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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc
molybdate in drinking water (10 mg/L) on the reproduction of mice over three generations. Because water consumption was not reported in the publication, daily molybdenum intake can only be estimated. Vyskocil and Viau (1999) estimated that a 20-mg mouse’s consumption of 3 mL of water (10 mg/L) daily would result in a dose of 1.5 mg/kg/day of molybdenum. At this dose, Schroeder and Mitchener (1971) reported some early deaths of offspring, dead litters, maternal deaths, and failure to breed.
Other Endpoints. There is no evidence that molybdenum causes cancer in humans or animals (Vyskocil and Viau, 1999). There are consistent findings of decreased hemoglobin concentration and hematocrit in rabbits (Arrington and Davis, 1953; McCarter et al., 1962; Ostrom et al., 1961; Valli et al., 1969). These effects were seen at doses of 25 mg/kg/day or more.
Growth depression has been noted in several studies with monogastric laboratory animals (Arthur, 1965; Jeter and Davis, 1954; Miller et al., 1956). In the study by Jeter and Davis (1954), rats were administered four different doses of molybdenum (20, 80, 140, and 700 mg/kg of diet) for 13 weeks. Growth depression was noted in female rats fed 80 mg/kg, which according to Vyskocil and Viau (1999), corresponds to 8 mg/kg/day of molybdenum. Miller and coworkers (1956) observed body weight loss and bone deformities in rats fed 75 and 300 mg/kg of diet molybdenum for 6 weeks. The lowest dose corresponds to 7.5 mg/kg/day according to Vyskocil and Viau (1999). Arthur (1965) fed guinea pigs diets containing various levels of molybdenum for 8 weeks. At the lowest dose (estimated to be 75 mg/kg/day), growth depression, loss of copper, and achromotrichia were observed.
Bioavailability and Toxicokinetics. Possible reasons for the presumed low toxicity of molybdenum include its rapid excretion in the urine, especially at higher intake levels (Miller et al., 1956; Turnlund et al., 1995b).
Because of the deficiencies in the study conducted in Armenia (Kovalsky et al., 1961), inadequate data exist to identify a causal association between excess molybdenum intake in normal, apparently healthy individuals and any adverse health outcomes. In addition, studies have identified levels of dietary molybdenum intake that appear to be associated with no harm (Deosthale and Gopalan,