Testing Information

Testing Status of Agents at NTP

CAS Registry Number: 13494-80-9 Toxicity Effects

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Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 1

Names (NTP)

  • Tellurium
  • AURUM PARADOXUM

Human Toxicity Excerpts

  • ... EXPOSURE TO TELLURIUM FUME OCCURRED ... POURING ... TELLURIUM-COPPER ALLOY ... ONLY ... SYMPTOM ... GARLIC ODOR. TELLURIUM WAS PRESENT IN URINE IN AMT FROM 0.008 TO 0.106 MG/L. SKIN LESIONS ... DRY, SCALY ITCHING PATCHES & LOSS OF SWEAT FUNCTION ... . [Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969., p. 315]**PEER REVIEWED**
  • Tellurium is one of the rarest elements on earth. Intoxications are rare & almost exclusively occupationally exposed workers are affected. Only a few cases of non- occupational poisoning have been reported so far. Severe poisoning results in respiratory depression & circulatory collapse. After occupational exposure main symptoms & signs include loss of appetite, dryness of the mouth, suppression of sweating, a metallic taste in the mouth, & most notable, a sharp garlic odor of the breath, sweat & urine. [Muller R et al; Klin Wochenschr 67 (22): 1152-5 (1989)]**PEER REVIEWED**
  • THE GARLIC ODOR OF SWEAT WAS A GOOD INDICATOR OF THE ABSORPTION OF TELLURIUM. [COOPER WC; TELLURIUM 313-21 (1971)]**PEER REVIEWED**
  • Exposure of iron foundry workers to concns of 0.01 & 0.1 mg Te/cu m for 22 months produced mild GI distress, the characteristic garlic odor, dryness of the mouth, metallic taste, & somnolence. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 486]**PEER REVIEWED**
  • May cause irritation of the respiratory system & lead to bronchitis & pneumonia. /Tellurium (dust or fume)/ [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3068]**PEER REVIEWED**
  • The capability of some metal compounds for inducing micronuclei (MN) in human lymphocytes was studied. In this investigation, Al (III), Cd (II), Hg (II), Sb (V), Te (VI), and Tl (I) salts were considered. The FISH (fluorescence in situ hybridization) technique with a centromeric probe was coupled with the MN assay in binucleated cells in order to detect both centromere-positive MN (C+ MN) due to malsegregation phenomena and centromere-negative MN (C- MN) due to chromosome breakage. The blood of two young nonsmoking male donors was employed for all experiments. In both donors, all the tested metal compounds, with the exception of Tl(2)SO(4), showed a statistically significant increase of MN compared to controls, at least at one dose. FISH analysis revealed an increase in the fraction of C+ MN for Al, Cd, and Hg compounds ... . A different efficiency was observed for the different metal compounds, in particular, KSbO(3) and CH(3)HgCl, which were highly genotoxic, whereas the others showed minimal effects. [Migliore L et al; Environ Mol Mutagen 34 (4): 279-84 (1999)]**PEER REVIEWED**
  • EFFECTS: GARLIC ODOR OF BREATH, METALLIC TASTE, NAUSEA, LOSS OF APPETITE, LIVER INJURY. /TELLURIUM FUMES/ [Dreisbach, R.H. Handbook of Poisoning. 12th ed. Norwalk, CT: Appleton and Lange, 1987., p. 239]**PEER REVIEWED**

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Non-Human Toxicity Excerpts

  • ... IN CATS, CHRONIC POISONING ... INDUCED BY INJECTION OF OILY SUSPENSION OF METALLIC TELLURIUM SC OR IM, & ... FOUND AFTER 3 MO TO CAUSE DEGENERATIVE CHANGES IN GANGLION CELLS OF RETINA & IN BRAIN ... RETINAL GANGLION CELLS ... DEVELOPED HONEYCOMBED VACUOLAR DEGENERATION ... . [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 887]**PEER REVIEWED**
  • ... POISONING OF MONKEYS ... PRODUCED ENCEPHALOPATHY & CHANGES IN RETINAL GANGLION CELLS, OPTIC NERVES, OPTIC TRACTS, & IN LATERAL GENICULATE BODIES. NO DESCRIPTION ... PUBLISHED ON EFFECTS ON VISION OR ON RELATED CLINICAL OBSERVATIONS. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 887]**PEER REVIEWED**
  • BRAINS OF RATS TREATED ORALLY WITH 0.2 G TELLURIUM DAY FOR 2-6 MO SHOWED INCR IN LIPOFUSCIN PIGMENTS IN NEURONAL PARENCHYMA. [MIYOSHI K ET AL; FOLIA PSYCHIATR NEUROL JPN 31 (1): 111 (1977)]**PEER REVIEWED**
  • RATS FED 0.2 G/DAY TELLURIUM SHOWED BLACK BRAIN CAUSED BY DARK TELLURIUM PARTICLES LOCALIZED IN LIPOFUSCIN GRANULES IN NEURON CYTOPLASM THROUGHOUT BRAIN, PROBABLY DUE TO EFFECTS OF TELLURIUM ON BRAIN MITOCHONDRIA. [DUCKETT S ET AL; BRAIN RES 73 (2): 205 (1974)]**PEER REVIEWED**
  • ELEMENTAL TELLURIUM FED TO GESTATING MAMMALS RESULTS IN HYDROCEPHALUS IN OFFSPRING. TELLURIUM REACHES FETAL BRAIN, INJURES EPENDYMAL CELLS, PRESUMABLY CSF-EPENDYMAL BARRIER, & POSSIBLY RESULTS IN DIMINUTION OF NEURAL CELLS. [DUCKETT S; ANN NY ACAD SCI 192: 220 (1972)]**PEER REVIEWED**
  • AFTER EXPOSURE TO 3300 PPM TELLURIUM IN DIET FOR 5 MO, RATS WERE MARKEDLY IMPAIRED IN ABILITY TO LEARN SEQUENCE OF BEHAVIORAL TASKS. [DRU D ET AL; PSYCHOPHARMACOLOGIA 24 (4): 508 (1972)]**PEER REVIEWED**
  • IM INJECTION OF METALLIC TELLURIUM (13 MG/KG) INTO RATS ON DAY 9 & 10 OF GESTATION PRODUCED HYDROCEPHALUS IN EMBRYOS. [AGNEW WF ET AL; EXPERIENTIA 28 (12): 1444 (1972)]**PEER REVIEWED**
  • TELLURIUM ENHANCED REDN OF METHEMOGLOBIN IN INTACT RAT ERYTHROCYTES. [IWATA H ET AL; EXPERIENTIA 33 (5): 678 (1977)]**PEER REVIEWED**
  • FEEDING OF ELEMENTAL TELLURIUM TO WEANLING RATS <3 WK OF AGE RESULTED IN PARALYSIS FROM SEGMENTAL DEMYELINATION OF SCIATIC NERVES & SPINAL ROOTS. RECOVERY FROM PARALYSIS & REMYELINATION OCCURRED DESPITE CONTINUED INGESTION OF TELLURIUM. [LAMPERT P ET AL; ACTA NEUROPATHOL 15 (4): 308 (1970)]**PEER REVIEWED**
  • ... NORMOCHROMIC, POSSIBLY HEMOLYTIC, ANEMIA /WAS REPORTED/ IN RATS EXPOSED TO TELLURIUM DIOXIDE & ELEMENTAL TELLURIUM AEROSOL (50-100 MG/CU M, 2 HR DAILY, 13-15 WK) INDICATED BY DOSE-RELATED REDUCTIONS IN HEMOGLOBIN & ERYTHROCYTES, & HEMATURIA. [Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. 541]**PEER REVIEWED**
  • The temporal relationships of blood nerve barrier breakdown, to metabolic & morphological changes in tellurium neuropathy were investigated in rats. 20 day old male Long Evans rats were fed diets containing 0 or 1.3% tellurium. Animals were observed for clinical signs of toxicity & were killed 12, 24, 48, 72, or 96 hr after starting the diet. The sciatic nerves were moved & examined for permeability of blood nerve barrier & cholesterol synthesis inhibition. Animals were injected iv with (125)iodine labeled albumin & horseradish peroxidase 24 hr before death. The effect of tellurium on the blood nerve barrier & the blood brain barrier was assessed by measuring uptake of (125)iodine & horseradish peroxidase. Sciatic nerve segments were incubated with (14)C labeled acetate & squalene to assess the effect on cholesterol synthesis. Other sciatic nerves were sectioned & examined for histopathological changes. Tellurium treated rats developed a garlic odor within 48 hr & usually developed hind-limb paresis within 72 hr. Exposed animals also gained less weight than controls. Progressive incrs in blood nerve barrier permeability occurred between 24 & 72 hr in rats given tellurium. The blood brain barrier was not affected by tellurium. Tellurium induced increased numbers of intracytoplasmic lipid droplets, intracytoplasmic membrane delimited clear vacuoles, & cytoplasmic excrescences within myelinating Schwann cells after 24 hr, axon demyelination after 48 hr, & endoneurial edema after 72 hr. Cholesterol synthesis was sharply inhibited after 12 hr. Squalene began accumulating in sciatic nerve segments at that time. /It was concluded/ that the initial Schwann cell injury seen in tellurium neuropathy may be due to factors other than blood nerve barrier breakdown & vasogenic endoneurial edema. Breakdown of the blood nerve barrier could have a synergistic effect on tellurium induced Schwann cell injury. [Bouldin TW et al; Neurotoxicology 10 (1): 79-89 (1989)]**PEER REVIEWED**
  • Exposure of weanling rats to a diet containing elemental tellurium results in a peripheral neuropathy characterized by segmental demyelination & minimal axonal degeneration. One of the earliest ultrastructural abnormalities in tellurium neuropathy is an increased number of cytoplasmic lipid droplets in myelinating Schwann cells. The pathogenesis of these lipid droplets was investigated using light & electron microscopic autoradiography. Nerve lipids were either "prelabeled" with (3)H acetate via in vivo intraneural injection 3 days before a 2 day exposure to tellurium, or "postlabeled" via in vivo intraneural injection or in vitro incubation with (3)H acetate following a 2 day exposure to tellurium. In the prelabeled nerves, myelin became heavily labeled, but the tellurium induced cytoplasmic lipid droplets were rarely labeled. In the postlabeled nerves, the tellurium induced cytoplasmic lipid droplets were the most heavily labeled structures within the nerve. These data indicate that the tellurium induced lipid droplets in Schwann cells are derived from newly synthesized lipid rather than from the early breakdown & internalization of myelin lipids. The earliest biochemical abnormality observed in tellurium neuropathy is an inhibition of cholesterol synthesis at the squalene epoxidase step. This leads to an accumulation of sequalene within the nerve. [Goodrum JF; J Neurochem 55 (6): 1928-32 (1990)]**PEER REVIEWED**
  • The signs of systemic toxicity of tellurium & its cmpd observed in acute & subacute studies incl listlessness, decr locomotor activity, somnolence, anorexia, loss of wt, & GI disturbances; changes in fur, & occasionally, epilation & paralysis of hind legs were noticed in rats. /Tellurium and its compounds/ [Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V2 540]**PEER REVIEWED**
  • Tellurium compounds are more toxic than the metal. Admin to pregnant rats of 500-3000 ppm tellurium in the diet resulted in high incidence of hydrocephalic offspring. Weaning rats fed elemental tellurium at a level of 1% (10,000 ppm) in the diet developed a neuropathy characterized by segmental demyelination; remyelination & functional recovery occurred despite continued admin of tellurium. /Tellurium and its compounds/ [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. ]**PEER REVIEWED**
  • Neonatal rats were exposed to tellurium, via the mother's milk, from the day of birth until sacrifice at 7, 14, 21, & 28 days of age. Light & electron microscopy revealed Schwann cell & myelin degeneration in the sciatic nerves at each age studied. ... In the CNS, hypomyelination of the optic nerves was demonstrated at 14, 21, & 28 days of age. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 486]**PEER REVIEWED**
  • In animals, repeated admin by the oral route has produced kidney & nerve damage in several species. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 486]**PEER REVIEWED**
  • Acute oral parenteral tellurium intoxication in animals resulted in restlessness, tremor, diminished reflexes, paralysis, convulsions, somnolence, coma, & death. Hematuria was prompt & occurred in all animals. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1489]**PEER REVIEWED**
  • Weanling rats fed elemental tellurium at 10,000 ppm in the diet developed neuropathy characterized by segment demyelination & remyelination; it is noteworthy that functional recovery occurred despite continual admin of tellurium. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1489]**PEER REVIEWED**
  • The capability of each of six trace elements added to a complete commercial ration to induce lesions of selenium vitamin-E deficiency in pigs was investigated. Forty two weanling pigs were fed for 10 weeks with a commercial ration adequate in selenium and vitamin-E, either alone or with supplements of silver, 3,000 mg/kg of feed, 500 mg/kg cobalt, 500 mg/kg tellurium , zinc 3,000 mg/kg, 500 mg/kg cadmium, or 200 mg/kg vanadium. Pigs were autopsied at death or after 10 weeks. The target organs of selenium/vitamin-E deficiency, liver, heart, and skeletal muscles, were especially examined for lesions and samples were histopathologically examined. Concentrations of blood glutathione-peroxidase and hepatic selenium were measured. Feed ingestion and body weight gains were reduced in all but control and zinc added animals. Silver fed pigs had high hepatic selenium concentrations; blood glutathione-peroxidase concentrations were significantly decreased for several weeks before death. Tellurium also markedly decreased blood glutathione-peroxidase activity after 4 weeks. Glutathione-peroxidase or hepatic selenium concentrations were not altered with other trace elements. Microscopically detected necrosis of cardiac and skeletal muscle was present in 50 to 65 percent of pigs fed cobalt or tellurium supplements. The authors conclude that characteristic lesions of selenium/vitamin-E deficiency are produced in pigs fed silver, cobalt, and tellurium and, at lower frequency, by added cadmium, vanadium, and tellurium. [Van Vleet JF et al; American Journal of Veterinary Research 42 (5): 789-799 (1981)]**PEER REVIEWED**
  • The tissue response to tellurium and tellurium-dioxide particulates retained in rat lungs following endotracheal introduction was studied. Male Harlan Wistar derived albino rats were administered single endotracheal injections of tellurium, tellurium-dioxide, or sodium-chloride, and were sacrificed 180 days later. Mean body weights of the treated rats were depressed in comparison to controls. Micropathological investigations revealed no difference in the lung tissue of the control and treated rats, except for those resulting from expected defensive mechanisms against any foreign material in the lungs. Black deposits were observed in the lung tissue of treated rats, indicating an inability of the clearance mechanisms of the lungs to remove all of the injected particulates within the 180 day study period. No evidence of a fibrotic tissue response was observed. Many internal organs of the rats treated with tellurium and tellurium-dioxide had a bluish tint, however, this discoloration was not accompanied by specific lesions. The 180 day study period was an insufficient time period to draw any conclusions regarding the absence of tumorigenic potential of these compounds. [Geary DL Jr et al; American Industrial Hygiene Association Journal 39 (2): 100-109 (1978)]**PEER REVIEWED**
  • The tissue response to tellurium and tellurium-dioxide particulates retained in rat lungs following endotracheal introduction was studied. Male Harlan Wistar derived albino rats were administered single endotracheal injections of tellurium, tellurium-dioxide, or sodium-chloride, and were sacrificed 180 days later. Mean body weights of the treated rats were depressed in comparison to controls. Micropathological investigations revealed no difference in the lung tissue of the control and treated rats, except for those resulting from expected defensive mechanisms against any foreign material in the lungs. Black deposits were observed in the lung tissue of treated rats, indicating an inability of the clearance mechanisms of the lungs to remove all of the injected particulates within the 180 day study period. No evidence of a fibrotic tissue response was observed. Many internal organs of the rats treated with tellurium and tellurium-dioxide had a bluish tint, however, this discoloration was not accompanied by specific lesions. The 180 day study period was an insufficient time period to draw any conclusions regarding the absence of tumorigenic potential of these compounds. [Geary DL Jr et al; American Industrial Hygiene Association Journal 39 (2): 100-109 (1978)]**PEER REVIEWED**
  • The peroxidation related effects of tellurium on the brain were studied in rats. Fifteen male Wistar-rats were given drinking water containing tellurium-tetrachloride at a concentration of 100 milligrams per liter. Control rats were given tap water. Rats were killed in groups of five after 7, 21, or 35 days of exposure. Blood, liver, kidney, and brain samples were analyzed for tellurium. Following preparation by acid treatment, analysis was performed by atomic absorption spectrophotometry. The left cerebral hemispheres were analyzed for glutathione, succinic-dehydrogenase, and creatine-kinase activities. Control animals showed a very low tellurium burden, whereas exposed rats accumulated relatively high concentrations. Blood had the highest tellurium concentrations, with an increasing trend according to the exposure period. Liver also showed a rapid increase, while the kidneys and brain had a continuous accumulation. Appreciable neurochemical effects were seen after the brain content exceeded 2 nanomoles per gram. Succinic-dehydrogenase activity was above the control range after 21 days, while creatine-kinase activity decreased or remained stable. Brain glutathione content was above the control range at 35 days, possibly as a result of attempts to counteract peroxidative effects associated with mitochondrial damage. The initially low uptake of tellurium in the brain may have been due to a blood/brain barrier. Once incorporated into the nervous system, accumulation apparently occurred because of the long half life of tellurium. [Valkonen S Bulletin of Environmental Contamination and Toxicology 34 (2): 170-174 (1985)]**PEER REVIEWED**
  • The developmental toxicity of tellurium was evaluated in Crl Sprague-Dawley rats and New Zealand white rabbits by means of standard segment II-type studies. Groups of pregnant rats were fed a diet containing 0, 30, 300, 3000, or 15,000 ppm of tellurium on Days 6 through 15 of gestation (microscopic detection of sperm in a smear of vaginal contents considered as Day 0), and artificially inseminated rabbits were fed a diet containing 0, 17.5, 175, 1750, and 5250 ppm of tellurium during Days 6 through 18 of gestation (day of insemination considered as Day 0). Signs of maternal toxicity were observed during the treatment period in a statistically significant and dose-related manner at dietary concentrations of 300 ppm and greater in rats and 1750 ppm and greater in rabbits. Exposure of these pregnant rats and rabbits to tellurium had no effect upon reproduction as measured by pregnancy rate, litter size, dead or resorbed implantations, or fetal sex ratio. Both skeletal (primarily skeletal maturational delays) and soft tissue malformations (primarily hydrocephalus) were noted in the offspring of pregnant rats exposed to the highest levels (3000 and 15,000 ppm) of tellurium. Rabbit fetuses of the highest dosage group (5250 ppm) had a slightly elevated evidence of skeletal delays and nonspecific abnormalities. Since maternal toxicity was observed at dosages that did not affect the developing conceptus, there were no indications of unique developmental susceptibility upon exposure of pregnant rats or rabbits to tellurium. [Johnson EM et al; Fundam Appl Toxicol 11 (4): 691-702 (1988)]**PEER REVIEWED**
  • The developmental toxicity of tellurium was evaluated in Crl Sprague-Dawley rats and New Zealand white rabbits by means of standard segment II-type studies. Groups of pregnant rats were fed a diet containing 0, 30, 300, 3000, or 15,000 ppm of tellurium on Days 6 through 15 of gestation (microscopic detection of sperm in a smear of vaginal contents considered as Day 0), and artificially inseminated rabbits were fed a diet containing 0, 17.5, 175, 1750, and 5250 ppm of tellurium during Days 6 through 18 of gestation (day of insemination considered as Day 0). Signs of maternal toxicity were observed during the treatment period in a statistically significant and dose-related manner at dietary concentrations of 300 ppm and greater in rats and 1750 ppm and greater in rabbits. Exposure of these pregnant rats and rabbits to tellurium had no effect upon reproduction as measured by pregnancy rate, litter size, dead or resorbed implantations, or fetal sex ratio. Both skeletal (primarily skeletal maturational delays) and soft tissue malformations (primarily hydrocephalus) were noted in the offspring of pregnant rats exposed to the highest levels (3000 and 15,000 ppm) of tellurium. Rabbit fetuses of the highest dosage group (5250 ppm) had a slightly elevated evidence of skeletal delays and nonspecific abnormalities. Since maternal toxicity was observed at dosages that did not affect the developing conceptus, there were no indications of unique developmental susceptibility upon exposure of pregnant rats or rabbits to tellurium. [Johnson EM et al; Fundam Appl Toxicol 11 (4): 691-702 (1988)]**PEER REVIEWED**
  • We present a cytological, immunocytochemical, and biochemical study of the cell death of mature myelinating Schwann cells (SCs) in the primary demyelinating neuropathy induced by tellurium (Te). Weaned rats were fed a diet containing 1.1% elemental Te. The animals were killed daily within the first week of Te diet. After 4 to 6 days of Te treatment some SCs underwent degeneration and necrosis. By electron microscopy analysis, degenerating SCs showed chromatin condensation, detachment from the nuclear envelope of condensed chromatin clumps, aggregation of interchromatin granule clusters, formation of intranuclear bundles of microfilaments, and cytoplasmic vesiculation. By confocal laser fluorescence microscopy, chromatin regions were stained with the TUNEL method for in situ labeling of DNA fragmentation and exhibited a progressive reduction of histone signal. In addition, splicing small nuclear ribonucleoprotein (snRNP) factors were redistributed in a few large nuclear domains and bright foci of intranuclear actin were observed. DNA electrophoresis revealed a smear pattern of DNA fragmentation in sciatic nerve samples from Te-treated animals. Upon Te treatment, no degradation of the caspase substrates poly (ADP-ribose) polymerase and lamin B was detected by Western blots or immunocytochemistry, respectively. The peculiar structural rearrangement of the transcription and splicing machinery as well as the vesicular degeneration of the cytoplasm in degenerating SCs support an autophagic cell death of the necrotic type. Unlike the apoptosis of pre-remyelinating SCs, this caspase independent cell death of necrotic type involves mature pre-demyelinating SCs and eliminates SCs injured by the neurotoxic effect of Te. [Berciano MT et al; J Neuropathol Exp Neurol 58 (12): 1234-43 (1999)]**PEER REVIEWED**
  • A diet containing 1.25% elemental tellurium (Te) when fed to rats in week 3 of life produces acute peripheral nervous system (PNS) demyelination. The purpose of this investigation was to determine whether Te has the same neurotoxic effect on Schwann cells and their associated myelin when located within the spinal cord. Schwann cells were induced into the CNS by irradiating the lumbosacral spinal cord of 3 day-old rats with 4000 rads of soft X-rays ... . At 22-28 days of age, a diet containing 1.25% Te was fed to half of these rats, and others were fed on rat chow alone. Non-irradiated rats of the same age were divided into two similarly fed groups. At intervals from 2 to 15 days after the initiation of this diet, the rats were perfused and the irradiated portion of the cord, or comparable level in non-irradiated rats, ... and processed for light and electron microscopy and immunocytochemistry. All rats fed Te became paretic by 6-7 days, and diffuse demyelination with obvious degenerative changes in Schwann cells was seen in the nerve roots. Immunocytochemical localization of Schwann cells and peripheral myelin in the spinal cord was demonstrated using Po antiserum, and in these areas the reduction of astrocytes and their processes was shown using sections incubated with GFAP antiserum. In these areas, as in the roots, there was myelin lamellar separation, and many Schwann cells contained cytoplasmic vacuoles, hypertrophied lysosomal structures and myelin debris. Adjacent oligodendrocytes and CNS myelin were apparently unaffected, confirming a differential susceptibility of oligodendrocytes and Schwann cells. There were no Schwann cell abnormalities in the non Te-fed irradiated rats. This experimental model provides a situation in which other neurotoxic compounds can be evaluated to compare their effects on CNS and PNS myelin. [Hammang JP et al; Neuropathol Appl Neurobiol 12 (4): 359-70 (1986)]**PEER REVIEWED**
  • Accumulation of squalene in the CNS is observed after administration of tellurium and squalene has been proposed to be a mediator of tellurium encephaloneuropathy. The aim of this study was to investigate the effects of squalene on the central and peripheral nervous systems in rat at the ultrastructural level. ... These alterations differ in some aspects (changes in endothelia, accumulation of lipid-like material) from the known features of tellurium encephaloneuropathy. [Gajkowska B; Exp Toxicol Pathol 51 (1): 75-80 (1999)]**PEER REVIEWED**
  • Rats fed a diet containing 1.25% elemental tellurium initiated on postnatal day 20 undergo a transient neuropathy characterized by synchronous demyelination of peripheral nerves. In sciatic nerve, the extent of demyelination was maximal after 5 days of tellurium exposure; there was a loss of 25% of the myelin, as assayed by concentration of myelin-specific P0 protein. Tellurium-induced alterations in the metabolic capacity of Schwann cells were examined by measuring the synthesis of myelin lipids in vitro in isolated sciatic nerve segments. Exposure to tellurium resulted in an early marked decrease of approximately 50% in overall incorporation of [14C]acetate into lipids, with a preferential depression in synthesis of cerebrosides, cholesterol, and ethanolamine plasmalogens (components enriched in myelin). Most dramatically, within 1 day of initiation of tellurium exposure, there was a profound increase in [14C]acetate-derived radioactivity in squalene; 23% of incorporated label was in this intermediate of cholesterol biosynthesis, compared to less than 0.5% in controls. In association with the remyelinating phase seen after 5 days of tellurium exposure, synthesis of myelin components gradually returned to normal levels. After 30 days, metabolic and morphologic alterations were no longer apparent. ... The sequence of metabolic events in sciatic nerve following tellurium treatment initially involves inhibition of the conversion of squalene to 2,3-epoxysqualene, and that this block in the cholesterol biosynthesis pathway results, either directly or indirectly, in the inhibition of the synthesis of myelin components and breakdown of myelin.[Harry GJ et al; J Neurochem 52 (3): 938-45 (1989)]**PEER REVIEWED**
  • Neonatal rats were exposed to Tellurium (Te), via the mother's milk, from the day of birth until sacrifice at 7, 14, 21, and 28 days of age. Light and electron microscopy revealed Schwann cell and myelin degeneration in the sciatic nerves at each age studied. These changes were similar to those described in weanling rats as a result of Te intoxication. In the CNS, hypomyelination of the optic nerves was convincingly demonstrated at 14, 21, and 28 days of age, accompanied by some evidence of myelin degeneration. These changes were also seen in the ventral columns of the cervical spinal cords, although less markedly, and were confirmed by quantitative methods. There was little evidence of oligodendrocyte pathology in the CNS, and it appears that degeneration of these cells is not the primary cause of the CNS hypomyelination, in contrast to the PNS where Schwann cell degeneration has been shown to precede the myelin pathology. [Jackson JP et al; Acta Neuropathol (Berl) 78 (3): 301-9 (1989)]**PEER REVIEWED**
  • An equal amount (per weight) of 127m tellurium (Te) was injected IP into weanling and adult rats, some intoxicated with a diet containing Te, others not. The young intoxicated rats presented a segmental demyelination of the sciatic nerve and paralysis of the hind limbs; the adult intoxicated rats did not. Quantitation of 127m Te in nervous and other tissues was done with a gamma counter. Correlative morphological examination of the nervous tissues was done with light and electron microscopy. This study shows that Te crosses the vascular wall without injuring endothelial cells and invades the surrounding sciatic nerve parenchyma following administration of 127 m Te to a weanling or adult rat. However, Te damages the endothelium, crosses the vascular wall of endo and perineurial vessels in weanling rats, causes a perivascular edema, cytoplasmic anomalies in the Schwann cells, destruction of myelin and apparently invades axones--according to autoradiographic studies--following the administration of 127 m Te plus the Te-diet. It is concluded that Te penetrates more quickly and in larger amounts the walls of blood vessels in the sciatic nerve of weanling rats intoxicated with Te, than the same nerve in the other weanling and adults rats. Te in the amounts indicated here penetrates the parenchyma of the CNS but apparently does not cause injury. [Duckett S; Neurotoxicology 3 (3): 63-73 (1983)]**PEER REVIEWED**
  • A compound may be "developmentally neurotoxic" because it interferes with a metabolic step exclusively or preferentially expressed during development in a particular class of neural cells. The initial metabolic specificity is often complicated by: (1) secondary responses in the affected cells, (2) involvement of other functionally-related cell types, and (3) the presence of compensatory and/or regenerative responses. In this context we study tellurium, which systemically blocks cholesterol biosynthesis at the squalene epoxidase step. Because of the high demand in developing peripheral nerves for newly synthesized cholesterol required for myelin assembly, this metabolic block leads to demyelination of the sciatic nerve. This insult is confounded by the fact that the myelin-forming Schwann cells do not upregulate their cholesterol biosynthetic pathway. This is contrary to expectations; liver (the main source of cholesterol for many tissues outside the nervous system) upregulates synthesis of cholesterol and overcomes the metabolic block. The shortage of cholesterol in Schwann cells results in an immediate secondary response down-regulation of steady-state mRNA levels for specific myelin proteins. Remyelination occurs after cessation of tellurium exposure. This model of primary demyelination allows study of Schwann-cell specific responses during the processes of myelin breakdown and subsequent steps leading to remyelination, without the complications of axonal degeneration and regeneration. Because tellurium specifically blocks the synthesis of a major required membrane component, it is also well suited for examining the coordinate control of membrane synthesis and assembly at the genomic level. [Morell P et al; Neurotoxicology 15 (1): 171-80 (1994)]**PEER REVIEWED**
  • We have used an experimental model of tellurium(Te)-induced demyelinating neuropathy in the rat to study cellular mechanisms involved in regulating Schwann cell (SC) numbers during remyelination. Starting at postnatal day 21, weaned rats were fed a diet containing 1.1% elemental Te. Following 7 days of Te treatment and at several time points of post-tellurium treatment (PTe), the animals were processed for ultrastructural analysis, SC nuclei quantification and teased fibre preparations. It is well-established that Te induces a transient demyelinating/remyelinating sequence in sciatic nerves. The loss of the myelin sheath in this neuropathy produces active proliferation and overproduction of immature SCs. By electron microscopy analysis most mitotic SCs were located along demyelinated segments. Quantitative determination of SC nuclei per transverse section of sciatic nerve revealed a dramatic increase of SCs at 2 days PTe relative to control nerves. The number of SC nuclei then decreased progressively during the long-term period of recovery studied (330 days PTe). In Te-treated rats, SCs undergoing cell death were regularly found within the nerve fibre compartment, especially on demyelinated segments. Dying cells exhibited morphological features of apoptosis and appeared enclosed by lamellar processes of adjacent healthy SCs in extracellular compartments. Both healthy immature SCs and endoneurial macrophages were involved in the phagocytosis of apoptotic SCs. Particularly during remyelination, supernumerary endoneurial SCs were observed surrounding myelinated fibres. These cells progressively became atrophic with a morphological phenotype similar so that of "onion bulb" cells. On the other hand, teased fibre measurements revealed a remarkable permanent internodal shortening in remyelinated fibres from Te-treated sciatic nerves. These results indicate that a portion of redundant immature SCs are susceptible to elimination by apoptosis. However, other distinct biological mechanisms such as the persistence of supernumerary SCs in the endoneurium and the shortening of internodal lengths are also involved in regulating SC numbers during the remyelination stage. [Berciano MT et al; Acta Neuropathol (Berl) 95 (3): 269-79 (1998)]**PEER REVIEWED**
  • The anatomical distribution and organization of the peripheral nervous system as well as its frequent ability to reflect neurotoxic injury make it useful for the study of nerve fiber and ganglionic lesions. Contemporary neuropathologic techniques provide sections with excellent light-microscopic resolution for use in making such assessments. The histopathologist examining such peripheral nerve samples may see several patterns of neurotoxic injury. Most common are axonopathies, conditions in which axonal alterations are noted; these axonopathies often progress toward the Wallerian-like degeneration of affected fibers. These are usually more severe in distal regions of the neurite, and they affect both peripheral and central fibers. Examples of such distal axonopathies are organophosphorous ester-induced delayed neuropathy, hexacarbon neuropathy, and p-bromophenylacetylurea intoxication. These axonopathies may have varying pathologic features and sometimes have incompletely understood toxic mechanisms. In such neuropathies with fiber degeneration, peripheral nerve axons may regenerate, which can complicate pathologic interpretation of neurotoxicity. On occasion neurotoxins elicit more severe injury in proximal regions of the fiber. Axonal pathology is also a feature of the neuronopathies, toxic states in which the primary injuries are found in neuronal cell bodies. This is exemplified by pyridoxine neurotoxicity, where there is sublethal or lethal damage to larger cytons in the sensory ganglia, with failure of such neurons to maintain their axons. Lastly, one may encounter myelinopathies, conditions in which the toxic effect is on the myelin-forming cell or sheath. An example of this is tellurium intoxication, where demyelination noted in young animals is coincident with toxin-induced interference of cholesterol synthesis by Schwann cells. In this paper, the above-noted examples of toxic neuropathy are discussed, with emphasis on mechanistic and morphologic considerations. [Jortner BS; Toxicol Pathol 28 (1): 54-69 (2000)]**PEER REVIEWED**
  • Tellurium compounds are more toxic than the metal. Admin to pregnant rats of 500-3000 ppm tellurium in the diet resulted in high incidence of hydrocephalic offspring. Weaning rats fed elemental tellurium at a level of 1% (10,000 ppm) in the diet developed a neuropathy characterized by segmental demyelination; remyelination & functional recovery occurred despite continued admin of tellurium. /Tellurium and its compounds/ [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. ]**PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LD50 Rat oral 83 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3068]**PEER REVIEWED**
  • LD50 Mouse oral 20 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3068]**PEER REVIEWED**
  • LD50 Rabbit oral 67 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3068]**PEER REVIEWED**
  • LD50 Guinea pig oral 45 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3068]**PEER REVIEWED**

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Absorption, Distribution and Excretion

  • In the nervous system, tellurium accumulates in the gray matter, not the white matter, when injected intracerebrally. The metal is found in phagocytic & ependymal cells & in lysosomes as fine needles. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 486]**PEER REVIEWED**
  • Elemental tellurium is poorly absorbed. ... Soluble tellurium can be absorbed through the skin, although ingestion or inhalation of fumes presents the greatest industrial hazard. A metallic taste in the mouth may result from excessive absorption. The characteristic sign of absorption is the garlic-like odor ... in the breath & sweat. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 486]**PEER REVIEWED**
  • Urinary, fecal, & biliary excretion also occur. Urinary excretion is probably more important than respiratory excretion in eliminating absorbed tellurium. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 485]**PEER REVIEWED**
  • EXCRETION BY BREATH ... IS NOT ... IMPORTANT CHANNEL. ... EXCRETION IN SALIVA ... SUGGESTED ... AS EXPLANATION OF METALLIC TASTE IN MOUTH ... . [Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969., p. 311]**PEER REVIEWED**
  • IN NERVOUS SYSTEM, TELLURIUM METAL ACCUMULATES IN GRAY MATTER ... NOT IN WHITE MATTER. WHEN INJECTED INTRACEREBRALLY, METAL IS LOCALIZED IN PHAGOCYTIC & EPENDYMAL CELLS. WHEN FED TO ANIMALS METAL ... IN LYSOSOMES AS FINE NEEDLES ... AMORPHOUS MATERIAL IN ENDOTHELIAL & GLIAL CELLS. [Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972., p. 199]**PEER REVIEWED**
  • GARLIC ODOR OF BREATH & SWEAT WERE GOOD INDICATORS OF ABSORPTION OF TELLURIUM. [COOPER WC; TELLURIUM: 313 (1971)]**PEER REVIEWED**
  • IN THE BLOOD, TELLURIUM IS COMPLEXED TO THE PLASMA PROTEINS, & VERY LITTLE ENTERS THE ERYTHROCYTES. [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978., p. 246]**PEER REVIEWED**
  • Tellurium is only slowly metabolized, & it is eliminated as methyl telluride in urine, sweat, & expired air. Tellurium concentrated in the liver, spleen, & kidney. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1489]**PEER REVIEWED**
  • Tellurium (Te) demonstrates properties similar to those of elements known to be toxic to humans, ... . It is relevant, therefore, to consider the tellurium physiology, toxicity, and methods for monitoring the element in biological and environmental specimens. Animal studies suggest that up to 25% of orally administered tellurium is absorbed in the gut. There is a biphasic elimination from the circulation with loss of about 50% within a short period, t1/2 = 0.81 d, and slower elimination of the residual Te, t1/2 = 12.9 d. Following a single ip, injection the largest proportion is in the kidney and bone, but with repeated oral administration, Te is found in the heart > > kidney, spleen, bone, and lung. Formation of dimethyl telluride is a characteristic feature of exposure, and gives a pungent garlic-like odor to breath, excreta, and the viscera. The main target sites for Te toxicity are the kidney, nervous system, skin, and the fetus (hydrocephalus). Te can be reliable measured in different specimens by several analytical techniques. Recent work has employed hydride generation atomic absorption spectrometry. [Taylor A; Biol Trace Elem Res 55 (3): 231-9 (1996)]**PEER REVIEWED**

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Metabolism/Metabolites

  • A very small amt of tellurium is exhaled (about 0.1%) presumably as dimethyltelluride ... in animals and man after exposure to elemental tellurium and tellurium(IV) cmpd. /Elemental tellurium & tellurium(IV) compounds/ [Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier Science Publishers B.V., 1986., p. V2 538]**PEER REVIEWED**

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TSCA Test Submissions

  • None found

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Footnotes

1 Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.

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Web page last updated on May 14, 2008