Journal
JOURNAL OF AEROSOL MEDICINE AND PULMONARY DRUG DELIVERY
Volume 21, Issue 1, Pages 145-154Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/jamp.2007.0655
Keywords
chemical composition; health effects; secondary organic aerosols
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Funding
- NERC [ncas10006] Funding Source: UKRI
- Natural Environment Research Council [ncas10006] Funding Source: researchfish
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Epidemiological studies show a clear link between increased mortality and enhanced. concentrations of ambient aerosols. The chemical and physical properties of aerosol particles causing these health effects remain unclear. A major fraction of the ambient aerosol particle mass is composed of secondary organic aerosol (SOA). Recent studies showed that. a significant amount of SOA consists of high molecular weight compounds (oligomers), which are chemically not well characterized. Within the POLYSOA project a large variety of state-ofthe-art analytical chemical methods were used to characterize the chemical composition of SOA particles with emphasis on the. oligomeric mass fraction. Mass spectrometric results showed that SOA oligomers are highly oxidized compounds and that hydroperoxides are formed, which is consistent with NMR results. This high molecular weight fraction accounts for up to 23% of the total organic 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-213, 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 addition, monolayers of the alveolar epithelial cell line A549 were used in an alveolar epithelial repair model. The lung cells were examined for morphological, biochemical, and physiological 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 concentrations comparable to environmental concentrations, may induce distinct effects in lung cells.
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