Abstract

This study examines the effects of nano-size particulate matter (nPM) exposure in the setting of murine reperfused stroke. Particulate matter is a potent source of inflammation and oxidative stress. These processes are known to influence stroke progression through recruitment of marginally viable penumbral tissue into the ischemic core. nPM was collected in an urban area in central Los Angeles, impacted primarily by traffic emissions. Re-aerosolized nPM or filtered air was then administered to mice through whole body exposure chambers for forty-five cumulative hours. Exposed mice then underwent middle cerebral artery occlusion/ reperfusion. Following cerebral ischemia/ reperfusion, mice exposed to nPM exhibited significantly larger infarct volumes and less favorable neurological deficit scores when compared to mice exposed to filtered air. Mice exposed to nPM also demonstrated increases in markers of inflammation and oxidative stress in the region of the ischemic core. The findings suggest a detrimental effect of urban airborne particulate matter exposure in the setting of acute ischemic stroke.

Highlights

  • Clinical and population based studies have established an association between acute stroke mortality and air pollution [1, 2]

  • These studies establish a relationship between air pollution exposure and acute stroke, consistent with associations previously noted in cardiovascular disease [5,6,7]

  • Our data suggests that subchronic nano-size particulate matter (nPM) exposure results in larger infarct volumes and less favorable neurological outcomes following reperfused stroke

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Summary

Introduction

Clinical and population based studies have established an association between acute stroke mortality and air pollution [1, 2]. Elevated post-stroke mortality has been documented in individuals living in close proximity to high-traffic roadways [4]. These studies establish a relationship between air pollution exposure and acute stroke, consistent with associations previously noted in cardiovascular disease [5,6,7]. Systematic reviews have demonstrated associations between PM2.5 and PM10 exposures and higher total cerebrovascular disease mortalities and established a concentration-response relationship between both short and long-.

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