UKPID MONOGRAPH
ANTIMONY TRIOXIDE
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
ST Beer BSc
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.
ANTIMONY TRIOXIDE
Toxbase summary
Type of product
Used mainly as a fire retardant in plastics, rubbers, textiles, paper
and paints.
Toxicity
Acute antimony trioxide poisoning is rare. Exposure may occur in
industry. Fatal dose not known.
Features
Topical
- Irritant to the skin and eyes.
- "Antimony spots" (papules and pustules around sweat and
sebaceous glands) may develop after repeated exposure,
particularly in warm conditions.
Ingestion
Moderate ingestions:
- Features usually occur within two hours with nausea,
vomiting, abdominal pain and diarrhoea. A garlic odour on
the breath has been described following ingestion of other
antimony salts.
Substantial ingestions:
- Severe vomiting and diarrhoea (which may contain blood) and
haemorrhagic gastritis may ensue. Myocardial depression,
vasodilation and fluid loss may cause shock with
hypotension, electrolyte disturbances and acute renal
failure. Cerebral oedema, coma and convulsions are possible.
A fatality occurred following ingestion of a soluble
antimony trioxide derivative (Miller, 1982).
Inhalation
- Irritant to the respiratory tract and mucous membranes
causing conjunctivitis, laryngitis, pharyngitis, tracheitis,
rhinitis bronchitis and rarely non-cardiogenic pulmonary
oedema.
- There may be radiological evidence of pneumonitis.
- Chronic occupational inhalation may cause pneumoconiosis
with cough, wheeze and diffuse, punctate opacities in the
middle and lower zones.
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.
4. A physician may need to examine the area if irritation or pain
persists after washing.
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 antimony concentration measurements
to confirm diagnosis although these assays are not widely
available. Check with NPIS.
5. Chelation therapy with dimercaprol, DMSA or DMPS may be
considered; seek specialist advice from an NPIS physician.
Inhalation
Acute exposure
1. Remove from exposure.
2. Secure cardiorespiratory stability.
3. Perform a chest X-ray in symptomatic patients.
4. Treat symptomatically.
5. If significant respiratory symptoms occur investigate for
systemic toxicity: ECG, biochemical and haematological profiles
and blood and urine samples for antimony concentration
determination.
Chronic exposure
1. Investigate as for other causes of pneumoconiosis.
2. Obtain blood and urine for antimony concentration measurements to
confirm diagnosis. However, these assays are not widely
available. Check with NPIS.
3. Consider the possibility of systemic toxicity.
References
Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J.
Experimental and human studies on antimony metabolism: their relevance
for the biological monitoring of workers exposed to inorganic
antimony.
Br J Ind Med 1991;48: 93-7.
Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L.
Oral antimony intoxications in man.
Crit Care Med 1990; 18: 324-6.
Miller JM.
Poisoning by antimony: a case report.
South Med J 1982; 75: 592.
Renes LE.
Antimony poisoning in industry.
Arch Ind Hyg Occup Med 1953; 7: 99-108.
Werrin M.
Chemical food poisoning.
Q Bull Assoc Food Drug Offic 1963; 27: 38-45.
White Jr GP, Mathias CGT, Davin JS.
Dermatitis in workers exposed to antimony in a melting process.
J Occup Med 1993; 35: 392-5.
Winship KA.
Toxicity of antimony and its compounds.
Adverse Drug React Acute Poisoning Rev 1987; 2: 67-90.
Substance name
Antimony trioxide
Origin of substance
Minerals such as senarmontite and valentinite.
(MERCK, 1996)
Manufactured by roasting antimony trisulphide ores.
(IARC, 1989)
Synonyms
Diantimony trioxide
Antimony white
Exitelite
Flowers of antimony
Valentinite (DOSE, 1992)
Chemical group
A compound of antimony, a group VA element
Reference numbers
CAS 1309-64-4 (DOSE, 1992)
1327-33-9 (CSDS, 1989)
RTECS CC 5650000 (CSDS, 1989)
UN 1549 (CSDS, 1989)
HAZCHEM NIF
Physicochemical properties
Chemical structure
Sb2O3 (DOSE, 1992)
Molecular weight
291.5 (DOSE, 1992)
Physical state at room temperature
Crystalline solid (CSDS, 1989)
Colour
White (CSDS, 1989)
Odour
None (CHRIS, 1997)
Viscosity
NA
pH
NIF
Solubility
Slightly soluble in water. Soluble in potassium hydroxide,
hydrochloric acid. Insoluble in organic solvents.
(CSDS, 1989)
Autoignition temperature
NA
Chemical interactions
Reacts with organic acids, alcohols, glycols, alpha-hydroxy
acids, o-dihydric phenols, sugar alcohols and other polyhydroxy
compounds. (OHM/TADS, 1997)
Major products of combustion
When heated to combustion emits toxic antimony fumes.
(HAZARDTEXT, 1997)
Explosive limits
NIF
Flammability
Ignites on heating in air. (CSDS, 1989)
Boiling point
1550°C (DOSE, 1992)
Density
5.2 (DOSE, 1992)
Vapour pressure
NA
Relative vapour density
NA
Flash Point
NA
Reactivity
Reacts explosively with chlorinated rubber.
Forms explosive mixtures with perchloric acid when hot.
(CSDS, 1989)
Uses
Fire retardant in plastics, rubbers, textiles, paper and paints.
(IARC, 1989)
In enamels and glass.
Tartar emetic (antimony potassium tartrate) manufacture.
(DOSE, 1992)
Hazard/risk classification
Index no. 051-005-00-X
Risk phases
Carc. Cat. 3; R40 - Possible risk of irreversible effects.
Xn; R40 - Harmful, possible risk of irreversible effects.
S(2-)22-36 - Keep out of reach of children. Do not breathe dust.
Wear suitable protective clothing.
EEC No. 215-175-0 (CHIP2, 1994)
INTRODUCTION
Antimony trioxide is a trivalent antimony compound which occurs
naturally as the ores valentinite and senarmontite. It is produced
commercially by the vapour phase reaction of antimony trisulphide and
oxygen.
It is used as a fire retardant and as an additive in enamel and glass
manufacture.
EPIDEMIOLOGY
The main route of antimony trioxide exposure is occupational
inhalation of dusts. Workers have been exposed in the production of
antimony trioxide (Renes, 1953; Schnorr et al, 1995) and from its
formation as a by-product of metal smelting (Gerhardsson et al, 1982;
Potkonjak and Pavlovich, 1983; Jones, 1994; Schnorr et al, 1995).
Other occupational exposure has occurred in the manufacture of
ceramics (Motolese et al, 1993), batteries (Kentner et al, 1995) and
alloys (White et al, 1993).
Accidental intoxication has been reported after leaching of antimony
from agate and ceramic containers into acidic beverages (Dunn, 1928;
Monier-Williams, 1934; Werrin, 1963).
It has been suggested that stibine generated from microbial growth on
cot mattresses containing antimony trioxide is a contributing factor
in sudden infant death syndrome (SIDS). Although there is some
evidence consistent with undue antimony exposure in infants who died
of SIDS (Taylor, 1996) other evidence disagrees such that it is most
unlikely stibine is the only cause of the syndrome (de Wolff, 1995). A
provisional comment by the Chair of the UK Expert Group on Cot Death
Theories states so far "there is no evidence of risk to babies" from
cot mattress PVC (Bradbury, 1997).
Historically, intoxication has resulted from the medical use of
antimony trioxide and potassium tartrate as tartar emetic in the
treatment of a variety of conditions including malaise, fever,
whooping cough and syphilis (Miller, 1982).
MECHANISM OF TOXICITY
The mechanism of toxicity of antimony compounds is unclear but may
involve disruption of thiol proteins via binding to sulphydryl groups
(de Wolff, 1995).
TOXICOKINETICS
Absorption
Antimony trioxide may be absorbed by inhalation and ingestion, though
gastrointestinal absorption in man is poor.
Distribution
Absorbed trivalent antimony readily enters red blood cells and
accumulates primarily in the spleen, liver and bone (IPCS, 1996).
Lauwers et al (1990) estimated that the total body antimony pool in a
patient who died following accidental antimony potassium tartrate
ingestion was only five per cent of the ingested dose with high
antimony concentrations in the liver, gall bladder and
gastrointestinal mucosa. This is consistent with antimony undergoing
enterohepatic circulation (see below).
Excretion
Antimony compounds are eliminated mainly in the urine, with small
amounts appearing in faeces via bile after conjugation with
glutathione. A significant amount of antimony excreted in bile
undergoes enterohepatic circulation (Bailly et al, 1991). Some 6-24
months after parenteral antimony therapy, Mansour et al (1967)
reported increased urine antimony concentrations (range 5.8-145.3
µg/L) compared to untreated controls (range 2.9-9.1 µg/L).
Gerhardsson et al (1982) reported significantly (p<0.001) higher
antimony concentrations in the lung tissue of 40 deceased smelter and
refinery workers who had been exposed to antimony for some 30 years,
compared to 11 unexposed controls. The time from last exposure to
death varied from 0-23 years. The antimony concentration in liver and
kidney was not significantly different between the two groups,
suggesting that following occupational inhalation antimony may be
retained in the lung for several years without significant systemic
distribution.
Kentner et al (1995) estimated a renal elimination half-life of four
days following occupational inhalation of antimony trioxide and
stibine in 21 employees of a starter battery manufacturing plant.
CLINICAL FEATURES: ACUTE EXPOSURE
Dermal exposure
Antimony trioxide is an irritant although antimony dermatitis
typically occurs during chronic occupational exposure.
Ocular exposure
Antimony trioxide is an eye irritant. Conjunctivitis and blurred
vision were reported in workers exposed to antimony trioxide fumes in
a smelter plant (Renes, 1953).
Ingestion
Acute poisoning is rare. Antimony trioxide is poorly soluble and is
not readily absorbed from the gastrointestinal tract. Cases have been
reported only when the compound has been leached into acidic beverages
or has been converted into a more soluble form.
Gastrointestinal toxicity
Ingestion of a substantial quantity of antimony trioxide may result in
nausea, vomiting and diarrhoea.
Over fifty people were "very sick" and treated in hospital after
drinking lemonade contaminated with 13 mg/L antimony. Antimony
trioxide had leached from an enamel container in which the drinks were
stored overnight. All the patients recovered completely within several
days (Dunn, 1928).
Similarly, antimony trioxide leached from enamel or ceramic glaze into
acidic beverages caused "a burning sensation in the stomach", colic,
nausea, vomiting and "collapse" (Monier-Williams, 1934).
One hundred and fifty children developed nausea, vomiting, abdominal
pain and diarrhoea some 15 minutes after drinking
antimony-contaminated lemonade. The lemonade had a pH of 2.5-3.1 and
leached an estimated 30 mg/L antimony into solution from an agate pot
in which it was stored for 20-22 hours. Most of the affected children
recovered within a few hours, the remainder recovering within a few
days (Werrin, 1963).
In 1982 Miller recounted the case of the author Oliver Goldsmith who
died after ingesting a mixture of antimony trioxide and potassium
tartrate. The estimated dose was 132-198 mg antimony. He succumbed
after 18 hours severe vomiting and diarrhoea.
Cardiovascular and peripheral vascular toxicity
Electrocardiographic abnormalities are associated typically with
chronic antimony exposure although have not been associated with
exposure to antimony trioxide alone.
Following acute antimony ingestion two patients had "moderate
bradyrhythmic dysfunctions" at presentation (Lauwers et al, 1990).
Phlebitis occurred in four patients who accidentally ingested antimony
potassium tartrate (Lauwers et al, 1990).
Inhalation
Pulmonary toxicity
Dusts and fumes of antimony trioxide are irritant to the respiratory
tract and mucous membranes and inhalation causes laryngitis (ranging
from hoarseness to aphonia), pharyngitis, tracheitis, rhinitis,
epistaxis, and bronchitis (Renes, 1953). Metal fume fever has been
described (Anonymous, 1984) though less frequently than following
exposure to zinc oxide.
Radiological evidence of pneumonitis was found in six workers exposed
to antimony smelter fumes for 2-12 hours. Inflammatory changes were
characteristically peri-hilar with no evidence of peripheral
parenchymal damage. Symptoms were alleviated by removal from exposure
(and treatment with penicillin aerosols). The average airborne
antimony concentration was 10-12 mg/m3 with a maximum measured
breathing zone concentration of 70.7 mg/m3 (Renes, 1953).
Gastrointestinal toxicity
Workers heavily exposed (not specified) to antimony trioxide in a
smelter plant developed "gastritis", abdominal pain, diarrhoea and
vomiting. Urine antimony concentrations ranged from a trace up to an
"exceptionally high" 600 mg/L (Renes, 1953).
Neurotoxicity
"Neuritis", dizziness and headache were reported amongst workers
exposed to antimony trioxide fumes at an antimony smelting plant
(Renes, 1953).
Nephrotoxicity
Albuminuria was reported in a "severely ill" worker with a urine
antimony concentration of 600 mg/L after exposure to antimony trioxide
in a smelting plant (Renes, 1953). Removal from exposure and
symptomatic treatment for several days "provided relief".
CLINICAL FEATURES: CHRONIC EXPOSURE
The major source of antimony trioxide exposure is as a by-product in
the smelting of metal ores (which may also contain arsenic) and in
industries such as ceramic, glass and alloy manufacture. Inhalation
and dermal contact are the most common routes of exposure.
Dermal exposure
Dermatitis following contact with antimony trioxide is well described
(Oliver, 1933; McCallum, 1989). Typical lesions arise on the arms,
legs and in the flexures, sparing the face, hands and feet (Renes,
1953; McCallum, 1989).
Papules and pustules predominate around sweat and sebaceous glands
with areas of eczema and lichenification (Paschoud, 1962). These so-
called "antimony spots" occur mainly in the summer (McCallum, 1989).
Skin lesions developed in 23 men employed at an antimony trioxide
production plant. Most of those affected were furnace workers with
lesions typically appearing within two weeks of exposure. Itching,
erythematous papules and pustular eruptions were characteristic,
usually on dust laden sweaty areas of skin. The lesions usually
resolved over two weeks in individuals removed to cooler parts of the
factory. Histological examination showed epidermal cellular necrosis
associated with an acute dermal inflammatory reaction. Antimony
trioxide patch testing was negative whilst injection of methacholine
into the affected areas caused enlargement of the lesions. The author
concluded that antimony trioxide dust initiated an irritant reaction
when it penetrated sweat ducts (Stevenson, 1965).
White et al (1993) described three cases of occupational antimony
dermatitis following several months exposure to antimony dust and
antimony trioxide fumes. Two of these patients also experienced
frequent nose bleeds. Both problems resolved when exposure ceased. In
one patient patch testing for antimony was negative and in another the
urine antimony concentration was 53.2 µg/L ("normal" < 1.0 µg/L).
Positive patch testing to antimony trioxide has been noted in
enamellers and decorators in the ceramics industry (Motolese et al,
1993).
Ocular exposure
Antimony trioxide is an irritant. Conjunctivitis was reported in 14 of
51 workers exposed to antimony trioxide dust in a smelting plant
(Potkonjak and Pavlovich, 1983).
Inhalation
Pulmonary toxicity
Chronic occupational antimony trioxide exposure may cause "antimony
pneumoconiosis" (Cooper et al, 1968; McCallum, 1989). Typical
radiological findings include diffuse, dense, punctate, non-confluent
opacities predominately in the middle and lower lung fields, sometimes
associated with pleural adhesions (Potkonjak and Pavlovich, 1983).
These changes developed after at least ten years working in an
antimony smelting plant where the dust contained nearly 90 per cent
antimony trioxide with some antimony pentoxide and small amounts (up
to five per cent) of silica (Potkonjak and Pavlovich, 1983). Cough (in
31 of 51 subjects) and exertional breathlessness (in 26 cases) were
the symptoms most frequently reported with wheeze, chest pain or
generalized weakness in a minority. Nine workers had obstructive lung
function defects with a combined restrictive/obstructive picture in
five cases but no isolated restrictive defects or radiological
evidence of diffuse fibrosis.
Pneumoconiosis was reported also in workers at an antimony oxide
production plant. Lung biopsies from two affected individuals revealed
antimony concentrations of 600-3000 µg/g (Le Bouffant et al, 1987)
Perforation of the nasal septum has been described in antimony workers
but these cases probably have involved concomitant arsenic exposure
(McCallum, 1989). There were no cases of nasal septum perforation in
51 workers employed at an antimony smelter for 9-31 years (mean 17.9
years) (Potkonjak and Pavlovich, 1983).
Cardiovascular toxicity
Although ECG changes have been reported in patients treated with
antimony drugs there are no reports following exposure to antimony
trioxide alone.
In the Czechoslovakian literature Klucik and Ulrich (1960) reported
subjective cardiac complaints and ECG changes (not specified in
English abstract) in 14 workers occupationally exposed to antimony
trioxide dust. However, significant antimony trisulphide exposure also
occurred.
Brieger et al (1954) attributed ECG T-wave changes and sudden deaths
to antimony-induced cardiotoxicity following occupational exposure to
antimony trisulphide although the reliability of this study has been
criticized (McCallum, 1989).
An epidemiological study of workers at an antimony processing plant
showed no excess deaths from ischaemic heart disease in workers
exposed to antimony trioxide compared with other employees at the same
site (McCallum, 1989).
Ingestion
Chronic ingestion is not a recognized toxicological hazard.
MANAGEMENT
Dermal exposure
Ensure adequate self protection before attempting treatment. 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. The most effective treatment for irritant antimony
dermatitis is removal from exposure.
Ocular exposure
Irrigate immediately with lukewarm water or preferably saline for at
least 10-15 minutes. A local anaesthetic may be indicated for pain
relief and to overcome blepharospasm. The use of fluorescein allows
detection of corneal damage. Specialist ophthalmological advice should
be sought if any significant abnormality is detected on examination
and in those whose symptoms do not resolve rapidly.
Ingestion
Following substantial ingestion of an antimony compound gastric lavage
may be considered if presentation is within the first hour. There are
no data to confirm that charcoal adsorbs antimony but the
administration to a co-operative patient of 50 g activated charcoal
within the first hour following a suspected substantial ingestion is
reasonable. Other symptomatic and supportive measures should be
dictated by the patient's condition. An ECG should be performed and
biochemical and haematological profiles monitored. Blood and urine
antimony concentrations are not widely available but may be of
interest retrospectively to confirm systemic uptake.
Inhalation
Removal from exposure and measures to secure cardiorespiratory
stability are the priority following acute inhalation of antimony
compounds. An ECG should be performed. Respiratory symptoms in those
with possible chronic antimony toxicity should be investigated as for
other cases of pneumoconiosis. Urine antimony concentrations may be
useful to monitor the initial extent of and subsequent reduction in
exposure but these assays are not widely available.
Antidotes
Dimercaprol (British anti-lewisite, BAL) (Thompson and Whittaker,
1947; Braun et al, 1946), dimercaptosuccinic acid (DMSA, Succimer)
(Basinger and Jones, 1981) and dimercaptopropane sulphonate (DMPS,
Unithiol) (Basinger and Jones, 1981; Hruby and Donner, 1987) have
antidotal activity in experimental systemic antimony poisoning (see
below). These findings have not been confirmed in controlled studies
in man.
Dimercaprol
In vitro studies
Using the pyruvate oxidase system of pigeon brains as a test model,
dimercaprol in a molar ratio of 6:1 dimercaprol: antimony was able to
protect the enzyme system from inhibition by several antimony salts
(Thompson and Whittaker, 1947).
Animal studies
The LD50 of intramuscular antimony tartrate administered to rabbits
was raised from 90 mg Sb/kg in controls to 160 mg Sb/kg in animals
treated with intramuscular dimercaprol (30 mg/kg one hour after
intoxication followed by 15 mg/kg at six, 24 and 48 hours) (Braun et
al, 1946). A total of 45 controls received 50-200 mg/kg antimony
tartrate with 56 treated animals receiving 125-200 mg/kg.
Clinical studies
Four adults with antimony poisoning following the inadvertent
consumption of antimony potassium tartrate were treated with
intramuscular dimercaprol 200-600 mg daily. Three patients made an
uneventful recovery but the fourth, who had a history of
cardiorespiratory disease, died on day three. There were no
pre-chelation antimony excretion data but in two survivors maximum
antimony urine concentrations of 1000 µg/L and 1500 µg/L were reported
some 36 and 72 hours after poisoning respectively. Urine volumes were
not stated (Lauwers et al, 1990).
Bailly et al (1991) reported a 24 year-old woman who made an
uneventful recovery after ingesting an undetermined amount of antimony
trisulphide. She was treated with dimercaprol 200 mg tds for five days
but there was no evidence of enhanced urinary antimony elimination
with therapy.
DMSA
Animal studies
DMSA was given intraperitoneally to mice at a molar ratio of 10:1
DMSA: antimony twenty minutes after administration of potassium
antimonyl tartrate (120 mg/kg; twice the LD50). The survival ratio
was 28/30 (Basinger and Jones, 1981).
Clinical studies
There are no human data.
DMPS
Animal studies
DMPS has been shown to be an effective chelating agent in mice
following intraperitoneal administration of potassium antimonyl
tartrate (120 mg/kg; twice the LD50). The survival rate was 19/30
when intraperitoneal DMPS was given twenty minutes after intoxication
at a molar ratio of 10:1 DMPS: antimony. However, DMSA was
significantly more effective under these conditions (see above)
(Basinger and Jones, 1981).
Clinical studies
There are no human data.
Antidotes: Conclusions and recommendations
1. Clinical data regarding antimony chelation are scarce.
2. Dimercaprol effectively chelates antimony but has been superseded
by the less toxic thiol antidotes DMPS and DMSA.
3. In limited animal studies DMSA is a more effective antimony
chelator than DMPS.
4. Parenteral or oral DMSA therapy may be considered in antimony
trioxide poisoning. The discussion of individual cases with an
NPIS physician is recommended.
MEDICAL SURVEILLANCE
Improved occupational health measures have reduced industrial airborne
antimony concentrations significantly but monitoring of ambient air
antimony concentrations remains important in some industries (Bailly
et al, 1991; Kentner et al, 1995).
Routine examination of the skin for "antimony spots" and chest
radiography for evidence of pneumoconiosis may also be useful. The
potential risk of pulmonary carcinogenicity should be remembered (see
below).
Although Bailly et al (1991) found that urine antimony excretion among
workers exposed to airborne antimony pentoxide and sodium antimoniate
correlated to the intensity of exposure, a recent publication from the
European Commission concluded "no indicator of effect is available"
for biological monitoring of antimony (Apostoli et al, 1994).
Normal concentrations in biological fluids
"Normal" serum and urine antimony concentrations are quoted as
approximately 3 µg/L and 0.8 µg/L respectively (Poisindex, 1997).
OCCUPATIONAL DATA
Maximum exposure limit
Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3
(Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There is some evidence that occupational antimony exposure is
associated with an increased risk of lung cancer although frequent
concomitant exposure to arsenic and other heavy metals precludes a
definitive conclusion about its carcinogenic potential (Gerhardsson et
al, 1982; McCallum, 1989; Gerhardsson and Nordberg, 1993; Jones 1994;
Schnorr et al, 1995).
Antimony also has been implicated in the aetiology of bladder tumours
in patients with schistosomiasis who have been treated with antimony
compounds (Winship, 1987).
The International Agency for Research on Cancer has concluded antimony
trioxide is "possibly carcinogenic to humans" (IARC, 1989).
Reprotoxicity
In the Russian literature women occupational exposed to antimony
aerosols were reported to have a higher incidence of spontaneous
abortion, premature births and menstrual disorders. Antimony was
present in the blood, urine, placentae, amniotic fluid and breast milk
of these women but further details were not available in the English
abstract (Belyaeva, 1967).
Genotoxicity
Bacillus subtilis: produced gene conversion and mitotic
recombination (DOSE, 1992).
Fish toxicity
LC50 (96 hr) bluegill sunfish, fathead minnow 530-833 mg/L (DOSE,
1992).
EEC Directive on Drinking Water Quality 80/778/EEC
Maximum admissible concentration 10 µg/L, as antimony (DOSE, 1992).
WHO Guidelines for Drinking Water Quality
Provisional guideline value 5 µg/L, as antimony (WHO, 1993).
AUTHORS
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
ST Beer BSc
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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