METABOLIC ACTIVATION OF AIR TOXICS IN ASTHMATIC MONKEYS

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 目的：许多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联。最近在幼年恒河猴中的研究表明，间歇性臭氧和屋尘螨过敏原（HDMA）暴露可诱发具有许多过敏性哮喘标志性体征的综合征。在该模型中观察到的几种结构改变发生在气道中，气道是肺异生物质代谢的主要部位。进行这些研究是为了检验以下假设：导致肺结构和功能发生根本改变的暴露也会改变代谢外源性物质的能力，重点是生物活化的外源性物质。

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.