 Hourly ice resurfacing by gas and propane fueled machines creates high levels of ultrafine and fine particulate matter PM1 in indoor ice rinks. PM1 exposure may disrupt the normal nitric oxide NOendothelin ET-1 vasodilation system and promote atherosclerosis, andor increase the risk of an acute cardiac event. Our specific aims are 1 to determine whether impaired endothelial-mediated vasodilation and forearm muscle tissue reoxygenation rate and blood volume change to reactive hyperemia following artery occlusion is associated with combustion-derived PM1 exposure, and 2 To characterize a PM1 induced mechanism of endothelial dysfunction which occurs via a leukotriene LT-associated, airway generated tumor necrosis factor-alpha TNF-a mediated pathway. Healthy low PM1 exposed males will be evaluated for endothelial dysfunction before and after artery occlusion using high resolution ultrasound and near-infrared spectroscopy NIRS, before and after moderate exercise in blinded high and low PM1. Endothelial dysfunction among chronically PM1 exposed ice rink athletes will be determined to evaluate the feasibility of using this population as a model in future studies. TNF-a, IL-8, LTB4, LTC4, LTD4, LTE4, ET-1, NO, and differential cell counts will be measured in sputum and serum. PM1 will be monitored and exposure levels will be typical of indoor ice rinks. LT involvement will be assessed in vivo by double-blind pharmacological manipulation during PM1 exposure during light exercise. Results will demonstrate whether endothelial-mediated vasodilation and muscle hemodynamics are influenced by PM1 exposure, and will elucidate an LT initiated TNF-a mediated pathway in ET-1 upregulation. Our results should provide information for understanding the effects of PM1 exposure on the atherosclerotic process and cardiovascular risk, and give insight to novel treatment and diagnostic modalities. 