Abstract
Correlations between short-term exposures to urban air particulate matter (PM) and increased morbidity and mortality for various cardiopulmonary diseases have been explained by the pro-inflammatory and pro-thrombotic effects of PM. This review updates a recent one by Scapellato and Lotti (Citation) and discusses the correlations between PM exposures, inflammatory endpoints and functional changes. Panel studies and controlled exposures to PM of various sizes in either healthy individuals, asthmatics and patients with coronary heart diseases, do not provide strong evidence of an inflammatory pathophysiology of PM toxicities. Contradictory results among reviewed studies could be explained by difficulties in dissecting inflammation brought about by PM from that of the ongoing diseases. However, other mechanisms, such as neurological ones, might be more relevant and co-exist with inflammation.
Acknowledgements
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.