Air Pollution and Cardiac Risk: Mechanisms & Time-course

空气污染和心脏风险：机制

• 批准号: 7265350
• 负责人: Duanping Liao
• 金额: $ 29.23万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-06-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7265350
• 关键词: Acute myocardial infarction; Address; Affect; Age; Air Pollutants; Air Pollution; Ambulatory Monitoring; Ammonium; Appendix; Archives; Arrhythmia; Arts; Binding; Biometry; Blood; Blood Pressure; Blood Pressure Monitors; Blood coagulation; Blood specimen; Budgets; Caliber; Carbon; Cardiac; Cardiovascular Diseases; Cardiovascular Models; Cardiovascular system; Certification; Characteristics; Chemicals; Clinical Trials; Coagulation Process; Coal; Complex; Condition; Congestive Heart Failure; Cross-Sectional Studies; Data; Data Collection; Data Quality; Data Set; Data Storage and Retrieval; Databases; Diabetes Mellitus; Diagnosis; Disease model; Disease regression; Echocardiography; Electrocardiogram; Elements; End Point; Enrollment; Environmental Health; Event; Exclusion Criteria; Exposure to; Fire - disasters; Frequencies; Health; Heart Atrium; Heart Rate; Heart Valve Diseases; Holter Electrocardiography; Hour; Hypertension; Hypertrophy; Individual; Inflammation; Inflammatory; Inorganic Sulfates; Interdisciplinary Study; Investigation; Laboratories; Laboratory Chemicals; Lead; Left; Left Ventricular Ejection Fraction; Left Ventricular Mass; Linear Regressions; Link; Liquid substance; Logistics; Manuscripts; Measurement; Measures; Metals; Methodology; Methods; Modeling; Modification; Monitor; Myocardial Ischemia; Nitrates; Nurses; Participant; Patients; Persons; Phase; Pollution; Population; Power Plants; Predisposition; Principal Investigator; Procedures; Protocols documentation; Publications; Purpose; Range; Recruitment Activity; Research; Research Personnel; Residual state; Resources; Risk; Series; Specialist; Standards of Weights and Measures; Statistical Models; System; Testing; Time; Time Series Analysis; Toxic effect; Training; Universities; Unspecified or Sulfate Ion Sulfates; Ventricular Premature Complexes; Water; Work; air pollution control; ambient particle; base; clinically relevant; congenital heart disorder; day; design; egg; functional status; indexing; markov model; nitrate; particle; response; time use; volunteer

DESCRIPTION (provided by applicant): Although consistent associations between ambient PM pollution and cardiovascular disease have been identified, the exact mechanisms, the time course by which PM causes the toxic effects, and effects of different PM species are not adequately understood. This study investigates clinically relevant arrhythmogenic, cardiac autonomic control, repolarization, myocardial ischemia, blood pressure (BP), inflammatory, coagulation, and fibrinolytic mechanisms and time course of PM2.5 effects (both concentration and species). Specifically, is personal short-term exposure to elevated ambient PM2.5 directly related to: (I) the onset of arrhythmic episodes (2) higher frequency of arrhythmias (3) lower heart rate variability (HRV) indices? (4) prolonged repolarization measured by QT index? (5) ST-segment level? Can this association be totally or partially attributed to the change of HRV and QT? (6) elevated ambulatory BP (SBP, DBP, and PP)? What are the time-courses (from minutes to hours) of the effects listed from 1-6 above? (7) Is personal short-term exposure to elevated ambient PM2.s (24-hour cumulative exposure) directly related to elevated markers of inflammation, blood coagulation, and fibrinolytic activity? (8) Are 24-hour cumulative concentrations of the ambient PM2.5 species, mostly emitted/formed from coal-fire power plant and vehicle combustion, associated with the above endpoints (Hypotheses 1-7)? (9) Are the associations between ambient PM2.5 concentration and cardiac endpoints (Hypotheses 1-7) modified by the types of PM2.5 spec/es? (10) Is there a synergistic interaction between PM2.5and long-term cardiac risk in the above relationships? (II) Are persons with older age, diabetes, and hypertension more susceptible to the above PM2.5 effects? We will (1) Recruit 100 patients with only arrhythmias of moderate frequency; (2) Perform a battery of cardiac tests to determine cardiac structural and functional status; (3) Measure concurrently 24-hour Holter ECG, ambulatory BP, and personal PM2.5 exposure, and derive real-time PM2.5 concentration, EGG, and BP data on each participant; (4) Analyze filters to assess major PM2.5 species; (5) Collect pre- and post- monitoring blood samples to assess inflammation and fibrinolytic activities; (6) Assess long-term risks of cardiac events; and (7) use time-series and cross-sectional analyses (both multivariable linear regression, transition models) to test the above research hypotheses. This study requires multidisciplinary collaborations of environmental, cardiovascular, and biostatistics researchers. The results will allow us to better understand the mechanisms and time course by which PM2.5 affects the cardiac system, and identify factors that lead to differential susceptibility to PM, and guide regulatory agencies in designing air pollution control standards.

描述（由申请人提供）：尽管已经确定了环境PM污染与心血管疾病之间的一致关联，但确切的机制，PM引起的毒性作用的时间过程以及不同PM物种的影响尚未充分理解。这项研究研究了临床相关的心律失常，心脏自主神经控制，复极化，心肌缺血，血压（BP），炎症，凝结和纤维蛋白分解机制以及PM2.5效应的时间过程（浓度和物种）。具体而言，个人短期暴露于升高的环境PM2.5是否与以下升高有关：（i）心律不齐发作的发作（2）心律失常的频率较高（3）较低的心率变异性（HRV）指数？ （4）通过QT指数测量的长时间复极化？ （5）ST细分级别？该关联可以完全或部分归因于HRV和QT的变化吗？ （6）高架门诊BP（SBP，DBP和PP）？从上面的1-6列出的效果的时间表（从几分钟到小时）是什么？ （7）个人短期暴露于升高的环境PM2.S（24小时累积暴露）是否与炎症，血液凝结和纤维蛋白水解活性的标记直接相关？ （8）环境PM2.5物种的累积浓度是24小时，主要由煤火电厂和车辆燃烧发射/形成，与上述端点相关（假设1-7）？ （9）环境PM2.5浓度与心脏终点（假设1-7）之间的关联是否通过PM2.5规格/ES的类型修饰？ （10）PM2.5与上述关系中的长期心脏风险之间是否存在协同的相互作用？ （ii）年龄较大，糖尿病和高血压的人是否更容易受到上述PM2.5影响？我们将（1）招募100例仅心律不齐的患者； （2）执行一系列心脏测试以确定心脏结构和功能状态； （3）同时测量每个参与者的PM2.5浓度，鸡蛋和BP数据，同时衡量24小时的ECG，门诊BP和个人PM2.5暴露； （4）分析过滤器以评估主要PM2.5种； （5）收集前后监测的血液样本以评估炎症和纤维蛋白水解活性； （6）评估心脏事件的长期风险； （7）使用时间序列和横截面分析（两个多变量线性回归，过渡模型）来检验上述研究假设。这项研究需要对环境，心血管和生物统计学研究人员进行多学科合作。结果将使我们能够更好地了解PM2.5影响心脏系统的机制和时间过程，并确定导致对PM敏感的因素的因素，并指导监管机构在设计空气污染控制标准时。