Potassium molybdate as a source of molybdenum added for nutritional purposes to food supplements

The toxicity of molybdates has been reviewed by several authorities including the SCF, and the UK Expert Group on Vitamins and Minerals (EVM). Overall these reviews indicate that the data documenting molybdenum toxicity in humans are limited. In studies conducted in a region of Armenia where levels of molybdenum in the soil are high, adults were found to have elevated plasma and urine concentrations of uric acid and gout-like symptoms. In these studies, the daily molybdenum intake for adults was estimated to be 10-15 mg. In animals, acutely toxic oral doses of molybdenum result in severe gastrointestinal irritation with diarrhea, coma and death from cardiac failure. Subchronic and chronic oral exposures can result in growth retardation, anaemia, hypothyroidism, bone and joint deformities, sterility, liver and kidney abnormalities, and death. In rabbit, two separate subchronic toxicological studies (4 and 6 months respectively) of molybdates indicated differences in the No-Observable-Adverse-Effect-Level (NOAEL) for ammonium and sodium molybdates (0.5 and 23 mg/kg bw/day, respectively). Regarding reproductive toxicity, male sterility and embryotoxic effects of sodium molybdate were observed in rats, and in particularly reduced foetal weight gain, delayed histological development of foetal structures and increased fetal resorption. The NOAEL of this study was 0.9 mg molybdenum/kg bw/day for reproductive toxicity. This study in rats was considered pivotal by the SCF, in its opinion on the tolerable intake level of molybdenum. There are no relevant studies of molybdenum or molybdate carcinogenicity in animals or humans. Regarding genotoxicity, both negative and positive responses on bacteria have been obtained with molybdates, as previously indicated by the SCF. Ammonium molybdate induced chromosome aberrations and sister-chromatid exchanges in human lymphocytes in vitro. Molybdenum trioxide but not ammonium molybdate induced chromosome damage in mouse bone marrow whereas dominant lethal mutations were induced in Drosophila exposed to ammonium molybdate. A study on the tolerable intake level of molybdenum, not available at the time of the SCF opinion was published, used the micronucleus assay in human lymphocytes. In this study, ammonium molybdate was more potent than sodium molybdate in inducing chromosome loss in cultured human lymphocytes. This study also assessed the genotoxicity of sodium molybdate in vivo by using the micronucleus assay in mouse bone marrow and the dominant lethal assay in mice, this study was used to assess the genotoxic effects of sodium molybdate in vivo. However, it provided a limited evidence of in vivo genotoxicity of this salt in mouse somatic and germ cells. The Panel concludes that the use of potassium molybdate, as a source of molybdenum, added for nutritional purposes in food supplements at the proposed use levels, is of no safety concern provided the applicable UL for molybdenum established by the SCF is not exceeded. The Panel notes that since the SCF adopted its opinion on molybdenum, new toxicological data have been made available on in vitro and in vivo genotoxicity of molybdenum that might need further investigation.