Toxicity Profiles

Condensed Toxicity Summary for MOLYBDENUM

NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.

JANUARY 1993

Prepared by: Dennis M. Opresko, Ph.D., Chemical Hazard Evaluation Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee.

Prepared for: Oak Ridge Reservation Environmental Restoration Program.

*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.

Molybdenum (Mo) occurs naturally in various ores; the principal source being molybdenite (MoS2) (Stokinger, 1981). Molybdenum compounds are used primarily in the production of metal alloys. Molybdenum is considered an essential trace element; the provisional recommended dietary intake is 75-250 g/day for adults and older children (NRC, 1989).

Water-soluble molybdenum compounds are readily taken up through the lungs and gastrointestinal tract; but insoluble compounds are not. Following absorption, molybdenum is distributed throughout the body with the highest levels generally found in the liver, kidneys, spleen, and bone (Wennig and Kirsch, 1988). Limited data suggest that 25 to 50% of an oral dose is excreted in the urine, with small amounts also eliminated in the bile. Biological half-life may vary from several hours in laboratory animals to as much as several weeks in humans (Friberg and Lener, 1986; Jarrell et al., 1980; Stokinger, 1981; Vanoeteren et al., 1982; Venugopal and Luckey, 1978).

Data documenting molybdenum toxicity in humans are limited. The physical and chemical state of the molybdenum, route of exposure, and compounding factors such as dietary copper and sulfur levels may all affect toxicity. Mild cases of molybdenosis may be clinically identifiable only by biochemical changes (eg., increases in uric acid levels due to the role of molybdenum in the enzyme xanthine oxidase). Excessive intake of molybdenum causes a physiological copper deficiency, and conversely, in cases of inadequate dietary intake of copper, molybdenum toxicity may occur at lower exposure levels.

There is no information available on the acute or subchronic oral toxicity of molybdenum in humans. In studies conducted in a region of Armenia where levels of molybdenum in the soil are high (77 mg Mo/kg), 18% of the adults examined in one town and 31% of those in another town were found to have elevated concentrations of uric acid in the blood and urine, increased blood xanthine oxidase activity, and gout-like symptoms such as arthralgia, articular deformities, erythema, and edema (Kovalskii et al., 1961). The daily molybdenum intake was estimated to be 10-15 mg. An outbreak of genu valgum (knock-knees) in India was attributed to an increase in Mo levels in sorgum, the main staple food of the region. The estimated daily Mo intake was 1.5 mg (Jarrell et al., 1980).

In animals, acutely toxic oral doses of molybdenum result in severe gastrointestinal irritation with diarrhea, coma and death from cardiac failure. Oral LD50 values of 125 and 370 mg Mo/kg for molybdenum trioxide and ammonium molybdate, respectively, have been reported in laboratory rats (Venugopal and Luckey, 1978). Subchronic and chronic oral exposures can result in gastrointestinal disturbances, growth retardation, anemia, hypothyroidism, bone and joint deformities, sterility, liver and kidney abnormalities, and death (Lloyd et al., 1976; Venugopal and Luckey, 1978; Valli et al., 1969; Fairhall et al., 1945; Rana and Kumar, 1980). Fatty degeneration of the liver occurred in rabbits dosed with 50 mg/kg/day for 6 mo (Asmangulyan, 1965) and in rats dosed with 5 mg/kg/day as ammonium molybdate for 1 year (Valjcuk and Sramko, 1973). Male sterility, was reported in rats fed diets containing 80 or 140 ppm Mo (Jeter and Davis, 1954). Teratogenic effects have not been observed in mammals, but embryotoxic effects, including reduced weight gain, reduced skeletal ossification, nerve system demyelinization, and reduced survival of offspring have been reported (Wide, 1984; Earl and Vish, 1979; Schroeder and Mitchener, 1971).

The chronic oral Reference Dose (RfD) for molybdenum and molybdenum compounds is 0.005 mg/kg/day, based on biochemical indices in humans (U.S. EPA, 1992). The subchronic RfD is also 0.005 mg/kg/day (U.S. EPA, 1992).

Information on the inhalation toxicity of molybdenum in humans following acute and subchronic exposures is not available. Studies of workers chronically exposed to Mo indicate a high incidence of weakness, fatigue, headache, irritability, lack of appetite, epigastric pain, joint and muscle pain, weight loss, red and moist skin, tremor of the hands, sweating, and dizziness (Akopajan, 1964; Ecolajan, 1965; Walravens et al., 1979). Elevated levels of Mo in blood plasma and urine and high levels of ceruloplasmin and uric acid in blood serum were reported for workers exposed to Mo (8-hr TWA 9.5 mg Mo/m3) (Walravens et al., 1979). Occupational exposure to molybdenum may also result in increased serum bilirubin levels and decreased blood IgA/IgG ratios due to a rise in alpha-immunoglobulins (Avakajan, 1966b; 1968). Direct pulmonary effects of chronic exposure to Mo have been reported in only one study in which 3 of 19 workers exposed to Mo and MoO3 (1 to 19 mg/m3) for 3-7 years were symptomatic and had X-ray findings indicative of pneumoconiosis (Mogilevskaya, 1963). Adverse reproductive or developmental effects have not been observed in molybdenum workers (Metreveli et al., 1985).

In animal studies, inhalation exposures to molybdenum compounds have resulted in respiratory tract irritation, pulmonary hemorrhages, perivascular edema, and liver and kidney damage (Mogilevskaya, 1963; Fairhall, et al., 1945). Other effects reported in animals include diarrhea, muscle incoordination, loss of hair, loss of weight (Fairhall et al., 1945), changes in ECG, increased arterial blood pressure, increased serum lactate dehydrogenase, increased cardiac adrenaline and noradrenaline levels (Babayan et al., 1984), and inflammation of the uterine horns with necrotic foci and endometrial atrophy (Metreveli and Daneliya, 1984). Some molybdenum compounds, such as molybdenum trioxide and sodium molybdate (Na2MoO4) are strong eye and skin irritants; however, others, such as calcium and zinc molybdates are not primary irritants.

Subchronic and chronic Reference Concentrations (RfC) for molybdenum are not available.

Information on the oral or inhalation carcinogenicity of molybdenum compounds in humans was not available, and animal data indicate that Mo may have an inhibitory effect on esophageal (Luo et al., 1983; van Rensburg et al., 1986; Komada, et al., 1990) and mammary carcinogenesis (Wei et al., 1987). However, intraperitoneal injections of MoO3 in mice produced a significant increase in the number of lung adenomas per mouse and an insignificant increase in the number of mice bearing tumors (Stoner et al., 1976). Molybdenum is placed in EPA Group D, not classifiable as to carcinogenicity in humans (U.S. EPA, 1990) and calculation of slope factors is not possible.

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