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Compelling evidence indicates that exposure to air pollutionparticulate matter (PM) affects human health. However, how PM compositioninteracts with PM-size to cause adverse health effects needs elucidation.In this study, we were also interested in the physicochemical characteristicsand toxicological end points of PM2.5–0.3samplesproduced in rural, urban, or industrial surroundings, thereby expectingto differentiate their respective in vitroadversehealth effects in human bronchial epithelial cells (BEAS-2B). Physicochemicalcharacteristics of the three PM2.5–0.3samples,notably their inorganic and organic components, were closely relatedto their respective emission sources. Referring also to the dose/responserelationships of the three PM2.5–0.3samples, themost toxicologically relevant exposure times (i.e., 24, 48, and 72h) and doses (i.e., 3.75 μg PM/cm2and 15 μgPM/cm2) to use to study the underlying mechanisms of actioninvolved in PM-induced lung toxicity were chosen. Organic chemicalsadsorbed on the three PM2.5–0.3samples (i.e., polycyclicaromatic hydrocarbons) were able to induce the gene expression ofxenobiotic-metabolizing enzymes (i.e., Cytochrome P4501A1 and 1B1,and, to a lesser extent, NADPH-quinone oxidoreductase-1). Moreover,intracellular reactive oxygen species within BEAS-2B cells exposedto the three PM2.5–0.3samples induced oxidativedamage (i.e., 8-hydroxy-2′-deoxyguanosine formation, malondialdehydeproduction and/or glutathione status alteration). There were alsostatistically significant increases of the gene expression and/orprotein secretion of inflammatory mediators (i.e., notably IL-6 andIL-8) in BEAS-2B cells after their exposure to the three PM2.5–0.3samples. Taken together, the present findings indicated that oxidativedamage and inflammatory response preceeded cytotoxicity in air pollutionPM2.5–0.3-exposed BEAS-2B cells and supported theidea that PM-size, composition, and origin could interact in a complexmanner to determine the in vitroresponsiveness toPM. [ABSTRACT FROM AUTHOR]