Tuesday, July 21, 2009

Tire Dust - Another Urban Air Particulate

Toxicology Letters
Volume 189, Issue 3, 28 September 2009, Pages 206-214
Lung toxicity induced by intratracheal instillation of size-fractionated tire particles

Paride Manteccaa, Giulio Sancinib, Elisa Moschinia, Francesca Farinab, Maurizio Gualtieria, Annette Rohrc, Giuseppe Miserocchib, Paola Palestinib and Marina Camatinia, Corresponding Author Contact Information, E-mail The Corresponding Author

aDepartment of Environmental Sciences, POLARIS Research Center, University of Milano-Bicocca, 1 piazza della Scienza, Milan 20126, Italy

bDepartment of Experimental Medicine, POLARIS Research Center, University of Milano-Bicocca, 48 via Cadore, Monza 20052, Italy

cAir Quality and Health, Electric Power Research Institute (EPRI), 3420 Hillview Avenue, Palo Alto, CA 94304, USA


Tire particles (TP) represent a significant component of urban air pollution (PM), constituting more than 10% of PM10 mass at urban locations with heavy traffic. The purpose of this study was to evaluate the effects of size-fractionated TP in an animal exposure model frequently used to assess the health effects of air pollutants. Potential pro-inflammatory and toxic effects of TP2.5 (<2.5 style="font-weight: bold; color: rgb(153, 0, 0);">Inflammatory cellular profiles showed dose-dependent responses after TP10 exposure, while strong cytotoxic effects, including increases in total protein, LDH and AP, were observed to be associated to TP2.5 exposure. Histologically, TP10-treated lungs mainly showed inflammatory tissue infiltration, in contrast to TP2.5-treated lungs, where lysis of the alveolar barrier appeared to be the most characteristic lesion. Our biochemical, cytological, and histological results indicated differential lung toxicity mechanisms elicited by size-fractionated, in agreement with other studies performed in in vivo systems that have shown that lung responses to inhaled or instilled particles are affected by particle size. We conclude that lung toxicity induced by TP10 was primarily due to macrophage-mediated inflammatory events, while toxicity induced by TP2.5 appeared to be related more closely to cytotoxicity.

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