Disrupted @entity842 Metabolism from XXXX and Acute Exposure to Particulate Air Pollution.

@entity2175 @entity455 @entity6 @entity63 @entity3542 @entity450 @entity842 @entity65
@entity2175 is an established cause of @entity455 . Particulate air pollution is known to exacerbate @entity65 , particularly in susceptible populations. This study set out to determine the impact of exposure to traffic pollution, with and without particle filtration, on vascular endothelial function in @entity2175 . Endothelial production of @entity842 (NO) has previously been linked to vascular health. @entity450 induces a significant increase in plasma @entity3542 , the proximal metabolite of NO, in healthy subjects, while @entity6 have a lower and more variable level of response. Twenty type II @entity6 and 20 controls (ages 46-70 years) were taken on a 1.5 hr roadway traffic air pollution exposure as passengers. We analyzed plasma @entity3542 , as a measure of vascular function, using forearm @entity63 to elicit a reactive hyperemic response before and after exposure to one ride with and one without filtration of the particle components of pollution. Control subjects displayed a significant increase in plasma @entity3542 levels during reactive @entity450 . This response was no longer present following exposure to traffic air pollution, but did not vary with whether or not the particle phase was filtered out. Diabetics did not display an increase in @entity3542 levels following reactive @entity450 . This response was not altered following pollution exposure. These data suggest that components of acute traffic pollution exposure diminish vascular reactivity in non- @entity6 individuals. It also confirms that type II @entity6 have a preexisting diminished ability to appropriately respond to a vascular challenge, and that traffic pollution exposure does not cause a further measureable acute change in plasma @entity3542 levels in @entity2175 .
