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ToxSci Advance Access published online on March 25, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg070
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received January 9, 2003; accepted February 11, 2003
© 2003 Society of Toxicology

Molecular and Genetic Toxicology

Genotoxicity of Samples of Nickel Refinery Dust

Farrah Clemens 1 Joseph R. Landolph 2*

1 Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California; USC/Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California
2 Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California; Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California; USC/Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California; Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, Los Angeles, California

* To whom correspondence should be addressed. E-mail: landolph{at}hsc.usc.edu.


  Abstract

In the INCO nickel refinery in Clydach, Wales, United Kingdom, which has operated since 1901, three hundred sixty-five respiratory cancers, including 85 nasal cancers and 280 lung cancers, occurred in workers since the l920s. From 1901 to 1923, incidences of these cancers were high. In 1923, the refining process was changed, eliminating a nickel arsenide, Ni5As2, called orcelite, from the refinery. Incidences of respiratory cancers decreased substantially from 1925-1930. Refinery dust samples were obtained in 1920 and in 1929. Both contain primarily nickel oxide (NiO). The 1920 sample also contains orcelite. The orcelite content of the l920 sample is ~10%; that of the l929 sample is ~1%. We hypothesized that orcelite in the 1920 sample was partially responsible for inducing nasal and lung cancers in the refinery workers, and we tested this hypothesis. The 1920 and 1929 samples and orcelite were phagocytosed by cultured C3H/10T1/2 Cl 8 (10T1/2) mouse embryo cells to similar extents and were similarly cytotoxic to 10T1/2 cells. The 1920 sample and orcelite induced dose-dependent morphological transformation of 10T1/2 cells; the l929 sample did not. The cell transforming ability of the 1920 sample, therefore its probable carcinogenicity, correlates with induction of respiratory cancers in refinery workers exposed to orcelite-containing nickel refinery dust before 1923. Inability of the 1929 sample to induce morphological transformation correlates with decreased human respiratory tumor incidence at this plant after 1923. This data supports our hypothesis that orcelite in the 1920 refinery sample contributed to its carcinogenicity to nickel refinery workers.

Orcelite, nickel arsenide, morphological cell transformation, C3H/10T1/2 mouse embryo cells, green (high temperature) nickel oxide .


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