Cancer of the lungs, nasal mucosa, and less frequently, of the larynx account for the most serious consequences of usually long-term occupational exposure to nickel.
The first cases of respiratory tract cancers were noted in 1932, in Clyclach (Wales) nickel refinery. It has been established that nickel sulfide and nickel oxide are the most carcinogenic agents of all the nickel compounds encountered. Workers engaged in nickel manufacturing and refining appear to run the highest risk of exposure to nickel compounds.
It emphasized the likelihood of nickel-exposed workers to develop lung cancer as significantly higher among smokers than nonsmokers, particularly asbestos workers.
Nickel, like beryllium compounds, has been capable of damaging DNA and impairing its synthesis in certain systems. Available data are considered inadequate for classifying it as convincingly genotoxic.
Apart from being carcinogenic, nickel is also a commonly known producer of local inflammatory reactions on the skin, chiefly due to sensitization. In workers of a nickel refinery, and even children residing in the vicinity of the plant, there were found to be significantly elevated levels of some serum proteins classed among so-called acute reactants.
Nickel and nickel compounds are known to play a significant role in the etiology of eczematous processes on the human skin. It is estimated that about 513of all cases of eczema are caused by contact with nickel or nickel compounds. Nickel dermatitis sometimes referred to as nickel itch, maybe both in occupationally and non occupationally exposed individuals, especially women as a result of direct contact with stainless steel and nickel-plated articles, such as coins, cooking utensils, watches, costume jewelry, etc. leaking of nickel from these metals assists in skin absorption resulting in allergic reactions and dermatitis and may be enhanced by sweat and cosmetics.
For the action of adverse biological effects of beryllium and nickel of primary importance is their solubility in water and serum and from the stomatoiogy’s viewpoint, in the saliva.
So far, no cases of malignant tumors at sites of dental prostheses have been reported, but local sarcomas have developed in humans and domestic animals at sites of metallic implants and prostheses mode of nickel, chromium, and cobalt alloys. The latency of the “implant” sarcomas varies within a wide range, mean ten years in humans. But the incidence of related tumors does not appear to be high since the metal pins, plates, screws, and joints have been implanted for the last 20 years in thousands of patients and domestic animals. Moreover, due to the multimetal composition of these devices, it is impossible to blame only nickel for the induction of tumors, as the other main components, chromium, and cobalt, also produce tumors in experimental animals. Nevertheless, among these metals nickel is the most potent carcinogen.
Examination of prostate tissue always shows nickel is present. For some reason, the metal nickel is always drawn to the prostate. Bacteria love and need nickel and are attracted to the prostate because of it. Nickel is the meal ticket causing prostatitis and urinary tract infections.
The above-mentioned adverse health effects, namely immunotoxicity and carcinogenicity of both metals, fully justify caution in their application of materials designed for the productions of prosthetics. They represent potential health risk aspects due to the usage of nickel alloys for these purposes and because of the high sensitization potential of beryllium.
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Brown, S.S., and Sunderman, F.W. Jr. Progress in Nickel Toxicology. Blackwell Sci. Publ., Oxford, 1985.
Kasprzak, K.S., Nickel in Genotoxic and Carcinogenic Metals: Environmental and Occupational Exposure. Fishbeib, L. Furst Princeton, N.J. 1987, p. 145-184
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Sunderman, F.F. Jr. Carcinogenic Risk of Metal Implants and Prostheses. In: Biocompatibility of CO-CR-NI Alloys H.F. Hilderbrand and M. Champy (Eds), Plenum Press, London, 1987.
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