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TELLURIUM HEXAFLUORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Tellurium hexafluoride is a colorless gas with a repulsive odor. It is a by-product of ore refining.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) F6-Te

Available Forms Sources

    A) FORMS
    1) Tellurium hexafluoride is a colorless gas with a repulsive odor (Budavari, 1989).
    B) SOURCES
    1) It is a by-product of ore refining (Hathaway et al, 1991).
    C) USES
    1) Little information is available on its effects in humans. This review is based on the known effects of TELLURIUM and FLUORIDE compounds in general, with specific effects attributed to TELLURIUM HEXAFLUORIDE indicated.
    2) Based on animal studies, tellurium hexafluoride is considered seriously toxic by inhalation and may produce pulmonary edema and death. Animal studies suggest that tellurium hexafluorid is five times more toxic than selenium hexafluoride and 2.5 times more toxic than ozone (ACGIH, 1986). Effects in humans exposed to tellurium hexafluoride have included headache, dyspnea, garlic breath odor, and bluish-black discoloration of the skin (Proctor et al, 1988).
    3) There have been no reports of workers dying or having serious symptoms from exposure to tellurium or its compounds (ACGIH, 1986). Tellurium is considered to be less toxic than selenium, but tellurites appear to be more toxic than selenites.
    4) A garlicky odor of the breath and perspiration are effects seen with tellurium and its compounds, and are considered good indicators of systemic tellurium absorption (HSDB , 1995). These effects are thought to be due to the generation of dimethyl telluride. This odor is also found in urine, feces, and internal organs of sacrificed animals (Steinberg et al, 1942; Nyska et al, 1989). Ingestion of as little as 40 mcg of soluble tellurium may cause the unusual breath odor.
    5) The ACGIH has established a Biological Exposure Index (BEI) for fluorides. See the BIOMONITORING section for more information.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Tellurium hexafluoride is considered seriously toxic by inhalation and may produce pulmonary edema and death. Little information is available on its effects in humans, and no data for chronic exposure were found.
    0.2.3) VITAL SIGNS
    A) Tachypnea and dyspnea have been observed in animals exposed to tellurium hexafluoride.
    0.2.4) HEENT
    A) Headache was reported following an exposure to hydrogen telluride. Dry mouth and throat have also been seen after exposure to this compound. Hair loss occurred in one case of acute intoxication.
    0.2.6) RESPIRATORY
    A) Tellurium hexafluoride is a respiratory irritant. It has produced signs of pulmonary edema and respiratory depression in animals, but this has not been documented in humans.
    0.2.7) NEUROLOGIC
    A) Headache has been reported from exposure to tellurium hexafluoride. Drowsiness has been seen as a symptom after human exposure to tellurium compounds. Malaise, weakness, and dizziness have also been seen. Lassitude may occur. Neuropathies have been reported in animals exposed to tellurium compounds.
    0.2.8) GASTROINTESTINAL
    A) Anorexia, nausea, vomiting, garlicky odor, metallic taste, and constipation have occurred from exposure to tellurium compounds. The garlic odor may occur from other routes of exposure besides ingestion.
    0.2.10) GENITOURINARY
    A) Kidney damage has been reported in animals.
    0.2.13) HEMATOLOGIC
    A) Hemolysis, reduced hemoglobin levels, or an increased MCV may be seen from exposure to tellurium compounds.
    0.2.14) DERMATOLOGIC
    A) Tellurium hexafluoride is highly irritating to the skin and mucous membranes. Dermatitis and blue-black skin discoloration have been reported to occur from exposure to tellurium hexafluoride. Alopecia has been reported after ingestion of tellurium.
    0.2.18) PSYCHIATRIC
    A) Lethargy has occurred following exposure to tellurium hexafluoride. Giddiness and fatigue have been reported after ingestion of tellurium.
    0.2.19) IMMUNOLOGIC
    A) Tellurium may be an immunomodulator; it has stimulated production of interleukin-2 in vitro.
    0.2.20) REPRODUCTIVE
    A) TELLURIUM HEXAFLUORIDE - No studies were found on the possible reproductive effects of tellurium hexafluoride in humans at the time of this review; however, it is possible that such effects might be similar to those of TELLURIUM and FLUORIDE.
    0.2.21) CARCINOGENICITY
    A) TELLURIUM HEXAFLUORIDE - No studies were found on the possible carcinogenic effects of tellurium hexafluoride in humans at the time of this review. Most information concerning tellurium compounds and sodium fluoride indicate that these substances are not clearly carcinogenic.
    0.2.22) OTHER
    A) Tellurium compounds may be absorbed by inhalation, dermal, or oral route. Because tellurium hexafluoride is a gas, significant oral exposure would not be expected. The exact mechanism of the toxicity of tellurium is not known.

Laboratory Monitoring

    A) No toxic levels of tellurium have been established. If there has been a significant exposure to tellurium hexafluoride, a chest x-ray may be necessary. Hematologic, liver, and kidney parameters should be monitored.

Treatment Overview

    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.
    B) Most cases require either no treatment or simple supportive care. There is no specific antidote or chelator. Treatment should be directed at maintaining respirations and monitoring kidney, hematologic, and liver function.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    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 tellurium produced the garlicky odor for 30 hours, and 15 mg produced an effect for 279 days. Tellurium hexafluoride produced breathing difficulties in four species of animals exposed to 1 ppm for 1 hour, and 1 ppm for 4 hours was fatal. Tellurites and tellurates in concentrations of 25 to 50 ppm in the diets of animals were toxic.

Clinical Effects

Summary Of Exposure

    A) Tellurium hexafluoride is considered seriously toxic by inhalation and may produce pulmonary edema and death. Little information is available on its effects in humans, and no data for chronic exposure were found.

Vital Signs

    3.3.1) SUMMARY
    A) Tachypnea and dyspnea have been observed in animals exposed to tellurium hexafluoride.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) TACHYPNEA - Increased respirations were seen in rabbits, guinea pigs, rats, and mice exposed to 1 ppm tellurium hexafluoride for one hour (ACGIH, 1991) Clayton & Clayton, 1994; (HSDB , 1999).
    2) DYSPNEA - Disturbed breathing was seen in four animal species exposed to 1 ppm tellurium hexafluoride for four hours (ACGIH, 1991).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) SWEATING - Tellurium inhibits sweating, whereas selenium does not (Blackadder & Manderson, 1975) Mullet et al, 1989).

Heent

    3.4.1) SUMMARY
    A) Headache was reported following an exposure to hydrogen telluride. Dry mouth and throat have also been seen after exposure to this compound. Hair loss occurred in one case of acute intoxication.
    3.4.2) HEAD
    A) WITH POISONING/EXPOSURE
    1) HEADACHE - has been reported in human exposures to tellurium hexafluoride (Hathaway et al, 1996).
    2) ALOPECIA - A 37-year-old with tellurium intoxication developed loss of hair and discoloration of new grown hair (Muller et al, 1989).
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CONJUNCTIVITIS - Tellurium hexafluoride is highly irritating to the eyes (HSDB , 1999).
    2) RETINAL CHANGES - have been observed in 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, 1986).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) METALLIC TASTE - One episode of acute inhalation of tellurium hexafluoride involving two persons produced metallic taste and a sour garlic odor on the breath (ACGIH, 1991) Clayton & Clayton, 1994).
    2) DRY MOUTH - Along with the characteristic garlic breath and metallic taste, dry mouth was reported in tellurium workers exposed to fumes and dust for several weeks or months (Finkel, 1983).

Respiratory

    3.6.1) SUMMARY
    A) Tellurium hexafluoride is a respiratory irritant. It has produced signs of pulmonary edema and respiratory depression in animals, but this has not been documented in humans.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Tellurium hexafluoride is a respiratory irritant (HSDB , 1999). Hydrogen telluride causes pulmonary irritation in animals (ACGIH, 1991). A dose of 40 mg of finely divided tellurium dioxide caused death in the animals receiving a single endotracheal injection, while a coarser material at 50 mg caused no effects. Elemental tellurium at 100 mg and the coarser tellurium dioxide also caused fatalities (ACGIH, 1991). Inflammation, but no fibrosis, was seen (Geary et al, 1978).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) LACK OF ADVERSE EFFECT
    1) In one incident of acute human exposure to tellurium hexafluoride, no respiratory effects were reported (ACGIH, 1991).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) A dose of 1.5 grams of tellurium salts given subcutaneously to dogs produced respiratory depression and asphyxia within three days (Mead & Giese, 1901).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ACUTE LUNG INJURY
    a) Disturbed breathing indicative of pulmonary edema was seen in four animal species exposed to 1 ppm tellurium hexafluoride for four hours (ACGIH, 1991).

Neurologic

    3.7.1) SUMMARY
    A) Headache has been reported from exposure to tellurium hexafluoride. Drowsiness has been seen as a symptom after human exposure to tellurium compounds. Malaise, weakness, and dizziness have also been seen. Lassitude may occur. Neuropathies have been reported in animals exposed to tellurium compounds.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported in human exposures to tellurium hexafluoride (Hathaway et al, 1996).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Drowsiness has been reported as a symptom after exposure. One man who was exposed to an unknown amount of tellurious oxide became drowsy and slept for 18 hours. This has been noted in animal studies (Steinberg et al, 1942).
    C) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Symptoms of CNS depression, including malaise, weakness, and dizziness, have been seen after exposure to hydrogen telluride (Clayton & Clayton, 1982).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS EFFECTS
    a) A dose of 1.5 grams of tellurium salts injected subcutaneously into dogs in a four-hour period produced within three days, restlessness, paralysis, seizures, drowsiness, and coma (Mead & Giese, 1901).
    b) Ingestion has resulted in "black brain" in rats (Finkel, 1983). Injection of 0.3 mcg potassium tellurite into rat tibial nerves resulted in rapid and progressive acute neurapraxia 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).
    c) Proliferation of myelinated, non-dividing intraspinal Schwann cells was observed in rats fed 1.25% 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) Anorexia, nausea, vomiting, garlicky odor, metallic taste, and constipation have occurred from exposure to tellurium compounds. The garlic odor may occur from other routes of exposure besides ingestion.
    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) Anorexia has been reported after exposure to tellurium and its compounds (Muller et al, 1989). It was among the symptoms reported in a human exposure in which 50 grams of tellurium hexafluoride leaked into a laboratory (Blackadder & Manderson, 1975).
    B) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may also be seen in tellurium compound exposures (Steinberg et al, 1942; Blackadder & Manderson, 1975; Muller et al, 1989).
    C) GARLIC BREATH
    1) WITH POISONING/EXPOSURE
    a) A garlic odor of breath and sweat and a metallic taste have been reported after exposure to tellurium and its compounds (Blackadder & Manderson, 1975; Muller et al, 1989).
    b) This odor may also be found in urine and feces, and is thought to be due to the metabolite dimethyl telluride (Steinberg et al, 1942; Muller et al, 1989).
    c) The metallic taste and garlicky odor may occur without ingestion (Clayton & Clayton, 1993).
    d) It has been suggested that the metallic taste caused by tellurium exposure may be due to salivary excretion (HSDB , 1991).
    D) CONSTIPATION
    1) WITH POISONING/EXPOSURE
    a) Constipation was noted in one patient who inhaled an unknown quantity of tellurious oxide (Steinberg et al, 1942).

Genitourinary

    3.10.1) SUMMARY
    A) Kidney damage has been reported in animals.
    3.10.2) CLINICAL EFFECTS
    A) DISORDER OF TESTIS
    1) WITH POISONING/EXPOSURE
    a) Ingestion of tellurium has resulted in black-colored testes in rats (Finkel, 1983).

Hematologic

    3.13.1) SUMMARY
    A) Hemolysis, reduced hemoglobin levels, or an increased MCV may be seen from exposure to tellurium compounds.
    3.13.2) CLINICAL EFFECTS
    A) INCREASED BLOOD ERYTHROCYTE VOLUME
    1) WITH POISONING/EXPOSURE
    a) ANTI-SICKLING - 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).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMOLYSIS
    a) Reduced hemoglobin levels and hemolysis have been reported in animal studies (Steinberg et al, 1942). This was especially true of hydrogen telluride (Finkel, 1983).

Dermatologic

    3.14.1) SUMMARY
    A) Tellurium hexafluoride is highly irritating to the skin and mucous membranes. Dermatitis and blue-black skin discoloration have been reported to occur from exposure to tellurium hexafluoride. Alopecia has been reported after ingestion of tellurium.
    3.14.2) CLINICAL EFFECTS
    A) DISCOLORATION OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Bluish-black discoloration of the skin in the webs of the fingers, and streaks on the neck and face, were noted in a single incident of acute exposure to tellurium hexafluoride (Blackadder & Manderson, 1975; ACGIH, 1991; Clayton & Clayton, 1993).
    B) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) In the same incident, dermatitis of a scaly, itchy type ensued. The dermatitis may have been due to reduction of sweating. In this case the exposure was thought to involve hydrogen telluride (Finkel, 1983).
    C) ALOPECIA
    1) WITH POISONING/EXPOSURE
    a) A 37-year-old female with tellurium intoxication developed loss of hair. Hair loss disappeared by eight weeks after evaluation and treatment with ascorbic acid 200 mg per day. New hair growth was noted to take a bright color (Muller et al, 1989).

Immunologic

    3.19.1) SUMMARY
    A) Tellurium may be an immunomodulator; it has stimulated production of interleukin-2 in vitro.
    3.19.2) CLINICAL EFFECTS
    A) DISORDER OF IMMUNE FUNCTION
    1) WITH POISONING/EXPOSURE
    a) IMMUNOMODULATION - The investigational immunomodulator AS-101, which is a tellurium compound, 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) TELLURIUM HEXAFLUORIDE - No studies were found on the possible reproductive effects of tellurium hexafluoride in humans at the time of this review; however, it is possible that such effects might be similar to those of TELLURIUM and FLUORIDE.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) TELLURIUM HEXAFLUORIDE - No studies were found on the possible reproductive effects of tellurium hexafluoride in humans at the time of this review; however, it is possible that such effects might be similar to those of TELLURIUM and FLUORIDE.
    2) Direct measurements showed that the fluoride ion passes into the fetal blood supply in humans and produced stronger teeth, but it was not clear whether or not birth defects were actually examined (Feltman & Kosel, 1961). Several epidemiological studies have found no correlation between the level of fluoride in drinking water (typically between 1 and 10 ppm) and birth defects (Knox, 1980; ERICKSON, 1976). In general, there appears to be no danger of osteosclerosis in the unborn even from high maternal exposure to fluoride, since this condition requires many years of high exposure to develop (Hodge & Macgregor, 1982).
    3) Fluoride at 8 ppm in the drinking water has been shown to have no effect on human reproduction (Hodge & Macgregor, 1982), while levels in the range of 12-18 ppm have rarely produced mottled deciduous (baby) teeth (Hodge & Macgregor, 1982).
    B) ANIMAL STUDIES
    1) TELLURIUM has produced a specific and characteristic hydrocephaly in rats from prenatal exposure (Barlow & Sullivan, 1982; Finkel, 1983; Garro & Pentschew, 1964; Agnew, 1968; Duckett, 1971). This hydrocephaly is not apparent until after birth and exposure to tellurium 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 rabbits (Garro & Pentschew, 1964).
    2) Skeletal malformations and delays in ossification were observed in the offspring of pregnant rats and rabbits given dietary tellurium 3,000 to 15,000 ppm for ten days. However, maternal toxicity was also seen at doses that had no effect on the fetuses (Johnson et al, 1988).
    3) In a study in which 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).
    a) 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).
    4) Fluoride has been tested in a variety of reproductive studies in experimental animals, generally at levels approximately 100 times higher than typical human intakes (Hodge & Smith, 1977). Sodium fluoride at 30 or 60 mg was embryotoxic to rats, at 10-66 mg/kg/2 months resulted in no conceptions in mice, and at 30 mg/kg/1 year reduced fertility and was embryotoxic in rabbits (Mandrik & Yakubovskaya, 1984).
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) Placental transfer does occur with tellurous acid in animals, but the transfer is slow. Animal studies have shown a high uptake in fetal brain tissue. Hydrocephalus has been noted in these studies (Barlow & Sullivan, 1982).
    2) FLUORIDE - Inorganic fluorides, in general, pose an enigma for evaluating potential human reproductive hazards. Fluoride seems to be required to some extent for normal human development, although its absolute requirement would be difficult to prove because of the ubiquitous presence of fluoride in the environment. The minimum daily requirement during pregnancy has been estimated to be 1.5 to 2 mg (GLENN, 1979).
    3) Sources of exposure to fluoride during pregnancy are food, occupation, and fluorine-containing anesthetics during labor and delivery. The latter source of exposure can be significant, achieving plasma levels approximately 20 times normal, but is of acute duration. There have been several reviews on reproductive issues of fluoride exposure (Stratmenn, 1979; Anon, 1967; Hodge & Macgregor, 1982).
    4) In general, fluoride metabolism is not affected by pregnancy (Maheshwari, 1981). The maternal level of fluoride in plasma decreases during pregnancy, presumably because the fetus extracts fluoride for normal development of bone and teeth (Hahijarvi, 1981). At low fluoride intake levels, the fetus concentrates fluoride (Gedalia et al, 1964), such that fetal plasma fluoride levels can exceed those of the mother by ten times (Louw & Van Wyk, 1984). Another study, however, found similar levels of plasma fluoride in maternal and cord blood (Teotia, 1979).
    5) A detailed analysis has concluded that a TLV level fluoride exposure presents no threat to pregnancy or the unborn (Hodge & Smith, 1977). Thus, at low levels, fluoride is beneficial; but, at high levels (which may vary from one individual to another, depending on other intrinsic and extrinsic factors), it can mottle the teeth of the offspring. Mottling of deciduous (baby) teeth is rare, and permanent skeletal abnormalities do not occur from prenatal exposure to fluoride, since the latter require many years of exposure (Hodge & Macgregor, 1982).
    a) However, fluoride at 8 ppm or greater in drinking water is known to cause mottled teeth if exposure occurs during the period of synthesis of the dental enamel (pre- and approximately 8 years post-birth) (Gedalia et al, 1964).
    6) Gynecological diseases, miscarriages, and problems with pregnancy were also reported (Danilov, 1975). An attempt was made to relate effects with specific levels of exposure, but the results are not available (Kuznetsova, 1969).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) Fluoride has been tested in a variety of reproductive studies in experimental animals, generally at levels approximately 100 times higher than typical human intakes (Hodge & Smith, 1977). Sodium fluoride at 30 or 60 mg was embryotoxic to rats, at 10-66 mg/kg/2 months resulted in no conceptions in mice, and at 30 mg/kg/1 year reduced fertility and was embryotoxic in rabbits (Mandrik & Yakubovskaya, 1984).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7783-80-4 (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) TELLURIUM HEXAFLUORIDE - No studies were found on the possible carcinogenic effects of tellurium hexafluoride in humans at the time of this review. Most information concerning tellurium compounds and sodium fluoride indicate that these substances are not clearly carcinogenic.
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECTS
    1) TELLURIUM compounds have not caused cancer in rats or mice (Friberg et al, 1986).

Genotoxicity

    A) TELLURIUM HEXAFLUORIDE - No studies were found on the possible genetic effects of tellurium hexafluoride in humans at the time of this review.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic levels of tellurium have been established. If there has been a significant exposure to tellurium hexafluoride, a chest x-ray may be necessary. Hematologic, liver, and kidney parameters should be monitored.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) No toxic levels of tellurium have been established.
    B) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, 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.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If there has been a significant exposure to tellurium hexafluoride, a chest x-ray may be necessary (Proctor et al, 1988).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic levels of tellurium have been established. If there has been a significant exposure to tellurium hexafluoride, a chest x-ray may be necessary. Hematologic, liver, and kidney parameters should be monitored.

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) SUPPORT
    1) Although there have been a significant number of adverse effects reported in animal studies, the actual number of serious overdoses with tellurium compounds is very small. Most cases have required either no treatment or simple supportive care. There is no specific antidote or chelator. Treatment should be directed at maintaining respirations and monitoring kidney, hematologic, and liver function.
    2) Although humans have experienced mild CNS depression, including dizziness, lethargy, and drowsiness, there has been none of the paralysis and tremors seen in severely poisoned animals. Nevertheless, severe CNS effects may be possible if exposures are high enough.
    B) 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).
    C) 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).
    D) CHELATION THERAPY
    1) There is no specific chelator which is effective for tellurium and its compounds.
    2) BAL - Although some early human cases were treated with BAL in oil, subsequent animal studies have found that BAL is of little value and may actually enhance toxicity (Amdur, 1958).
    3) ASCORBIC ACID - Oral vitamin C at doses up to 10 milligrams/kilogram/day has been suggested to treat the garlicky odor resulting from tellurium ingestion (DeMeio, 1947; Muller et al, 1989). Its effects are questionable, and its use should be limited to those cases where the odor presents a severe social problem (ITI, 1985).

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).
    6.8.2) TREATMENT
    A) OBSERVATION REGIMES
    1) Observe patient for signs of systemic effects and follow treatment recommendations in the DERMAL EXPOSURE section where appropriate.

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).
    6.9.2) TREATMENT
    A) SUPPORT
    1) Although there have been a significant number of adverse effects reported in animal studies, the actual number of serious overdoses with tellurium compounds is very small. Most cases have required either no treatment or simple supportive care. There is no specific antidote or chelator. Treatment should be directed at maintaining respirations and monitoring kidney, hematologic, and liver function.
    2) Although humans have experienced mild CNS depression, including dizziness, lethargy, and drowsiness, there has been none of the paralysis and tremors seen in severely poisoned animals. Nevertheless, severe CNS effects may be possible if exposures are high enough.
    B) 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).
    C) CHELATION THERAPY
    1) There is no specific chelator which is effective for tellurium and its compounds.
    2) BAL - Although some early human cases were treated with BAL in oil, subsequent animal studies have found that BAL is of little value and may actually enhance toxicity (Amdur, 1958).
    3) ASCORBIC ACID - Oral vitamin C at doses up to 10 milligrams/kilogram/day has been suggested to treat the garlicky odor resulting from tellurium ingestion (DeMeio, 1947; Muller et al, 1989). Its effects are questionable, and its use should be limited to those cases where the odor presents a severe social problem (ITI, 1985).

Range Of Toxicity

Summary

    A) As little as 0.5 mcg tellurium produced the garlicky odor for 30 hours, and 15 mg produced an effect for 279 days. Tellurium hexafluoride produced breathing difficulties in four species of animals exposed to 1 ppm for 1 hour, and 1 ppm for 4 hours was fatal. Tellurites and tellurates in 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.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Tellurites and tellurates in concentrations of 25 to 50 ppm placed in the diets of animals proved toxic. Elemental tellurium had only a slight effect on growth at 1500 ppm (ACGIH, 1991).
    2) As little as 0.5 microgram produced the garlicky odor for 30 hours. An estimated dose of 15 milligrams produced an effect for 279 days (Blackadder & Manderson, 1975; Steinberg et al, 1942).

Workplace Standards

    A) ACGIH TLV Values for CAS7783-80-4 (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 hexafluoride, as Te
    a) TLV:
    1) TLV-TWA: 0.02 ppm
    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): LRT irr
    d) Molecular Weight: 241.61
    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 CAS7783-80-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Tellurium hexafluoride
    2) REL:
    a) TWA: 0.02 ppm (0.2 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7783-80-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Tellurium hexafluoride, as Te
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Tellurium hexafluoride
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7783-80-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Tellurium hexafluoride (as Te)
    2) Table Z-1 for Tellurium hexafluoride (as Te):
    a) 8-hour TWA:
    1) ppm: 0.02
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.2
    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) Reference: RTECS, 1999

Physicochemical

Physical Characteristics

    A) Tellurium hexafluoride exists as a colorless gas at standard temperature and pressure. It is noncombustible and has a repulsive odor (ACGIH, 1991; Budavari, 1996).

Molecular Weight

    A) 241.59 (Budavari, 1996)

References

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