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Size-partitioning of an urban aerosol to identify particle determinants involved in the proinflammatory response induced in airway epithelial cells

Kiran Ramgolam1, Olivier Favez2, Hélène Cachier2, Annie Gaudichet3, Francelyne Marano1, Laurent Martinon4 and Armelle Baeza-Squiban1*

Author Affiliations

1 Univ Paris Diderot, Paris 7, Laboratory of Molecular and Cellular Responses to Xénobiotics, Unit of Functional and Adaptive Biology affiliated to CNRS, 5 rue Thomas Mann, case courrier 7073, 75013 Paris, France

2 Laboratoire des Sciences du Climat et de l'Environnement (LSCE/IPSL), Laboratoire CEA-CNRS-UVSQ, CEA Orme des Merisiers, 91191 Gif-sur-Yvette, France

3 Laboratoire Interuniversitaire des Systèmes Atmosphériques (LISA), Université Paris 12, 61 avenue du Général de Gaulle, 94010 Créteil Cedex, France

4 Laboratoire d'Etude des Particules Inhalées (LEPI), Ville de Paris, 11 rue George Eastman, 75013 Paris, France

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Particle and Fibre Toxicology 2009, 6:10 doi:10.1186/1743-8977-6-10

Published: 23 March 2009

Abstract

Background

The contribution of air particles in human cardio-respiratory diseases has been enlightened by several epidemiological studies. However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear. The aim of the present study is to determine which size fraction from a chemically characterized background aerosol has the most important short term biological effect and to decipher the determinants of such a behaviour.

Results

Ambient aerosols were collected at an urban background site in Paris using four 13-stage low pressure cascade impactors running in parallel (winter and summer 2005) in order to separate four size-classes (PM0.03–0.17 (defined here as ultrafine particles), PM0.17–1 (fine), PM1–2.5(intermediate) and PM2.5–10 (coarse)). Accordingly, their chemical composition and their pro-inflammatory potential on human airway epithelial cells were investigated. Considering isomass exposures (same particle concentrations for each size fractions) the pro-inflammatory response characterized by Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) release was found to decrease with aerosol size with no seasonal dependency. When cells were exposed to isovolume of particle suspensions in order to respect the particle proportions observed in ambient air, the GM-CSF release was maximal with the fine fraction. In presence of a recombinant endotoxin neutralizing protein, the GM-CSF release induced by particles is reduced for all size-fractions, with exception of the ultra-fine fraction which response is not modified. The different aerosol size-fractions were found to display important chemical differences related to the various contributing primary and secondary sources and aerosol age. The GM-CSF release was correlated to the organic component of the aerosols and especially its water soluble fraction. Finally, Cytochrome P450 1A1 activity that reflects PAH bioavailability varied as a function of the season: it was maximal for the fine fraction in winter and for the ultrafine fraction in summer.

Conclusion

In the frame of future regulations, a particular attention should thus be paid to the ultrafine/fine (here referred to as PM1) fraction due to their overwhelming anthropogenic origin and predominance in the urban aerosol and their pro-inflammatory potential.