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Title: Unusual inflammatory and fibrogenic pulmonary responses to single-walled carbon nanotubes in mice
Date: 11/2005
  Link to Journal Abstract
Abstract: Single-walled carbon nanotubes (SWCNT) are new materials of emerging technological importance. As SWCNT are introduced into the life cycle of commercial products, their effects on human health and environment should be addressed. We demonstrated that pharyngeal aspiration of SWCNT elicited unusual pulmonary effects in C57BL/ 6 mice that combined a robust but acute inflammation with early onset yet progressive fibrosis and granulomas. A dose-dependent increase in the protein, LDH, and gamma-glutamyl transferase activities in bronchoalveolar lavage were found along with accumulation of 4-hydroxynonenal ( oxidative biomarker) and depletion of glutathione in lungs. An early neutrophils accumulation ( day 1), followed by lymphocyte ( day 3) and macrophage ( day 7) influx, was accompanied by early elevation of proinflammatory cytokines ( TNF-alpha, IL-1 beta; day 1) followed by fibrogenic transforming growth factor ( TGF)-beta 1 ( peaked on day 7). A rapid progressive fibrosis found in mice exhibited two distinct morphologies: 1) SWCNT-induced granulomas mainly associated with hypertrophied epithelial cells surrounding SWCNT aggregates and 2) diffuse interstitial fibrosis and alveolar wall thickening likely associated with dispersed SWCNT. In vitro exposure of murine RAW 264.7 macrophages to SWCNT triggered TGF-beta 1 production similarly to zymosan but generated less TNF-alpha and IL-1 beta. SWCNT did not cause superoxide or NO (.) production, active SWCNT engulfment, or apoptosis in RAW 264.7 macrophages. Functional respiratory deficiencies and decreased bacterial clearance ( Listeria monocytogenes) were found in mice treated with SWCNT. Equal doses of ultrafine carbon black particles or fine crystalline silica ( SiO2) did not induce granulomas or alveolar wall thickening and caused a significantly weaker pulmonary inflammation and damage.
Content Emphasis Peer Reviewed Journal Article
Exposure Or Hazard Target Mammalian
Exposure Pathway Multiple
Method Of Study Multiple
Paper Type Hazard
Particle Type Carbon
Production Method Engineered
Risk Exposure Group General Population
Target Audience Technical Research
Citation: American Journal of Physiology-Lung Cellular and Molecular Physiology 2005, 289, (5), L698-L708.
Publication: American Journal of Physiology-Lung Cellular and Molecular Physiology
Author: Shvedova AA, Kisin ER, Mercer R, Murray AR, Johnson VJ, Potapovich AI,Tyurina YY, Gorelik O, Arepalli S, Schwegler-Berry D, Hubbs AF, Antonini J, Evans DE, Ku B, Ramsey D, Maynard A, Kagan VE, Castranova V, Baron P
Volume: 289
Number: 5
Pages: L698-L708
     


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This work is supported in part by the Nanoscale Science and Engineering Initiative of the National Science Foundation
under NSF Award Number EEC-0118007.

 		 
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