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    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
         1150C                                  (CSDS, 1989)

    Density
         4.63 at 20C                            (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
    g/L) compared to untreated controls (range 2.9-9.1 g/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 g/L, dropping to 2 g/L 20
    hours post ingestion, then falling to 1.5 g/L during the course of
    treatment. The corresponding urine antimony concentration rose to
    600 g/L 20 hours after ingestion and fell to <100 g/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 g/L ("normal" <1.0 g/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 g/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 g/L and 1500 g/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 g/L and 0.8 g/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 g/L, as antimony (DOSE, 1992).

    WHO Guidelines for Drinking Water Quality

    Provisional guideline value 5 g/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

    REFERENCES

    Apostoli P, Porru S, Alessio L.
    Antimony. In: Alessio L, Berlin A. Roi R, van der Venne MT, eds.
    Biological indicators for the assessment of human exposure to
    industrial chemicals.
    Luxembourg: Office for Official Publications of the European
    Communities, 1994.

    Anonymous.
    Metals and the lung.
    Lancet 1984; 2: 903-4.

    Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J.
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    See Also:
       Toxicological Abbreviations