Pulmonary Immunotoxicity of Inhaled Ammonium Metavanadate in Fisher 344 Rats |
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Authors: | COHEN, MITCHELL D. YANG, ZIJIAN ZELIKOFF, JUDITH T. SCHLESINGER, RICHARD B. |
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Affiliation: | Department of Environmental Medicine, New York University Medical Center Long Meadow Road, Tuxedo, New York, 10987 Received March 1, 1996; accepted July 30, 1996 |
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Abstract: | Male Fisher 344 rats were exposed to 2 mg vanadium(V)/m3 (asammonium metavanadate NH4VO3, 0.32 µm MMD) atmospheresfor 8 hr/day for 4 days in a nose-only exposure system. In exposedrats, lung V burdens increased in a time-dependent fashion.Analysis of lung cells and lavage fluid 24 hr after the finalexposure suggested that tissue damage and a strong inflammatoryresponse was elicited; numbers of neutrophil and small macrophages(M), as well as levels of lavageable protein and lactate dehydrogenase,were significantly elevated as compared with levels observedwith air-exposed rats. Vanadium also affected pulmonary alveolarM (PAM) capacities to produce and respond to immunoregulatingcytokines. Inducible PAM production of tumor necrosis factor-awas significantly inhibited, as was the ability to increasecell surface Class II/I-A molecule expression in response tointerferon- (rFN- ). PAM from V-exposed hosts were also inhibitedin their ability to be primed by EFN- to produce superorideanion and hydrogen peroxide in response to stimulation withopsonized zy-mosan. These studies indicate that short-term repeatedexposure of rats to atmospheric V, at levels encountered inan occupational setting, can alter host pulmonary immunomocompetence,with one major effect occurring at the level of cytokine-relatedfunctions. These alterations may be underlying mechanisms forthe well-documented increases in bronchopulmonary infectionsand cancers in workers chronically exposed to V-containing atmospheres. |
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