UKPID MONOGRAPH
ANTIMONY
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
Toxbase summary
Type of product
Used in alloys, textiles, catalysts, enamels, ceramics, fireworks and
pigments. Antimony salts are used in the treatment of leishmaniasis
and schistosomiasis.
Toxicity
A fatality has occurred following the mistaken ingestion of tartar
emetic (antimony potassium tartrate). Antimony toxicity more typically
follows the parenteral administration of antimony pharmaceuticals in
the treatment of schistosomiasis and leishmaniasis.
Features
Topical
- Irritant to the skin and eyes.
- Ocular exposure to antimony pentachloride or antimony
trichloride fumes have produced corneal burns.
- "Antimony spots" (papules and pustules around sweat and
sebaceous glands) may develop after repeated exposure.
Ingestion
Moderate ingestions:
- Features usually start within 30 minutes to 2 hours with a
metallic taste, nausea, vomiting, abdominal pain and
diarrhoea. There may be a garlic odour on the breath.
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.
Death may occur from ventricular fibrillation.
- Chronic ingestion may result in anorexia, weight loss,
diarrhoea, peripheral neuropathy, palmar keratosis and skin
rash.
Inhalation
- Irritant to the respiratory tract and mucous membranes:
Conjunctivitis, laryngitis, pharyngitis, tracheitis,
rhinitis and bronchitis, rarely 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.
Injection
- The treatment of leishmaniasis and schistosomiasis has been
associated with anorexia, nausea, vomiting, abdominal pain,
a metallic taste, diarrhoea, pancreatitis, reversible
elevations of liver enzyme activities, myalgia, arthralgia,
proteinuria, ECG changes (T wave inversion, Q-T interval
prolongation, S-T segment abnormalities), phlebitis,
uveitis, optic atrophy and rarely anaphylactic shock, acute
renal failure, hepatic necrosis and bone marrow hypoplasia.
Management
Topical
- Surface decontamination with soap and water where
appropriate.
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.
5. Chelation therapy with dimercaprol, DMSA or DMPS may be
considered, but only after specialist advice from the NPIS.
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.
3. Consider the possibility of systemic toxicity.
Injection
- Discontinue therapy if adverse effects occur and monitor as
above.
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.
Hepburn NC, Siddique I, Howie AF, Beckett GJ, Hayes PC.
Hepatotoxicity of sodium stibogluconate in leishmaniasis.
Lancet 1993; 342: 238-9.
Hepburn NC, Nolan J, Fenn L, Herd RM, Neilson JM, Sutherland GR,
Fox KA.
Cardiac effects of sodium stibogluconate: myocardial,
electrophysiological and biochemical studies.
QJM 1994; 87: 465-72.
Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L.
Oral antimony intoxications in man.
Crit Care Med 1990; 18: 324-6.
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
Origin of substance
Found in many naturally occuring minerals, stibnite (SbS3) is
the major source of the metal.
Synonyms
Antimony black
Antimony black
Stibium (CSDS, 1989)
Chemical group
A group V element
Reference Numbers
CAS 7440-36-0 (CSDS, 1989)
RTECS CC4025000 (RTECS, 1996)
UN 2871 (CSDS, 1989)
HAZCHEM CODE 2Z (CSDS, 1989)
Physico-chemical properties
Chemical structure
Antimony, Sb (DOSE, 1992)
Molecular weight
121.75 (DOSE, 1992)
Physical state at room temperature
Solid
Colour
Silvery white (CSDS, 1989)
Odour
NIF
Viscosity
NA
pH
NA
Solubility
Insoluble in hot or cold water. (HSDB, 1996)
Soluble in hot concentrated sulphuric acid.
(CSDS, 1989)
Autoignition temperature
NIF
Chemical interactions
Finally divided antimony will react violently with nitric acid,
and ammonium nitrate. (NFPA, 1986)
Fumes of antimony hydride may be released on contact with acids.
(Sax, 1984)
Explosive reactions will follow contact of bromoazide with
antimony. (NFPA, 1986)
Antimony will burn spontaneously in gaseous chlorine, fluorine or
bromine. (NFPA, 1986)
Nascent hydrogen will react with antimony to form toxic stibine.
(DOSE, 1992)
Major products of combustion
NIF
Explosive limits
NIF
Flammability
May burn, but will not ignite readily. (HSDB, 1996)
Boiling point
1635°C (CSDS, 1989)
Density
6.684 at 25°C (CSDS, 1989)
Vapour pressure
133.3 Pa at 886°C (CSDS, 1989)
Relative vapour density
NA
Flash Point
NA
Reactivity
NIF
Uses
The most important use of antimony is as an alloying ingredient
with metals such as lead, tin and copper.
Antimony trioxide is used as a flame retardant in textiles, as a
catalyst, and as an opacifier in glass, enamels and ceramics.
Antimony tetroxide is used as an oxidation catalyst.
Antimony trisulphide is used in fireworks, matches, as a pigment,
and in the manufacture of ruby glass.
Antimony pentasulphide is used in vulcanization processes.
Pentavalent antimony preparations (including sodium
stibogluconate) are still used in the treatment of leishmaniasis.
Trivalent compounds (especially antimony potassium tartrate)
inactivate schistosomes by inhibiting the activity of
phosphofructokinase. (Bueding and Fisher, 1966; PATTY, 1994)
Hazard/risk classification
NIF
INTRODUCTION
Antimony is a metalloid since it has properties of both metals and
non-metals. It exists in a trivalent and pentavalent state and forms
inorganic and organic compounds.
Examples of trivalent antimony compounds are antimony trioxide,
antimony trisulphide, antimony trichloride, antimony potassium
tartrate (tartar emetic) and stibine (SbH3).
Pentavalent antimony compounds include antimony pentasulphide and
antimony pentoxide.
Sodium stibogluconate (sodium antimony gluconate) exists with antimony
in both the trivalent and pentavalent forms.
Elemental antimony oxidises slowly in moist air to form a mixture of
antimony and antimony oxide and burns in air to form antimony trioxide
vapour.
Pentavalent antimony is an oxidising agent.
Historically, the systemic administration of antimony compounds has
been used in the treatment of many conditions including syphilis,
whooping cough and gout and topical antimony compounds were believed
to improve herpetic lesions, leprosy, mania and epilepsy. Antimony has
been used also as an emetic, a decongestant and a sedative and still
has a role in the treatment of tropical infections.
Industrial exposure to antimony occurs mainly by inhalation of dust or
fumes during the processing or packaging of antimony compounds.
Antimony poisoning also has occurred following the misuse of
pharmaceuticals.
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 compounds may be absorbed by inhalation and ingestion, though
gastrointestinal absorption in man is poor necessitating parenteral
administration of antimony pharmaceuticals.
Distribution
Absorbed trivalent and pentavalent antimony compounds differ
significantly in their distribution; trivalent compounds have an
affinity for red blood cells whereas pentavalent antimony is found in
the plasma.
Following injection or oral administration significant antimony
concentrations can be found in the liver, kidney, thyroid, adrenals
and bone (Winship, 1987).
Some pentavalent antimony is reduced to the trivalent form in the
liver (Winship, 1987).
Lauwers et al (1990) estimated that the total body pool of antimony 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). Rees et al
(1980) demonstrated that some 80-90 per cent of an intramuscular dose
of sodium stibogluconate was recovered in the urine within six hours
of administration. However, even 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 higher antimony
(p<0.001) concentrations in 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 and its compounds are skin irritants although antimony
dermatitis typically occurs during chronic occupational exposure (see
below) (Poisindex, 1996).
Ocular exposure
Exposure to high concentrations of antimony pentachloride or antimony
trichloride fumes produces severe eye irritation and sometimes corneal
burns (Grant and Schuman, 1993).
Ingestion
Gastrointestinal toxicity
One hundred and fifty children who drank lemon which had been
refrigerated for 20 hours in a large agate pot experienced nausea,
vomiting and diarrhoea which was found to be due to the leaching of
antimony from the agate lining (Werrin, 1963).
In 1982 Miller recounted the death of the author Oliver Goldsmith, who
committed suicide in 1774 by ingesting a mixture of antimony oxide
(antimony trioxide) and potassium tartrate and succumbed after 18
hours from severe vomiting and diarrhoea.
More recently, Lauwers et al (1990) reported four adults who presented
with similar gastrointestinal features having mistaken "tartar emetic"
(antimony potassium tartrate) for "cream of tartar". Three of them
made an uneventful recovery but the fourth died from haemorrhagic
gastritis complicated by cardiorespiratory failure.
A 24 year-old woman who attempted suicide by ingesting an unknown
quantity of antimony trisulphide presented within one hour complaining
of a metallic taste, epigastric pain and dysphagia. She made an
uneventful recovery (Bailly et al, 1991).
Cardiovascular and peripheral vascular toxicity
Electrocardiographic abnormalities are associated typically with
chronic antimony exposure. 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 and its compounds are irritant to the
respiratory tract and mucous membranes and inhalation causes
conjunctivitis, laryngitis, pharyngitis, tracheitis, rhinitis and
bronchitis (Renes, 1953; Taylor, 1966). Metal fume fever has been
described (Anonymous, 1984) though less frequently than following
exposure to zinc oxide.
There may be radiological evidence of pneumonitis which resolves upon
removal from exposure (Renes, 1953).
Inhalation of antimony pentachloride has resulted in pulmonary oedema
(Cordasco, 1974).
Gastrointestinal toxicity
In addition to respiratory tract irritation, seven men exposed to
antimony trichloride fumes also experienced abdominal pain, anorexia,
and vomiting (Taylor, 1966) . Renes (1953) reported similar symptoms
in association with diarrhoea, headache and dizziness, in smelter
workers exposed to antimony fumes.
Injection
Hepatotoxicity
A 27 year-old woman with cutaneous leishmaniasis developed a transient
rise in alaninine aminotransferase activity (to 2.4 times the upper
limit of normal) when she was inadvertently given ten times the
intended dose of parenteral pentavalent sodium stibogluconate
(Herwaldt et al, 1992) but hepatotoxicity is more typically observed
during prolonged therapy with antimony pharmaceuticals.
Cardiovascular toxicity
No cardiovascular complications arose in a patient who accidentally
was given ten times the intended intravenous dose of sodium
stibogluconate (Herwaldt et al, 1992).
CLINICAL FEATURES: CHRONIC EXPOSURE
Dermal exposure
Dermatitis following contact with antimony compounds is well described
although this is not usually a problem after contact with the metal
(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. These so-called "antimony
spots" occur mainly in the summer (McCallum, 1989).
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).
Inhalation
Pulmonary toxicity
Chronic occupational exposure to antimony and its compounds may cause
"antimony pneumoconiosis" (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,
generalised weakness or conjunctivitis 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.
Perforation of the nasal septum has been described in antimony workers
but these cases probably have involved concomitant exposure to arsenic
(McCallum, 1989). There were no cases of nasal perforation in 51
workers employed at an antimony smelter for 9-31 years (mean 17.9
years) (Potkonjak and Pavlovich, 1983).
Brieger et al (1954) attributed ECG T-wave changes and sudden deaths
to antimony-induced cardiotoxicity following occupational exposure to
antimony trisulphide (Sb2S3) although the reliability of this study
has been criticised (McCallum, 1989).
Injection
Dermal toxicity
Davis (1968) reported antimony dermatitis in some four per cent of 160
patients treated with antimonial drugs.
Gastrointestinal toxicity
Patients treated for some one to two weeks with parenteral antimony
compounds frequently reported anorexia, nausea and vomiting with some
complaints of abdominal pain, a metallic taste and diarrhoea (Davis,
1968).
Pancreatitis also has been reported as a complication of parenteral
therapy with stibogluconate or meglumine antimonate (McCarthy et al,
1993; de Lalla et al, 1993; Gasser et al, 1994).
Hepatotoxicity
Parenteral treatment with antimony compounds has caused hepatic
necrosis although reversible elevations of liver enzyme activities are
more typical (Winship, 1987; Saenz et al, 1991; Hepburn et al, 1993).
Nephrotoxicity
In a review of 92 patients with visceral leishmaniasis (kala-azar)
treated with sodium stibogluconate, two developed renal toxicity
manifest as renal casts, proteinuria and an increased serum urea
concentration although these patients were also receiving
intramuscular pentamidine which is recognised renal toxin (Chunge et
al, 1984).
Other patients treated with sodium stibogluconate have developed acute
renal failure (Balzan and Fenech, 1992; Rai et al, 1994b).
Renal tubular acidosis and tubular necrosis have also been described
(Horber et al, 1991; Rai et al, 1994a).
Cardiovascular and peripheral vascular toxicity
ECG changes following exposure to antimony compounds are seen
typically in patients with leishmaniasis or schistosomiasis who have
been treated with parenteral antimony compounds. Typical features
include T wave inversion or amplitude reduction, Q-T interval
prolongation and S-T segment abnormalities (Davis, 1968; Chulay et al,
1985; Henderson and Jolliffe, 1985). These effects usually reverse
when treatment is discontinued.
In 12 soldiers with cutaneous leishmaniasis treated with sodium
stibogluconate Hepburn et al (1994) found that although a reversible
decrease in T-wave amplitude occurred during treatment there were no
significant changes in echocardiographic induces of left ventricular
function, arrhythmia frequency or heart-rate variability. The authors
concluded that 20 mg/kg/day sodium stibogluconate for 20 days had no
cardiac side-effects in most fit, young patients.
Gupta (1990) similarly noted that T-wave changes induced by antimony
therapy were not associated with a deterioration in cardiac function.
In a review of 160 patients with schistosomiasis treated with
antimonal drugs (Davis, 1968) retrosternal chest pain was reported by
27 individuals. In three cases this was associated with acute vascular
collapse immediately after intravenous drug administration (after the
first dose in one case) suggesting an anaphylactic-type response.
Phlebitis occurred in 31 patients receiving intravenous sodium
stibogluconate in the treatment of visceral leishmaniasis (Chunge et
al, 1984) and in one patient administered antimony sodium tartrate in
the treatment of urinary schistosomiasis (Davis, 1968).
Neurotoxicity
Rai et al (1994b) described combined ninth and tenth cranial nerve
palsies in a patient with kala-azar treated with parenteral
stibogluconate.
Haemotoxicity
Mallick (1990) described bone marrow hypoplasia as a complication of
sodium stibogluconate administration and other authors have described
leucopenia (Hiēsönmez et al, 1988; Saenz et al, 1991) or recurrent
episodes of thrombocytopenia (Braconier and Miörner, 1993) during
parenteral antimonial therapy.
Chunge et al (1984) also reported epistaxis in 13 patients, in three
cases associated with pancytopenia.
Musculoskeletal toxicity
Myalgia and arthralgia are reported frequently by patients with
leishmaniasis or schistosomiasis treated with parenteral antimony
compounds (Davis, 1968; Winship, 1987; Castro et al, 1990; Saenz et
al, 1991).
Ocular toxicity
Parenteral treatment with antimony potassium tartrate (tartar emetic)
in the treatment of leishmaniasis has resulted in bilateral blindness
with dilated unreactive pupils and optic atrophy (Grant and Schuman,
1993).
In a review of 92 patients with visceral leishmaniasis treated with
parenteral stibogluconate, eight developed eye disease (after
completion of treatment and apparent cure) including uveitis and
retinal haemorrhages (Chunge et al, 1984).
Forsyth (1958) reported one patient who developed transient retinal
haemorrhages and exudates and another in whom the fundus was described
as 'granular' following parenteral sodium antimony tartrate therapy
for schistosomiasis. Visual acuity was diminished in both cases but
returned to normal within six months.
Three children who received repeated courses of parenteral tartar
emetic in the treatment of schistosomiasis developed irreversible
optic atrophy (Kassem et al, 1976).
MANAGEMENT
Ingestion
Decontamination
Following 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
cooperative 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.
Inhalation
Removal from exposure and measures to secure cardiorespiratory
stability are the priority following acute inhalation of antimony
compounds. 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.
Antidotes
Dimercaprol (Thompson and Whittaker, 1947; Braun et al, 1946), DMSA
(Basinger and Jones, 1981) and DMPS (Basinger and Jones, 1981; Hruby
and Donner, 1987) have antidotal activity in experimental systemic
antimony poisoning (see below) but these findings have not been
confirmed in controlled studies in man.
Dimercaprol
Using the pyruvate oxidase system of pigeon brains as a test model,
dimercaprol was able to protect the enzyme system from inhibition by
several antimony salts (Thompson and Whittaker, 1947). 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. In two survivors treatment was associated
with an apparent increased urine antimony excretion (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 for five days (200 mg
tds) but there was no evidence of enhanced urinary antimony
elimination with therapy.
DMSA and DMPS
The antidotal efficacy of thiol chelating agents was examined in
animal survival experiments. Twenty minutes following intraperitoneal
administration to mice of potassium antimonyl tartrate at twice the
LD50 (120 mg/kg), DMSA or DMPS were given intraperitoneally at a
molar ratio of 10:1 chelating agent: antimony. The overall survival
rates were 28/30 and 19/30 respectively, indicating that both
chelating agents were effective, with DMSA superior in the conditions
of this study (Basinger and Jones, 1981). There are no human data.
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.
Although Bailly et al, (1991) found that the urinary antimony
excretion of workers exposed to airborne antimony pentoxide and sodium
antimoniate correlated to the intensity of exposure, a recent
publication from the European Commission concluded there is "no
indicator of effect is available" for biological monitoring of
antimony (Alessio et al, 1994).
'Normal' serum and urine antimony concentrations are approximately 3
µg/L and 0.8 µg/L respectively (Poisindex, 1996).
OCCUPATIONAL DATA
Occupational exposure standard
Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3
(Health and Safety Executive, 1995).
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 the bladder
tumours in patients with schistosomiasis who have been treated with
antimony compounds (Winship, 1987).
Reprotoxicity
Women occupationally 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,
placenta, amniotic fluid and breast milk of these women (Belyaeva,
1967).
Genotoxicity
NIF
Fish toxicity
LC50 (28 day) rainbow trout 0.66 mg/L (DOSE, 1992).
EEC Directive on Drinking Water Quality 80/778/EEC
Maximum admissible concentration 10 µg/L (DOSE, 1992).
AUTHORS
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
16/7/96
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Experimental and human studies on antimony metabolism: their relevance
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Acute renal failure in visceral leishmaniasis treated with sodium
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Structural requirements for chelate antidotal efficacy in acute
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