The current understanding of the carcinogenic potential of the most prominent Ni species in sulfidic Ni (Ni subsulphide
([Ni.sub.3][S.sub.2]), Ni oxide (NiO), Ni metal ([Ni.sup.0]), and soluble Ni (primarily Ni sulfate, NiS[O.sub.4]) has been determined through studies based on a combination of animal testing (of pure compounds) and human epidemiological data .
The single dose oral [LD.sub.50] in rats for the less soluble nickel oxide and subsulphide were > 3,600 mg Ni/kg b wt, whereas the oral [LD.sub.50] for the more soluble nickel sulphate and nickel acetate ranged from 39 to 141 mg Ni/kg b wt in rats and mice (40).
Nickel subsulphide (1.8 mg nickel/[m.sup.3]) decreased activity levels of natural killer cells while both nickel oxide (0.47, 2.0, and 7.9 mg nickel/[m.sup.3]) and nickel subsulphate (0.45 and 1.8 mg nickel/[m.sup.3]) inhibited phagocytic ability of alveolar macrophages (50).
The NTP (63-65) studies allow for the comparison of the toxicity of nickel sulphate, nickel subsulphide, and nickel oxide in rats and mice.
Gene mutation frequency was not affected in transgenic mouse and rat respiratory tissue following inhalation exposure to nickel subsulphide (84).
Testicular degeneration was observed in rats and mice exposed to nickel sulphate ([greater than or equal to] 1.4 mg Ni/[m.sup.3]) and nickel subsulphide ([greater than or equal to]1.83 mg Ni/[m.sup.3] for rats and [greater than or equal to]3.65 mg Ni/[m.sup.3] for mice) 6 h/day for 12 days over a 16-day period (63-65).
A number of animal studies have examined the carcinogenic potential of nickel subsulphide, nickel oxide, and nickel sulphate.
Studies in rats and mice demonstrate that chronic active inflammation in the lungs is the most prominent effect following inhalation exposure to nickel sulphate, nickel subsulphide, or nickel oxide.
Immunopathologic effects of nickel subsulphide on the primate pulmonary immune system.
NTP technical report on the toxicology and carcinogenesis studies of nickel subsulphide (CAS No.