Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.

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