Biological mechanisms linking inhaled particles to cardiovascular morbidity and mortality. Several hypotheses have been proposed for the means by which inhaled particles have actions on the cardiovascular system. These include: the passage of biological mediators (e.g. not only inflammatory mediators but also unidentified mediators that are not traditional cytokines) from the lung into the circulation; activation of alveoli sensory receptors leading to triggering of neural afferents which can alter the activity of the autonomic nervous system or release of endocrine molecules; direct passage of particles (or chemicals eluting from particles) into the circulation to directly impair cardiovascular function. We emphasize that there is considerable interplay between the four pathways shown, with inflammation and oxidative stress, in particular, having the capacity to amply different stages of each pathways. The diagram also highlights that urban PM exerts many pathophysiological changes on different aspects of the cardiovascular system that ultimately increases cardiovascular morbidity and mortality.