ACUTE PULMONARY TOXICITY OF COPPER GALLIUM DISELENIDE, COPPER INDIUM DISELENIDE, AND CADMIUM TELLURIDE INTRATRACHEALLY INSTILLED INTO RATS

Citation
Dl. Morgan et al., ACUTE PULMONARY TOXICITY OF COPPER GALLIUM DISELENIDE, COPPER INDIUM DISELENIDE, AND CADMIUM TELLURIDE INTRATRACHEALLY INSTILLED INTO RATS, Environmental research, 71(1), 1995, pp. 16-24
Citations number
14
Categorie Soggetti
Public, Environmental & Occupation Heath","Environmental Sciences
Journal title
ISSN journal
00139351
Volume
71
Issue
1
Year of publication
1995
Pages
16 - 24
Database
ISI
SICI code
0013-9351(1995)71:1<16:APTOCG>2.0.ZU;2-F
Abstract
Acute toxicity studies were conducted on copper gallium diselenide (CG S), copper indium diselenide (CIS), and cadmium telluride (CT), three novel compounds used in the photovoltaic and semiconductor industries. Female Sprague-Dawley rats (six rats/dose) were administered 0, 12, 2 5, 50, or 100 mg/kg body wt of CGS, CIS, or CT by intratracheal instil lation. At 72 hr after treatment, body weight gain was significantly d ecreased in the 100 mg/kg CIS group and in all CT dose groups. Lung we ights were increased in most chemical-treated rats, with CT causing th e greatest increase. Total numbers of cells in bronchoalveolar lavage fluid (BALF) were significantly increased in treated rats and were gre atest in the 100 mg/kg CIS group. Differential cell counts of BALF dem onstrated a marked decrease in the percentage of alveolar macrophages and an increase in the percentage of polymorphonuclear leukocytes in a ll dose groups of all three chemicals. Slight to moderate increases in lactate dehydrogenase activity were observed in BALF from CGS- and CI S-treated rats; marked increases were observed in CT-treated rats. BAL F protein was significantly increased in rats treated with CIS and CT. Microscopic examination revealed lymphoid hyperplasia in lungs of rat s treated with all three chemicals. CT caused necrosis of the terminal bronchiolar epithelium and epithelium of the alveolar duct region wit h inflammation, prominent fibrin exudates, and type II cell hyperplasi a. CGS and CIS also caused intraalveolar inflammation and type II cell hyperplasia, but did not cause the necrosis and fibrin exudate observ ed in lungs of CT-treated rats. Based on changes in lung weight, BALF indices, and histopathology, CT was the most toxic for the lung; CIS h ad intermediate toxicity and CGS was the least toxic. The solubilities of CGS and CIS were relatively low and similar at both pH levels and do not readily explain the observed differences in pulmonary toxicity. The solubility of CdTe was considerably greater than that of CGS and CIS and likely contributed to the greater toxicity of this compound. ( C) 1995 Academic Press, Inc.