1997 Volume 35 Issue 1 Pages 69-77
Acute and subacute lung toxicity of nickel fumes was examined by single and repeated intratracheal instillation of nickel fumes and Ni2O3 and NiO powders in the rat. LD50 of nickel fumes was estimated as 38.2mg/kg body weight (b.w.) according to the method of Litchfield and Wilcoxon. Body weight gain was retarded as in the order of a single dose of 13.0mg Ni2O3/kg>14.3 mg nickel fumes/kg>1.4mg Ni2O3/kg>13.0mg NiO/kg b.w. compared to controls. The histopathological changes in the lungs of the 14.3mg nickel fumes/kg-dosed rats were milder than those induced by administration of 13.0mg Ni2O3/kg but severer than those induced by administration of 1.4mg Ni2O3/kg b.w. A single administration of NiO powder did not produce any histopathological effects on the lungs. The repeated administration of nickel fumes produced persistent edema and proteinosis in the alveoli. The nickel fumes, which were chemically composed of 97% of NiO and 3% of Ni2O3, were very fine particles about 5-10nm in diameter, partly aggregated into larger particles and spherical particles about 0.6μm in diameter. Solubility in distilled water and saline was in the order of nickel fumes>Ni2O3 powder_??_NiO powder. It was suggested that a toxic Ni2O3 component and very fine particles of nickel fumes are involved in the acute lung toxicity of nickel fumes. The epithelial injury induced by reactive oxygen and hydroxy radicals, which would be produced during the process of conversion of Ni(III) to Ni(II) and phagocytosis of nickel fumes by macrophages and polymorphonuclear cells, are presumed to be involved in the pathogenesis of nickel fumes-induced lung lesion.
