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

Exposures to fine particulate matter (PM 1) have been associated with health impacts, but the understanding of the PM 1 concentration-response (PM 1 -CR) relationships, especially at low PM 1 , remains incomplete. Here, we present novel data using a methodology to mimic lung exposure to ambient air (2 < PM1< 60 μ g m - 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 -CR curves are interpreted as a result of the interplay between the aerosol total oxidative potential (OP t) and its distribution across particle size (d p). A d p -dependent condensation sink (CS) is assessed together with the distribution with d p of reactive species. Urban ambient aerosol high in OP 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 concentrations (< 5 μ g m - 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 with d p also at relatively low PM 1 .