UKPID MONOGRAPH
ANTIMONY TRISULPHIDE
WN Harrison PhD
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 TRISULPHIDE
Toxbase summary
Type of product
Used as a plasticizer and pigment, and in pyrotechnics and explosives.
Toxicity
Acute antimony trisulphide 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,
especially in warm conditions.
Ingestion
Moderate ingestions:
- Features usually occur within 2 hours with a metallic taste,
nausea, vomiting, abdominal pain and diarrhoea. A garlic
odour on the breath has been described following ingestion
of other antimony compounds.
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.
Inhalation
- Irritant to the respiratory tract and mucous membranes
causing conjunctivitis, laryngitis, pharyngitis, tracheitis,
rhinitis and 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 on chest X-ray.
- ECG T-wave changes and sudden deaths attributed to antimony-
induced cardiotoxicity have been reported rarely following
occupational exposure.
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.
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 trisulphide
Origin of substance
Produced by the addition of sodium thiosulphate to antimony
potassium tartrate. Occurs naturally as the ore stibnite.
IARC, 1989)
Synonyms
Antimonous sulphide
Antimony vermilion
Antimony glance
Diantimony trisulphide
Antimony orange (CSDS, 1989)
Chemical group
A compound of antimony, a group VA element
Reference numbers
CAS 1345-04-6 (CSDS, 1989)
RTECS C 9450000 (CSDS, 1989)
UN 1549 (CSDS, 1989)
HAZCHEM NIF
Physicochemical properties
Chemical structure
Sb2S3 (CSDS, 1989)
Molecular weight
339.68 (HSDB, 1997)
Physical state at room temperature
Crystalline powder (CSDS, 1989)
Colour
Grey-black (CSDS, 1989)
Odour
NIF
Viscosity
NA
pH
NIF
Solubility
Practically insoluble in water, soluble in concentrated
hydrochloric acid or excess alkali. (CSDS, 1989)
Autoignition temperature
NA
Chemical interactions
Reacts with water or steam to produce flammable vapours of
hydrogen sulphide. (HSDB, 1997)
Major products of combustion
When heated to decomposition emits fumes of sulphur and antimony
oxides. (HSDB, 1997)
Explosive limits
NA
Flammability
Burns with blue flame. (HSDB, 1997)
Boiling point
1150°C (CSDS, 1989)
Density
4.63 at 20°C (CSDS, 1989)
Vapour pressure
NA
Relative vapour density
NA
Flash point
NA
Reactivity
Reacts violently with water and oxidizing agents.
(HSDB, 1997)
Uses
Used in pyrotechnics and explosives.
Plasticizer and pigment in the rubber industry.
(CSDS, 1989)
Hazard/risk classification
NIF
INTRODUCTION
Antimony trisulphide is a trivalent antimony compound which occurs
naturally as the ore stibnite. It is used in the production of
antimony trioxide and often is associated with arsenic. It is produced
also by the addition of sodium thiosulphate to a solution of an
antimony salt.
Antimony trisulphide is used as a primer in ammunition and smoke
markers. It is used also in red and yellow pigments and in ruby glass
manufacture.
EPIDEMIOLOGY
The main source of antimony trisulphide exposure is in the milling and
refining of stibnite for antimony trioxide production (Renes, 1953;
Schnorr et al, 1995). Exposure has occurred also in the production
(Bulmer and Johnston, 1948) and use (Brieger et al, 1954) of antimony
trisulphide powder in industry.
lntentional ingestion of a veterinary preparation containing antimony
trisulphide has been reported (Bailly et al, 1991). Accidental
intoxication has also occurred after antimony leached from an agate
container into an acidic beverage (Werrin, 1963).
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 trisulphide 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 at a starter battery manufacturing plant.
CLINICAL FEATURES: ACUTE EXPOSURE
Dermal exposure
Antimony trisulphide is an irritant although antimony dermatitis
typically occurs during chronic occupational exposure to antimony
trioxide.
Ocular exposure
Antimony trisulphide is an eye irritant.
Ingestion
Acute poisoning is rare. Antimony trisulphide is poorly soluble and is
not absorbed readily from the gastrointestinal tract.
Gastrointestinal toxicity
A 24 year-old woman was admitted to hospital within an hour of
ingesting an unknown quantity of antimony trisulphide used in
veterinary practice. The patient complained of epigastric pain,
dysphagia and a metallic taste although clinical examination was
normal. Immediate gastric lavage was followed by forced diuresis
(10-14 L/24 h), repeated gastric aspiration and chelation therapy with
dimercaprol 200 mg tds for five days. At presentation the blood
antimony concentration was approximately 5 µg/L, dropping to 2 µg/L 20
hours post ingestion, then falling to 1.5 µg/L during the course of
treatment. The corresponding urine antimony concentration rose to
600 µg/L 20 hours after ingestion and fell to <100 µg/L over the next
six days. Routine biological tests remained in the normal range. No
clinical signs of intoxication developed and the patient was
discharged after six days (Bailly et al, 1991).
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).
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 trisulphide are irritant to the
respiratory tract and mucous membranes and inhalation causes
laryngitis, pharyngitis, tracheitis, rhinitis, epistaxis and
bronchitis (Renes, 1953). However, most reports are of concomitant
exposure to antimony trioxide produced from smelting antimony
trisulphide ore. 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
supportive care for several days "provided relief".
CLINICAL FEATURES: CHRONIC EXPOSURE
The major source of antimony trisulphide exposure is as an ore (which
may also contain arsenic) used in the production of antimony and
antimony trioxide. Inhalation and dermal contact are the most common
routes of exposure.
Dermal exposure
Dermatitis following contact with antimony compounds is well described
(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, 1963). These so-
called "antimony spots" occur mainly in the summer (McCallum, 1989)
and are usually associated with antimony trioxide exposure.
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 skin areas. 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 cause enlargement of the lesions. The author concluded
that antimony trioxide dust initiated an irritant reaction when it
penetrated the 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. Symptoms 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 compounds are irritant to the eye. 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 exposure to antimony 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 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)
No symptoms of respiratory and mucous membrane irritation usually
associated with antimony exposure were reported in 125 workers exposed
to 3.0-5.5 mg/m3 antimony trisulphide. However, an increased
incidence of gastric ulcer, abnormal ECG changes and sudden deaths was
noted as discussed below (Brieger et al, 1954).
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
In the Czechoslovakian literature Klucik and Ulrich (1960) reported
subjective cardiac complaints and ECG changes (not specified in the
English abstract) in 14 workers occupationally exposed to antimony
trisulphide.
Brieger et al (1954) attributed ECG T-wave changes and sudden deaths
to antimony-induced cardiotoxicity following occupational exposure to
antimony trisulphide. This compound replaced lead in a resin grinding
process exposing 125 workers to some 3.0-5.5 mg/m3 for eight months
to two years. Six sudden deaths and two deaths from chronic heart
disease occurred during this period compared to one death (from
coronary thrombosis) in the previous 16 years. One hundred and
thirteen employees were examined; 14 had a blood pressure over 150/90
mmHg and 24 under 110/70 mmHg. A further 37 of 75 workers examined
showed "significant" ECG changes, mostly of the T-waves. Random urine
samples contained 0.8-9.6 mg Sb/L. No further cardiovascular related
deaths were reported following removal of antimony trisulphide from
the process though ECG changes persisted in 12 of 56 individuals
examined several years later.
Gastrointestinal toxicity
"Gastrointestinal disturbances" were reported in workers exposed to
3.0-5.5 mg/m3 antimony trisulphide for between eight months and two
years. Radiological studies revealed peptic ulcers in seven of 111
individuals examined (6.3 per cent) compared to 1.5 per cent in the
total plant population (Brieger et al, 1954).
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 antimony induced irritant dermatitis
and "antimony spots" 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
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
Antimony trisulphide is not classifiable as to its carcinogenicity to
humans (IARC, 1989).
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).
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. Further details were not available in the English
abstract (Belyaeva, 1967).
Genotoxicity
NIF
Fish toxicity
Rainbow trout: LC50 for trivalent antimony 0.66 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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