Ultrafine Particulate Matter & Cardiorespiratory Health

超细颗粒物

基本信息

批准号：
7267656
负责人：
RALPH J DELFINO
金额：
$ 44.7万
依托单位：
UNIVERSITY OF CALIFORNIA-IRVINE
依托单位国家：
美国
项目类别：
财政年份：
2003
资助国家：
美国
起止时间：
2003-09-30 至 2010-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7267656
关键词：
Acute Acute-Phase Proteins Address Admission activity Adult Age Age-Years Air Air Pollutants Air Pollution Airborne Particulate Matter Ambulatory Monitoring Animals Area Arrhythmia Atherosclerosis Automobile Driving Biochemical Biological Markers Blood Blood Pressure C-reactive protein Caliber California Carboxylic Acids Cardiac Cardiopulmonary Cardiovascular Physiology Cardiovascular system Cause of Death Cell Adhesion Molecules Cessation of life Characteristics Chemistry Cholesterol Clinical Clinical Data Coagulation Process Cohort Studies Collection Communities Congestive Heart Failure Coronary Coronary Occlusions Coronary heart disease County Daily Data Deposition Diagnosis Diastolic blood pressure EKG ST Segment Depression Elderly Electrocardiogram Endothelin-1 Ensure Epidemiologic Studies Epidemiologist Event Exercise Exercise stress test Exhalation Exposure to Fibrin fragment D Fibrin split products Fibrinogen Fibrinolysis Fire - disasters Future Gases Goals Government Health Heart Heart Diseases Heart Rate Hemostatic Agents Home environment Hospital Mortality Hospitalization Hospitals Hour Hypertension Incidence Individual Inflammation Inflammatory Inflammatory Response Injury Intercellular adhesion molecule 1 Interleukin-6 Interleukins Investigation Ischemia Knowledge Lead Life Link Literature Los Angeles Lung Measurement Measures Metals Methods Metric Modeling Monitor Morbidity - disease rate Myocardial Infarction National Research Council Netherlands Nitric Oxide Nitroglycerin Numbers Oranges Outcome Oxidants Particle Size Particulate Particulate Matter Patients Personal Behavior Persons Petroleum Physical condensation Physiological Plasma Plasminogen Pneumonia Population Populations at Risk Principal Investigator Process Prohibit Publishing Reliance Reporting Research Personnel Research Priority Retirement Risk Risk Factors Route Sampling Series Serum Serum amyloid A protein Site Smog Smoke Source Subgroup Surface Symptoms Testing Thinking Thrombophilia Thrombosis Time Tobacco smoke Tracer Transition Elements Tumor Necrosis Factor-alpha Tumor Necrosis Factors Ultrafine Vascular Endothelium Vasoconstrictor Agents Vehicle Emissions Ventricular Arrhythmia Viscosity Week Wood material aged airway inflammation base biological adaptation to stress cardiovascular risk factor clinically relevant cooking cysteine rich protein cytokine day design exposed human population forest hemodynamics human TNF protein interest levoglucosan mortality non-smoker non-smoking particle particle exposure pollutant programs prospective receptor respiratory size trafficking ultrafine particle urban area

项目摘要

DESCRIPTION: (provided by applicant) Heart disease is the leading cause of death and hospitalization among the elderly population, which makes the identification of preventable causes for heart disease morbidity and mortality a major goal of epidemiologic research. Numerous studies have shown associations of outdoor particulate matter (PM) air pollution with cardiovascular hospital admissions and mortality. The causal pollutant components and physiologic mechanisms for these associations are not fully understood. There is evidence that airway inflammation resulting from airway deposition of ultrafine particles (< 0.1 mu/m in diameter) could lead to an increase in thrombogenic and inflammatory activity in the blood, and to a disturbance in cardiovascular function, resulting from oxidant stress responses at extra-pulmonary sites, including the vascular endothelium of the heart. This is expected to increase the risk of adverse cardiovascular outcomes, particularly in people with underlying coronary heart disease (CHD). We propose to conduct a panel study with repeated measurements to evaluate acute cardiovascular and respiratory health effects of ultrafine PM personal, indoor and outdoor exposures. Over seven month periods, we will follow 72 nonsmoking elderly individuals with CHD living in areas with high air pollution levels in the Los Angeles Air Basin of California. The design will maximize the utility of intensive exposure assessments by measuring multiple interrelated clinical, physiological and biochemical outcomes. The specific aims will address the following hypotheses: 1) Exposure to ultrafine particles will be associated with increased circulating biomarkers of inflammation and thrombosis, increased blood pressure, adverse cardiac clinical outcomes, and increases in a biomarker of airway inflammation, exhaled nitric oxide; and 2) These associations will be stronger for measurements of particle components and certain ambient sources thought to influence inflammatory processes through oxidant damage. We will also evaluate relationships of outcomes with accumulation mode PM (0.18-2.5 mu/m) and coarse mode PM (2.5-10 fm). We will assess whether estimates of association for predicted (adjusted) personal or indoor exposure to ultrafine or accumulation mode PM of outdoor origin are stronger than estimates of association for unadjusted (raw) personal or indoor exposures. Results of this study will advance knowledge on the cardiovascular and respiratory effects of ultrafine particles. Our results are expected to clarify findings in the literature of associations between ambient particulate air pollution (PM10 and PM2.5) and severe cardiovascular outcomes, including mortality and hospital admissions.

描述：（由申请人提供）心脏病是老年人群死亡和住院的主要原因，这使得确定心脏病发病率和死亡率的可预防原因成为流行病学研究的主要目标。大量研究表明室外颗粒物 (PM) 空气污染与心血管疾病住院率和死亡率之间存在关联。这些关联的致病污染物成分和生理机制尚未完全了解。有证据表明，超细颗粒（直径<0.1μ/m）气道沉积引起的气道炎症可能导致血液中血栓形成和炎症活动增加，并导致心血管功能紊乱，这是由氧化应激反应引起的肺外部位，包括心脏的血管内皮。预计这会增加不良心血管结局的风险，尤其是患有潜在冠心病（CHD）的人。我们建议开展一项重复测量的小组研究，以评估个人、室内和室外接触超细颗粒物对心血管和呼吸系统健康的急性影响。在七个月的时间里，我们将追踪居住在加利福尼亚州洛杉矶空气盆地空气污染严重地区的 72 名患有先天性心脏病的不吸烟老年人。该设计将通过测量多种相互关联的临床、生理和生化结果，最大限度地提高强化暴露评估的效用。具体目标将解决以下假设：1）暴露于超细颗粒将与炎症和血栓形成的循环生物标志物增加、血压升高、不良心脏临床结果以及气道炎症生物标志物呼出一氧化氮的增加相关； 2）对于颗粒成分和某些被认为通过氧化损伤影响炎症过程的环境来源的测量，这些关联会更强。我们还将评估结果与累积模式 PM (0.18-2.5 mu/m) 和粗略模式 PM (2.5-10 fm) 的关系。我们将评估预测（调整后）个人或室内暴露于室外来源的超细或累积模式 PM 的关联估计是否强于未调整（原始）个人或室内暴露的关联估计。这项研究的结果将增进人们对超细颗粒对心血管和呼吸系统影响的认识。我们的研究结果有望澄清文献中有关环境颗粒物空气污染（PM10 和 PM2.5）与严重心血管结局（包括死亡率和入院率）之间关联的发现。