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Carcinogenesis cobalt

Cobalt compounds can be classified as relatively nontoxic (33). There have been few health problems associated with workplace exposure to cobalt. The primary workplace problems from cobalt exposure are fibrosis, also known as hard metal disease (34,35), asthma, and dermatitis (36). Finely powdered cobalt can cause siUcosis. There is Htfle evidence to suggest that cobalt is a carcinogen in animals and no epidemiological evidence of carcinogenesis in humans. The LD q (rat) for cobalt powder is 1500 mg/kg. The oral LD q (rat) for cobalt(II) acetate, chloride, nitrate, oxide, and sulfate are 194, 133, 198, 1700, 5000, and 279 mg/kg, respectively the intraperitoneal LD q (rat) for cobalt(III) oxide is 5000 mg/kg (37). [Pg.379]

Gilman JPW, Ruckerbauer GM. 1962. Metal carcinogenesis I Observations on the carcinogenicity of a refinery dust, cobalt oxide and colloidal thorium dioxide. Cancer Res 22 152-156. [Pg.138]

Gilman JPW. 1962. Metal carcinogenesis. 11. A study on the carcinogenic activity of cobalt, copper, iron and nickel compounds. Cancer Res 22 159-162. [Pg.233]

Pauli BU. 1990. Carcinogenesis testing of sintered porous (Co Cr Mo) cobalt-chromium-molybdenum implants. U.S. Department of Agriculture/Current Research Information System. Database, July 19,... [Pg.452]

A number of metals (cadmium, cliromium, nickel, and cobalt) and related compounds have been implicated as carcinogens based upon epidemiological and experimental evidence. These metals are thought to act as primary carcinogens since no metabolic activation appears to bq involved. A characteristic of a primary metal carcinogen is that cancers are produced at the point of application. The carcinogenesis of nickel... [Pg.73]

Kazantzis G. 1981. Role of cobalt, iron, lead, manganese, mercury, platinum, selenium, and titanium in carcinogenesis. Environ Health Perspect 40 143-161. [Pg.619]

The wear products of MOM joint articulahon are transported systemically and are manifested in elevated chromium and cobalt levels in a patient s serum and urine, raising the potential risk for carcinogenesis (Jacobs et al. 1996, Jacobs et al. 1998, Jacobs et al. 1999). However, epidemiological studies of cancer risk in patients with MOM remain inconclusive, because of the relatively small... [Pg.100]

The wear products of MOM joint articulation are transported systemically and are manifested in elevated chromium and cobalt levels in a patient s serum and urine, raising the pKJtential risk for carcinogenesis [36, 69, 70]. However, epidemiological studies of cancer risk in patients with MOM remain inconclusive, due to the relatively small patient populations evaluated, the Scandinavian basis of the studies, and the typically rare incidence of the disease [35, 72]. There have also been reports of metal hypersensitivity associated with the implantation of MOM pros-theses, but the incidence of this complication is reported to be extremely rare [73]. Hypersensitivity may manifest itself in the form of an allergic response on the patient s skin however, there is no accepted clinical test to reliably test a patent s sensitivity to metals [74]. It remains unclear whether metal hypersensitivity is a contributing factor to implant performance or survivorship. [Pg.61]


See other pages where Carcinogenesis cobalt is mentioned: [Pg.6]    [Pg.48]    [Pg.68]    [Pg.4821]    [Pg.2998]    [Pg.1372]    [Pg.47]    [Pg.48]    [Pg.349]    [Pg.351]    [Pg.365]    [Pg.280]   
See also in sourсe #XX -- [ Pg.447 ]

See also in sourсe #XX -- [ Pg.185 ]




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