Respiratory toxicity of Diesel exhaust particles: cellular and molecular mechanisms

Particulate air pollution has been incriminated by epidemiologists to be re sponsible for increased mortality and morbidity due to cardiovascular and r espiratory disorders. Diesel exhaust particles (DEP) are one of the main co ntributers to atmospheric particles. article we review the effects of DEP o n the cells of the respiratory tract, especially the inflammatory response elicited by these particles. DEP increase the release of proinflammatory cy tokines, chemokines and adhesion molecules, responsible for the recruitment and the activation of inflammatory cells. Furthermore DEP act as an adjuva nt which may enhance allergic inflammation. These responses are linked to t he activation of the expression of certain genes. They may result from the direct or indirect production of reactive oxygen species bp the different c omponents-of DEP which are the carbonaceous core, the adsorbed organics and metallic contaminants. We discuss the different molecular and cellular mec hanisms involved in this inflammatory response which may include the metabo lic activation of DEP.