Proinflammatory effect of fine and ultrafine particulate matter using size-resolved urban aerosols from Paris Original Research Article

Epidemiological and experimental studies have underlined that exposure to particulate matter (PM) leads mainly to airway inflammation, but the roles of particle size and chemical composition associated to such adverse health outcomes need to be better investigated. This study was performed to validate novel strategies of particle sampling, recovery and cell exposure in order to evaluate the pro-inflammatory potential of fine and ultrafine particles from a fractionated aerosol. Samplings of Paris background aerosols using 13-stage low pressure impactors (0.03–10 μm) gave bimodal mass distributions with an accumulation mode centered on a median diameter of 0.42 μm and a coarse one on 3.25 μm. PM1 accounted for 70% and PM0.1 for 12% of PM10. The latter mainly comprised carbon-chained aggregates. The development of an efficient and reproducible method to recover fine (PM1–0.1) and ultrafine (PM0.1–0.03) particulate matter has permitted experimental comparison of the impact of such particles on human bronchial epithelial cells (HBECs). In this study we have compared the relative effects of fine and ultrafine particles at non-cytotoxic concentrations over 24 h on the production of the pro-inflammatory cytokine GM-CSF by HBECs. Combining two cell exposure strategies to the size-fraction particles according to either their proportion (isovolume exposure) or their quantity in the aerosol (isomass exposure), we showed that both ultrafine and fine particles induced a concentration-dependent GM-CSF release by HBECs which is significant from 1 μg cm−2. In conclusion, short duration samplings using 13-stage impactors enable to obtain size-resolved PM in sufficient quantities to carry out toxicological investigations. These findings are promising in view to conduct a more intensive study joining chemical and toxicological assays.