Toxicity of fine and quasi-ultrafine particles: focus on the effects of extractable and non-extractable matter fractions

Abstract

Air pollution represents today one of the major risk factors for human health. An important part of this threat is due to the presence in the atmosphere of fine particulate matter (PM$_{2.5}$). PM$_{2.5}$ forms a heterogeneous mixture of inorganic pollutants (metals, ions…), organic pollutants (volatile organic compounds (VOC), polycyclic aromatic hydrocarbons (PAHs), dioxins, polychlorobiphenyls (PCBs)…), and biological contaminants (pollen, bacteria, fungi…). To date many studies have demonstrated the toxicity of PAHs and some metals, but so far, no study has been able to clearly attribute the toxicological effects observed to a class of pollutants. Therefore, this study aims to determine the physicochemical characteristics of PM$_{2.5-0.3}$ and PM$_{0,3}$ and to compare the toxicity of native PM$_{2.5-0.3}$, organic fractions of fine (EOM$_{2.5-0.3}$) and quasi ultrafine particles (OEM$_{0.3}$), and PM$_{2.5-0.3}$ freed from this organic fraction (dPM$_{2.5-0.3}$) on BEAS-2B cells in culture. Fine and quasi-ultrafine particles were sampled in the southern suburb of Beirut, Lebanon. Chemical characterization showed that quasi-ultrafine particles were about 40 times more concentrated in PAHs than fines one suggesting a significant influence of anthropogenic activities and combustion sources (industries, road traffic and electric generators) on the emission of quasi-ultrafine particles. The influence of combustion sources was confirmed by investigation of PAHs diagnostic ratios. In addition, BEAS-2B cells exposed to PM$_{2.5-0.3}$, dPM$_{2.5-0.3}$, EOM$_{2.5-0.3}$ and EOM$_{0.3}$ lead to different results concerning metabolic activation of PAHs pathway and proteins expression of biomarkers implicated in the pathway of genotoxicity. Globally, EOM$_{0.3}$ was the most inducer for phase I and phase II enzymes implicated in the metabolic activation of PAHs (AhR, AhRR, ARNT, Cyp1A1, Cyp1B1, EPHX-1, GSTA-4) and EOM$_{0.3}$ induced DNA damage, felt by ATR and followed by a cascade of protein phosphorylations contributing to the cell cycle arrest (P21 and P53 induction)