Exposure to urban nanoparticles at low PM1 concentrations as a source of oxidative stress and inflammation

Exposures to fine particulate matter (PM1 ) have been associated with health impacts, but the understanding of the PM1 concentration-response (PM1-CR) relationships, especially at low PM1 , remains incomplete. Here, we present novel data using a methodology to mimic lung exposure to ambient air (2< PM1 < 60 μg 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 PM1-CR curves are interpreted as a result of the interplay between the aerosol total oxidative potential (OPt ) and its distribution across particle size (dp ). A d p-dependent condensation sink (CS) is assessed together with the distribution with d p of reactive species . Urban ambient aerosol high in OPt , as indicated by the DTT assay, with (possibly copper-containing) nanoparticles, shows higher pro-inflammatory and oxidative responses, this occurring at lower PM1 concentrations (< 5 μg 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 OPt with d p also at relatively low PM1.