Exposure to diesel
engine exhaust particles (DEPs), representing a complex and variable mixture of components, has been linked with cellular production and release of several types of mediators related to
pulmonary inflammation. A key challenge is to identify the specific components, which may be responsible for these effects. The aim of this study was to compare the proinflammatory potential of two
DEP-samples with contrasting contents of
polycyclic aromatic hydrocarbons (PAHs) and metals. The
DEP-samples were compared with respect to their ability to induce cytotoxicity, expression and release of proinflammatory mediators (IL-6, IL-8), activation of
mitogen-activated protein kinases (MAPKs) and expression of
CYP1A1 and
heme oxygenase-1 (HO-1) in human bronchial epithelial (BEAS-2B) cells. In addition,
dithiothreitol and
ascorbic acid assays were performed in order to examine the oxidative potential of the PM samples. The
DEP-sample with the highest PAH and lowest
metal content was more potent with respect to cytotoxicity and expression and release of proinflammatory mediators,
CYP1A1 and HO-1 expression and MAPK activation, than the
DEP-sample with lower PAH and higher
metal content. The
DEP-sample with the highest PAH and lowest
metal content also possessed a greater oxidative potential. The present results indicate that the content of organic components may be determinant for the proinflammatory effects of
DEP. The findings underscore the importance of considering the chemical composition of
particulate matter-emissions, when evaluating the potential health impact and implementation of air pollution regulations.