Exposure to urban nanoparticles at low PM$$_1$$ concentrations as a source of oxidative stress and inflammation

Abstract

AbstractExposures to fine particulate matter (PM$$_1$$ 1 ) have been associated with health impacts, but the understanding of the PM$$_1$$ 1 concentration-response (PM$$_1$$ 1 -CR) relationships, especially at low PM$$_1$$ 1 , remains incomplete. Here, we present novel data using a methodology to mimic lung exposure to ambient air (2$$<PM_1<$$ < P M 1 < 60 $$\upmu$$ μ g m$$^{-3}$$ - 3 ), with minimized sampling artifacts for nanoparticles. A reference model (Air Liquid Interface cultures of human bronchial epithelial cells, BEAS-2B) was used for aerosol exposure. Non-linearities observed in PM$$_1$$ 1 -CR curves are interpreted as a result of the interplay between the aerosol total oxidative potential (OP$$_t$$ t ) and its distribution across particle size (d$$_p$$ p ). A d$$_p$$ p -dependent condensation sink (CS) is assessed together with the distribution with d$$_p$$ p of reactive species . Urban ambient aerosol high in OP$$_t$$ t , as indicated by the DTT assay, with (possibly copper-containing) nanoparticles, shows higher pro-inflammatory and oxidative responses, this occurring at lower PM$$_1$$ 1 concentrations (< 5 $$\upmu$$ μ g m$$^{-3}$$ - 3 ). Among the implications of this work, there are recommendations for global efforts to go toward the refinement of actual air quality standards with metrics considering the distribution of OP$$_t$$ t with d$$_p$$ p also at relatively low PM$$_1$$ 1 .