Since my postdoctoral position, I have used a variety of cellular and molecular approaches, and both human and animal models, to study mechanisms underlying cardiovascular disease (CVD). My current interests focus on the role of environmental exposures in promoting CVD. In early work we determined that exposure to airborne particulate matter (PM_2.5) induced vascular dysfunction, altered the abundance and functionality of endothelial progenitor cells, promoted inflammatory responses, and induced defects in hematopoiesis and insulin signaling. Using mice, we have determined that means taken to limit oxidative stress can mitigate these adverse outcomes and we have recently completed a randomized human clinical trial examining the efficacy of carnosine supplementation in doing the same. As PM_2.5 exposures do not occur in isolation but are often in combination with volatile organics (VOCs), we have also examined the effects of inhalation exposure to acrolein and benzene in mice. As with PM_2.5, exposure to these two VOCs disrupts glucose homeostasis and vascular repair processes. Current studies examine the toxicity of environmentally abundant microplastics (MP). In preliminary mouse studies, we determined that polystyrene consumption promotes adiposity, hyperglycemia, elevated HOMA IR scores and potentiates atherosclerotic lesion size in disease prone strains as well. We are attmpting to further characterize these effects, identify their mechanistic basis, and explore potential interventional approaches.