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Inhalation Toxicology
International Forum for Respiratory Research
Volume 21, 2009 - Issue 12
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Research Article

Associations of urban air particulate composition with inflammatory and cytotoxic responses in RAW 246.7 cell line

, , , , , , , , , , & show all
Pages 994-1006 | Received 16 Sep 2008, Accepted 16 Dec 2008, Published online: 23 Sep 2009
 

Abstract

Epidemiological studies show heterogeneities in the particulate pollution-related exposure–effect relationships among cardiorespiratory patients, but the connection to chemical composition and toxic properties of the inhaled particles is largely unknown. To identify the chemical constituents and sources responsible for the diverse inflammatory and cytotoxic effects of urban air, fine (PM2.5–0.2) and coarse (PM10–2.5) particulate samples were collected during contrasting air pollution situations. We exposed mouse RAW 246.7 macrophages for 24 hrs to PM2.5–0.2 and PM10–2.5 samples from six European cities. The concentrations of proinflammatory cytokines (IL-6, TNFα), chemokine (MIP-2), and nitric oxide were measured from the cell culture medium, and the cytotoxicity was assayed. Spearman’s correlations between the chemical constituents and cellular responses were analyzed. In the PM2.5–0.2 size range, the tracers of photo-oxidation of organics in the atmosphere (oxalate, succinate, malonate), some transition metals (Ni, V, Fe, Cu, Cr), and insoluble soil constituents (Ca, Al, Fe, Si) correlated positively with the response parameters. In contrast, the tracers of incomplete biomass (monosaccharide anhydrides) and coal (As) combustion, and polycyclic aromatic hydrocarbons (PAHs), had negative correlations with the inflammatory activity. The compositions of PM10–2.5 samples were more uniform and there were only occasional high correlations between the chemical constituents, endotoxin, and the response parameters. The present results suggest that the local sources of incomplete combustion and resuspended road dust are important producers of harmful fine particulate constituents that may, however, operate via diverse toxicity mechanisms. The results agree well with our recent findings in the mouse lung.

Acknowledgements

The authors are grateful for funding by the EC-FP5 Quality of Life and Management of Living Resources Programme (QLK4-CT-2001-00423), the Academy of Finland (contracts 201701 and 53307), and Tekes (contract 40715/01), and for conduction of field campaigns by the PAMCHAR partners in the six European cities (www.pamchar.org).

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