METABOLIC ACTIVATION OF AIR TOXICS IN ASTHMATIC MONKEYS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 目的：大量流行病学研究已经注意到暴露于环境空气污染物(VOC、颗粒物、臭氧)与哮喘发病率和严重程度之间的关系。最近对幼年恒河猴的研究表明，间歇性臭氧和室内尘螨过敏原(HDMA)暴露可诱发具有过敏性哮喘许多特征迹象的综合征。在这个模型中观察到的几个结构变化发生在呼吸道，这是肺内异物代谢的主要部位。进行这些研究是为了检验这样一种假设，即暴露导致肺结构和功能的根本改变也会改变代谢异生物质的能力，重点是生物活性异生物质。

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. Objective: Numerous epidemiologic studies have noted associations between exposures to ambient air pollutants (VOC, particulates, ozone) and asthma incidence and severity. Recent work in juvenile rhesus macaques has shown that a syndrome having many of the hallmark signs of allergic asthma can be induced by intermittent ozone and house dust mite allergen (HDMA) exposures. Several of the structural alterations observed in this model occur in the airways, a primary site for pulmonary xenobiotic metabolism. These studies were conducted to test the hypothesis that exposures resulting in fundamental alterations in the structure and function of the lung also alter the ability to metabolize xenobiotics, with a focus on bioactivated xenobiotics.