| Titolo | Lung toxicity induced by intratracheal instillation of size-fractionated tire particles |
|---|---|
| Tipo di pubblicazione | Articolo su Rivista peer-reviewed |
| Anno di Pubblicazione | 2009 |
| Autori | Mantecca, P., Sancini G., Moschini E., Farina F., Gualtieri Maurizio, Rohr A., Miserocchi G., Palestini P., and Camatini M. |
| Rivista | Toxicology Letters |
| Volume | 189 |
| Paginazione | 206-214 |
| ISSN | 03784274 |
| Parole chiave | air pollutant, Air Pollutants, Air pollution, alkaline phosphatase, animal experiment, animal model, animal tissue, Animalia, Animals, Antioxidants, article, beta glucuronidase, Bronchoalveolar Lavage Fluid, Cell Count, Cell Survival, concentration response, controlled study, Cytokines, Cytotoxicity, electron, environmental exposure, glutathione, histopathology, in vivo study, Inbred BALB C, inflammation, inflammatory cell, inflammatory infiltrate, Intratracheal, Intubation, lactate dehydrogenase, lung, Lung Diseases, lung lavage, lung toxicity, macrophage activation, macrophage inflammatory protein 2, male, Mice, Microscopy, mouse, Mus, nonhuman, Occupational, Oxidation-Reduction, Oxidative stress, particle size, particulate matter, pneumonia, priority journal, Protein, protein analysis, Rubber, Scanning, superoxide dismutase, tire particle, tumor necrosis factor alpha |
| Abstract | 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 μm) and TP10 (<10 μm) were investigated through instillation of suspensions of these materials in BALB/c mice. Bronchoalveolar lavage fluid (BALF) was screened for total protein, lactate dehydrogenase (LDH), alkaline phosphatase (AP), and β-glucuronidase (B-Gluc) as markers of cytotoxicity; glutathione (GSH) and superoxide dismutase (SOD) as markers of oxidative potential; and tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-2 (MIP-2), and inflammatory cells as markers of inflammation. Concomitantly, histological analysis of TP-exposed lungs was performed. A single intratracheal instillation of 10 μg/100 μl, 100 μg/100 μl or 200 μg/100 μl was performed, and after 24 h mice were euthanized and BALF examined. 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 TP, 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. © 2009 Elsevier Ireland Ltd. |
| Note | cited By 29 |
| URL | https://www.scopus.com/inward/record.uri?eid=2-s2.0-67650022863&doi=10.1016%2fj.toxlet.2009.05.023&partnerID=40&md5=3a782046b247f6ed24379bc376cbc47f |
| DOI | 10.1016/j.toxlet.2009.05.023 |
| Citation Key | Mantecca2009206 |
