Airborne Particulate Matter (PM) is an important risk factor for human health. In spite of the numerous studies that have been carried out, the underlying mechanisms of action involved in particulate matter physiopathological effects are still unclear. In this work, PM samples were collected in two urban sites (Fann and Faidherbe) in Dakar (Senegal) and in a rural site (Ngaparou). The two urban sites mainly differ in the type of motor vehicles circulating in the area : most of the traffic is made of buses in Fann, whereas they are absent from Faidherbe. The physical characterization of the three samples showed their fine size distribution (96% < 2,5 μm), with surface areas ranging from 8 to 13m²/g. Collected PM were then able to reach deep lung, and to adsorb potentially toxic substances. Their chemical composition, rich in inorganic and organic compounds demonstrated the diversity of emission sources. After assessing their cytotoxicity in human epithelial bronchial cells (BEAS-2B), we showed that these PM could induce gene expression of metabolizing enzymes CYP1A1, 1B1 and NQO1, and therefore the metabolic activation of their organic fraction. No significant response to oxidative damage through lipid peroxidation (MDA) or glutathione status modification (GSSG/GSH) was observed after cells exposure to particulate matter. However, this exposure induced an inflammatory response by a significant increase in expression and secretion of cytokines TNF-α, IL-1β, IL-6 and IL-8.
