U. Baltensperger, J. Dommen, M Alfarra, J. Duplissy, K. Gäggeler, A. Metzger, M. Facchini, S. Decesari, E. Finessi, C. Reinnig, M. Schott, J. Warnke, T. Hoffmann, B. Klatzer, H. Puxbaum, M. Geiser, M. Savi, D. Lang, M. Kalberer, T. Geiser:
"Combined Determination of the Chemical Composition and of Health Effects of Secondary Organic Aerosols: The POLYSOA Project";
Journal of Aerosol Medicine and Pulmonary Drug Delivery, 21 (2008), 1; S. 145 - 154.

Kurzfassung englisch:
Epidemiol. studies show a clear link between increased mortality and enhanced concns. of ambient aerosols. The chem. and phys. properties of aerosol particles causing these health effects remain unclear. A major fraction of the ambient aerosol particle mass is composed of secondary org. aerosol (SOA). Recent studies showed that a significant amt. of SOA consists of high mol. wt. compds. (oligomers), which are chem. not well characterized. Within the POLYSOA project a large variety of state-of-the-art anal. chem. methods were used to characterize the chem. compn. of SOA particles with emphasis on the oligomeric mass fraction. Mass spectrometric results showed that SOA oligomers are highly oxidized compds. and that hydroperoxides are formed, which is consistent with NMR results. This high mol. wt. fraction accounts for up to 23 of the total org. carbon in SOA particles. These well-characterized SOA particles were deposited on three lung cell culture systems (microdissected respiratory epithelia from porcine tracheae, the human bronchial epithelial cell line BEAS-2B, and porcine lung surface macrophages obtained by bronchoalveolar lavage) in a newly constructed particle deposition chamber with the goal to eventually identify particle components that are responsible for cell responses leading to adverse health effects. In addn., monolayers of the alveolar epithelial cell line A549 were used in an alveolar epithelial repair model. The lung cells were examd. for morphol., biochem., and physiol. changes after exposure to SOA. Analyses of the lung cells after exposure to SOA are ongoing. First data give evidence for a moderate increase of necrotic cell death as measured by lactate dehydrogenase release and for effects on the alveolar epithelial wound repair mainly due to alterations of cell spreading and cell migration at the edge of the wound. Thus, these first results indicate that SOA, in concns. comparable to environmental concns., may induce distinct effects in lung cells.

Indexing -- Section 59 (Air Pollution and Industrial Hygiene)

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