of this pervasive disease will be valuable for public health protection strategies, especially for susceptible population such as patients with atherosclerosis. Here we propose a longitudinal cohort study and present an overarching hypothesis that long-term exposure to air pollutants alter coronary biological process, accelerate disease progression, and contribute to CHD morbidity and mortality. This study builds upon a well-selected 3500 patients with atherosclerosis in Beijing retrieved from an existing cohort and will add two waves of clinic visits in 1100 subpopulation to examine disease progression. The cohort includes extensive data of novel subclinical markers from computed tomography angiography (CTA) reflecting plaque morphology, plaque vulnerability, vascular stenosis, and coronary inflammation, and also collects biomarkers related to their mechanistic pathways. We also propose to add state-of-the art air pollution exposure assessment to determine individual level of outdoor and indoor air pollution exposure of the highest quality to address our study hypotheses. Firstly, we will determine the impact of outdoor and indoor air pollution exposures on coronary events and total cardiovascular mortality. Secondly, we will investigate the effects of exposure to air pollution on atherosclerosis progression and high-risk plaque formation characterized by CTA outcomes. Thirdly, we will examine the effects of air pollution on biological markers of inflammation pathways and explore whether these pathways mediate any response of disease progression to air pollution exposure. Lastly, we will take the unique opportunity of the most stringent regulation period on air pollution in Beijing and assess whether long-term decline in ambient air pollution change the worsening of the disease progression and biological responses as our secondary hypothesis. Apart from the main analysis, we will also explore the potential of joint effects of air pollutant mixtures and independent effects of air pollution exposure from traffic noise on CHD. Findings from this study will not only extend scientific knowledge on air pollution and CHD physiopathology, but will provide information to guide public policy and inform clinical management for individuals at-risk of CHD.

抽象的 心血管健康是全球公共卫生的重点。动脉粥样硬化是最常见的冠状动脉形式 每年在全球范围内占1750万死亡的心脏病（CHD）。全球，户外和 室内空气污染物被称为冠心病负担的主要贡献者。尽管基于人群 证据表明暴露于环境空气污染物并将固体燃料用于烹饪原因增加 冠心病的死亡率对空气污染对冠心病发病率和进展的影响鲜为人知。 例如，暴露于空气污染的程度会加速动脉粥样硬化，启动斑块不稳定性 破裂和发展冠状动脉事件，下面的机械途径在很大程度上是未知的。一个 更好地理解空气污染物是这种普遍性发展和发展的潜在因素 疾病对于公共卫生保护策略很有价值，特别是对于易感人群（例如 动脉粥样硬化的患者。在这里，我们提出了一项纵向队列研究，并提出了总体 假设长期暴露于空气污染物改变冠状动脉生物学过程，加速疾病 进展，并导致冠心病发病率和死亡率。这项研究建立在经过良好选择的3500的基础上 从现有队列中检索的北京动脉粥样硬化的患者将增加两波诊所就诊 在1100个亚群中检查疾病进展。该队列包括新型亚临床的广泛数据 来自计算机断层扫描（CTA）的标志物，反映了斑块形态，斑块脆弱性， 血管狭窄和冠状动脉炎症，还收集与机械的生物标志物 途径。我们还建议添加最先进的空气污染暴露评估以确定个体 最高质量的室外和室内空气污染水平，以解决我们的研究假设。 首先，我们将确定室外和室内空气污染暴露对冠状动脉事件的影响 心血管死亡率。其次，我们将研究暴露于空气污染对动脉粥样硬化的影响 以CTA结果为特征的进展和高风险斑块形成。第三，我们将检查 空气污染对炎症途径的生物标记物的影响，并探索这些途径是否 调解疾病进展对空气污染暴露的任何反应。最后，我们将采取独特 最严格的北京空气污染法规时期的机会，并评估是否长期 周围空气污染的下降改变了疾病进展的恶化和生物学反应的恶化 我们的次要假设。除了主要分析外，我们还将探索空气联合影响的潜力 污染物混合物和空气污染暴露于交通噪声的独立影响。来自 这项研究不仅将扩展有关空气污染和冠心病生理学的科学知识，而且还将提供 指导公共政策并为冠心病患者提供临床管理的信息。