UKPID MONOGRAPH
TELLURIUM
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service
(Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
This monograph has been produced by staff of a National Poisons
Information Service Centre in the United Kingdom. The work was
commissioned and funded by the UK Departments of Health, and was
designed as a source of detailed information for use by poisons
information centres.
Peer review group: Directors of the UK National Poisons Information
Service.
TELLURIUM
Toxbase summary
Type of product
Tellurium and its compounds are industrial chemicals used in metal
alloys, "daylight lamps" and the electronics industry.
Toxicity
Acute poisoning is rare. Two men died after 2g sodium tellurite was
mistakenly injected during retrograde pyelography (Keall et al, 1946).
Exposure may occur occupationally, particularly during the production
of metal alloys and electrolytic copper refining.
Features
Topical
- Irritant to skin and eyes.
- May cause dermal discolouration.
Inhalation
- A garlic odour to the breath, sweat and urine is
characteristic of tellurium exposure.
- A metallic taste, nausea, loss of appetite, tiredness,
reduced sweating and unspecified ECG changes have been
reported.
- May cause respiratory tract irritation, although reports of
significant pulmonary toxicity are rare.
Ingestion
- A garlic odour of the breath, sweat, urine and faeces is
characteristic of tellurium exposure.
- Initial symptoms of nausea, vomiting and a metallic taste
develop within hours.
- Fever, hair loss, weight loss and fatigue may occur days to
weeks after substantial ingestion.
Injection
- A garlic odour of the breath and body secretions is
characteristic after systemic administration of tellurium.
- Loin pain, nausea, vomiting, confusion, dyspnoea and
cyanosis occurred in two patients following accidental
intraureteric injection of 2g sodium tellurite; both died
(Keall et al, 1946).
Management
Dermal
1. If possible the patient should remove soiled clothing and wash
him/herself.
2. Wash contaminated hair and skin with soap and copious amounts of
water.
3. Pay special attention to skin folds, fingernails and ears.
Ocular
1. Immediately irrigate the affected eye thoroughly with tepid water
or 0.9% saline for at least 10-15 minutes.
2. Any particles lodged in the conjunctival recesses should be
removed.
3. Continue irrigation with saline infusion using drip tubing.
4. Repeated instillation of local anaesthetic may reduce discomfort
and help more thorough decontamination.
5. Corneal damage may be detected by instillation of fluorescein.
6. Patients with corneal damage and those whose symptoms do not
resolve rapidly should be referred for ophthalmological
assessment.
Ingestion
Minor ingestions (very mild or no symptoms):
1. Gastrointestinal decontamination is unnecessary.
2. Symptomatic and supportive measures only.
Moderate/substantial ingestions:
1. Gastric lavage should be considered only if the patient presents
within one hour; its value is unproven.
2. Symptomatic and supportive measures as dictated by the patient's
condition.
3. Monitor the ECG, biochemical and haematological profiles.
4. Collect urine and blood for tellurium concentration measurements
to confirm diagnosis although these assays are not widely
available. Check with NPIS.
5. It has been suggested that ascorbic acid may reduce the garlic
odour from tellurium intoxication (De Meio, 1947) but this has
not been confirmed.
6. Dimercaprol increases tellurium toxicity and should not be used.
Inhalation
1. Remove from exposure
2. Treat symptomatically and supportively.
3. If symptoms occur perform a chest X-ray, ECG, biochemical and
haematological profiles.
4. Collect urine and blood for tellurium concentration measurements
to confirm diagnosis although these assays are not widely
available. Check with NPIS.
5. It has been suggested that ascorbic acid may reduce the garlic
odour from tellurium intoxication (De Meio, 1947) but this has
not been confirmed.
6. Dimercaprol increases tellurium toxicity and should not be used.
Injection
1. Symptomatic and supportive care as dictated by the patients
condition.
2. Monitor the ECG, biochemical and haematological profiles.
3. Collect urine and blood for tellurium concentration measurements
to confirm diagnosis although these assays are not widely
available. Check with NPIS.
4. It has been suggested that ascorbic acid may reduce the garlic
odour from tellurium intoxication (De Meio, 1947) but this has
not been confirmed.
5. Dimercaprol increases tellurium toxicity and should not be used.
REFERENCES
Blackadder ES, Manderson WG.
Occupational absorption of tellurium: a report of two cases.
Br J Ind Med 1975; 32: 59-61.
De Meio RH.
Tellurium. II. Effect of ascorbic acid on the tellurium breath.
J Ind Hyg Toxicol 1947; 29: 393-5.
Keall JHH, Martin NH, Tunbridge RE.
A report of three cases of accidental poisoning by sodium tellurite.
Br J Ind Med 1946; 3: 175-6.
Kron T, Hansen C, Werner E.
Renal excretion of tellurium after peroral administration of tellurium
in different forms to healthy human volunteers.
J Trace Elem Electrolytes Health Dis 1991; 5: 239-44.
Müller R, Zschiesche W, Steffen HM, Schaller KH.
Tellurium-intoxication.
Klin Wochenschr 1989; 67: 1152-5.
Substance name
Tellurium
Origin of substance
Usually found naturally as the telluride of gold (calverite). It
is produced as a by-product of the smelting of copper and other
metals. (Gerhardsson et al, 1986)
Synonyms
Aurum paradoxum
Metalum problematum (DOSE, 1994)
Chemical group
A group VIA element
Reference numbers
CAS 13494-80-9 (DOSE, 1994)
RTECS WY 2625000 (RTECS, 1997)
UN 3284 (HAZARD TEXT, 1997)
HAZCHEM CODE NIF
Physicochemical properties
Chemical structure
Te (DOSE, 1994)
Molecular weight
127.60 (DOSE, 1994)
Physical state at room temperature
Crystalline solid or amorphous powder.
(Gerhardsson et al, 1986)
Colour
Crystals are silvery white, powder is black.
(Gerhardsson et al, 1986)
Odour
Odourless (HSDB, 1997)
Viscosity
NIF
pH
NIF
Solubility
Elemental tellurium is insoluble in water.
(Gerhardsson et al, 1986)
Autoignition temperature
NIF
Chemical interactions
Tellurium is not attacked by hydrochloric acid. It reacts with
nitric acid and with concentrated or fuming sulphuric acid. In
the presence of air, it dissolves in potassium hydroxide with
formation of a deep-red solution. (HSDB, 1997)
Major products of combustion
Tellurium dioxide. (HSDB, 1997)
Explosive limits
NIF
Flammability
Burns slowly in air. (HSDB, 1997)
Boiling point
990°C. (DOSE, 1994)
Density
6.2 (Gerhardsson et al, 1986)
Vapour pressure
133.3 Pa at 520°C (DOSE, 1994)
Relative vapour density
NIF
Flash point
NIF
Reactivity
A finely divided suspension of elemental tellurium in air can be
exploded.
The fire hazard of tellurium is moderate in the form of dust when
exposed to heat or flame or by chemical reaction with oxidizing
agents.
Reactions with zinc, chlorine, fluorine, and solid sodium are
vigorous and have a potential to cause fires (HSDB, 1997).
Uses
Additive to metal alloys.
Vulcanization of rubber.
Semiconductors and electronic devices.
Catalyst.
Tellurium vapour is used in "daylight lamps".
Used in blast caps.
Limited use in pottery glazes. (PATTY, 1993)
Hazard/Risk Classification
NIF
INTRODUCTION
Tellurium has the appearance and physical properties of a metal yet
has the chemical properties of a non-metal. It forms compounds in
oxidation states -2, +2, +4 and +6. Of toxicological interest are
elemental tellurium, tellurium dioxide, the gases hydrogen telluride
and tellurium hexafluoride, and the water soluble salts of tellurous
and telluric acid. It also forms a number of organometallic complexes
(Gerhardsson et al, 1986). There is no evidence that tellurium is an
essential trace element.
Tellurium exposure is characterized by a distinctive garlic odour
which is due to formation of the hepatic metabolite dimethyl
telluride.
EPIDEMIOLOGY
Tellurium is used as an additive in many metallurgical processes such
that it is often involved in multiple metal exposures, notably with
lead, zinc, arsenic, selenium, cadmium and thallium. Tellurium
exposure also occurs during electrolytic copper refining where
tellurium is formed in the anode slime. Tellurium intoxication is
rare, though acute (Gerhardsson et al, 1986; Blackadder and Manderson,
1975) and chronic (Keall et al, 1946; Shie and Deeds, 1920)
occupational exposure has been reported.
An isolated case of poisoning from tellurium-contaminated meat has
been reported (Müller et al, 1989). The source of contamination is
unknown.
The only reported deaths from tellurium intoxication occurred when two
men were mistakenly injected with some 2 g sodium tellurite during
retrograde pyelography (Keall et al, 1946).
MECHANISMS OF TOXICITY
There are few data on the mechanism of toxicity of tellurium or its
compounds. Animal studies suggest tellurium may affect the conversion
of squalene to cholesterol so interfering with neurotransmission via
demyelination (Gerhardsson et al, 1986).
Impaired secretory nerve neurotransmission is the proposed mechanism
of impaired saliva and sweat secretion in humans and of reduced
gastric acid secretion in animals poisoned with tellurium (Shie and
Deeds, 1920).
There is some evidence that the aroma of fresh garlic is caused by a
high tellurium content. This may contribute to garlic's cholesterol-
lowering properties (Larner, 1995).
In vitro studies demonstrate that tellurite (Te4+) ions can
penetrate the erythrocyte membrane and, in the presence of reduced
glutathione, form telluride (Te2+) which causes irreversible membrane
damage and hence haemolysis (De Meio and O'Leary, 1975; Kurantsin-
Mills et al, 1988). Tellurate (Te6+) ions do not penetrate the
erythrocyte membrane. Haemolysis has been observed in animals poisoned
with tellurium (Shie and Deeds, 1920), but not as a feature of
tellurium intoxication in man.
TOXICOKINETICS
Absorption
The mean (± SD) gastrointestinal absorption in healthy volunteers
ingesting between 15 and 57 µg has been estimated as ten per cent (± 4
per cent) for elemental tellurium, 23 per cent (± 9 per cent) for
tellurate and 21.5 per cent (no SD given) for tellurite (Kron et al,
1991).
Ingestion of 0.5 µg tellurium oxide produced a garlic breath odour
within 75 minutes which lasted for 30 hours (Reisert, 1884).
Tellurium dusts and fumes can be absorbed via the lung. Workers
exposed to tellurium concentrations up to 0.1 mg/m3 had urine
tellurium concentrations of up to 0.06 mg/L (Steinberg et al, 1942).
Organometallic complexes of tellurium and soluble tellurium salts can
be absorbed through the skin (Blackadder and Manderson, 1975).
Distribution
Tellurium is distributed widely with high concentrations particularly
in kidneys, liver, bone, brain and testes (Meditext, 1997).
Excretion
Excretion is mainly renal although small amounts of tellurium are
exhaled as dimethyl telluride which has a distinctive garlic odour
which may persist for many days; Reisert (1884) reported garlic breath
odour for 237 days following ingestion of 15 mg tellurium oxide. The
susceptibility to this effect varies considerably between individuals
and is exacerbated by alcohol consumption (Cerwenka and Cooper, 1961).
The whole body retention time of tetravalent tellurium has been
estimated as more than two months (Kron et al, 1991).
CLINICAL FEATURES: ACUTE EXPOSURE
Dermal exposure
Although it has been claimed that some tellurium compounds give rise
to skin burns or rashes following dermal contact (Gerhardsson et al,
1986), no original case data were cited in support.
Blue-black patches in the webs of the fingers and streaks on the neck
were observed in two postgraduate chemists who handled volatile
tellurium esters. The discolouration was believed to be due to
deposition of elemental tellurium in the dermis and subcutaneous
tissue (Blackadder and Manderson, 1975).
Ocular exposure
Some tellurium compounds are irritant although there are no reports of
ocular exposure to tellurium or its compounds producing adverse
effects.
Exposure to either hydrogen telluride or to shampoo containing
tellurium oxide has not caused eye problems (Grant and Schuman, 1993).
Inhalation
Reports from the Russian literature state that tellurium dust or fumes
and hydrogen telluride are irritant to the respiratory tract
(Gerhardsson et al, 1986).
No pulmonary features were reported when two postgraduate chemists
were exposed to some 50 g tellurium hexafluoride gas which leaked from
a cylinder into a small laboratory. The first individual developed a
metallic taste, anorexia and tiredness and, after two days, an
erythematous papular vesicular rash on the hands, arms and neck. This
was diagnosed as contact dermatitis, possibly from wearing rubber
gloves, although the ability of tellurium to inhibit sweating may have
contributed. The second person affected experienced only a metallic
taste and somnolence. Both patients developed a garlic odour to the
breath, sweat and urine which persisted for several weeks (Blackadder
and Manderson, 1975). Haematological and biochemical profiles and
chest X-ray were normal.
Three workers exposed to tellurium fumes for ten minutes developed a
garlic breath odour and experienced a metallic taste, headache and
"epigastric distress" within 24 hours. Twenty-four hour urine
tellurium concentrations in collections commenced some 48 hours post
exposure varied between 7.7 µg/L and 12.0 µg/L. The full blood count
in each case showed a mild lymphocytosis (40-51 per cent of the total
white cells). All recovered fully without treatment but were given an
eight day course of dimercaprol in an attempt to clear the garlic
odour, which disappeared one to four days after cessation of treatment
(Amdur, 1947). No tellurium was detectable in the urine 17 days after
presentation.
Two cases of occupational exposure to tellurium vapour have been
reported in the Russian literature (Gerhardsson et al, 1986). Features
included a garlic breath odour with general weakness, pallor, cough,
shivering, fever, sinus tachycardia, amnesia and black-green
discolouration of the mucosa of the tongue and the nasopharynx.
Ingestion
A 37 year-old woman developed characteristic symptoms of tellurium
exposure "only hours" after eating a small piece of meat containing
800-1000 µg/kg tellurium of unknown origin. Initially she experienced
nausea, vomiting, a metallic taste and a garlic odour of the breath,
sweat, urine and faeces. The next day she developed a fever which
resolved over some five days as the gastrointestinal features
subsided. The patient noticed hair loss two weeks after intoxication
and was referred to hospital after four weeks with weight loss,
fatigue and a persistent garlic breath odour. Examination was normal
except for the strong garlic odour. Gastroscopy showed petechial
bleeding in the gastric fundus. Serum and urine tellurium
concentrations were 27.6 µg/L (normal = 1.0 µg/L) and 3.1-3.2 µg/L
(normal = 1.0 µg/L) respectively. The patient was given ascorbic acid
200 mg per day and discharged. Hair loss ceased eight weeks after
intoxication with a "bright colour" to new grown hair. The garlic
odour persisted for some ten months, intensifying after alcohol
intake. No persistent health effects were reported. (Müller et al,
1989).
Injection
Three patients were accidentally poisoned when sodium tellurite was
administered instead of sodium iodide during retrograde pyelography
(Keall et al, 1946). Two of these patients who each received an
estimated 2 g tellurite died.
A garlic odour was observed around the first patient, a 40 year old
male, some 90 minutes after sodium tellurite was injected into the
left ureter. After a further 75 minutes the patient complained of
severe discomfort in the left loin and subsequently vomited. Four
hours after the procedure he became deeply cyanosed and dyspnoeic and
died twenty minutes later (Keall et al, 1946).
The second patient, a 31 year old male, developed a garlic odour
within an hour of undergoing pyelography. He became confused and
progressively cyanosed with only partial relief from oxygen therapy.
Spectroscopy of the patient's blood revealed an abnormal pigment which
was not methaemoglobin and could not be identified. The patient died
six hours after sodium tellurite injection (Keall et al, 1946).
At autopsy both patients showed marked cyanosis of the head and neck.
An intense yellow colour was observed in body fat and a deep brown
colour in muscles. Black deposits were found in the mucosa of the
bladder and in the injected ureter. Congestion was noted in the lungs,
liver, spleen and kidneys with marked fatty degeneration and oedema in
the liver. A garlic odour was emitted from all tissues (Keall et al,
1946).
The third patient, a 21 year old male, received a smaller (unknown)
dose of sodium tellurite due to a blocked catheter. After four days a
garlic odour was noticed and the patient became slightly cyanosed,
complained of a "nasty taste" in the mouth and was administered
intravenous fluids. He vomited the following day but recovered fully
by day seven. The garlic odour disappeared after 12 days (Keall et al,
1946).
CLINICAL FEATURES: CHRONIC EXPOSURE
Exposure to tellurium compounds is most likely to occur in the form of
dusts and fumes in industry. Only hydrogen telluride, tellurium
dioxide and potassium tellurite are of occupational significance
(Glover, 1983). No deaths or permanent health effects have been
reported following exposure.
Inhalation
Thirteen individuals working near the blast furnaces in a lead
refinery were examined for signs of tellurium exposure (Shie and
Deeds, 1920). The workers were believed to have been exposed to
hydrogen telluride though no exposure data were given. Seven had a
garlic odour to the breath, sweat and urine, and dryness and a
metallic taste in the mouth. Five had "considerable inhibition of the
sweat function" and three developed dry and itchy skin, anorexia,
nausea, vomiting, depression and somnolence.
A survey of ninety-eight workers exposed to 0.01-0.1 mg/m3 tellurium
for 22 months revealed similar effects. The most common findings were
a garlic odour of the breath (84 individuals), dryness of the mouth
(32), a metallic taste (27) and garlic odour of the sweat (20). Other
symptoms included somnolence (16), loss of appetite (9) and nausea
(3). No evidence of sweat suppression was found. Urinalysis revealed
increased tellurium concentrations (0.01 to greater than 0.06 mg/L) in
the exposed group compared to controls. Symptoms occurred even in
those with urine tellurium concentrations less than 0.01 mg/L, though
the frequency increased at higher tellurium concentrations with
somnolence and a garlic sweat odour occurring only in workers with a
urine tellurium concentration greater than 0.01 mg/L (Steinberg et al,
1942).
MANAGEMENT
Dermal exposure
If possible the patient should remove any contaminated clothing
him/herself. Affected areas of skin should be washed with copious
quantities of water. Pay special attention to skin folds, fingernails
and ears. Burns should be treated conventionally as for thermal burns
(e.g. silver sulphadiazine dressing).
Ocular exposure
Irrigate immediately with lukewarm water or preferably saline for at
least 10-15 minutes. Specialist ophthalmological advice should be
sought if any abnormality is detected or suspected on examination and
in those whose symptoms do not resolved rapidly.
Inhalation
Immediate management involves removal from exposure, establishment of
a clear airway and administration of supplemental oxygen if necessary.
Mechanical ventilation may be required. Other symptomatic and
supportive measures should be dictated by the patients condition.
Ingestion
Gastric lavage may be considered if presentation is within the first
hour, though there are no clinical data regarding its value. It is not
known whether activated charcoal will adsorb tellurium. Symptomatic
and supportive measures should be employed. An ECG should be performed
and biochemical and haematological profiles undertaken. Blood and
urine tellurium concentrations are not widely available but may be of
interest retrospectively to confirm systemic uptake.
Injection
The management of a patient following injection of tellurium is
symptomatic and supportive as dictated by the patient's condition.
Monitoring and investigations are as for tellurium ingestion.
Antidotes
Animal studies
Four guinea pigs were administered 5 mg intramuscular dimercaprol
eight hours prior to the intramuscular injection of 75 mg tellurium
oxide. A second group of four similarly poisoned guinea pigs received
dimercaprol eight hours after tellurium oxide injection. Both groups
then received dimercaprol 5 mg tds for 24 hours and 5 mg bd for a
further 24 hours. There was 100 per cent mortality in the two
dimercaprol administered groups (n=8) within 48 hours (and all animals
showed pronounced haematuria) whereas the 48 hour survival rate in
control animals (n=4) administered tellurium oxide alone was 75 per
cent. A single guinea pig administered only intramuscular dimercaprol
5 mg every eight hours for 24 hours remained healthy. The weights of
the animals were not stated (Armdur, 1958).
Clinical studies
Three men exposed to tellurium fumes developed a strong garlic breath
odour and were treated with 2.5 mg/kg dimercaprol intramuscularly
every four hours for 24 hours, every six hours for a further 24 hours
and then daily for six days. Each patient reported accentuation of the
garlic odour following the injection and the odour disappeared one to
four days after the cessation of treatment. There was no evidence of
enhanced tellurium elimination with therapy (Amdur, 1947).
Ascorbic acid
Animal studies
The reduction in garlic odour from rabbits and guinea pigs intoxicated
with tellurium following administration of ascorbic acid (route not
described) has been reported. The proposed mechanism is reduction of
ionized to elemental tellurium with decreased dimethyl telluride
formation (De Meio, 1947).
Intramuscular ascorbic acid 25 mg tds for 24 hours then 25 mg bd for a
further 24 hours did not increase the one week survival of guinea pigs
injected intramuscularly with 75 mg tellurium oxide compared to
controls (Amdur, 1958).
Clinical studies
Workers exposed to tellurium dust were treated with 8-10 mg/kg
ascorbic acid (route not stated) one to three times daily. A reduction
in the garlic odour of the breath was noted which recurred on
cessation of treatment (De Meio, 1947).
A 37 year old woman who ingested an unknown amount of tellurium was
treated with ascorbic acid 200 mg daily (route not stated). She
recovered fully though a garlic odour of the breath persisted from
some ten months (Müller et al, 1989).
Antidotes: Conclusions and recommendations
1. Animal studies suggest dimercaprol increases tellurium toxicity
and, as there is no evidence that it enhances tellurium
elimination, it should not be employed.
2. Ascorbic acid may decrease the extent of garlic odour in persons
with tellurium intoxication although this has not been confirmed
in controlled studies.
MEDICAL SURVEILLANCE
The most obvious indication of tellurium exposure is a garlic odour to
the breath, which occurs in association with urine tellurium
concentrations greater than 1 µg/L (Gerhardsson et al, 1986). This
clinical indication of tellurium exposure may be masked in those with
badly smelling breath (i.e. bronchiectasis, grossly carious teeth,
severe gingivitis) (Gerhardsson et al, 1986).
Normal concentrations in biological fluids
The "upper normal limits" for tellurium in non-occupationally exposed
individuals have been reported as 1.0 µg/L in serum and 1.0 µg/L in
urine (Müller et al, 1989).
OCCUPATIONAL DATA
Occupational exposure standard
Tellurium and compounds, except hydrogen telluride. Long-term exposure
limit 0.1 µg/m3 (as Te) (Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There are no reports associating tellurium or its compounds with the
development of cancer in humans.
Reprotoxicity
There are no reports of exposure to tellurium or its compounds causing
reproductive effects in humans although pregnant rats fed diets
containing 500 to 3500 ppm tellurium gave birth to hydrocephalic (non-
obstructive) offspring, the incidence of hydrocephalus being
proportional to the tellurium dose (Duckett, 1970). The mechanism of
this effect is not known.
Genotoxicity
An increase in the incidence of chromosome breakage was found when
in vitro human leukocytes were treated for 48 hours with 1.2 x 10-8
mol/L sodium tellurite and 2.4 x 10-7 mol/L ammonium tellurite (Paton
and Allison, 1972).
Fish toxicity
NIF
EC Directive on Drinking Water Quality 80/778/EEC
NIF
WHO Guidelines for Drinking Water Quality
NIF
AUTHORS
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service (Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
UK
This monograph was produced by the staff of the Birmingham Centre of
the National Poisons Information Service in the United Kingdom. The
work was commissioned and funded by the UK Departments of Health, and
was designed as a source of detailed information for use by poisons
information centres.
Date of last revision
28/1/98
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Tellurium. Accidental exposure and treatment with BAL in oil.
Occup Med 1947; 3: 386-91.
Amdur ML.
Tellurium oxide: an animal study in acute toxicity.
Arch Ind Health 1958; 17: 665-7.
Blackadder ES, Manderson WG.
Occupational absorption of tellurium: a report of two cases.
Br J Ind Med 1975; 32: 59-61.
Cerwenka EA, Cooper WC.
Toxicology of selenium and tellurium and their compounds.
Arch Environ Health 1961; 3: 189-200.
De Meio RH.
Tellurium. II. Effect of ascorbic acid on the tellurium breath.
J Ind Hyg Toxicol 1947; 29: 393-5.
De Meio RH, O'Leary DJ.
Hemolysis by tellurium compounds: Telluride and tellurate, effect on
reduced glutathione.
J Am Osteopath Assoc 1975; 75: 430-1.
DOSE/Dictionary of substances and their effects. Vol 7.
Cambridge: Royal Society of Chemistry, 1994.
Duckett S
Fetal encephalopathy following ingestion of tellurium.
Experientia 1970; 26: 1239-41.
Gerhardsson L, Glover JR, Nordberg GF, Vouk V.
Tellurium.
In: Friberg L, Nordberg GF, Vouk VB, eds. Handbook on the toxicology
of metals. Vol 2. 2nd ed.
Amsterdam: Elsevier Science Publishers, 1986; 532-48.
Glover JR.
Tellurium and compounds.
In: Parmeggiani L, ed. Encyclopaedia of occupational health and
safety. Vol 2. 3rd ed.
Geneva: International Labour Organisation, 1983; 2156-7.
Grant WM, Schuman JS.
Toxicology of the eye. 4th ed.
Illinois: Charles C Thomas, 1993.
HAZARDTEXT.
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Health and Safety Executive.
EH40/97: Occupational exposure limits 1997.
Sudbury: HSE Books, 1997.
HSDB/Hazardous Substances Data Bank.
In: Tomes plus. Environmental Health and Safety Series 1. Vol 32.
National Library of Medicine, 1997.
Keall JHH, Martin NH, Tunbridge RE.
A report of three cases of accidental poisoning by sodium tellurite.
Br J Ind Med 1946; 3: 175-6.
Kron T, Hansen C, Werner E.
Renal excretion of tellurium after peroral administration of tellurium
in different forms to healthy human volunteers.
J Trace Elem Electrolytes Health Dis 1991; 5: 239-44.
Kurantsin-Mills J, Klug RK, Lessin LS.
Irreversible erythrocyte volume expansion induced by tellurite.
Br J Haematol 1988; 70: 369-74.
Larner AJ.
How does garlic exert its hypocholesterolaemic action? The tellurium
hypothesis.
Med Hypotheses 1995; 44: 295-7.
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Müller R, Zschiesche W, Steffen HM, Schaller KH.
Tellurium-intoxication.
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Phosphorus, selenium, tellurium, and sulfur. In: Clayton GD, Clayton
FE, eds. Patty's industrial hygiene and toxicology. Vol 2. 4th ed.
New York: John Wiley & Sons, Inc., 1993; 783-829.
Paton GR, Allison AC.
Chromosome damage in human cell cultures induced by metal salts.
Mutat Res 1972; 16: 332-6.
Reisert W.
The so-called bismuth breath.
Am J Pharm 1884; 56: 177-80.
RTECS/Registry of Toxic Effects of Chemical Substances.
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National Institute for Occupational Safety and Health (NIOSH), 1997.
Shie MD, Deeds FE.
The importance of tellurium as a health hazard in industry - a
preliminary report.
Public Health Rep 1920; 35: 939-54.
Steinberg HH, Massari SC, Miner AC, Rink R.
Industrial exposure to tellurium: atmosphere studies and clinical
evaluation.
J Ind Hyg Toxicol 1942; 24: 183-92.