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Particles containing vanadium are emitted into the air from fuel oil and coal combustion, and may be inhaled by man. Because such particles are within the respirable size, vanadium may be deposited in the alveolar region of the lung and come into contact with the pulmonary alveolar macrophage. In order to evaluate vanadium cytotoxicity, pulmonary alveolar macrophages were lavaged from dogs, rabbits and rats and then incubated with various concentrations of vanadium pentoxide. The minimum vanadium pentoxide concentration which reduced cell viability from control was 1 mg/m1 for dog macrophages, 2.5 mg/ml for rabbit macrophages and 10 mg/ml for rat macrophages. The concentration of vanadium pentoxide which reduced cell viability by 50% for dog, rabbit and rat macrophages was 33 +_ 4 mg/ml, 29 +_ 6 mg/ml and 569 +_ 62 mg/ml respectively. Lipid metabolism by alveolar macrophages from dogs, rabbits and rats was evaluated in vitro at vanadium pentoxide concentrations which caused cell death in less than 10% of the cell population and at vanadium concentrations which reduced cell viability by 50%. Following a 20-h incubation with vanadium pentoxide, 3H-palmitateand 14C-glucose were added to the incubation medium. The incorporation of 3H-palmitate into phospholipid decreased by at least 64% from the control values at 30 mg vanadium pentoxide pentoxide/ml for rat macrophages. At these same concentrations for all three species, the incorporation of 14C-glucose into total lipid decreased by at least 49% from the control values. A decline in lipid synthesis by the pulmonary alveolar macrophages may interfere with cell membrane integrity and therefore result in a decline in pulmonary defense.

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This research was conducted under the Contract EY-76-04-1013 between the United States Department of Energy and the Lovelace Biomedical and Environmental Research Institute, in the facilities fully accredited by the American Association for Accrediation of Laboratory Animal Care. I wish to thank my committee members, Dr. R.O. McClellan, Dr. R.C. Pfleger, Dr. M.L. Riedesel and Dr. G.V. Johnson for their assistance throughout the study. I am indebted to Dr. J.O. Hill, Dr. R.F. Henderson, Dr. T.R. Henderson and Dr. S.H. Weissman for their scientific aid and Mr. W.C. Griffith for his assistance with statistical analysis of the data. I thank Mr. J.J. Waide, Mr. M.L. Binette, Ms. V.A. White, Ms. C.L. Elmquist and Ms. S.A. Felicetti for their technical assistance, Mr. R.E. Dudley and Ms. S.A. Felicetti for their critical review of the thesis and Mr. E.E. Goff for his assistance in the preparation of illustrations. Finally, special appreciation goes to my family whose support and encouragement sustained me throughout the completion of this thesis.



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UNM Biology Department

First Committee Member (Chair)

Roger Orville McClellan

Second Committee Member

Marvin LeRoy Riedesel

Third Committee Member

Gordon Verle Johnson

Fourth Committee Member

Raymond Charles Pfleger

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