ULTRAFINE PARTICULATE MATTER & CARDIORESPIRATORY HEALTH
超细颗粒物
基本信息
- 批准号:7606628
- 负责人:
- 金额:$ 0.12万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2006
- 资助国家:美国
- 起止时间:2006-12-01 至 2007-11-30
- 项目状态:已结题
- 来源:
- 关键词:AcuteAddressAdmission activityAirAir PollutionAreaBiochemicalBiological MarkersBloodBlood PressureCaliberCaliforniaCardiacCardiovascular PhysiologyCardiovascular systemCause of DeathCharacteristicsClinicalComputer Retrieval of Information on Scientific Projects DatabaseCoronary heart diseaseCountyDepositionElderlyEnd PointEpidemiologic StudiesExhalationExposure toFundingGoalsGrantHealthHeartHeart DiseasesHospital MortalityHospitalizationHospitalsIndividualInflammationInflammatoryInstitutionKnowledgeLeadLifeLiteratureLos AngelesLungMeasurementMeasuresMediator of activation proteinMorbidity - disease rateNitric OxideOrangesOutcomeOxidantsParticulateParticulate MatterPhysiologicalPopulationPopulations at RiskProcessResearchResearch PersonnelResourcesRiskSiteSmogSourceThinkingThrombosisUltrafineUnited States National Institutes of HealthVascular Endotheliumagedairway inflammationbiological adaptation to stressdesignmortalityparticlepollutantreceptorrespiratoryultrafine particle
项目摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
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. However, 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 (defined herein as < 0.18 m in diameter) could lead to an increase in thrombogenic and inflammatory activity in the blood, and to a disturbance in cardiovascular function. This is believed to result from oxidant stress responses at extra-pulmonary sites, including the vascular endothelium of the heart. Changes in intermediary endpoints such as inflammatory mediators are 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. We will study two regions of southern California with differing air pollution profiles: areas of Los Angeles County and North Orange County (pollutant emissions source sites with freshly emitted PM) and more inland areas of Eastern Los Angeles County, San Bernardino and Riverside Counties (down-wind smog receptor sites with aged PM). This will enhance variability in characteristics of ultrafine and accumulation mode particles, and enhance the external validity of findings to populations at risk.
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 m) and coarse mode PM (2.5-10 m). 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.
该副本是利用众多研究子项目之一
由NIH/NCRR资助的中心赠款提供的资源。子弹和
调查员(PI)可能已经从其他NIH来源获得了主要资金,
因此可以在其他清晰的条目中代表。列出的机构是
对于中心,这不一定是调查员的机构。
心脏病是老年人口死亡和住院的主要原因,这使得鉴定出心脏病发病率和死亡率的可预防原因是流行病学研究的主要目标。许多研究表明,室外颗粒物(PM)空气污染与心血管医院入院和死亡率的关联。 但是,这些关联的因果污染物成分和生理机制尚不完全了解。 有证据表明,由超铁颗粒的气道沉积引起的气道炎症(此处定义为直径<0.18 m)可能导致血液中血栓形成和炎症活性的增加,并导致心血管功能的干扰。 据信这是由于肺部外部位(包括心脏的血管内皮)的氧化应激反应引起的。 炎症介质等中介终点的变化有望增加心血管不良后果的风险,尤其是在潜在的冠心病(CHD)的人中。
我们建议进行一项针对重复测量的小组研究,以评估Ultrafine PM个人,室内和室外暴露的急性心血管和呼吸健康影响。 在七个月的时间里,我们将跟随72名不吸烟的老年人,居住在加利福尼亚州洛杉矶空中盆地高空气污染水平的地区。 我们将研究南加州的两个区域,具有不同的空气污染概况:洛杉矶县和北奥兰治县(污染物排放量新鲜发射的PM)以及更多的内陆洛杉矶县,洛杉矶县,圣贝纳迪诺和河滨县的内陆地区(带有老年PM的柔软烟雾受体)。 这将提高超级法和累积模式颗粒特征的变化,并提高发现对处于风险的人群的外部有效性。
该设计将通过测量多个相互关联的临床,生理和生化结果来最大程度地提高强化暴露评估的效用。
具体目的将解决以下假设:
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有关,血压升高,心脏不良临床结果以及气道炎症的生物标志物增加,呼出的一氧化氮;和
2)这些关联将对粒子成分的测量和某些被认为会通过氧化剂损伤影响炎症过程的环境来源更强。
我们还将评估结果与累积模式PM(0.18-2.5 m)和粗模式PM(2.5-10 m)的关系的关系。 我们将评估预测(调整后的)个人或室内暴露于Ultrafine或累积模式PM的估计值是否比未经调整的(原始)个人或室内暴露的关联估计更强。 这项研究的结果将提高有关超细颗粒心血管和呼吸作用的知识。 预计我们的结果将阐明在环境颗粒空气污染(PM10和PM2.5)与严重心血管结局(包括死亡率和住院)之间的关联文献中的发现。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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RALPH J DELFINO其他文献
RALPH J DELFINO的其他文献
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{{ truncateString('RALPH J DELFINO', 18)}}的其他基金
Acute Asthma Outcomes, Endotoxin and Oxidative Potential of Pollutant Particles
急性哮喘结果、内毒素和污染物颗粒的氧化电位
- 批准号:
8032030 - 财政年份:2011
- 资助金额:
$ 0.12万 - 项目类别:
Acute Asthma Outcomes, Endotoxin and Oxidative Potential of Pollutant Particles
急性哮喘结果、内毒素和污染物颗粒的氧化电位
- 批准号:
8207940 - 财政年份:2011
- 资助金额:
$ 0.12万 - 项目类别:
Pediatric asthma, photochemical oxidant air pollutants, and climate change vulner
小儿哮喘、光化学氧化剂空气污染物和气候变化脆弱性
- 批准号:
8305466 - 财政年份:2011
- 资助金额:
$ 0.12万 - 项目类别:
Pediatric asthma, photochemical oxidant air pollutants, and climate change vulner
小儿哮喘、光化学氧化剂空气污染物和气候变化脆弱性
- 批准号:
8152473 - 财政年份:2011
- 资助金额:
$ 0.12万 - 项目类别:
Air Pollution and Peripheral Blood Gene Expression in Subjects with Coronary Arte
空气污染与冠心病患者外周血基因表达
- 批准号:
7661193 - 财政年份:2009
- 资助金额:
$ 0.12万 - 项目类别:
Air Pollution and Peripheral Blood Gene Expression in Subjects with Coronary Arte
空气污染与冠心病患者外周血基因表达
- 批准号:
7846833 - 财政年份:2009
- 资助金额:
$ 0.12万 - 项目类别:
Transcriptomic, Oxidative Stress, and Inflammatory Responses to Air Pollutants
对空气污染物的转录组、氧化应激和炎症反应
- 批准号:
8258226 - 财政年份:2003
- 资助金额:
$ 0.12万 - 项目类别:
Transcriptomic, Oxidative Stress, and Inflammatory Responses to Air Pollutants
对空气污染物的转录组、氧化应激和炎症反应
- 批准号:
8415850 - 财政年份:2003
- 资助金额:
$ 0.12万 - 项目类别:
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