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MOLYBDENUM

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Molybdenum is an essential trace element for humans and mammals.

Specific Substances

    A) MOLYBDENUM
    1) Molybdate
    2) Molecular Formula: Mo
    3) MCHVL
    4) TSM1
    5) CAS 7439-48-7 (metal)
    6) NIOSH/RTECS QA 4680000
    AMMONIUM MOLYBDATE
    1) Ammonium molybdate
    2) Molybdic acid, diammonium salt
    3) Diammonium molybdate
    4) Molecular Formula: (NH4)2MoO4
    5) CAS 13106-76-8
    6) NIOSH/RTECS QA 4900000
    AMMONIUM PARAMOLYBDATE
    1) Molybdic acid, commercial
    2) Molecular Formula: (NH4)6Mo7O24.4H2O
    CALCIUM MOLYBDATE
    1) Molecular Formula: CaMoO4
    LEAD-MOLYBDENUM CHROMATE
    1) Molybdenum orange
    2) Molybdenum-lead chromate
    3) C.I. pigment red 104
    4) Wulfenite
    5) Lead chromate, sulfate and molybdate
    6) CAS 12709-98-7
    7) NIOSH/RTECS OG 1625000
    MOLYBDATE ORANGE
    1) Chrome vermillion
    2) C.I. pigment red 104
    3) Mineral fire red 5DDS
    4) Mineral fire red 5GS
    5) Molybdate red
    6) Molybdenum red
    7) Molybden red
    8) NCI-c 54626
    9) CAS 12656-85-8
    10) NIOSH/RTECS QA 4660000
    MOLYBDENUM CHLORIDE
    1) Molybdenum dichloride
    2) Molecular Formula: MoCl2
    MOLYBDENUM DISULFIDE
    1) Molybdic sulfide
    2) Molybdenum glance
    3) Natural molybdenite
    4) Molybdenite
    5) Molykote
    6) Mopolm
    7) Molecular Formula: MoS2
    8) NIOSH/RTECS QA 4697000
    MOLYBDENUM PENTACHLORIDE
    1) Molecular Formula: MoCl5
    2) CAS 10241-05-1
    3) NIOSH/RTECS QA 4690000
    MOLYBDENUM TRIOXIDE
    1) Molybdic anhydride
    2) Molybdic trioxide
    3) Molybdenum anhydride
    4) Molybdenum (VI) oxide
    5) Molybdic oxide
    6) Molybdic acid anhydride
    7) Molybdite
    8) Natural molybdite
    9) Molecular Formula: MoO3
    10) CAS 1313-27-5
    11) NIOSH/RTECS QA 4725000
    MOLYBDIC (VI) ACID
    1) Molecular Formula: H2MoO4
    MOLYBDIC ACID, 85%
    1) CAS 7782-91-4
    SODIUM MOLYBDATE
    1) Molybdic acid, disodium salt
    2) Molecular Formula: Na2MoO4
    SODIUM MOLYBDATE DIHYDRATE
    1) Disodium molybdate dihydrate
    2) Molecular Formula: Na2MoO4.(H2O)2
    3) CAS 10102-40-6

    1.2.1) MOLECULAR FORMULA
    1) Mo

Available Forms Sources

    A) FORMS
    1) SOLUBLE COMPOUNDS
    a) Sodium molybdate, ammonium dimolybdate, and ammonium heptamolybdate are highly soluble molybdenum salts (solubility greater than 100 mg/L). These compounds will dissociate into the molybdate anion [MoO4]2- under physiological conditions. Molybdenum is taken up into organisms and is present in blood as molybdate. Molybdenum trioxide, a moderately soluble compound, reacts with water under acidification to molybdate anions (International Molybdenum Association (IMOA), 2013; Hathaway et al, 1996). These compounds are readily absorbed from the gastrointestinal tract (Friberg et al, 1986).
    2) INSOLUBLE COMPOUNDS
    a) Calcium molybdate, molybdenum halides, molybdenum disulfide, molybdenum dioxide are insoluble compounds (Hathaway et al, 1996).
    B) SOURCES
    1) ENVIRONMENTAL/INDUSTRIAL/FOOD/WATER SOURCES
    a) SUMMARY: Trace amounts of soluble molybdate can be found in foods and drinking water. Occupational exposure to molybdenum from mining operations and industrial sources have also been reported. The main routes of exposure are via inhalation and dermal contact. Since dermal absorption is negligible, inhalational exposure is the main concern. Mineral supplements can also contain trace amounts of sodium molybdate and ammonium dimolybdate (International Molybdenum Association (IMOA), 2013).
    b) AIR: Over 90% of samples had less than 0.01 mcg/m3 Mo (Jarrell et al, 1980). Higher concentrations (0.01 to 0.03 mcg/m3) found in urban compared with rural areal (0.001 to 0.0032 mcg/m3) (Barceloux, 1999). Ash contains 10 to 40 mcg/g Mo. USSR steel foundry air Mo increased from 1.4 mg/m(3) during production of 4% Mo steel to 5.4 mg/m(3) during production of 17% Mo steel. Breathing zone air Mo of workers averaged 0.2 mg/m(3), occasionally peaking at 0.4 to 0.5 (Lener & Bibr, 1984).
    c) WATER: Mean Mo concentration in rivers averaged 0.5, in brines 1.7, in the ocean 11, and in thermal waters 20 mcg/L (Wedepohl, 1978). Most natural waters contain less than 3 mcg/L; near industrial sources molybdenum concentration in surface and ground water may reach 0.2 to 0.4 mg/L and 25 mg/L respectively (Barceloux, 1999).
    d) SOIL: Mo less than 0.2 mg/kg is considered deficient and greater than 0.7 mg/kg excessive (Barceloux, 1999; Lener & Bibr, 1984). Mo is more available from neutral or alkaline soils. Average soil concentration is 1 to 2 mg/kg. Municipal sewage sludge contains molybdenum concentrations from 1 to 40 mg/kg (average 15 mg/kg) (Barceloux, 1999).
    e) FOOD: Above ground plant sources have higher Mo than food from plant roots. Grains, legumes, and cauliflower are particularly high (Barceloux, 1999; Schroeder et al, 1970; Lener & Bibr, 1984). Mineral supplements can also contain trace amounts of sodium molybdate and ammonium dimolybdate (International Molybdenum Association (IMOA), 2013).
    f) AVERAGE DAILY INTAKE: Was estimated at 160 mcg in children and 200 to 500 mcg in adults in the USSR and 128 and 335 mcg in adults in England and the USA (Lener & Bibr, 1984). In general, vegetarians consume more molybdenum in the diet (Holzinger et al, 1998).
    C) USES
    1) Molybdenum is an essential trace element for humans and mammals. The main commercial source is molybdenite (MoS2) (Tallkvist & Oskarsson, 2015; International Molybdenum Association (IMOA), 2013).
    2) Molybdenum compounds (Mo, MoO3, MoS2) are used for a variety of applications. They are used as catalysts, in ceramics, labeling glass containers, fertilizers as a trace element, electroplating, and the tanning of skins (Langard, 2001).
    3) Molybdenum inorganic and organic complexes are used for color (pigments, insoluble dyes, mordants) (Langard, 2001).
    4) Molybdenum metal is used for electronic parts. Molybdenum steel is used in the manufacture of parts for missiles and aircraft (Langard, 2001).
    5) MOLYBDENUM ACETLYACETONATE is a catalyst for the polymerization of ethylene and the production of polyurethane foam (Barceloux, 1999).
    6) MOLYBDENUM DISULFIDE (molybdenite) is used as a lubricant which does not require a water film for lubrication and can therefore be used in a vacuum (Langard, 2001).
    7) AMMONIUM TETRATHIOMOLYBDATE has been used an experimental copper chelating agent for the treatment of Wilson's disease (Barceloux, 1999).
    8) MOLYBDENUM TRIOXIDE is used as a corrosion inhibitor and a reagent for chemical analysis (Barceloux, 1999).
    9) ZINC MOLYBDATE is used as a stabilizer and anticorrosive in paint (Barceloux, 1999).
    10) FERTILIZERS: Standard commercial fertilizers contain 2 to 6 ppm molybdenum (Barceloux, 1999).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Molybdenum is an essential trace element for humans and mammals. The main commercial source is molybdenite (MoS2). Molybdenum compounds (Mo, MoO3, MoS2) are used as catalysts, lubricants (molybdenum disulfide), corrosion inhibitors (molybdenum trioxide), and stabilizers (zinc molybdate). They are also used in ceramics, labeling glass containers, fertilizers as a trace element, and electroplating. Molybdenum metal is used for electronic parts and molybdenum steel is used in the manufacture of parts for missiles and aircraft. Molybdenum inorganic and organic complexes are used for color (pigments, insoluble dyes, mordants).
    B) TOXICOLOGY: Sodium molybdate, ammonium dimolybdate, and ammonium heptamolybdate are highly soluble molybdenum salts. Other soluble molybdenum include ammonium molybdate and molybdenum trioxide. Soluble molybdenum compounds are readily absorbed from the gastrointestinal tract. Calcium molybdate, molybdenum halides, molybdenum disulfide, molybdenum dioxide are insoluble compounds. The main routes of exposure are via inhalation and dermal contact. Since dermal absorption is negligible, inhalational exposure is the main concern. There seems to be a reciprocal relationship between molybdenum and copper. In ruminants (especially cattle and sheep), intake of herbage with a high molybdenum content produces "scouring" disease (diarrhea). A copper deficiency aggravates this disease and administration of copper salts alleviates the disease. Evidence suggests that excess molybdenum promotes binding of copper to a serum protein, thus limiting uptakes of copper in tissue. Molybdenum is a cofactor of xanthine oxidase. Excess molybdenum may induce xanthine oxidase.
    C) EPIDEMIOLOGY: Exposure to molybdenum is common. Trace amounts of soluble molybdate can be found in foods and drinking water. Mineral supplements can also contain trace amounts of sodium molybdate and ammonium dimolybdate. Occupational exposure to molybdenum from mining operations and industrial sources have also been reported.
    D) WITH POISONING/EXPOSURE
    1) There are few reports of human toxicity. Toxicity information is mostly based on animal data. Molybdenum can produce mild eye, nose, throat, and skin irritations. Elevated liver enzymes, diarrhea, weakness, fatigue, anorexia, headache, joint and muscle pain, tremor, pneumoconiosis, and/or chest pain have been reported in workers exposed to molybdenum. Pancytopenia was reported in 2 patients who received copper chelator tetrathiomolybdate. High dietary intake of molybdenum may alter copper balance, increase serum ceruloplasmin, and theoretically predispose some individuals to anemia. Hypothyroidism may also occur. Molybdenum toxicity is associated with copper and sulfate deficiency in animals. Diarrhea, anorexia, listlessness, fatty degeneration of the liver, dystrophic changes and kidney cell swelling, and anemia have been reported in animals.
    0.2.20) REPRODUCTIVE
    A) Molybdenum or its compounds have produced mixed reproductive effects in exposed experimental animals. In earlier studies, molybdenum was found to be embryotoxic, fetotoxic, and teratogenic in animals. However, no reproductive effects were observed in more recent studies. Reproductive effects of molybdenum should be interpreted with respect to the copper content of the diet.
    0.2.21) CARCINOGENICITY
    A) In an earlier case-control study, a weak association between occupational exposure to molybdenum and the development of primary lung cancer was observed; however, data are limited and molybdenum has not been systematically evaluated for carcinogenicity in humans.

Laboratory Monitoring

    A) Plasma concentrations are not readily available or clinically useful in the management of molybdenum exposure.
    B) Monitor uric acid, CBC with differential, liver enzymes, and renal function in symptomatic patients, particularly with chronic, excessive exposure.
    C) Monitor serum electrolytes in patients with severe diarrhea.
    D) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe vomiting.
    B) DECONTAMINATION
    1) Acute toxicity is unlikely; gastrointestinal decontamination is generally not necessary. For patients with ingestion, dilution with milk or water (no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children) may decrease symptoms. EYE/DERMAL EXPOSURE: Molybdenum can produce mild eye, nose, throat, and skin irritations. Flush eyes with copious amounts of water. Skin should be thoroughly irrigated. Contact dermatitis may arise after repeated exposure to irritants.
    C) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with severe respiratory distress.
    D) ANTIDOTE
    1) None.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home. For patients with a minor eye or dermal exposure, flush the eyes with copious amounts of water. Skin that has become reddened and/or irritated should be gently cleansed with a mild soap and water. Ongoing symptoms may require further evaluation by a healthcare provider.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.
    3) ADMISSION CRITERIA: Patients with severe symptoms despite treatment should be admitted.
    4) CONSULT CRITERIA: Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    F) PITFALLS
    1) Missing an ingestion of another chemical or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    G) DIFFERENTIAL DIAGNOSIS
    1) Patients with severe vomiting/diarrhea and underlying cardiac dysrhythmias or electrolyte imbalance, may develop more severe symptoms.
    H) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Most of the range of toxicity data are estimates which have been calculated from limited human and animal data. Industrial toxicology reports indicate that in general molybdenum compounds exhibit a low order of toxicity. The toxicity of molybdenum compounds may vary, with the trioxide and ammonium molybdate possibly being more toxic than molybdenum disulfide, molybdenum metal or molybdenum dioxide. INGESTION: A LOAEL (Lowest Observable Adverse Effect Level) has been designated as 0.14 mg/kg/day in adults, based on long term exposure. A NOAEL (No Observable Adverse Effect Level) for adults has been reported as 4 mcg/kg/day to 8 mcg/kg/day. INHALATION: Airborne concentrations which are designated as IDLH (Immediately Dangerous to Life or Health) in industrial settings are MOLYBDENUM METAL: 5000 mg/m(3), as molybdenum and SOLUBLE MOLYBDENUM COMPOUNDS: 1000 mg/m(3), as molybdenum. Threshold Limit Value-Time-Weighted Average (TLV-TWA) = 10 mg/m(3) (inhalable particulate mass) and 3 mg/m(3) (respirable particulate mass); mild eye, nose, throat, and skin irritation

Clinical Effects

Summary Of Exposure

    A) USES: Molybdenum is an essential trace element for humans and mammals. The main commercial source is molybdenite (MoS2). Molybdenum compounds (Mo, MoO3, MoS2) are used as catalysts, lubricants (molybdenum disulfide), corrosion inhibitors (molybdenum trioxide), and stabilizers (zinc molybdate). They are also used in ceramics, labeling glass containers, fertilizers as a trace element, and electroplating. Molybdenum metal is used for electronic parts and molybdenum steel is used in the manufacture of parts for missiles and aircraft. Molybdenum inorganic and organic complexes are used for color (pigments, insoluble dyes, mordants).
    B) TOXICOLOGY: Sodium molybdate, ammonium dimolybdate, and ammonium heptamolybdate are highly soluble molybdenum salts. Other soluble molybdenum include ammonium molybdate and molybdenum trioxide. Soluble molybdenum compounds are readily absorbed from the gastrointestinal tract. Calcium molybdate, molybdenum halides, molybdenum disulfide, molybdenum dioxide are insoluble compounds. The main routes of exposure are via inhalation and dermal contact. Since dermal absorption is negligible, inhalational exposure is the main concern. There seems to be a reciprocal relationship between molybdenum and copper. In ruminants (especially cattle and sheep), intake of herbage with a high molybdenum content produces "scouring" disease (diarrhea). A copper deficiency aggravates this disease and administration of copper salts alleviates the disease. Evidence suggests that excess molybdenum promotes binding of copper to a serum protein, thus limiting uptakes of copper in tissue. Molybdenum is a cofactor of xanthine oxidase. Excess molybdenum may induce xanthine oxidase.
    C) EPIDEMIOLOGY: Exposure to molybdenum is common. Trace amounts of soluble molybdate can be found in foods and drinking water. Mineral supplements can also contain trace amounts of sodium molybdate and ammonium dimolybdate. Occupational exposure to molybdenum from mining operations and industrial sources have also been reported.
    D) WITH POISONING/EXPOSURE
    1) There are few reports of human toxicity. Toxicity information is mostly based on animal data. Molybdenum can produce mild eye, nose, throat, and skin irritations. Elevated liver enzymes, diarrhea, weakness, fatigue, anorexia, headache, joint and muscle pain, tremor, pneumoconiosis, and/or chest pain have been reported in workers exposed to molybdenum. Pancytopenia was reported in 2 patients who received copper chelator tetrathiomolybdate. High dietary intake of molybdenum may alter copper balance, increase serum ceruloplasmin, and theoretically predispose some individuals to anemia. Hypothyroidism may also occur. Molybdenum toxicity is associated with copper and sulfate deficiency in animals. Diarrhea, anorexia, listlessness, fatty degeneration of the liver, dystrophic changes and kidney cell swelling, and anemia have been reported in animals.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Molybdenum metal implanted in rabbits' eyes produced no effect (Grant & Schuman, 1993).
    2) Molybdenum can produce mild eye, nose, throat, and skin irritations (Occupational Safety & Health Administration (OSHA), 2012).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Molybdenum can produce mild eye, nose, throat, and skin irritations (Occupational Safety & Health Administration (OSHA), 2012).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Molybdenum can produce mild eye, nose, throat, and skin irritations (Occupational Safety & Health Administration (OSHA), 2012).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PNEUMOCONIOSIS
    1) WITH POISONING/EXPOSURE
    a) Molybdenum exposure can produce respiratory irritation (Hazardous Substances Databank (HSDB), 2010).
    b) Dry cough and chest pains may develop after chronic industrial exposure to 1 to 19 mg/m(3) metallic molybdenum and molybdenum oxides (Lener & Bibr, 1984; Hazardous Substances Databank (HSDB), 2010).
    c) Another publication summarized a document translated from Russian (unavailable for our review) which reported early signs of pneumoconiosis in workers exposed to molybdenum compounds, and dyspnea, cough, and/or chest pain in 2 individuals exposed to molybdenum trioxide for 5 to 7 yrs (ACGIH, 1991).
    d) Dyspnea, weakness, and dizziness developed in a 44-year-old woman exposed to metallic molybdenum and molybdenum trioxide dust at 1 to 3 mg/m(3) with occasional excursions of 25 mg/m(3) or higher of molybdenum trioxide for 5 years (Hazardous Substances Databank (HSDB), 2010).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) High concentrations have produced respiratory tract irritation in animals exposed to insoluble molybdenum compounds (Hathaway et al, 1996).
    2) OTHER NON-SPECIFIC
    a) Moderate amounts of bronchial and alveolar exudate were present in animals exposed to molybdenum by inhalation exposure (Fairhall LT, Dunn RC & Sharpless NE et al, 1945).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Weakness, fatigue, anorexia, headache, joint and muscle pain and hand tremor were reported in USSR miners and metallurgy workers chronically exposed to 60 to 600 mg/m(3) (Lener & Bibr, 1984; Hathaway et al, 1996; Hazardous Substances Databank (HSDB), 2010).
    b) CASE REPORT: A man developed anxiety, agitation, visual and auditory hallucination, excessive craving for salt, insomnia, diarrhea, and painful and cold extremities after taking an average of 7 to 8 molybdenum tablets per day for 18 days (total cumulative dose: 13.5 mg). On day 22, he developed petit mal seizures and became suicidal. His condition deteriorated further and he developed coma after receiving medications for a grand mal seizure. His blood molybdenum concentration was 7.7 ng/mL on day 25 and 1.7 ng/mL about 6 weeks after starting molybdenum supplements. Treatment with chelation therapy (calcium ethylene diamine tetraacetic acid (CaEDTA)) improved his symptoms; however neuropsychological tests and Spectral Emission Computer Tomography images (SPECT) revealed frontal cortical damage of the brain. A year later, he was diagnosed with toxic encephalopathy, learning disability, major depression, and post-traumatic stress disorder (Momcilovic, 1999). A causal relationship could not be established.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) Anorexia or loss of appetite was reported in molybdenum poisoned guinea pigs (Langard, 2001).
    2) MALAISE
    a) Listlessness and reduced growth rate occurred in guinea pigs due to molybdenum poisoning (Langard, 2001).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Diarrhea was reported in 5 of 25 molybdenum roasting plant workers (Walravens et al, 1979).
    b) CASE REPORT: Diarrhea developed in a man who ingested an average of 7 to 8 molybdenum tablets per day for 18 days (total cumulative dose: 13.5 mg) (Momcilovic, 1999).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) Loss of appetite, diarrhea, and reduced growth rate are signs of molybdenum poisoning in animals (Pitt, 1976).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Evidence suggests that molybdenum may produce liver dysfunction. Workmen in Russia Mo-Cu plant reported a fall in A/G ratios due to a rise in globulins, primarily alpha-globulins that has been interpreted as evidence of liver dysfunction (Stokinger, 1982).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER FATTY
    a) Fatty degeneration of the liver was reported in animals severely poisoned (Fairhall LT, Dunn RC & Sharpless NE et al, 1945; Friberg L, Boston P & Nordberg G et al, 1975). Fatty liver changes have been reported in guinea pigs exposed to the fumes from arcing molybdenum metal (US DHHS, 1981).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Dystrophic changes and swelling of kidney cells were reported (Fairhall LT, Dunn RC & Sharpless NE et al, 1945; Friberg L, Boston P & Nordberg G et al, 1975).
    b) GUINEA PIGS: Fatty changes in the kidneys developed in guinea pigs which had been exposed to fume from arcing molybdenum metal (US DHHS, 1981).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) PANCYTOPENIA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Pancytopenia resulted in 2 patients receiving the copper chelator tetrathiomolybdate (Harper & Walshe, 1986).
    B) ANEMIA
    1) WITH POISONING/EXPOSURE
    a) Data in humans suggests that high dietary molybdenum potentially can produce mineral imbalances (eg, copper deficiency) which may predispose some individuals to hypochromic microcytic anemia (IRIS , 1995).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANEMIA
    a) A hypochromic, microcytic anemia is characteristic of molybdenum toxicity and has been produced in many animal species by high molybdenum exposure (Friberg L, Boston P & Nordberg G et al, 1975). Low hemoglobin concentration and reduced red cell counts and red cell survival time may occur (Langard, 2001).
    b) MECHANISM OF ANEMIA: Molybdenum is required for the release of Fe from intestinal mucosa and ferritin. Excess molybdenum interferes with copper absorption producing anemia, due to the copper requirement for Fe uptake by transferrin. Molybdenum interferes with Copper incorporation into ceruloplasmin (Friberg L, Boston P & Nordberg G et al, 1975; Langard, 2001).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DISORDER OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Molybdenum can produce mild eye, nose, throat, and skin irritations (Occupational Safety & Health Administration (OSHA), 2012).
    b) CASE SERIES: Eight of 25 Mo roasting plant workers reported skin or hair changes (Walravens et al, 1979). The resident physician at the molybdenum plant in Climax, Colorado noted no dermatitis among workers whose skins were covered with molybdenum disulfide (Langard, 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ALOPECIA
    a) Dermatosis, hair loss, and hair depigmentation were reported in several animal species exposed to high dietary molybdenum (Pitt, 1976).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) ACQUIRED MUSCULOSKELETAL DEFORMITY
    1) WITH POISONING/EXPOSURE
    a) Genu valgum (knock knee) was seen in 10 to 25-yr-olds living in an area of India where fluorosis is endemic. Their staple food was grain which had a higher molybdenum concentration than in other areas of the country (Anon, 1975).
    B) JOINT PAIN
    1) WITH POISONING/EXPOSURE
    a) Pain of the joints of the knees, hands and feet and back as well as articular deformities, erythema and edema of the joint areas were reported in 8 of 25 molybdenum roasting plant workers and in people in a Mo-rich settlement in Armenia who also had increased blood uric acid levels (Walravens et al, 1979; Langard, 2001; IRIS , 1995).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ARTHROPATHY
    a) Deformities of the joints of the extremities have occurred in cattle, chicks, and rabbits which had high dietary molybdenum (Friberg L, Boston P & Nordberg G et al, 1975; Pitt, 1976).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOTHYROIDISM
    1) WITH POISONING/EXPOSURE
    a) Hypothyroidism may occur (Stokinger, 1982).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) IMMUNE SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) LACK OF EFFECT
    1) None of 50 recipients of total joint replacements containing molybdenum showed Mo sensitivity (Elves et al, 1975).

Reproductive

    3.20.1) SUMMARY
    A) Molybdenum or its compounds have produced mixed reproductive effects in exposed experimental animals. In earlier studies, molybdenum was found to be embryotoxic, fetotoxic, and teratogenic in animals. However, no reproductive effects were observed in more recent studies. Reproductive effects of molybdenum should be interpreted with respect to the copper content of the diet.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Molybdenum or its compounds have produced mixed reproductive effects in exposed experimental animals. In earlier studies, molybdenum was found to be embryotoxic, fetotoxic, and teratogenic in animals (Schroeder & Mitchener, 1971; Mills & Fell, 1960; O'Dell, 1968; O'Dell, 1968; Ridgway & Karnofsky, 1952). However, no reproductive effects were observed in more recent studies (International Molybdenum Association (IMOA), 2013).
    2) SODIUM MOLYBDATE: In a prenatal developmental toxicity study, rats were given 3, 10, 20, and 40 mg/kg/day of sodium molybdate during gestational days 6 through 20. No biological or statistical differences among groups for the number of fetuses, fetal sex ratios, fetal body weights, fetal external, visceral or skeletal malformations or variations per female at any dose were observed at any dose. However, there were significant increases in copper concentrations in kidneys and livers at 40 mg Mo/kg/day. The NOAEL and NOEL for maternal toxicity were 40 mg Mo/kg/day and 20 mg Mo/kg/day (International Molybdenum Association (IMOA), 2013).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) SODIUM MOLYBDATE: In a prenatal developmental toxicity study, rats were given 3, 10, 20, and 40 mg/kg/day of sodium molybdate during gestational days 6 through 20. No treatment or dose-related effects on maternal body weights, weight changes, feed consumption in grams/day or grams/kg, body weight/day, or on maternal clinical observations, pregnancy indices, or maternal organ weights were observed at any dose. The NOAEL and NOEL for maternal toxicity were 40 mg Mo/kg/day and 20 mg Mo/kg/day, respectively (International Molybdenum Association (IMOA), 2013).
    3.20.5) FERTILITY
    A) SEMEN QUALITY AND BLOOD TESTOSTERONE
    1) In a fertility study of 219 men, high blood molybdenum concentrations were associated with lower semen quality and blood testosterone levels (Tallkvist & Oskarsson, 2015).
    B) ANIMAL STUDIES
    1) SODIUM MOLYBDATE DIHYDRATE: In a 90-day oral repeated-dose toxicity study, rats were given 5, 17, or 60 mg/kg/day of sodium molybdate dihydrate. No changes in the male or female reproductive tissues, vaginal cytology and oestrous cycles, organ weight of testes or secondary sex organ, spermatid or sperm counts, or motility or morphology were observed at any dose. The NOAEL for effects on reproductive organs, sperm and oestrous cycle was 60 mg Mo/kg/day (International Molybdenum Association (IMOA), 2013).
    2) SODIUM MOLYBDATE: In a prenatal developmental toxicity study, rats were given 3, 10, 20, and 40 mg/kg/day of sodium molybdate during gestational days 6 through 20. No biological or statistical differences among groups for the numbers of ovarian corpora lutea/female, for uterine implantation sites, or for uterine implantation losses per female were observed. The NOAEL and NOEL for maternal toxicity were 40 mg Mo/kg/day and 20 mg Mo/kg/day, respectively (International Molybdenum Association (IMOA), 2013).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7439-98-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) In an earlier case-control study, a weak association between occupational exposure to molybdenum and the development of primary lung cancer was observed; however, data are limited and molybdenum has not been systematically evaluated for carcinogenicity in humans.
    3.21.3) HUMAN STUDIES
    A) LUNG CANCER
    1) A case-control study found a weak association between occupational exposure to molybdenum and the development of primary lung cancer, odds ratio after more than 21 years of exposure was 3.3 (95% CI 1.3 to 8.3). Exposure to molybdenum was assessed by job-task exposure matrix rather than any form of occupational or biologic monitoring (Droste et al, 1999). However, data are limited and molybdenum has not been systematically evaluated for carcinogenicity in recent years (Tallkvist & Oskarsson, 2015).
    3.21.4) ANIMAL STUDIES
    A) SARCOMA
    1) Subcutaneous sarcomas were noted after local injection of molybdenum orange (Langard, 2001).
    2) MOLYBDENUM TRIOXIDE: Molybdenum trioxide was weakly carcinogenic in mice given 19 IP injections over 30 weeks (Stoner et al, 1976). To the contrary, esophageal cancer incidence negatively correlated with Mo in water, cereals and tissues. Molybdenum supplementation decreased cancer incidence in mice (Luo et al, 1981).
    B) CARCINOMA
    1) In mice, chronic inhalation of molybdenum trioxide was associated with an increase in the incidence of alveolar/bronchiolar adenoma or carcinoma (combined). In exposed rats the incidence of alveolar/bronchiolar adenoma or carcinoma (combined) was marginally increased in males but not females (Chan et al, 1998).
    C) LACK OF EFFECT
    1) MOLYBDENUM TRIOXIDE was not carcinogenic in 2-year inhalation animal studies following doses up to 100 mg MoO3/m(3) (67 mg Mo/m(3)). All molybdenum substances are considered to have no carcinogenic potential based on these results (International Molybdenum Association (IMOA), 2013).

Genotoxicity

    A) SODIUM MOLYBDATE was not genotoxic/mutagenic in a bacterial reverse mutation assay/Ames test with multiple strains of Salmonella typhimurium, in an in vitro induction test of micronuclei in culture human peripheral blood lymphocytes, and in an vitro test at the thymidine kinase locus of mouse lymphoma cells (International Molybdenum Association (IMOA), 2013; Tallkvist & Oskarsson, 2015).
    B) AMMONIUM MOLYBDATE demonstrated mutagenic potential in a bacterial system (Nishioka, 1975). Sodium molybdate was a comutagen at concentrations equal or greater than 100 uM (Rossman & Molina, 1986).
    C) MOLYBDENUM CHLORIDE had mutagenic activity in the Drosophila wing spot test system (Ogawa et al, 1994).
    D) MOLYBDENUM TRIOXIDE: Mutagenic effects were not observed in any of 5 strains of Salmonella typhimurium. In addition, sister chromatic exchange or chromosomal aberrations in cultured Chinese hamster ovary cells were not observed in vitro (Tallkvist & Oskarsson, 2015).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma concentrations are not readily available or clinically useful in the management of molybdenum exposure.
    B) Monitor uric acid, CBC with differential, liver enzymes, and renal function in symptomatic patients, particularly with chronic, excessive exposure.
    C) Monitor serum electrolytes in patients with severe diarrhea.
    D) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Atomic absorption, neutron activation, and other analytical procedures are replacing older spectrophotometric (eg, thiocyanate) methods. Atomic absorption can be used to measure tap water Mo and airborne/soluble Mo compounds leached into aqueous solutions from collection fibers (Barceloux, 1999).
    2) Thiocyanate method (blood) has a limit of detection of 0.5 mcg Mo/100 mL (Stokinger, 1982).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe symptoms despite treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home. For patients with a minor eye or dermal exposure, flush the eyes with copious amounts of water. Skin that has become reddened and/or irritated should be gently cleansed with a mild soap and water. Ongoing symptoms may require further evaluation by a healthcare provider.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate overdose, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.

Monitoring

    A) Plasma concentrations are not readily available or clinically useful in the management of molybdenum exposure.
    B) Monitor uric acid, CBC with differential, liver enzymes, and renal function in symptomatic patients, particularly with chronic, excessive exposure.
    C) Monitor serum electrolytes in patients with severe diarrhea.
    D) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Acute toxicity is unlikely; gastrointestinal decontamination is generally not necessary.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) EYE/DERMAL EXPOSURE: Molybdenum can produce mild eye, nose, throat, and skin irritations. Flush eyes with copious amounts of water. Skin should be thoroughly irrigated. Contact dermatitis may arise after repeated exposure to irritants.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Acute toxicity is unlikely; gastrointestinal decontamination is generally not necessary.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea.
    B) MONITORING OF PATIENT
    1) Plasma concentrations are not readily available or clinically useful in the management of molybdenum exposure.
    2) Monitor uric acid, CBC with differential, liver enzymes, and renal function in symptomatic patients, particularly with chronic, excessive exposure.
    3) Monitor serum electrolytes in patients with severe diarrhea.
    4) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory signs or symptoms.
    C) COPPER
    1) In animals with molybdenum excess in the food supply, copper added to the diet alleviated toxicity (Barceloux, 1999).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

Summary

    A) TOXICITY: Most of the range of toxicity data are estimates which have been calculated from limited human and animal data. Industrial toxicology reports indicate that in general molybdenum compounds exhibit a low order of toxicity. The toxicity of molybdenum compounds may vary, with the trioxide and ammonium molybdate possibly being more toxic than molybdenum disulfide, molybdenum metal or molybdenum dioxide. INGESTION: A LOAEL (Lowest Observable Adverse Effect Level) has been designated as 0.14 mg/kg/day in adults, based on long term exposure. A NOAEL (No Observable Adverse Effect Level) for adults has been reported as 4 mcg/kg/day to 8 mcg/kg/day. INHALATION: Airborne concentrations which are designated as IDLH (Immediately Dangerous to Life or Health) in industrial settings are MOLYBDENUM METAL: 5000 mg/m(3), as molybdenum and SOLUBLE MOLYBDENUM COMPOUNDS: 1000 mg/m(3), as molybdenum. Threshold Limit Value-Time-Weighted Average (TLV-TWA) = 10 mg/m(3) (inhalable particulate mass) and 3 mg/m(3) (respirable particulate mass); mild eye, nose, throat, and skin irritation

Therapeutic Dose

    7.2.1) ADULT
    A) DIETARY REFERENCE INTAKE
    1) ADULTS
    a) ESTIMATED AVERAGE REQUIREMENT (EAR): 34 mcg/day (0.034 mg/day; 0.00049 mg/kg body weight per day assuming 70 kg body weight) (Hays et al, 2016; Turnlund et al, 1995; International Molybdenum Association (IMOA), As accessed 2016-08-18).
    b) RECOMMENDED DIETARY ALLOWANCE (RDA): 45 mcg/day (0.045 mg/day; 0.00064 mg/kg body weight per day) (Hays et al, 2016; International Molybdenum Association (IMOA), As accessed 2016-08-18)
    c) TOLERABLE UPPER INTAKE LEVEL (UL): 2 mg/day (2000 mcg/day; 0.03 mg/kg body weight per day assuming 68 kg body weight) (Hays et al, 2016; International Molybdenum Association (IMOA), As accessed 2016-08-18)
    2) PREGNANCY
    a) ESTIMATED AVERAGE REQUIREMENT (EAR): 40 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    b) RECOMMENDED DIETARY ALLOWANCE (RDA): 50 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    c) TOLERABLE UPPER INTAKE LEVEL (UL): 1700 mcg/day for 14 to 18 years old; 2000 mcg/day for 19 years and greater (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    3) LACTATION
    a) ESTIMATED AVERAGE REQUIREMENT (EAR): 35 mcg/day for 14 to 18 years old; 36 mcg/day for 19 years and greater(International Molybdenum Association (IMOA), As accessed 2016-08-18)
    b) RECOMMENDED DIETARY ALLOWANCE (RDA): 50 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    c) TOLERABLE UPPER INTAKE LEVEL (UL): 1700 mcg/day for 14 to 18 years old; 2000 mcg/day for 19 years and greater (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    B) TOLERABLE DAILY INTAKE (TDI)
    1) 0.01 mg/kg body weight per day for oral exposures based on kidney effects in rats (Hays et al, 2016)
    C) CHRONIC ORAL REFERENCE DOSE (RFD)
    1) 0.005 mg/kg/day based on a study in which the most sensitive endpoint was increased serum uric acid levels (Hays et al, 2016)
    7.2.2) PEDIATRIC
    A) 14 to 18 YEARS OLD
    1) ESTIMATED AVERAGE REQUIREMENT (EAR): 33 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    2) RECOMMENDED DIETARY ALLOWANCE (RDA): 43 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    3) TOLERABLE UPPER INTAKE LEVEL (UL): 1700 mcg/day(International Molybdenum Association (IMOA), As accessed 2016-08-18)
    B) 9 TO 13 YEARS OLD
    1) ESTIMATED AVERAGE REQUIREMENT (EAR): 26 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    2) RECOMMENDED DIETARY ALLOWANCE (RDA): 34 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    3) TOLERABLE UPPER INTAKE LEVEL (UL): 1100 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    C) 4 TO 8 YEARS OLD
    1) ESTIMATED AVERAGE REQUIREMENT (EAR): 17 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    2) RECOMMENDED DIETARY ALLOWANCE (RDA): 22 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    3) TOLERABLE UPPER INTAKE LEVEL (UL): 600 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    D) 1 TO 3 YEARS OLD
    1) ESTIMATED AVERAGE REQUIREMENT (EAR): 13 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    2) RECOMMENDED DIETARY ALLOWANCE (RDA): 17 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    3) TOLERABLE UPPER INTAKE LEVEL (UL): 300 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    E) 7 TO 12 MONTHS OLD
    1) ADEQUATE INTAKE (AI): 3 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)
    F) 0 TO 6 MONTHS OLD
    1) ADEQUATE INTAKE (AI): 2 mcg/day (International Molybdenum Association (IMOA), As accessed 2016-08-18)

Minimum Lethal Exposure

    A) IDLH/INHALATION
    1) NIOSH Immediately Dangerous to Life or Health (IDLH) concentration (NIOSH , 1996; Hazardous Substances Databank (HSDB), 2010):
    a) MOLYBDENUM METAL: 5000 mg/m(3), as molybdenum (Occupational Safety & Health Administration (OSHA), 2012)
    b) SOLUBLE MOLYBDENUM COMPOUNDS: 1000 mg/m(3), as molybdenum (NIOSH , 1996).
    B) ANIMAL DATA
    1) Injected molybdenum produced death in 2 to 4 days in guinea pigs, depending on the dose given (Stokinger, 1982).
    2) Lethal doses of molybdenum and its salts by oral or parenteral exposure are above 100 mg/kg in the animal species tested. Intratracheal instillation would be expected to possess a lower lethal dose (molybdenum powder LDLo was 70 mg/kg in the rabbit; (Friberg L, Boston P & Nordberg G et al, 1975).

Maximum Tolerated Exposure

    A) RANKING OF TOXICITY
    1) Industrial toxicology reports indicate that in general molybdenum compounds exhibit a low order of toxicity. The trioxide and ammonium molybdate are generally more toxic than the ore (molybdenite), the metal, molybdenum disulfide or molybdenum dioxide (ACGIH, 1991; Stokinger, 1982; ACGIH, 1991).
    B) INGESTION
    1) A LOAEL (Lowest Observable Adverse Effect Level) has been designated as 0.14 mg/kg/day in adults, based on long term exposure. A NOAEL (No Observable Adverse Effect Level) for adults has been reported as 4 mcg/kg/day to 8 mcg/kg/day (IRIS , 1995) or 22 to 1500 mcg/day (Turnlund et al, 1995).
    2) SODIUM MOLYBDATE DIHYDRATE: In a 90-day oral repeated-dose toxicity study, rats were administered 5, 17, or 60 mg/kg/day of sodium molybdate dihydrate. Reduced body weight gains and kidney effects (slight diffuse hyperplasia of the proximal tubules) were observed only following 60 mg/kg/day dose. The NOAEL for this dose was 17 mg Mo/kg/day (International Molybdenum Association (IMOA), 2013).
    3) CASE REPORT: A man developed anxiety, agitation, visual and auditory hallucination, excessive craving for salt, insomnia, diarrhea, and painful and cold extremities after taking an average of 7 to 8 molybdenum tablets per day for 18 days (total cumulative dose: 13.5 mg). On day 22, he developed petit mal seizures and became suicidal. His condition deteriorated further and he developed coma after receiving medications for a grand mal seizure. His blood molybdenum concentration was 7.7 ng/mL on day 25 and 1.7 ng/mL about 6 weeks after starting molybdenum supplements. Treatment with chelation therapy (calcium ethylene diamine tetraacetic acid (CaEDTA)) improved his symptoms; however neuropsychological tests and Spectral Emission Computer Tomography images (SPECT) revealed frontal cortical damage of the brain. A year later, he was diagnosed with toxic encephalopathy, learning disability, major depression, and post-traumatic stress disorder (Momcilovic, 1999). A causal relationship could not be established.
    C) INHALATION
    1) NIOSH Immediately Dangerous to Life or Health (IDLH) concentration (NIOSH , 1996; Hazardous Substances Databank (HSDB), 2010):
    a) MOLYBDENUM METAL: 5000 mg/m(3), as molybdenum (Occupational Safety & Health Administration (OSHA), 2012)
    b) SOLUBLE MOLYBDENUM COMPOUNDS: 1000 mg/m(3), as molybdenum (NIOSH , 1996).
    2) Threshold Limit Value-Time-Weighted Average (TLV-TWA) = 10 mg/m(3) (inhalable particulate mass) and 3 mg/m(3) (respirable particulate mass); mild eye, nose, throat, and skin irritation (Hazardous Substances Databank (HSDB), 2010; Occupational Safety & Health Administration (OSHA), 2012).
    3) MOLYBDENUM TRIOXIDE: In a 13-week inhalation toxicity study, animals were exposed to 0, 1, 3, 10, 30, and 100 mg MoO3/m(3) for 6.5 hours/day, 5 days/week for 13 weeks. No treatment-related effects were observed at all concentrations. A true NOAEC (No Observed Adverse Effect Concentration) was determined to be 100 mg MoO3/m(3) (corresponding to 66.7 mg Mo/m(3). In 2-year inhalation studies, animals received 0, 10, 30, and 100 mg MoO3/m(3) of molybdenum trioxide. Although no adverse effects were observed, significant increases in liver copper concentrations were observed following exposure to 30 mg/m(3) and 100 mg/m(3). A NOAEC of 100 mg MoO3/m(3) (corresponding to 66.7 mg Mo/m(3)) and a NOEC (No Observed Effect Concentration) of 10 mg MoO3/m(3) (corresponding to 6.7 mg Mo/m(3)) were observed (International Molybdenum Association (IMOA), 2013).
    4) MOLYBDENUM TRIOXIDE: In repeated-dose animal toxicity studies, molybdate blood concentrations in rats following the inhalation of 100 mg/m(3) molybdenum trioxide (67 mg Mo/m(3)) were similar to those resulting from dietary exposure to 17 to 20 mg Mo/kg body weight/day (in the form of sodium molybdate in the diet) (International Molybdenum Association (IMOA), 2013).
    D) RELATIVE TOXICITY
    1) MOLYBDENUM DISULFIDE & MOLYBDENUM METAL: Molybdenum disulfide by oral exposure or inhalation was found to be relatively non-toxic in animals. Rats showed no toxicity while ingesting up to 500 mg daily for 44 days. Increased respiration was observed in guinea pigs inhaling 286 mg/m(3) Mo for 1 hour daily 5 days weekly for 5 weeks. Daily IP injection produced 17% mortality in 4 days and 25% mortality in 4 months in guinea pigs at a daily dosage of 800 mg/kg. Survivors gained weight and remained well (Fairhall LT, Dunn RC & Sharpless NE et al, 1945).
    2) MOLYBDENUM OXIDES/METAL DUSTS
    a) MoO3 dust by inhalation exposure for 1 hour daily at 205 mg Mo/m(3) in guinea pigs was extremely irritating. Anorexia and weight loss, diarrhea, muscular incoordination as well as loss of hair was reported. Death occurred in 26 of 51 (51%) animals. Freshly generated MoO3 fume (190 mg/m(3) Mo) was found to be less toxic under the same exposure conditions, with only 8.3% mortality. No mortality occurred when exposure was decreased to 53 mg Mo/m(3) (Fairhall LT, Dunn RC & Sharpless NE et al, 1945).
    b) Under conditions as MoO3 dust, 20.8% mortality occurred (N=24 guinea pigs) for CaMoO4 dust at 159 mg Mo/m(3) without showing any toxic signs (Fairhall LT, Dunn RC & Sharpless NE et al, 1945).
    c) No toxic effects were seen in rats after a single inhalation exposure to 3 to 30 g/m(3) metallic molybdenum or Mo compounds. A single intratracheal dose of 50 mg Mo or MoO3 suspension produced emphysema, interstitial fibrosis and regional lymph node changes in rats. Similarly exposed rabbits showed diffuse pneumoconiosis and interstitial pneumonitis several months later (Lener & Bibr, 1984).
    3) CALCIUM & ZINC MOLYBDATES: Acute toxicity tests in laboratory animals showed Ca and Zn molybdates were "practically nontoxic" orally, percutaneously, and by inhalation according to the definition of the Federal Hazardous Substance Labeling Act for purposes of labeling for Climax Molybdenum between 1957 and 1963. No skin or eye irritation was found (Stokinger, 1982).
    4) HEXAVALENT MO/AMMONIUM MO/DIHYDRATE MO SALT: Hexavalent compounds given orally to rats produced an LD50 of 101 mg/kg for CaMoO4, 125 mg/kg for MoO3 and 333 mg/kg for (NH4)2MoO4 (Fairhall LT, Dunn RC & Sharpless NE et al, 1945). Ammonium molybdate (25 mg/kg) added to rat feed for 100 days had little effect whereas 50 mg/kg slightly decreased weight gain. The dihydrate salt (Na2MoO4(2H2O)) fed to rabbits in the diet at 0.1% and higher was uniformly fatal within weeks. When copper was added to this diet, toxicity was prevented (Stokinger, 1982).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) SERUM/BLOOD
    a) Serum molybdenum concentrations averaged 1 to 3 mcg/dL and whole blood molybdenum concentrations averaged 7 mcg/dL in a Los Angeles study. Whole blood molybdenum was below the detection limit (0.5 mcg/dL) in 181 of 229 people in a national study; with values up to 41 mcg/dL in the remaining persons (Butt et al, 1964; Allaway et al, 1968).
    2) PLASMA
    a) Plasma molybdenum in 25 Mo roasting plant workers was 0.9 to 36.5 mcg/dL (10 controls ranged from 0 to 3.4 mcg/dL); 14 were below the limit of detection (0.5 mcg/dL). Residents of Morich Armenia who had gout-like symptoms (arthralgia, joint inflammation) and elevated blood uric acid concentrations (IRIS , 1995) had molybdenum concentrations averaging 31 mcg/dL vs 17 mcg/dL in healthy inhabitants and 6 mcg/dL in controls (Walravens et al, 1979).

Workplace Standards

    A) ACGIH TLV Values for CAS7439-98-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Molybdenum, as Mo; soluble compounds
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: R
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    c) TLV Basis - Critical Effect(s): LRT irr
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Adopted Value
    1) Molybdenum, as Mo; metal and insoluble compounds
    a) TLV:
    1) TLV-TWA: 10 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: I
    3) Definitions:
    a) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    c) TLV Basis - Critical Effect(s): LRT irr
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    c) Adopted Value
    1) Molybdenum, as Mo; metal and insoluble compounds
    a) TLV:
    1) TLV-TWA: 3 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: R
    3) Definitions:
    a) R: Respirable fraction; see Appendix C, paragraph C (of TLV booklet).
    c) TLV Basis - Critical Effect(s): LRT irr
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7439-98-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Molybdenum and insoluble compounds (as Mo)
    2) REL:
    a) TWA: NIOSH REL*:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D; [*Note: The REL and PEL also applies to other insoluble molybdenum compounds (as Mo).],
    3) Listed as: Molybdenum (soluble compounds, as Mo)
    4) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix D
    5) IDLH:
    a) IDLH: 5000 mg Mo/m3
    b) Note(s): Not Listed
    6) IDLH:
    a) IDLH: 1000 mg Mo/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7439-98-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Molybdenum, as Mo; soluble compounds
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Molybdenum, as Mo; metal and insoluble compounds
    3) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Molybdenum, as Mo; metal and insoluble compounds
    4) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Molybdenum
    5) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    6) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Molybdenum and insoluble compounds (as Mo)
    7) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Molybdenum (soluble compounds, as Mo)
    8) MAK (DFG, 2002): Not Listed
    9) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7439-98-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Molybdenum (as Mo) (Soluble compounds)
    2) Table Z-1 for Molybdenum (as Mo) (Soluble compounds):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 5
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Listed as: Molybdenum (as Mo) (Insoluble compounds) (Total dust)
    4) Table Z-1 for Molybdenum (as Mo) (Insoluble compounds) (Total dust):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 15
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) SODIUM MOLYBDATE (ANHYDROUS): 4233 mg/kg (International Molybdenum Association (IMOA), 2013)
    B) LD50- (ORAL)RAT:
    1) AMMONIUM DIMOLYBDATE: 3883 mg/kg (International Molybdenum Association (IMOA), 2013)
    C) LD50- (SKIN)RAT:
    1) SODIUM MOLYBDATE (ANHYDROUS): Greater than 2000 mg/kg (International Molybdenum Association (IMOA), 2013)
    D) LD50- (SKIN)RAT:
    1) AMMONIUM DIMOLYBDATE: Greater than 2000 mg/kg (International Molybdenum Association (IMOA), 2013)

Pharmacology Toxicology

Toxicologic Mechanism

    A) There seems to be a reciprocal relationship between molybdenum and copper. In ruminants (especially cattle and sheep) intake of herbage with a high molybdenum content produces "scouring" disease (diarrhea). A copper deficiency aggravates this disease and administration of copper salts alleviates the disease. Evidence suggests that excess molybdenum promotes binding of copper to a serum protein, thus limiting uptakes of copper in tissue (Stokinger, 1982).
    B) Molybdenum appears not to induce copper deficiency in animals with normal copper stores and toxicity is prevented by sulfate. In a copper depleted rat, molybdenum produces a greater copper deficiency which is exacerbated by sulfate. This suggests that ruminants with their multiple stomachs have a greater capacity to retain copper than nonruminant animals (Stokinger, 1982).
    C) Molybdenum is a cofactor of xanthine oxidase. Excess molybdenum may induce xanthine oxidase. Sulfite to sulfate reaction is catalyzed by molybdenum. An increase in molybdenum intake decreases the availability of sulfite producing an excess of hydrogen sulfide and rendering copper inactive by forming insoluble CuS. Molybdenum toxicity is reduced by thiol compounds (cysteine, methionine). Sulfoxidase oxidizes thiols to sulfate and molybdenum inhibits this enzyme. The inhibition of sulfoxidase is reversed in rats by excess sulfate and copper is a cofactor (Stokinger, 1982).
    D) Small doses of chronically administered MoO4(-2) salts inactivate glutaminases significantly. Vitamin A status is affected by small amounts of molybdenum salts (like those of copper, vanadium, selenium) by imparing the efficiency of intestinal utilization of carotene precursors (Stokinger, 1982).

Physicochemical

Physical Characteristics

    A) Molybdenum is a dark-gray or black powder with metallic luster or a coherent mass of silver-white color; body-centered cubic structure (HSDB, 2005; Budavari, 1996).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 95.94

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) Ruminants are much more sensitive than non-ruminants to Mo toxicity. Toxicity is primarily expressed as copper deficiency.
    B) Renal calculi increase in cattle feeding on Mo-deficient pastures.
    C) Cattle grazing on grass containing 20 to 100 mcg/kg dry weight Mo (normal = 3 to 5) developed molybdenosis (heart disease, peat scours-also seen in sheep but not horses or swine) characterized by diarrhea (scouring), weight loss, joint and bone abnormalities, hair loss and anemia. This was seen in Somerset, England; Kern County, California; and New Zealand (Lener & Bibr, 1984).
    D) Forage may contain up to 100 mg/kg Mo in parts of the San Joaquin Valley of California and on some of the Eocene shales of the western USA.
    E) Dietary intake of 2 to 5 mg/kg Mo can decrease plasma Cu and produce Cu deficiency. Herbage with a Cu:Mo ratio less than 2 resulted in Mo toxicity (Pitt, 1976).
    F) Cattle grazing for over 2 weeks on grass contaminated with molybdenum disulfide supplemented motor oil developed motor excitation, appetite loss, hind limb weakening, diarrhea, weak hind limb reflexes and muscle fibrillation. Two died showing Cu deficiency, low ceruloplasmin activity and a hypochromic microcytic anemia (Sas, 1989).
    G) Cattle fed 100 mg/kg Mo (sodium molybdate) for 11 months demonstrated diarrhea as soon as 18 days, significant elevation of plasma Mo by 1 month, achromatrichia (bleached hair) and decreased hematocrit by 2 months, increased plasma Cu by 4 months, and growth suppression due to inefficient feed utilization (Lesperance et al, 1985).
    11.1.9) OVINE/SHEEP
    A) Lambs grazing where soil Mo was 2.5 times Cu developed enzootic ataxia in 15 to 39% of cases (Lener & Bibr, 1984).
    B) Ammonium heptamolybdate (100 mg IV daily for 28 days to 45 kg sheep) decreased hemoglobin and mean corpuscular hemoglobin and elevated erythrocyte sedimentation rate, copper, sorbitol dehydrogenase, lactate dehydrogenase and glutamate dehydrogenase. The results suggested a Mo-induced hypochromic normocytic anemia and hepatotoxicity (Auza et al, 1989).

Treatment

    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) Dietary Cu antagonized Mo toxicity in sheep and cattle. Addition of Cu sulfate to the diet or as a drench should decrease diarrhea within days. Sulfate protected against Mo toxicity in monogastric animals but enhanced Mo toxicity in ruminants (Pitt, 1976).
    2) Addition of 0.5% (Na) sulfate reduced the elevated plasma Mo produced by consumption of 100 mg/kg sodium molybdate in the diet of cattle. Addition of 2.7 kg pelleted alfalfa to a diet containing 100 mg/kg sodium molybdate enhanced metabolic status and reduced liver Mo (Lesperance et al, 1985).
    3) Removal of animals from high Mo pastures results in rapid recovery due to the rapid excretion of Mo.
    4) A Cu:Mo feed ratio of 2:1 should be maintained.

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