Exposure to urban nanoparticles at low PM $$_1$$ 1 concentrations as a source of oxidative stress and inflammation

Abstract

Abstract Exposures 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 .