Particulate exposure and cardiovascular inflammation

Abstract

The cardiovascular complications following pulmonary exposure to a variety of unrelated materials can manifest as adverse outcome events. While the specific underlying mechanisms are yet to be fully elucidated the cardiovascular system response to exposures is manifested as a more robust response. In this chapter we describe cardiovascular responses to ambient particulate matter (PM) CeO 2, Printex 90 (P90), and multi-walled carbon nanotube (MWCNT) nanoparticles. The inherent complexity of ambient sources of PM and the growing diversity of specifically engineered PM reinforce a need to understand the broader impact of exposures. Mice were exposed to 100 μg of PM or vehicle by intratracheal instillation. MWCNT, P90, and ambient PM all increased the ischemic-reperfusion injury compared to vehicle. Ambient PM and P90 decreased total blood leukocyte counts, while MWCNT induced a larger increase in plasma fibrinogen than ambient PM. Only ambient PM affected blood palette numbers and endothelial mediated relaxations. MWCNT exposure augmented the constrictor response but had no effect on endothelial dependent responses. These results illustrate our increasing yet limited understanding of the integrative nature of the cardiovascular system with neural, humeral, and immune systems and only begins to hint at the importance of a hypersensitive state on physiological and pathophysiological processes.