title: Prooxidant and proinflammatory potency of air pollution particulate matter (PM₂.₅₋₀.₃) produced in rural, urban, or industrial surroundings in human bronchial epithelial cells (BEAS-2B).
abstract: Compelling evidence indicates that exposure to air pollution particulate matter (PM) affects human health. However, how PM composition interacts with PM-size to cause adverse health effects needs elucidation. In this study, we were also interested in the physicochemical characteristics and toxicological end points of PM₂.₅₋₀.₃ samples produced in rural, urban, or industrial surroundings, thereby expecting to differentiate their respective in vitro adverse health effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics of the three PM₂.₅₋₀.₃ samples, notably their inorganic and organic components, were closely related to their respective emission sources. Referring also to the dose/response relationships of the three PM₂.₅₋₀.₃ samples, the most toxicologically relevant exposure times (i.e., 24, 48, and 72 h) and doses (i.e., 3.75 μg PM/cm² and 15 μg PM/cm²) to use to study the underlying mechanisms of action involved in PM-induced lung toxicity were chosen. Organic chemicals adsorbed on the three PM₂.₅₋₀.₃ samples (i.e., polycyclic aromatic hydrocarbons) were able to induce the gene expression of xenobiotic-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 exposed to the three PM₂.₅₋₀.₃ samples induced oxidative damage (i.e., 8-hydroxy-2'-deoxyguanosine formation, malondialdehyde production and/or glutathione status alteration). There were also statistically significant increases of the gene expression and/or protein secretion of inflammatory mediators (i.e., notably IL-6 and IL-8) in BEAS-2B cells after their exposure to the three PM₂.₅₋₀.₃ samples. Taken together, the present findings indicated that oxidative damage and inflammatory response preceeded cytotoxicity in air pollution PM₂.₅₋₀.₃-exposed BEAS-2B cells and supported the idea that PM-size, composition, and origin could interact in a complex manner to determine the in vitro responsiveness to PM.
authors.affiliation: Université Lille Nord de France, Lille, France.
authors.forename: Mona
authors.initials: M
authors.lastname: Dergham
authors.forename: Capucine
authors.initials: C
authors.lastname: Lepers
authors.forename: Anthony
authors.initials: A
authors.lastname: Verdin
authors.forename: Sylvain
authors.initials: S
authors.lastname: Billet
authors.forename: Fabrice
authors.initials: F
authors.lastname: Cazier
authors.forename: Dominique
authors.initials: D
authors.lastname: Courcot
authors.forename: Pirouz
authors.initials: P
authors.lastname: Shirali
authors.forename: Guillaume
authors.initials: G
authors.lastname: Garçon
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D001189:Aryl Hydrocarbon Hydroxylases / Q000378:metabolism; D001980:Bronchi / Q000166:cytology* / Q000187:drug effects; D002460:Cell Line; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D065633:Cytochrome P-450 CYP1B1; D004249:DNA Damage / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D007221:Industry; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D052638:Particulate Matter / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012424:Rural Population; D014505:Urban Population
chemical_list: D000393:Air Pollutants; D015850:Interleukin-6; D016209:Interleukin-8; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D001189:Aryl Hydrocarbon Hydroxylases; C585496:CYP1B1 protein, human; D019363:Cytochrome P-450 CYP1A1; D065633:Cytochrome P-450 CYP1B1; D016660:NAD(P)H Dehydrogenase (Quinone)