Metal passivity as mechanism of metal carcinogenesis: Chromium,nickel, iron,copper, cobalt,platinum, molybdenum

For the transition metals chromium, nickel, iron, copper, cobalt, platinum, and molybdenum, mechanisms of stable bonding in biochemistry (emphasis on carcinogenic mechanisms), chemistry, industrial chemistry, as well as epidemiological, occupational, orthopedic (implant devices) effects related to carcinogenesis, were reviewed. Hypothetically, the propensity to stable bonding (inertness), which ensures the metals’ performance capacity for consumers and industrial application, relates to their carcinogenicity. For chromium, a relationship between industrial/chemical and biological reactivity was noted for the tendency of Cr(III) ions to cause hydrolysis previous to stable bonding, as occurs during anodic passivation, leather tanning, and as indicated in biochemical studies pertaining to a mechanism of DNA condensation, which was suggested as a carcinogenic mechanism. The involvement of metal hydrolysis in both anodic passivation and biochemistry was noted also for nickel, iron, and platinum; the DNA interaction of platinum (cis-platin) is known to depend on hydrolysis. For nickel, issues of potential (V) were found important in both passivation and carcinogenicity. Comparably, the passivity behavior of cobalt and copper was found atypical, and their carcinogenicity yet unclear. Molybdenum, contained in passivated metallic implants, may relate to implant-associated carcinogenesis. Occupational carcinogenic effects were indicated for chromium, nickel, iron, and cobalt as caused by both reactive and passivated metal species. Exposure to acids and chronic respiratory irritation/infection/inflammation in workers were important cofactors in metal carcinogenesis. For wood and leather workers exposed to dust, the assumed presence in dust of metal particles abraded from alloys (sawing or cutting blades) may be a carcinogenic exposure hazard.