Review
Update on the genotoxicity and carcinogenicity of cobalt
compounds
D Lisona, M De Boeckb, V Verougstraetea, M Kirsch-Voldersb
a Industrial
Toxicology and Occupational Medicine Unit, Université catholique de
Louvain, Clos Chapelle-aux-Champs 3054, 1200 Bruxelles, Belgium, b Laboratory of Cell Genetics, Vrije Universiteit
Brussel, Brussels, Belgium
Correspondence to: Dr D Lison lison{at}toxi.ucl.ac.be
Accepted 17 April
2001
OBJECTIVE
To integrate
recent understandings of the mechanisms of genotoxicity and
carcinogenicity of the different cobalt compounds.
METHODA narrative
review of the studies published since the last IARC assessment in 1991 (genotoxicity, experimental carcinogenesis, and epidemiology).
RESULTSTwo different
mechanisms of genotoxicity, DNA breakage induced by cobalt metal and
especially hard metal particles, and inhibition of DNA repair by cobalt
(II) ions contribute to the carcinogenic potential of cobalt compounds.
There is evidence that soluble cobalt (II) cations exert a genotoxic
and carcinogenic activity in vitro and in vivo in experimental systems
but evidence in humans is lacking. Experimental data indicate some
evidence of a genotoxic potential for cobalt metal in vitro in human
lymphocytes but there is no evidence available of a carcinogenic
potential. There is evidence that hard metal particles exert a
genotoxic and carcinogenic activity in vitro and in human studies,
respectively. There is insufficient information for cobalt oxides and
other compounds.
CONCLUSIONAlthough
many areas of uncertainty remain, an assessment of the carcinogenicity
of cobalt and its compounds requires a clear distinction between the
different compounds of the element and needs to take into account the
different mechanisms involved.
Keywords: cobalt; DNA breakage; inhibition of DNA repair
© 2001 by Occupational and Environmental Medicine
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