Aruni Bhatnagar

TL;DR: It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM2.5 exposure and cardiovascular morbidity and mortality.

TL;DR: Treatment with AR inhibitors prevents vascular smooth muscle cell growth and endothelial cell apoptosis in culture and inflammation and restenosis in vivo, and additional studies indicate that the antioxidant and signaling roles of AR are interlinked and that AR regulates protein kinase C and nuclear factor-kappaB via redox-sensitive mechanisms.

TL;DR: Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes, which could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

TL;DR: Results demonstrate that, in conscious rabbits, up-regulation of COX-2 plays an essential role in the cardioprotection afforded by the late phase of ischemic PC.

TL;DR: Additional studies are urgently needed to identify the contribution of individual pollutants to specific aspects of cardiovascular disease and establish causality; elucidate the underlying physiological and molecular mechanisms; and determine whether pollutant exposure are risk correlates.