Experimental Exposure to Air Pollutants and Sympathetic Nerve Activity in Human Subjects

人类受试者暴露于空气污染物和交感神经活动的实验

• 批准号: 213733301
• 负责人: Professor Dr. Jens Jordan
• 金额: --
• 依托单位: Fraunhofer-Institut für Toxikologie und Experimentelle Medizin (ITEM)
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2012
• 资助国家: 德国
• 起止时间: 2011-12-31 至 2014-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/213733301?language=en
• 关键词: Experimental; Exposure; Air; Pollutants; Sympathetic

Air pollution is the 13th leading cause of mortality worldwide largely through excess cardiovascular mortality. Sympathetic activation is implicated by the rapid onset of the cardiovascular risk increase after exposure and changes in heart rate variability. Therefore, we will test the hypothesis that ultrafine particle exposure increases sympathetic nervous system activity in human subjects and that ozone-induced airway inflammation augments autonomic dysregulation. Participants will be exposed to clean air, ultrafine particles, or ultrafine particles and ozone in a randomized, double-blind, and cross-over fashion. We will determine blood pressure, heart rate, respiration, cardiac output and directly record sympathetic vasomotor tone using microneurography. To elucidate the underlying mechanisms through which particles and ozone affect the autonomic nervous system, we will assess the local and systemic inflammatory response as well as the changes in neurotrophic factors in sputum and blood. Changes in sympathetic activity will be correlated with the degree of airway inflammation and oxidative stress assessed in induced sputum as well as in blood and urine. Our study will provide insight in the mechanisms through which air pollution, particularly ultrafine particle exposure, increases cardiovascular risk in human subjects and generate a human model for mechanistic and therapeutic studies.

空气污染是全球第13大死亡原因，主要是心血管死亡率过高。交感神经激活与暴露后心血管风险增加的快速发作和心率变异性的变化有关。因此，我们将测试的假设，超细颗粒暴露增加人类受试者的交感神经系统活动和臭氧诱导的气道炎症增强自主神经失调。参与者将以随机、双盲和交叉的方式暴露于清洁空气、超细颗粒或超细颗粒和臭氧中。我们将测定血压、心率、呼吸、心输出量，并使用显微神经造影术直接记录交感血管紧张度。为了阐明颗粒物和臭氧影响自主神经系统的潜在机制，我们将评估局部和全身炎症反应以及痰液和血液中神经营养因子的变化。交感神经活性的变化将与诱导痰以及血液和尿液中评估的气道炎症和氧化应激的程度相关。我们的研究将深入了解空气污染，特别是超细颗粒暴露，增加人类受试者心血管风险的机制，并为机制和治疗研究建立人类模型。

项目成果

Inflammatory response to the exposure with ultra-fine particles and ozone

暴露于超细颗粒和臭氧的炎症反应

• DOI: 10.1183/13993003.congress-2016.pa1836
• 发表时间: 2016
• 期刊: European Respiratory Journal
• 影响因子: 24.3
• 作者: Holz O;Heusser K;Gaida A;Allers M;Zimmermann S;Müller M;Schichardt S;Schindler C;Tank J;Jordan J;Hohlfeld J
• 通讯作者: Hohlfeld J