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TUNGSTEN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Tungsten, a transition element on the periodic table, is an extremely hard, resistant metal naturally occurring as a mineral.

Specific Substances

    1) Tungsten
    2) Wolfram
    3) VA
    4) Molecular Formula = W
    5) 7440-33-7 CAS
    1.2.1) MOLECULAR FORMULA
    1) W

Available Forms Sources

    A) FORMS
    1) Tungsten is available in the following grades (Lewis, 1993):
    1) Technical
    2) Powder
    3) Single crystals
    4) Ultra-pure granules of 50 to 600 microns
    B) SOURCES
    1) The earth's crust contains approximately 1.5 ppm of tungsten, with the chief tungsten ores being wolframite and scheelite (Budavari, 1996). Tungsten occurs naturally in Bolivia, Canada, China, Malaya, Mexico, Peru, Portugal, South America, Thailand, the former USSR, and the United States (Budavari, 1996; Lewis, 1993). Tungsten deposits are also found throughout the world occurring with metamorphic and granite igneous rocks (HSDB , 2002).
    2) TUNGSTEN CARBIDE - Tungsten carbide is manufactured by the mixing of tungsten and carbon, heating by induction in covered graphite pots, and followed by crushing and mixing with cobalt powder to form the cemented carbide (HSDB , 2002). The pulmonary fibrosis associated with chronic exposure of tungsten carbide is believed to be due to exposure of the cobalt. Please refer to the COBALT management for further information.
    C) USES
    1) Tungsten is used in light filaments, heating elements, electrical contacts, welding electrodes, rocket nozzles, phonograph needles, solar energy devices, ferrous and non- ferrous alloys (especially high-speed tool steel), shell steel, hard-facing rods, high- speed rotors as in gyroscopes, x-ray and electron tubes, chemical apparatus, mill products, and in the manufacture of abrasives, tools, textiles, ceramics, and pigments for dyes and paints. It is used to increase the hardness, toughness, elasticity, and tensile strength of steel (Bingham et al, 2001; Lee, 1998; Budavari, 1996; Hathaway et al, 1996; Ashford, 1994; Lewis, 1993) ACGIH, 1991). The metal powder is also used in mixtures with barium chromate and potassium chlorate as a pyrotechnic fuse (Urban, 1995).

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: Tungsten is a greyish-white lustrous metal that is solid at room temperature and is a naturally occurring element found in rocks and minerals combined with other chemicals but never occurs as a pure metal. Tungsten is used many products and has included electrical products (ie, lighting, electronic devices), welding electrodes, phonograph needles, solar energy devices, ferrous and non- ferrous alloys, high-speed rotors as in gyroscopes, x-ray and electron tubes and mill products. It is used to increase the hardness, toughness, elasticity, and tensile strength of steel. In more recent years, the military has used tungsten to replace other heavy metals including lead and uranium. Heavy metal tungsten alloys have been used in helicopter rotors, guided missiles and kinetic energy penetrators for defeating heavy armor.
    B) EPIDEMIOLOGY: Exposure may occur; however, toxicity has been rarely reported. There is very limited data following human exposure to tungsten metal.
    C) WITH POISONING/EXPOSURE
    1) EXPOSURE: Overall, significant exposure is uncommon.
    2) BACKGROUND LEVEL: As a naturally occurring element, tungsten is present in the air, water and food but at very low levels.
    3) OCCUPATIONAL: Occupational exposure can occur in metallurgy workers exposed to tungsten carbide and usually results in inhalation or dermal exposure. Tungsten metal dust is an eye, skin, and respiratory irritant.
    a) INHALATION: Chronic occupational exposure to hard metals involving cemented tungsten carbide (a mixture containing cobalt, used as a binding agent, and tungsten carbide) may result in lung fibrosis and is attributed to exposure to the cobalt. Please refer to the COBALT management for further information.
    b) DERMAL: Workers exposed to tungsten carbide may develop dermatitis and similar to inhalation the events are likely related to cobalt.
    4) ACUTE TOXICITY: Limited human information. Acute toxicity is rare.
    a) INGESTION: Ingestion of 25 to 80 g as a radiocontrast agent had no ill effect. Ingestion of ethanol reportedly contaminated with tungsten has been associated with the development of nausea and vomiting, seizures, metabolic acidosis, renal failure, rhabdomyolysis, clouded consciousness leading to coma and encephalopathy.
    5) ANIMAL DATA: In animals, other reported effects following exposure to tungsten include anorexia, colic, weight loss, incoordination, trembling, and dermatitis.
    0.2.7) NEUROLOGIC
    A) Seizures, headache, and coma have been reported following acute exposure to tungsten.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no studies were found on the potential reproductive effects of tungsten in humans.
    B) Oral administration of tungsten to female rats prior to mating was associated with post-implantation mortality of the fetus and resulted in musculoskeletal developmental abnormalities of the fetus.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of tungsten in humans.

Laboratory Monitoring

    A) Serum tungsten levels are useful in confirming diagnosis following significant exposures, but are not readily available.
    B) Monitor renal function tests and urine output after significant exposures or in symptomatic patients.
    C) If severe vomiting occurs following significant exposure to tungsten, monitor fluid and electrolyte levels.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Limited human experience following tungsten ingestion. Treatment is symptomatic and supportive. Monitor fluids and electrolytes in patients that develop significant vomiting. Administer IV fluids and replace electrolytes as indicated. In case of tungsten ingestion (very rare reports), activated charcoal and good supportive care may be indicated.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Limited human experience. Treatment is symptomatic and supportive. SEIZURES: Initially treat with benzodiazepines (eg, diazepam, lorazepam). Consider phenobarbital or propofol if seizures recur after diazepam. CHRONIC: OCCUPATIONAL EXPOSURE: Tungsten metal dust is an eye, skin, and respiratory irritant. Chronic occupational exposure to hard metals involving cemented tungsten carbide (a mixture containing cobalt, used as a binding agent, and tungsten carbide) may result in lung fibrosis and is attributed to exposure to the cobalt. Please refer to the COBALT management for further information when necessary.
    C) DECONTAMINATION
    1) PREHOSPITAL: Consider activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. INHALATION: Immediately remove patient from exposure and evaluate respiratory effort.
    2) HOSPITAL: Consider activated charcoal if the overdose is recent, the patient is not vomiting, and is able to maintain airway. INHALATION: Monitor respiratory effort and assess airway. Begin oxygen as indicated.
    D) AIRWAY MANAGEMENT
    1) Tungsten is a respiratory irritant. Airway support and management may be necessary if exposed to tungsten fumes (eg. welding)
    E) ANTIDOTE
    1) There is no known antidote.
    F) ENHANCED ELIMINATION
    1) Enhanced elimination is unlikely to be beneficial.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Tungsten exposure is likely to only occur in an occupational setting and home management is not indicated.
    2) OBSERVATION CRITERIA: Limited human experience, acute toxicity has been reported rarely. 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 including possible seizures, renal insufficiency, CNS toxicity 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.
    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: A specific lethal or minimum toxic dose has not been established. Acute tungsten toxicity is extremely rare. Chronic toxicity due to occupational exposure to tungsten is usually associated with the effects of cobalt which is often combined with tungsten carbide in metallurgy.

Clinical Effects

Summary Of Exposure

    A) USES: Tungsten is a greyish-white lustrous metal that is solid at room temperature and is a naturally occurring element found in rocks and minerals combined with other chemicals but never occurs as a pure metal. Tungsten is used many products and has included electrical products (ie, lighting, electronic devices), welding electrodes, phonograph needles, solar energy devices, ferrous and non- ferrous alloys, high-speed rotors as in gyroscopes, x-ray and electron tubes and mill products. It is used to increase the hardness, toughness, elasticity, and tensile strength of steel. In more recent years, the military has used tungsten to replace other heavy metals including lead and uranium. Heavy metal tungsten alloys have been used in helicopter rotors, guided missiles and kinetic energy penetrators for defeating heavy armor.
    B) EPIDEMIOLOGY: Exposure may occur; however, toxicity has been rarely reported. There is very limited data following human exposure to tungsten metal.
    C) WITH POISONING/EXPOSURE
    1) EXPOSURE: Overall, significant exposure is uncommon.
    2) BACKGROUND LEVEL: As a naturally occurring element, tungsten is present in the air, water and food but at very low levels.
    3) OCCUPATIONAL: Occupational exposure can occur in metallurgy workers exposed to tungsten carbide and usually results in inhalation or dermal exposure. Tungsten metal dust is an eye, skin, and respiratory irritant.
    a) INHALATION: Chronic occupational exposure to hard metals involving cemented tungsten carbide (a mixture containing cobalt, used as a binding agent, and tungsten carbide) may result in lung fibrosis and is attributed to exposure to the cobalt. Please refer to the COBALT management for further information.
    b) DERMAL: Workers exposed to tungsten carbide may develop dermatitis and similar to inhalation the events are likely related to cobalt.
    4) ACUTE TOXICITY: Limited human information. Acute toxicity is rare.
    a) INGESTION: Ingestion of 25 to 80 g as a radiocontrast agent had no ill effect. Ingestion of ethanol reportedly contaminated with tungsten has been associated with the development of nausea and vomiting, seizures, metabolic acidosis, renal failure, rhabdomyolysis, clouded consciousness leading to coma and encephalopathy.
    5) ANIMAL DATA: In animals, other reported effects following exposure to tungsten include anorexia, colic, weight loss, incoordination, trembling, and dermatitis.

Heent

    3.4.3) EYES
    A) IRRITATION
    1) Dryness, irritation, or a burning sensation of the eyes may occur following exposure to tungsten dust or tungsten fumes generated during welding (MSDS, 1996; MSDS, 1991).
    2) RABBITS: In the standard Draize test, mild irritation was reported following ocular tungsten exposure (RTECS , 2002).
    B) LACK OF EFFECT: A particle of tungsten, less than 1 millimeter in diameter, was inserted into the midvitreous region of eye of two rabbits. Weekly and monthly examinations for one year showed that the tungsten metal was "completely inert" (Bingham et al, 2001).
    3.4.5) NOSE
    A) Nasal dryness or irritation may occur following inhalational exposure to tungsten metal dust or tungsten fumes generated during welding (MSDS, 1996; MSDS, 1991).
    3.4.6) THROAT
    A) Inhalational exposure to tungsten metal dust or tungsten fumes generated during welding may result in throat dryness or irritation (MSDS, 1996; MSDS, 1991).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Difficulty in breathing may occur following inhalational exposure to tungsten fumes generated during welding (MSDS, 1996).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PNEUMONITIS
    a) GUINEA PIGS: Focal interstitial pneumonitis and bronchiolitis were reported in guinea pigs following intratracheal administration of tungsten metal in 3 50-mg doses (HSDB , 2002; Hathaway et al, 1996).
    2) DYSPNEA
    a) GUINEA PIGS: Dyspnea was reported in guinea pigs following oral or intravenous administration of tungsten (Hathaway et al, 1996).

Neurologic

    3.7.1) SUMMARY
    A) Seizures, headache, and coma have been reported following acute exposure to tungsten.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old man ingested 250 mL of wine which had flowed through the barrel of a gun that had been recently fired and, 15 minutes later, developed seizures that lasted for 25 minutes. The seizures resolved following intravenous administration of diazepam. On day 1 of presentation, laboratory analysis showed a blood ethanol level of 0.31 g/L and elevated tungsten levels in serum (5 mg/L), urine (101 mg/L), and gastric contents (8 mg/L). A high concentration of tungsten was found in the wine that the patient had consumed (1540 mg/L; dose ingested was approximately 385 mg) (Marquet et al, 1997).
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may occur following exposure to tungsten fumes generated during the welding process (MSDS, 1996).
    C) COMA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old military recruit became comatose (stage I coma) approximately 35 minutes after consuming 250 mL of ethanol that flowed through a recently fired gun barrel. The patient was mechanically ventilated and subsequently progressed to stage II coma. An EEG revealed diffuse slow waves. Laboratory analysis showed an ethanol level of 0.31 g/L and elevated tungsten levels in serum (5 mg/L), urine (101 mg/L), and gastric contents (8 mg/L). A high concentration of tungsten was found in the wine that the patient had consumed (1540 mg/L; dose ingested was approximately 385 mg). The patient gradually recovered following supportive care (Marquet et al, 1997).
    b) Inhalational exposure to tungsten fumes generated during welding may result in unconsciousness (MSDS, 1996).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TREMOR
    a) GUINEA PIGS: Incoordination and trembling were observed in guinea pigs following oral or intravenous administration of tungsten (Hathaway et al, 1996).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Nausea and vomiting were reported in a 19-year-old military recruit following ingestion of 250 mL ethanol that flowed through a recently fired gun barrel and was reportedly contaminated with tungsten (Marquet et al, 1997).
    b) Nausea may occur following inhalational exposure to tungsten fumes generated during welding (MSDS, 1996).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) GUINEA PIGS: Anorexia, weight loss, and colic were reported in guinea pigs following oral or intravenous administration of tungsten (Hathaway et al, 1996).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Renal failure, with a serum creatinine of 160 mcmol/L and a BUN of 6.4 mmol/L, occurred in a 19-year-old man who ingested 250 mL ethanol that flowed through a recently fired gun barrel and was reportedly contaminated with tungsten. Serum tungsten levels on day 1 of admission were 4960 mcg/L. Optic microscopy of a kidney biopsy showed extensive tubular necrosis with interstitial inflammatory infiltrate. The patient recovered following hemodialysis and diuresis, with a serum tungsten level of less than 50 mcg/L on day 14 (Marquet et al, 1997).
    B) POLYURIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old developed polyuria (4 L in the first few hours after admission) that subsequently progressed to anuria following ingestion of 250 mL ethanol reportedly contaminated with tungsten. The patient gradually recovered following hemodialysis and administration of bumetanide (Marquet et al, 1997).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Metabolic acidosis (pH of 7.17 and bicarbonate level of 10 mmol/L) occurred in a 19-year-old man following ingestion of 250 mL ethanol reportedly contaminated with tungsten. The patient recovered following hemodialysis (Marquet et al, 1997).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Skin irritation may occur following dermal exposure to tungsten metal dust (MSDS, 1991).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RASH
    a) RABBITS: In the standard Draize test, mild dermal irritation has been reported following tungsten application (RTECS , 2002).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old military recruit developed mild rhabdomyolysis (CPK of 1287 IU/L) after drinking 250 mL ethanol through a recently fired gun barrel. Serum tungsten levels on day 1 of admission were 4960 mcg/L. The patient's CPK levels normalized (42 IU/L) on day 12 following hemodialyses (Marquet et al, 1997).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no studies were found on the potential reproductive effects of tungsten in humans.
    B) Oral administration of tungsten to female rats prior to mating was associated with post-implantation mortality of the fetus and resulted in musculoskeletal developmental abnormalities of the fetus.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) RATS - Oral administration of tungsten to female rats, 1160 micrograms/kilogram 30 weeks prior to mating and the first twenty days of gestation, resulted in musculoskeletal developmental abnormalities of the fetus (RTECS , 2002).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) RATS - Oral administration of tungsten to female rats, 1160 micrograms/kilogram 30 weeks prior to mating and the first twenty days of gestation, resulted in musculoskeletal developmental abnormalities of the fetus (RTECS , 2002).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7440-33-7 (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) At the time of this review, no studies were found on the possible carcinogenic activity of tungsten in humans.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) RATS - The incidence of N-nitroso-N-methylurea-induced mammary carcinomas in female rats increased following the addition of tungsten (150 ppm) to the drinking water of rats (Bingham et al, 2001).

Genotoxicity

    A) At the time of this review, no genetic studies were found for tungsten.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Serum tungsten levels are useful in confirming diagnosis following significant exposures, but are not readily available.
    B) Monitor renal function tests and urine output after significant exposures or in symptomatic patients.
    C) If severe vomiting occurs following significant exposure to tungsten, monitor fluid and electrolyte levels.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Marquet et al (1997) described a quantitative assay of tungsten in biological fluids, hair, and nails, using an inductively coupled plasma (ICP) emission spectrometer. The ICP emission spectrometer had a 50 mcg/L limit of detection in biological fluids (Marquet et al, 1997).

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 including possible seizures, renal insufficiency, CNS toxicity despite treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Tungsten exposure is likely to only occur in an occupational setting and home management is not indicated.
    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) Limited human experience, acute toxicity has been reported rarely. Patients with a deliberate overdose, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.

Monitoring

    A) Serum tungsten levels are useful in confirming diagnosis following significant exposures, but are not readily available.
    B) Monitor renal function tests and urine output after significant exposures or in symptomatic patients.
    C) If severe vomiting occurs following significant exposure to tungsten, monitor fluid and electrolyte levels.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Limited human experience following tungsten ingestion. Treatment is symptomatic and supportive. Monitor fluids and electrolytes in patients that develop significant vomiting. Administer IV fluids and replace electrolytes as indicated.
    b) In case of tungsten ingestion (very rare reports), activated charcoal and good supportive care may be indicated (van der Voet et al, 2007).
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Limited human experience. Treatment is symptomatic and supportive. SEIZURES: Initially treat with benzodiazepines (eg, diazepam, lorazepam). Consider phenobarbital or propofol if seizures recur after diazepam. CHRONIC: OCCUPATIONAL EXPOSURE: Tungsten metal dust is an eye, skin, and respiratory irritant. Chronic occupational exposure to hard metals involving cemented tungsten carbide (a mixture containing cobalt, used as a binding agent, and tungsten carbide) may result in lung fibrosis and is attributed to exposure to the cobalt. Please refer to the COBALT management for further information when necessary.
    B) MONITORING OF PATIENT
    1) Serum tungsten levels are useful in confirming diagnosis following significant exposures, but are not readily available.
    2) Monitor renal function tests and urine output after significant exposures or in symptomatic patients.
    3) If severe vomiting occurs following significant exposure to tungsten, monitor fluid and electrolyte levels.
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

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) 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).

Enhanced Elimination

    A) SUMMARY
    1) Enhanced elimination is unlikely to be beneficial.
    B) HEMODIALYSIS
    1) A total of 9 sessions of hemodialysis were performed on a 26-year-old man between days 3 and 19 after ingesting approximately 250 mL of ethanol contaminated with tungsten. Despite this treatment, tungsten levels were still detectable in plasma and urine until days 12 and 33, respectively. Dialysance clearance of tungsten was not calculated (Marquet et al, 1996).

Range Of Toxicity

Summary

    A) TOXICITY: A specific lethal or minimum toxic dose has not been established. Acute tungsten toxicity is extremely rare. Chronic toxicity due to occupational exposure to tungsten is usually associated with the effects of cobalt which is often combined with tungsten carbide in metallurgy.

Minimum Lethal Exposure

    A) SUMMARY
    1) A specific lethal dose has not been established.
    B) ACUTE
    1) The probable minimum lethal oral exposure ranges from 0.5-5 g/kg (1 oz-1 pt (or 1 lb) for a 70 kg (150 lb) person) (HSDB , 1997).

Maximum Tolerated Exposure

    A) SUMMARY
    1) The maximum tolerated human exposure to tungsten has not been delineated.
    2) Acute tungsten toxicity is extremely rare. Chronic toxicity due to occupational exposure to tungsten is usually associated with the effects of cobalt which is often combined with tungsten carbide in metallurgy (van der Voet et al, 2007).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ADULT
    a) CASE REPORT - Serum tungsten levels in a 26-year-old, who ingested approximately 250 milliliters of ethanol that flowed through a recently fired gun barrel, were 4960 micrograms/liter on day 1 post-ingestion (Marquet et al, 1997).

Workplace Standards

    A) ACGIH TLV Values for CAS7440-33-7 (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) Tungsten, soluble compounds, as W
    a) TLV:
    1) TLV-TWA: 1 mg/m(3)
    2) TLV-STEL: 3 mg/m(3)
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): CNS impair; pulm fibrosis
    d) Molecular Weight: Varies
    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) Tungsten, metal and insoluble compounds, as W
    a) TLV:
    1) TLV-TWA: 5 mg/m(3)
    2) TLV-STEL: 10 mg/m(3)
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): LRT irr
    d) Molecular Weight: Varies
    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) Under Study
    1) Tungsten carbide
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    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 CAS7440-33-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Tungsten
    2) REL:
    a) TWA: 5 mg/m(3)
    b) STEL: 10 mg/m(3)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL also applies to other insoluble tungsten compounds (as W).],
    3) Listed as: Tungsten (soluble compounds, as W)
    4) REL:
    a) TWA: 1 mg/m(3)
    b) STEL: 3 mg/m(3)
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    5) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS7440-33-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tungsten, soluble compounds, as W
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tungsten, metal and insoluble compounds, as W
    3) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tungsten carbide
    4) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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: Tungsten
    7) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Tungsten (soluble compounds, as W)
    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 CAS7440-33-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2002 Lewis, 1996
    1) LD50- (INTRAPERITONEAL)RAT:
    a) 5 g/kg

Physicochemical

Physical Characteristics

    A) Tungsten is a steel-gray to tin-white, hard, brittle metal with a body centered cubic structure and atomic number 74 (Budavari, 1996) Hathaway, 1996; (Lewis, 1993) ACGIH, 1991). Lewis (1996) states that it is "cuttable, forgeable, and spinnable" and that it is "fairly soft when pure."
    B) The naturally occurring isotopes are 180 (0.135%), 182 (26.4%), 183 (14.4%), 184 (30.6%), and 186 (28.4%) (Budavari, 1996).
    C) It occurs in the 0, 2+, 4+, 5+, and 6+ valence states with 6+ being the most stable and occurring the most frequently in the tungsten compounds (Budavari, 1996; Clayton & Clayton, 1994; Lewis, 1993) ACGIH, 1991).
    D) Tungsten forms the carbide, carbonyl, chloride, fluoride, oxide, oxychloride, silicide, sulfide, tungstate, and tungstic acid compounds (Hathaway, 1996; ACGIH, 1991).
    E) It has high electrical conductivity and the highest melting point of all the metals (Ashford, 1994; Lewis, 1993) ACGIH, 1991).

Molecular Weight

    A) 183.85

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