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Toxicity of gallium oxide particles following a 4-week inhalation exposure

โœ Scribed by R. K. Wolff; R. F. Henderson; A. F. Eidson; J. A. Pickrell; S. J. Rothenberg; F. F. Hahn


Publisher
John Wiley and Sons
Year
1988
Tongue
English
Weight
986 KB
Volume
8
Category
Article
ISSN
0260-437X

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โœฆ Synopsis


To evaluate the inhalation toxicity of Ga103, F344 rats were exposed nose-only to 0.2 p m GazO, particles 2 h/day, 5 daydweek for 4 weeks. The exposure concentration was 23 2 5 mg/m3 (mean I+-SD) resulting in lung burdens of 0.8 I+-0.1 mg Gaz03/lung (mean i-I SE) at the end of 4 weeks of exposure. Analysis of bronchoalveolar lavage fluid of exposed rats showed marked responses. One day after termination of exposure, lactate dehydrogenase was increased 6-fold, and the lysosomal enzyme, beta-glucuronidase, was increased 38fold in rats exposed to Ga203 compared to sham exposed controls. Alkaline phosphatase, glutathione reductase, glutathione peroxidase, white blood cells, acid proteinase, and protein were increased 3-to 4-fold. Responses remained elevated 6 and 12 months after exposure. Lung clearance of radiolabeled tracer particles was evaluated 4 days and 6 months after the end of 4 weeks of Gaz03 exposures. Long-term clearance half-times were significantly longer1 ( 3 4 fold, P <0.01) in rats exposed to Gaz03 than in the sham-exposed control rats at both 4 days and 6 months, indicating persistent impairment of particle clearance. Histopathological lesions consisted primarily of alveolar proteinosis 1 day after 4 weeks exposure, progressing in severity to large focal lesions of alveolar histiocytosis and septa1 fibrosis 6 and 12 months after exposure. Inhaled Gaz03 produced cytotoxic, inflammatory, and fibrogenic responses of comparable or greater magnitude than those seen after similar exposures of rats to inhaled quartz particles in other studies. These data show that inhaled Ga203 particles produce considerable toxicity and exposures in the work place should be limited. 16. The Health Effects Institute (HEI), is an organization jointly funded by the United States Environmental Protection Agency (EPA) (Assistance Agreement X-812059) and automotive manufacturers. The contents of this article do not nccessarily reflect the views of the HEI, nor do they necessarily reflect the policies of EPA, or automotive manufacturers. Research conducted in facilities fully accredited by the American Association for Accreditation of Laboratory Animal Care.


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