Air Pollution and Cardiac Risk: Mechanisms & Time-course

空气污染和心脏风险：机制

• 批准号: 7816698
• 负责人: Duanping Liao
• 金额: $ 27.18万
• 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 2011-10-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7816698
• 关键词: Acute myocardial infarction; Address; Affect; Age; Air Pollutants; Air Pollution; Ambulatory Blood Pressure Monitoring; Ammonium; Archives; Arrhythmia; Arts; Binding; Biometry; Blood; Blood Pressure; Blood coagulation; Blood specimen; Budgets; Caliber; Carbon; Cardiac; Cardiovascular Diseases; Cardiovascular Models; Cardiovascular system; Certification; Characteristics; Chemicals; Clinical Trials; Coagulation Process; Coal; Complex; Congestive Heart Failure; Cross-Sectional Studies; Data; Data Collection; Data Quality; Data Set; Data Storage and Retrieval; Databases; Diabetes Mellitus; Diagnosis; Disease model; Echocardiography; Electrocardiogram; Elements; Enrollment; Environmental Health; Event; Exclusion Criteria; Exposure to; 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; Power Plants; Predisposition; Principal Investigator; Procedures; Protocols documentation; Publications; Recruitment Activity; Research; Research Personnel; Residual state; Resources; Risk; Series; Specialist; 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; clinically relevant; congenital heart disorder; design; egg; functional status; heart rate variability; indexing; inflammatory marker; markov model; particle; population based; 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)：尽管环境PM污染和心血管疾病之间的一致联系已经被确定，但确切的机制，PM引起毒性影响的时间过程，以及不同PM种类的影响还没有被充分了解。本研究调查了PM2.5的临床相关致心律失常、心脏自主神经控制、复极、心肌缺血、血压、炎症、凝血和纤溶机制以及PM2.5作用的时间进程(包括浓度和种类)。具体地说，个人短期暴露于升高的环境PM2.5是否与：(1)心律失常发作的开始(2)心律失常的频率增加(3)心率变异性(HRV)指数降低？(4)QT指数测量的复极延长？(5)ST段水平？这种关联是否完全或部分归因于HRV和QT的改变？(6)动态血压升高(SBP、DBP和PP)？上述1-6种影响的时间进程(从几分钟到几小时)是什么？(7)个人短期暴露于升高的环境PM2(24小时累积暴露)是否与炎症、凝血和纤溶活性的升高的标志物直接相关？(8)环境PM2.5的24小时累积浓度，主要来自燃煤电厂和车辆燃烧，与上述终点相关(假设1-7)？(9)环境PM2.5浓度和心脏终点(假设1-7)之间的关系是否被PM2.5的类型改变？(10)在上述关系中，PM2.5和长期心脏风险之间是否存在协同作用？(Ii)年龄较大、患有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名仅有中频性心律失常的患者；(2)进行一系列心脏测试，以确定心脏的结构和功能状态；(3)同时测量24小时动态心电图、动态血压和个人PM2.5暴露，并获得每个参与者的PM2.5浓度、心电图和血压的实时数据；(4)分析过滤器，以评估主要的PM2.5种类；(5)收集监测前后的血液样本，以评估炎症和纤溶活动；(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(多变量线性回归、转换模型)对上述研究假设进行检验。这项研究需要环境、心血管和生物统计学研究人员的多学科合作。研究结果将使我们更好地了解PM2.5影响心脏系统的机制和时间过程，并确定导致PM不同易感性的因素，并指导监管机构制定空气污染控制标准。

项目成果

Acute effects of fine particulate air pollution on ST segment height: a longitudinal study.

• DOI: 10.1186/1476-069x-9-68
• 发表时间: 2010-11-08
• 期刊: Environmental health : a global access science source
• 作者: He F;Shaffer ML;Rodriguez-Colon S;Bixler EO;Vgontzas AN;Williams RW;Wu R;Cascio WE;Liao D
• 通讯作者: Liao D

Acute adverse effects of fine particulate air pollution on ventricular repolarization.

• DOI: 10.1289/ehp.0901648
• 发表时间: 2010-07
• 期刊: Environmental health perspectives
• 影响因子: 10.4
• 作者: Liao D;Shaffer ML;Rodriguez-Colon S;He F;Li X;Wolbrette DL;Yanosky J;Cascio WE
• 通讯作者: Cascio WE

Fine particulate air pollution is associated with higher vulnerability to atrial fibrillation--the APACR study.

• DOI: 10.1080/15287394.2011.556056
• 发表时间: 2011
• 期刊: Journal of toxicology and environmental health. Part A
• 作者: Liao D;Shaffer ML;He F;Rodriguez-Colon S;Wu R;Whitsel EA;Bixler EO;Cascio WE
• 通讯作者: Cascio WE

The circadian pattern of cardiac autonomic modulation in a middle-aged population.

• DOI: 10.1007/s10286-010-0112-4
• 发表时间: 2011-06
• 期刊: CLINICAL AUTONOMIC RESEARCH
• 影响因子: 5.8
• 作者: Li, Xian;Shaffer, Michele L.;Rodriguez-Colon, Sol;He, Fan;Wolbrette, Deborah L.;Alagona, Peter, Jr.;Wu, Chuntao;Liao, Duanping
• 通讯作者: Liao, Duanping