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Citation
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HERO ID
56067
Reference Type
Journal Article
Title
Increased inflammation and altered macrophage chemotactic responses caused by two ultrafine particle types
Author(s)
Renwick, LC; Brown, D; Clouter, A; Donaldson, K
Year
2004
Is Peer Reviewed?
1
Journal
Occupational and Environmental Medicine
ISSN:
1351-0711
EISSN:
1470-7926
Volume
61
Issue
5
Page Numbers
442-447
Language
English
PMID
15090666
DOI
10.1136/oem.2003.008227
Web of Science Id
WOS:000220887400011
URL
http://www.ncbi.nlm.nih.gov/pubmed/=15090666
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Abstract
Background: Ultrafine particles have been hypothesised to be an important contributing factor in the toxicity and adverse health effects of particulate air pollution (PM10) and nanoparticles are used increasingly in industrial processes.
Aims: To compare the ability of ultrafine and fine particles of titanium dioxide and carbon black to induce inflammation, cause epithelial injury, and affect the alveolar macrophage clearance functions of phagocytosis and chemotaxis in vivo.
Methods: Rats were instilled with fine and ultrafine carbon black and titanium dioxide. Inflammation was quantified by bronchoalveolar lavage; the ability of the macrophages to phagoytose indictor fluorescent beads and to migrate towards aC5a were determined.
Results: Ultrafine particles induced more PMN recruitment, epithelial damage, and cytotoxicity than their fine counterparts, exposed at equal mass. Both ultrafine and fine particles significantly impaired the phagocytic ability of alveolar macrophages. Only ultrafine particle treatment significantly enhanced the sensitivity of alveolar macrophages to chemotact towards C5a.
Conclusions: Ultrafine particles of two very different materials induced inflammation and epithelial damage to a greater extent than their fine counterparts. In general, the effect of ultrafine carbon black was greater than ultrafine titanium dioxide, suggesting that there are differences in the likely harmfulness of different types of ultrafine particle. Epithelial injury and toxicity were associated with the development of inflammation after exposure to ultrafines. Increased sensitivity to a C5a chemotactic gradient could make the ultrafine exposed macrophages more likely to be retained in the lungs, so allowing dose to accumulate.
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