Relationship between physicochemical characterization and toxicity of fine particulate matter (PM2.5) collected in Dakar city (Senegal)

The massive increase in emissions of air pollutants due to economic and industrial growth in developing countries has made air quality a crucial health problem in this continent. Hence, it is somewhat critical to have a better knowledge on the air pollution in Sub-Saharan Africa countries. Three air pollution PM2.5 samples were also collected in two urban sites (i.e. Fann and Faidherbe) in Dakar (Senegal) and in a rural site near Dakar (i.e. Ngaparu). The two urban sites mainly differ in the type of used vehicles: in Fann, most of the traffic is made of buses, which are absent, in Faidherbe. The physicochemical characteristics of the three PM2.5 samples revealed their high heterogeneities and complexities, related to the multiple natural and anthropogenic emission sources. Results from 5-bromodeoxyuridine incorporation into DNA, mitochondrial dehydrogenase activity, and extracellular lactate dehydrogenase activity in PM2.5-exposed BEAS-2B cells suggested the exposure conditions (i.e. 3 and 12 μg PM/cm² during 24, 48, and 72 h) to further consider. The organic fractions (i.e. mainly PAHs) of the PM2.5 samples were able to induce a time and/or concentration-dependent gene expression of CYP1A1 and CYP1B1, and, to a lesser extent, NQO1. There was a time and/or dose-dependent increase of both the gene expression and/or protein secretion of inflammatory mediators (i.e. TNF-α, IL-1β, IL-6, and/or IL-8) in PM2.5-exposed BEAS-2B cells. In agreement with the physicochemical characterization, urban PM2.5 samples caused greater biological responses in BEAS-2B cells than the rural one. Variable concentrations of transition metals (i.e. Fe, Al, Pb, Mn, Zn) and organic compounds (i.e. PAHs) founded in the three PM2.5 samples might be firmly involved in a time- and/or dose-dependent toxicity, relying on inflammatory processes.

► Better knowledge on the air pollution in Sub-Saharan Africa countries.
► Physico-chemical characterization of three air pollution PM2.5 samples.
► Metabolic activation of the PAH-coated onto PM2.5 in BEAS-2B cells.
► Oxidative damage and cytokine secretion induced by the exposure to PM2.5.
► Relationship between metals and organics in the three PM2.5 samples and toxicity.