ABSTRACT
Three hypotheses have been put forth in the past few years to explain the mechanisms of cardiotoxicity by ambient particulate matter (PM). Namely, that the cardiac effects of PM are mediated by: (i) increased autonomic influence on the heart, (ii) proinflammatory cytokines or chemokines produced by lung cells and released into the blood stream, and/or (iii) direct effect of ultrafine particles or soluble particle components that could leach out of the particles and reach the heart.
