Very few epidemiological studies have been conducted to determine the relationship between minerals and the incidence of cancer in humans. This is due partly to the difficulty of identifying populations with significantly different intakes of the various minerals. In contrast, there have been numerous studies in laboratory animals. In these investigations, the carcinogenic effects of many metals, administered at high doses to the animals parenterally, have been well established and have been reviewed extensively (Furst, 1979; Sunderman,1977). However, the results of these studies have shed little light on the potential carcinogenic risk posed by trace elements in the amounts occurring naturally in the diet of humans.
Very few feeding studies have been conducted to test the carcinogenicity of trace elements in animals. The carcinogenic action of these elements is difficult to test in animals because some of them are toxic at levels that exceed dietary requirements, and because it is difficult to control synergistic interactions of the element under investigation with other elements that may contaminate air, diet, and drinking water. This chapter contains an evaluation of a few of those trace elements that are nutritionally significant and suspected of playing a role in carcinogenesis. The committee sought evidence primarily from those experiments in which the element was fed
to the animal or from epidemiological reports of exposure through diet. Results obtained from laboratory experiments using other routes of exposure, or evidence from occupational exposure of humans, are described briefly when sufficient information about dietary exposure could not be found. The effects of both the deficiencies as well as excessive intakes of minerals are also discussed in this chapter. Schroeder and his associates investigated the carcinogenicity of trace elements in a series of large experiments extending over 15 years (Kanisawa and Schroeder, 1967; Schroeder and Mitchener, 1971a,b, 1972; Schroeder et al., 1964, 1965, 1968, 1970). Animals were raised in an environment that permitted maximum control of trace element contamination; they were fed one diet of known composition; and they were observed
for their lifetime. The following elements were studied in at least 50 mice and/or rats per treatment: fluorine, titanium, vanadium, chromium, nickel, gallium, germanium, arsenic, selenium, yttrium, zirconium, niobium, rhodium, palladium, cadmium, indium, tin, antimony, tellurium, and lead. These elements were added to the drinking water at levels of 5 mg/liter, except for selenium (3 mg/liter) and tellurium (2 mg/liter). These levels (approximately 100 times greater than the concentrations present naturally in the diet) did not significantly affect
growth and survival of the animals. The interpretation of these findings of no effects or minimally significant effects must be cautious, in view of the small number of animals used. Only rhodium and palladium (tested in mice only) showed any signs of carcinogenicity, but as Schroeder and Michener (1971a) stated, “The results were at a minimally significant level of confidence.” Further studies are needed to confirm these findings. Schroeder also reported that selenate, but not selenite, increased the incidence of spontaneous malignant mammary and subcutaneous tumors in rats after lifetime exposure (11 in 75 controls vs 20 in 73 selenate-fed animals). These results were not confirmed in similar studies in mice. (The effects of selenium on carcinogenesis are discussed in further detail below.) None of the remaining elements examined increased tumor incidence. A significant reduction in tumor incidence was observed in mice fed arsenic and cadmium and in mice and rats fed lead.
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