Chemical characterization and in vitro toxicity on human bronchial epithelial cells BEAS-2B of PM$_{2.5}$ from an urban site under industrial emission influence

Particulate Matter (PM) is one of the most relevant environment-related health issues all over the world. In 2013, the International Agency for Research on Cancer (IARC) has classified air pollution and PM as a carcinogen for humans [1]. However, the mechanisms involved in the toxicity of these particles remains poorly understood, mainly because PM are uniquely complex owing to their physicochemical characteristics. In this study, fine particles were collected in the city center of Dunkirk, northern France using a 5 stages high volume cascade impactor (Staplex® 235, 68m3/h) and a Digitel DA80 high volume sampler (30m3/h).Samples were extensively characterized for their physico-chemical properties, including trace metals, water-soluble ions and organic species. Normal human bronchial epithelial cells (BEAS-2B) were used as cell model for toxicological analysis. Cytotoxicity, PAHs-metabolizing enzymes gene expression and genotoxic alterations were evaluated after 24, 48 or 72 h of exposure considering increasing concentrations of PM$_{2.5-0.3}$, organic extracts (OE) and water-soluble fraction (WF) of PM$_{2.5-0.3}$ and PM$_{2.5}$. Several sources such as road traffic, industrial activities mainly related to steelmaking, marine emissions including sea-salts and shipping, as well as soil resuspension were found to contribute to the PM$_{2.5}$ composition. Cytotoxicity assessment results showed time and dose dependent responses, with effects mainly related to PAH compounds in PM$_{2.5}$ OE in which their content were 12 times higher than in PM$_{2.5-0.3}$ one [2]. Differences in the induction of CYP1A1, CYP1B1 and NQO1 genes expression involved in the metabolic activation of organic compounds, as well as genotoxic effects (oxidative DNA adducts, H2A.X phosphorylation) were also evidenced after cells exposure to OE and PM$_{2.5-0.3}$ [3]. These results confirm the major effect of organic compounds on toxic effects, but also the potential contribution of the inorganic fraction of the PM which maintains longer the effects in exposed cells.