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TELLURIUM AND COMPOUNDS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Tellurium is a non-metallic element, or metalloid, in group 6A (Lee, 1998). Its major compounds are tellurides (Clayton & Clayton, 1993).

Specific Substances

    A) AS-101
    1) Ammonium trichloro(dioxyethylene-O,O')tellurate
    POTASSIUM TELLURITE
    1) Molecular Formula: K2-Te-O3
    TELLURIUM
    1) Te
    2) Aurum paradoxum
    3) Metallum problematum
    4) CAS 13494-80-9
    HYDROGEN TELLURIDE
    1) CAS 7783-09-7
    TELLURIC ACID
    1) CAS 7803-68-1
    TELLURIUM DIBROMIDE
    1) CAS 7789-50-0
    TELLURIUM DICHLORIDE
    1) CAS 10025-7-5
    TELLURIUM DIOXIDE
    1) CAS 7446-07-3
    TELLURIUM HEXAFLUORIDE
    1) CAS 7783-80-4
    TELLURIUM TETRABROMIDE
    1) CAS 10031-27-3
    TELLURIUM TETRACHLORIDE
    1) CAS 10026-07-0
    TELLURIUM TETRAIODIDE
    1) CAS 7790-48-9
    TELLUROUS ACID
    1) CAS 10049-23-7
    GENERAL TERMS
    1) TELLURIUM COMPOUND, N.O.S.
    2) TELLURIUM COMPOUND, TOXIC, N.O.S.
    3) TELLURIC ACID, DISODIUM SALT

    1.2.1) MOLECULAR FORMULA
    1) Te

Available Forms Sources

    A) FORMS
    1) Elemental tellurium has a bright luster, is brittle, readily powders, and burns slowly in air. It exists in 2 allotropic forms, as a powder and in the hexagonal crystalline form (isomorphous) with gray selenium (Bingham et al, 2001).
    B) SOURCES
    1) Tellurium is contained in the earth's crust at a concentration of about 0.002 ppm. During the refining of blister copper, tellurium is recovered from anode muds. It is also found in various sulfide ores along with selenium; it is produced as a by-product of metal refineries (Bingham et al, 2001).
    C) USES
    1) It is used as a coloring agent in chinaware, porcelains, enamels, and glass; reagent in producing black finish on silverware; in the manufacture of special alloys of marked electrical resistance; and in semiconductor research (Budavari, 1996).
    2) It is also used as a secondary rubber vulcanizing agent; in the manufacture of iron and stainless-steel castings; in thermoelectric devices; as a catalyst; and used with lithium in storage batteries for spacecraft (Lewis, 1993).
    3) INDUSTRIAL USES (Bingham et al, 2001; ITI, 1995; Clayton & Clayton, 1993; Blackadder & Manderson, 1975):
    a) VULCANIZATION OF RUBBER: Tellurium increases heat, abrasion, and aging resistance.
    b) COLORING AGENT: Tellurium is used in the glass and ceramics industry as a coloring agent.
    c) CATALYST: Tellurium is a catalyst in the chemical industry.
    d) LAMPS: Tellurium vapor is used in daylight lamps.
    e) Elemental tellurium is used as an additive to copper and iron, as a coloring agent in ceramics, in thermoelectric devices, in vulcanizing rubber, and in storage batteries.
    f) METAL ALLOYS: Tellurium is alloyed with iron, steel, and copper to improve machinability and improve surface resistance to wear and corrosion.
    4) MEDICINAL USES (Blackadder & Manderson, 1975):
    a) NO LONGER RECOMMENDED: Tellurium compounds have been used as a sedative and as a treatment for night sweats in phthisis and to treat syphilis.
    b) INVESTIGATIONAL: Selected tellurium compounds have been studied as immunomodulators (Sredni et al, 1987; Nyska et al, 1989) and as anti-sickling agents (Kurantsin-Mills et al, 1988).
    c) BACTERIOLOGY: Tellurium is used in diagnostic tests for diphtheria.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) There have been no reports of workers dying or having serious poisoning from exposure to tellurium or its compounds. However, accidental deaths have occurred. Two of three patients accidentally injected with sodium tellurite in place of sodium iodide died. Tellurium is considered to be less toxic than selenium, but tellurides appear to be more toxic than selenurites.
    B) ACUTE EXPOSURE effects may include acute respiratory irritation followed by the development of garlicky odor of the breath and sweat. The skin may develop a blue-black discoloration. Systemic effects may consist of fatigue, somnolence, dizziness, alopecia, headache, and gastritis.
    C) CHRONIC EXPOSURE effects may include garlic breath, metallic taste, decreased sweating, dry mouth, fatigue, lassitude, anorexia and nausea.
    D) A garlicky odor of the breath and sweat is an effect seen with tellurium and its compounds, and is considered a good indicator of tellurium absorption. It is thought to be due to the generation of dimethyl telluride. This odor is also found in urine, feces, and internal organs of sacrificed animals. Ingestion of as little as 40 mcg of soluble tellurium may cause the unusual breath odor.
    E) ANIMALS - Tellurium hexafluoride is considered seriously toxic by inhalation and may produce respiratory depression, pulmonary edema, cardiovascular collapse and death in experimental animals. Tellurium hexafluoride is five times as potent as selenium hexafluoride at the same concentrations. Adverse neurologic and reproductive effects have been seen in experimental animals, but not in humans.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Dry mouth and throat may be seen following exposure to hydrogen telluride. Retinal changes have been observed in experimental animals.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Hydrogen telluride causes pulmonary irritation and edema in experimental animals, which may also occur in humans. Two patients developed no pulmonary symptoms associated with a tellurium hexafluoride leak.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Drowsiness, headache, malaise, lassitude, weakness, and dizziness may occur. Neuropathies have been reported in experimental animals.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Anorexia, nausea, vomiting, garlicky odor, metallic taste, dry mouth and constipation have occurred.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Hemolysis and an increased MCV were reported in animal studies.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Dermatitis and blue-black skin discoloration may occur from exposure to tellurium hexafluoride.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for tellurium in humans.
    B) Congenital abnormalities have been reported in experimental animals.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the carcinogenic potential of tellurium in humans.

Laboratory Monitoring

    A) No toxic levels of tellurium have been established in biological specimens.
    B) If there has been a significant exposure to tellurium hexafluoride, monitor chest x-ray and arterial blood gases or pulse oximetry.
    C) Hematologic parameters should be monitored.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL - There are no data on adsorption of tellurium to activated charcoal.
    1) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    B) No specific chelator is effective for tellurium or its compounds.
    0.4.3) INHALATION EXPOSURE
    A) Most cases require no treatment or simple supportive care. Treatment should be directed at maintaining respirations for those agents which are pulmonary irritants and for monitoring kidney, hematologic, and liver function.
    B) 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) As little as 0.5 mcg produced the garlicky odor for 30 hours. Fifteen mg produced an effect for 279 days.
    B) No specific toxic level has been established for tellurium or its compounds. Workers exposed to 0.01 to 0.1 mL/m(3) developed a garlic-odor of sweat and breath, somnolence, anorexia, nausea, and urinary levels up to 0.06 mg/L.
    C) ANIMAL DATA - Tellurite and tellurate concentrations of 25 to 50 ppm in the diets of animals were toxic.

Clinical Effects

Summary Of Exposure

    A) There have been no reports of workers dying or having serious poisoning from exposure to tellurium or its compounds. However, accidental deaths have occurred. Two of three patients accidentally injected with sodium tellurite in place of sodium iodide died. Tellurium is considered to be less toxic than selenium, but tellurides appear to be more toxic than selenurites.
    B) ACUTE EXPOSURE effects may include acute respiratory irritation followed by the development of garlicky odor of the breath and sweat. The skin may develop a blue-black discoloration. Systemic effects may consist of fatigue, somnolence, dizziness, alopecia, headache, and gastritis.
    C) CHRONIC EXPOSURE effects may include garlic breath, metallic taste, decreased sweating, dry mouth, fatigue, lassitude, anorexia and nausea.
    D) A garlicky odor of the breath and sweat is an effect seen with tellurium and its compounds, and is considered a good indicator of tellurium absorption. It is thought to be due to the generation of dimethyl telluride. This odor is also found in urine, feces, and internal organs of sacrificed animals. Ingestion of as little as 40 mcg of soluble tellurium may cause the unusual breath odor.
    E) ANIMALS - Tellurium hexafluoride is considered seriously toxic by inhalation and may produce respiratory depression, pulmonary edema, cardiovascular collapse and death in experimental animals. Tellurium hexafluoride is five times as potent as selenium hexafluoride at the same concentrations. Adverse neurologic and reproductive effects have been seen in experimental animals, but not in humans.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Tellurium inhibits sweating, whereas selenium does not (Blackadder & Manderson, 1975; Muller et al, 1989).
    2) CASE REPORT - FEVER was reported in a 37-year-old female 2 days after eating meat contaminated with tellurium. Fever subsided within 5 days (Muller et al, 1989).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Dry mouth and throat may be seen following exposure to hydrogen telluride. Retinal changes have been observed in experimental animals.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) RETINOPATHY has been observed in experimental animals. Chronic experimental poisoning with metallic tellurium in cats has caused degenerative changes in the ganglion cells of the retina. This has not been reported in humans (Grant & Schuman, 1993).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) DRY MOUTH and throat were seen in some workers exposed to hydrogen telluride (Steinberg et al, 1942).
    2) A metallic taste and a sharp garlic odor of the breath may be present following tellurium intoxication, and is enhanced following alcohol ingestion (Muller et al, 1989; Larner, 1995; Bingham et al, 2001). The characteristic garlic odor is a result of the metabolism of tellurium to dimethyl telluride.
    3) Dysphagia, a persistent garlic odor, and a blackened tongue were observed in an infant who ingested an unknown quantity of silver blackening solution containing 1.7% tellurium dioxide in 60% HCl (Higgins et al, 1999).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Severe tellurium poisoning, which is rare, may result in respiratory depression and circulatory collapse (HSDB , 2001).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hydrogen telluride causes pulmonary irritation and edema in experimental animals, which may also occur in humans. Two patients developed no pulmonary symptoms associated with a tellurium hexafluoride leak.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Tellurium fumes are absorbed through the respiratory tract and may result in pulmonary irritation (Lewis, 1990).
    B) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) Severe tellurium poisoning, which is rare, may result in respiratory depression and circulatory collapse (HSDB , 2001).
    C) LACK OF EFFECT
    1) WITH POISONING/EXPOSURE
    a) In two human cases where 50 g of tellurium hexafluoride accidentally leaked into a laboratory room, no pulmonary symptoms developed.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) ANIMALS - Hydrogen telluride causes pulmonary irritation in experimental animals (Bingham et al, 2001; ACGIH, 1991). 40 mg of finely divided tellurium dioxide caused death in animals receiving a single endotracheal injection, while a coarser material at 50 mg caused no effects. 100 mg of elemental tellurium and the coarser tellurium dioxide also caused fatalities (ACGIH, 1991). Inflammation, but no fibrosis, was seen (Geary et al, 1978).
    2) HYPERVENTILATION
    a) Tachypnea was noted in experimental animals exposed to 1 ppm of tellurium hexafluoride for four hours, but no mortality was seen. Daily one hour exposures for five days produced no recognizable injury.
    3) PULMONARY EDEMA
    a) Pulmonary edema was noted in experimental animal studies when 1 ppm of tellurium hexafluoride was administered for four hours. Exposures at 5, 10, 25, 50 and 100 ppm were fatal. 1.5 g of tellurium salts given subcutaneously to dogs produced respiratory depression and asphyxia within three days (Mead & Giese, 1901).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Drowsiness, headache, malaise, lassitude, weakness, and dizziness may occur. Neuropathies have been reported in experimental animals.
    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Drowsiness/weakness has been reported after tellurium exposure. One man who was exposed to an unknown amount of tellurious oxide became drowsy and slept for 18 hours.
    1) This has also been borne out in experimental animal studies (Steinberg et al, 1942).
    B) MALAISE
    1) WITH POISONING/EXPOSURE
    a) Malaise, weakness, and dizziness have also been reported after exposure to hydrogen telluride (Clayton & Clayton, 1993).
    C) FATIGUE
    1) WITH POISONING/EXPOSURE
    a) Lassitude was noted in two human cases of exposure to 50 g of tellurium hexafluoride that had leaked into a laboratory room.
    b) CASE REPORT - Giddiness, fatigue and weight loss were reported in a 37-year-old female exposed to tellurium in a piece of meat she tasted containing 800 to 1000 micrograms tellurium/kg of meat (Muller et al, 1989).
    D) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may occur following exposure to hydrogen telluride (Bingham et al, 2001; Clayton & Clayton, 1993).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) 1.5 g of tellurium salts injected subcutaneously into dogs in a four-hour period produced restlessness, paralysis, seizures, drowsiness, and coma within three days (Mead & Giese, 1901). Ingestion has resulted in "black brain" and black testes in rats (Lee, 1998).
    2) NEUROPATHY PERIPHERAL
    a) RATS - Injection of 0.3 mcg potassium tellurite into rat tibial nerves resulted in rapid and progressive acute neuropraxia within six hours. Focal demyelination and intraneuronal accumulation of myelin debris were also seen. Recovery with remyelination had begun within 9 days (Uncini et al, 1988).
    b) RATS - A significant peripheral neuropathy, characterized by a transient demyelinating/remyelinating sequence, is produced in rats fed a diet high in tellurium. This occurs secondary to inhibition of squalene epoxidase which results in decreased synthesis of cholesterol and cerebrosides, lipids in high concentrations in myelin. Synthesis of phosphatidylcholine is unaffected. Myelin protein mRNA steady state levels are down regulated (Morell et al, 1994; Wagner et al, 1995; Larner, 1995).
    3) NEUROPATHY
    a) RATS - Proliferation of myelinated, non-dividing intraspinal Schwann cells was observed in rats fed 1.25 percent tellurium in the diet. This is thought to be due to initial tellurium-induced demyelination, which would provide a stimulus for Schwann cell division (Hammang et al, 1988).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Anorexia, nausea, vomiting, garlicky odor, metallic taste, dry mouth and constipation have occurred.
    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Anorexia has been a symptom reported after exposure to tellurium and its compounds (Muller et al, 1989). It was one of the symptoms noted in a human exposure incident where 50 g of tellurium hexafluoride leaked into a laboratory room.
    B) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting and nausea may also be seen in tellurium compound exposures, although they are not always present (Yarema & Curry, 2005; Steinberg et al, 1942; Blackadder & Manderson, 1975; Muller et al, 1989).
    C) BREATH SMELLS UNPLEASANT
    1) WITH POISONING/EXPOSURE
    a) A garlic odor of the breath and sweat and a metallic taste have been reported after exposure to tellurium and its compounds (Blackadder & Manderson, 1975; Muller et al, 1989; Higgins et al, 1999; Bingham et al, 2001). Dry mouth is typical. This odor may also be found in urine and feces (Steinberg et al, 1942; Muller et al, 1989).
    b) The metallic taste and garlicky odor may occur with chronic exposure to metallic dusts and fumes (HSDB , 2001; Clayton & Clayton, 1993).
    c) Garlicky breath odor was reported in two children (a 20-month-old boy and a 21-month-old boy) after ingesting metal-oxidizing solutions (containing 1.7% and 5.86% tellurium; 60% and 31.9% hydrochloride acid, respectively). Following supportive care, both patients recovered without further sequelae. On follow-up 7 months later, one patient still had a garlic breath odor (Yarema & Curry, 2005).
    D) CONSTIPATION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Constipation was noted in one patient who inhaled an unknown quantity of tellurious oxide, but it is not a common complaint (Steinberg et al, 1942).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Liver damage may occur following chronic exposure to tellurium fumes in occupational settings (HSDB , 2001).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL COLOR
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - The mucosa of the ureter and bladder was discolored in the two human fatal cases injected with tellurium (Keal et al, 1946).
    B) ABNORMAL URINE
    1) WITH POISONING/EXPOSURE
    a) Tellurium poisoning, by ingestion and chronic exposure to fumes, most notably results in a sharp, garlic odor of the urine (Bingham et al, 2001; HSDB , 2001).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Kidney damage has been reported after repeated oral exposure in animals (Clayton & Clayton, 1993).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Hemolysis and an increased MCV were reported in animal studies.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Reduced hemoglobin levels and hemolysis have been reported in experimental animal studies (Steinberg et al, 1942). This was especially true of hydrogen telluride (Bingham et al, 2001; Hathaway et al, 1996).
    2) ANEMIA HYPOCHROMIC
    a) Potassium tellurite has been shown to increase MCV and decrease MCHC in a time and concentration-dependent fashion, without affecting MCH. For this reason, it has been studied as an anti-sickling agent (Kurantsin-Mills et al, 1988).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Dermatitis and blue-black skin discoloration may occur from exposure to tellurium hexafluoride.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Dermatitis was noted in two patients exposed to 50 g of tellurium hexafluoride which leaked into a laboratory room (Blackadder & Manderson, 1975).
    1) The reduction of sweating may result in scaly, dry skin and resultant dermatitis (HSDB , 2001; Hathaway et al, 1996).
    B) DISCOLORATION OF SKIN
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Bluish-black patches were noted on the skin of the fingers, neck, and face in a case report where two patients were inadvertently exposed to 50 g of tellurium hexafluoride (Blackadder & Manderson, 1975).
    b) CASE REPORT - Blackening of the dorsal surface of the tongue was reported in an infant following ingestion of a silver blackening solution containing 1.7% tellurium dioxide (Higgins et al, 1999).
    c) Black discoloration of the oral mucosa was reported in two children (a 20-month-old boy and a 21-month-old boy) after ingesting metal-oxidizing solutions (containing 1.7% and 5.86% tellurium; 60% and 31.9% hydrochloride acid, respectively). Following supportive care, both patients recovered without further sequelae (Yarema & Curry, 2005).
    C) ALOPECIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 37-year-old patient with tellurium intoxication developed loss of hair and discoloration of new grown hair (Muller et al, 1989).
    D) CYANOSIS
    1) WITH POISONING/EXPOSURE
    a) Marked cyanosis may occur following severe tellurium toxicity (Muller et al, 1989).
    E) ANHIDROSIS
    1) WITH POISONING/EXPOSURE
    a) Decreased sweating and dry skin is characteristic of tellurium poisoning, as is a garlicky odor to the skin and breath (Blackadder & Manderson, 1975; Muller et al, 1989; Lewis, 1990).
    F) ABNORMAL BODY ODOR
    1) WITH POISONING/EXPOSURE
    a) A garlic-like odor in the sweat, attributed to dimethyltelluride, is characteristic of tellurium absorption, and may persist for many days after exposure (Bingham et al, 2001).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) DISORDER OF IMMUNE FUNCTION
    1) WITH POISONING/EXPOSURE
    a) IMMUNOMODULATION - The investigational immunomodulator AS-101 has been shown to stimulate proliferation and interleukin-2 production in human lymphocytes in vitro, and the production of interleukin-2 and colony stimulating factor in murine spleen cells (Sredni et al, 1987; Nyska et al, 1989).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for tellurium in humans.
    B) Congenital abnormalities have been reported in experimental animals.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) CONGENITAL ANOMALY
    a) RATS - Specific developmental abnormalities of the central nervous and musculoskeletal systems, the craniofacial area (including nose and tongue), fetotoxicity, and other neonatal effects were found in rat studies. Effects on post-implantation were also observed (RTECS, 1998).
    b) RATS - When pregnant rats were exposed to tellurium dioxide 10 to 1,000 mcmol/kg for 4 days, fetal pups were noted to have dose-related effects of hydrocephalus, edema, exophthalmia, ocular hemorrhage, umbilical hernia, undescended testis, and small kidneys (Perez-D'Gregorio & Miller, 1988).
    1) At maternal doses of 500 mcmol/kg, the incidence of these abnormalities was 100 percent. No maternal toxicity or fetal mortality were observed (Perez-D'Gregorio & Miller, 1988).
    c) Tellurium has produced specific and characteristic HYDROCEPHALY in rats with prenatal exposure (Garro & Pentschew, 1964; Agnew, 1968; Duckett, 1971). This hydrocephaly is not apparent until after birth, and treatment on a single day (during day 9 or 10) of gestation is sufficient to induce the defect (Agnew & Curry, 1972). CNS behavioral effects have also been produced in prenatally-exposed rabbits (Garro & Pentschew, 1964).
    2) SKELETAL MALFORMATION
    a) Skeletal malformations and skeletal maturational delays were observed in the offspring of pregnant rats and rabbits given dietary tellurium doses of 3,000 to 15,000 ppm for ten days. Maternal toxicity was also seen at doses that had no effect on the fetuses (Johnson et al, 1988).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) PLACENTAL BARRIER
    a) Placental transfer occurs with tellurious acid in experimental animals, but is slow. Experimental animal studies have shown a high uptake in fetal brain tissue. Hydrocephalus has been noted in these studies (Barlow & Sullivan, 1982). No human data were found.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS13494-80-9 (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 carcinogenic potential of tellurium in humans.
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Tellurium compounds did not cause cancer in rats or mice (Friberg et al, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic levels of tellurium have been established in biological specimens.
    B) If there has been a significant exposure to tellurium hexafluoride, monitor chest x-ray and arterial blood gases or pulse oximetry.
    C) Hematologic parameters should be monitored.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) No toxic levels of tellurium have been established in biological specimens
    B) HEMATOLOGIC
    1) A CBC with differential may be useful to monitor for adverse hematologic effects.
    C) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) A background urinary level for tellurium is approximately 0.2 to 1.0 mcg/mL of urine.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.
    2) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    b) Pulse oximetry monitoring is an alternative to arterial blood gases.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If there has been significant exposure to tellurium hexafluoride, monitor chest x-ray.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) URINE - Determination and quantification of tellurium in urine has been performed by hydrid atomic absorption spectrometry and the concentration in urine was measured directly (Muller et al, 1989).
    2) SERUM AND HAIR - Serum and hair were digested first with nitric and sulfuric acid under a time-temperature program. Digestion residue was dissolved in HCl, and sodium boron hydrid was used as reducing agent. Hydrid atomic absorption spectrometry was then used for quantification of tellurium (Muller et al, 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic levels of tellurium have been established in biological specimens.
    B) If there has been a significant exposure to tellurium hexafluoride, monitor chest x-ray and arterial blood gases or pulse oximetry.
    C) Hematologic parameters should be monitored.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Elemental tellurium is poorly absorbed, but its more soluble compounds may undergo some oral absorption.
    B) ACTIVATED CHARCOAL
    1) There are no studies on the use of activated charcoal in tellurium overdoses. However, due to the low toxicity of activated charcoal, it should be tried if significant amounts of tellurium compounds have been ingested.
    2) 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).
    3) 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) There are no studies on the use of activated charcoal in tellurium overdoses. However, due to the low toxicity of activated charcoal, it should be tried if significant amounts of tellurium compounds have been ingested.
    2) 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.
    3) 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) CHELATION THERAPY
    1) No specific chelator is effective for tellurium and its compounds.
    2) DIMERCAPROL/BAL: Although some early human cases were treated with BAL in oil, subsequent experimental animal studies have found that BAL is of little value and may actually enhance toxicity (Amdur, 1958).
    B) ASCORBIC ACID
    1) 10 milligrams/kilogram/day of vitamin C has been suggested to treat the garlicky odor resulting from tellurium ingestion (ITI, 1995). Its effects are questionable, and its use should be limited to those cases where the odor presents a severe social problem.
    C) SUPPORT
    1) Most cases of exposure to tellurium and its compounds have resulted in minimal signs and symptoms. Patients should be monitored for adequate renal function, liver function, and for hematologic abnormalities, as these have been reported in severely poisoned experimental animals.
    2) Although humans have experienced mild CNS depression, including dizziness, lethargy, and drowsiness, paralysis and tremors as seen in severely poisoned experimental animals have not been reported.

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.
    6.7.2) TREATMENT
    A) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).

Abstracts

Case Reports

    A) ADULT
    1) A 37-year-old female recalled the onset of symptoms of nausea, vomiting, metallic taste in the mouth, and a sharp garlic odor of the breath, sweat, and excrement beginning hours after she tasted a piece of meat that was contaminated with 800 to 1000 mcg of tellurium/kg meat.
    2) She presented to a health care facility complaining of weight loss, fatigue, and a garlic odor of breath of 4 weeks duration. Two weeks prior to presentation she observed hair loss. Toxicologic analysis of serum, urine, hair, and the implicated meat detected tellurium in concentrations of 27.6 mcg/L in serum, 3.2 mcg/L in urine, not detected in hair, and 800 to 1000 mcg/kg meat.
    3) Therapy consisted of ascorbic acid 200 mg/day. Hair loss disappeared by eight weeks after evaluation. New hair growth was noted to take a bright color. The garlic odor became less apparent but was still noticeable 9 months later (Muller et al, 1989).

Range Of Toxicity

Summary

    A) As little as 0.5 mcg produced the garlicky odor for 30 hours. Fifteen mg produced an effect for 279 days.
    B) No specific toxic level has been established for tellurium or its compounds. Workers exposed to 0.01 to 0.1 mL/m(3) developed a garlic-odor of sweat and breath, somnolence, anorexia, nausea, and urinary levels up to 0.06 mg/L.
    C) ANIMAL DATA - Tellurite and tellurate concentrations of 25 to 50 ppm in the diets of animals were toxic.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) CASE REPORTS
    1) The following information is for TELLURIUM AND ITS COMPOUNDS -
    a) Two fatalities occurred after unintentional treatment with 2 grams of sodium tellurite by ureteral catheter. The patients died 6 hours post-treatment after experiencing emesis, dyspnea, cyanosis, loss of consciousness, stupor, and renal pain. Autopsy revealed acute fatty degeneration and edema of the liver (ACGIH, 1991).
    C) ANIMAL DATA
    1) RATS - Intratracheal instillation of 100 mg doses of tellurium caused fatalities in rats (ACGIH, 1991).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) SPECIFIC SUBSTANCE
    1) The following information is for TELLURIUM AND ITS COMPOUNDS -
    a) Tellurites and tellurates in concentrations of 25 to 50 ppm placed in the diets of animals proved toxic (ACGIH, 1991).
    b) One study determined that the oxide (TeO2) was more toxic to rats than elemental tellurium after intratracheal instillation, but particle size appeared to be the critical factor. Deaths followed intratracheal instillation of 40 mg of finely divided tellurium oxide (TeO2), while the animals survived after 50 mg of coarse material. In addition, 100 mg of tellurium, as well as of the less finely divided TeO2 also caused fatalities (ACGIH, 1991; Geary et al, 1978).
    c) As little as 0.5 mcg produced the garlicky odor for 30 hours. Fifteen mg produced an effect for 279 days (Blackadder & Manderson, 1975; Steinberg et al, 1942).
    C) OCCUPATIONAL
    1) Iron foundry workers exposed to concentrations between 0.01 and 0.1 mg/m(3) complained of a garlic odor of the breath and sweat, dryness of the mouth and a metallic taste, somnolence, anorexia, and occasional nausea. Urinary concentrations ranged from 0 to 0.06 mg/L (Hathaway et al, 1996).
    D) ANIMAL DATA
    1) Elemental tellurium had only a slight effect on the growth of rats after feeding at concentrations up to 1500 ppm (ACGIH, 1991).
    2) Dietary administration of 500 to 3000 ppm tellurium to pregnant rats resulted in an increased incidence of fetal encephalopathy (ACGIH, 1991).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) Muller et al (1989) measured urine and serum levels of tellurium 4 weeks following ingestion of a small piece of meat that contained 800 to 1000 micrograms/kilogram tellurium by an adult. Urine level was 3.2 micrograms/liter and serum level was 27.6 micrograms/liter.
    b) Following the ingestion of an unknown quantity of silver blackening solution, containing 1.7% tellurium dioxide in 60% HCl, an infant was reported to have a serum tellurium level of 200 micrograms/liter (33 micrograms/liter average) and a urine level of 56 micrograms/liter (normal 0.2-1.0 microgram/liter) (Higgins et al, 1999).
    2) OCCUPATIONAL
    a) One study attempted to associate urine levels of exposed workers with symptoms. A garlicky odor occurred at urinary levels less that 0.01 mg/L and increased in intensity as the urinary concentration increased. Metallic taste, somnolence, and body odor appeared at approximately 0.01 mg/L of tellurium (Steinberg et al, 1942). A "background" level of tellurium in normal individuals is 0.2 to 1.0 mcg/mL.
    b) Workers in an iron foundry who were exposed to airborne tellurium concentrations of approximately 0.01 to 0.1 mg/m(3) developed garlic-odor of sweat and breath, somnolence, anorexia, nausea and a urinary level varying in proportion to exposure and ranging up to 0.06 mg/L (Steinberg et al, 1942).

Workplace Standards

    A) ACGIH TLV Values for CAS13494-80-9 (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) Tellurium and compounds (NOS), as Te, excluding hydrogen telluride
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    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): Halitosis
    d) Molecular Weight: 127.6
    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) Tellurium and compounds (NOS), as Te, excluding hydrogen telluride
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    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): Halitosis
    d) Molecular Weight: 127.6
    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 CAS13494-80-9 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Tellurium and compounds (as Te)
    2) REL:
    a) TWA: 0.1 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL and PEL also applies to other tellurium compounds (as Te) except Tellurium hexafluoride and Bismuth telluride.]
    3) IDLH:
    a) IDLH: 25 mg Te/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS13494-80-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tellurium and compounds (NOS), as Te, excluding hydrogen telluride
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tellurium and compounds (NOS), as Te, excluding hydrogen telluride
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Tellurium and compounds (as Te)
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS13494-80-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Tellurium and compounds (as Te)
    2) Table Z-1 for Tellurium and compounds (as Te):
    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: 0.1
    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) References: Lewis, 1996 RTECS, 2001
    1) LD50- (ORAL)MOUSE:
    a) 20 mg/kg
    b) > 5 g/kg
    2) LD50- (ORAL)RAT:
    a) 83 mg/kg
    b) > 5 g/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) No studies have been done to evaluate the exact mechanism by which tellurium produces its toxicity in experimental animals. Initial work seems to indicate that the somnolence and other CNS effects may be due to a reduction of cortical irritability (Steinberg et al, 1942).
    B) NEUROPATHY - Rat studies have shown a decreased synthesis of cholesterol and cerebrosides (myelin lipids). Myelin protein mRNA steady state levels are down regulated. The synthesis of free fatty acids and cholesterol esters increases to some degree, and there is a marked increase in squalene, a precursor of cholesterol. These biochemical findings reveal that there are a variety of lipid abnormalities, and the concurrent increase in squalene and decrease in cholesterol suggest that tellurium or one of its derivatives may interfere with the normal conversion of squalene to cholesterol. This process interferes with neurotransmission and causes a severe peripheral neuropathy in animals (Morell et al, 1994).

Physicochemical

Physical Characteristics

    A) DESCRIPTION
    1) Tellurium is a grayish- or silvery-white, lustrous, brittle, solid. It has 2 allotropic forms: a hexagonal, rhombohedral crystalline structure, or a dark-gray to brown, amorphous powder with metal characteristics (Clayton & Clayton, 1993; Budavari, 1996). Tellurium is a nonmetallic element with many properties similar to those of selenium and sulfur (Lewis, 1996).
    2) Tellurium burns slowly in air with a greenish-blue flame, forming the dioxide (Budavari, 1996; Clayton & Clayton, 1993).
    3) Tellurium is diatomic (Te2) in the vapor state (Budavari, 1996).
    4) There are eight stable isotopes: 120, 122 to 126, 128, and 130. The artificial radioactive isotopes are 114 to 119, 121, 127, 129, and 131 to 134 (Budavari, 1996).
    5) The concentration of tellurium in the earth's crust is 0.002 ppm (Budavari, 1996).
    6) Tellurium occurs as tellurides in combination with metals in the minerals tetradymite, altaite, and coloradolite; is found as the dioxide, tellurite; and is found also native, associated with silver and gold (Budavari, 1996).
    7) The major compounds of tellurium are tellurides, including the unstable gas hydrogen telluride (H2Te), halides, oxides, sulfides, and tellurites and tellurates. In these compounds, the valence of tellurium may be 2, 4, or 6 (ACGIH, 1991).
    8) Tellurium is recovered from anode muds during the refining of blister copper. It is also found in various sulfide ores along with selenium and is produced as a byproduct of metal refineries. The USA, Canada, Peru, and Japan are the largest producers (Clayton & Clayton, 1993).
    9) TELLURIUM HEXAFLUORIDE is a colorless, non-combustible gas with an unpleasant odor.
    B) ODOR: Tellurium is odorless (HSDB , 2001). However, after ingestion, tellurium causes a garlic-like odor on the breath (Lewis, 1996; HSDB , 2001).
    C) TASTE: No information on the taste of tellurium was found in available references at the time of this review.
    D) COLOR: Tellurium is a grayish-white solid or a dark-gray to brown powder (Budavari, 1996).

Ph

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

Molecular Weight

    A) TELLURIUM (ELEMENTAL): 127.6 (atomic weight) (Budavari, 1996)
    B) TELLURIUM HEXAFLUORIDE: 241.61 (Budavari, 1996)

References

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