Inflammatory mediators induced by coarse (PM2.5-10) and fine (PM2.5) urban air particles in RAW 264.7 cells.

Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of urban air particles with an aerodynamic diameter <10 micron, PM10 and <2.5 micron, PM2.5. Respirable particles reach the lower respiratory tract where they are phagocytized by alveolar macrophages. Depending on particle composition, exposed macrophages may produce inflammatory mediators. A cascade impactor sampler was used to collect size-fractionated urban air particles. Particulate matter from the city of Rome (Italy) were collected onto stainless steel plates, and recovered using alcohol. The murine monocytic/macrophagic RAW 264.7 cell line was used to compare the ability of PM2.5-10, PM2.5 and carbon black to cause cell injury, such as arachidonic acid (AA) release, tumour necrosis factor alpha (TNF alpha) and interleukin (IL)-6 production. All test particles have been used at the same concentrations 30 and 120 microg/ml. Treatment with PM2.5-10 and PM2.5 induced significant AA release after 5 h of exposure at both concentrations, while carbon black was effective only at the higher concentration. After 5 h of incubation, PM2.5-10 and PM2.5 at 120 microg/ml induced 10 times the amount of TNF alpha than carbon black particles. The urban air particles-stimulated TNF alpha production decreased after 24 h of incubation while carbon black-stimulated TNF alpha was not. IL-6 production was induced by PM2.5 and by PM2.5-10 but not by carbon black. Carbon black was consistently less effective than the urban particles, suggesting that, the contaminants adsorbed on the particles are responsible for the release of inflammatory mediators.