SM Bradberry BSc MB MRCP
    ST Beer BSc

    National Poisons Information Service
    (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    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


    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.


    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.



         -    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.


    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


         -    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.


         -    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.



         -    Surface decontamination with soap and water where


    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
    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.


    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

    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.


         -    Discontinue therapy if adverse effects occur and monitor as


    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
    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


    Origin of substance

         Found in many naturally occuring minerals, stibnite (SbS3) is
         the major source of the metal.


         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

         Silvery white                           (CSDS, 1989)




         Insoluble in hot or cold water.         (HSDB, 1996)
         Soluble in hot concentrated sulphuric acid.
                                                 (CSDS, 1989)

    Autoignition temperature

    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

    Explosive limits

         May burn, but will not ignite readily.  (HSDB, 1996)

    Boiling point
         1635°C                                  (CSDS, 1989)

         6.684 at 25°C                           (CSDS, 1989)

    Vapour pressure
         133.3 Pa at 886°C                       (CSDS, 1989)

    Relative vapour density

    Flash Point



         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



    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

    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


    The mechanism of toxicity of antimony compounds is unclear but may
    involve disruption of thiol proteins via binding to sulphydryl groups
    (de Wolff, 1995).



    Antimony compounds may be absorbed by inhalation and ingestion, though
    gastrointestinal absorption in man is poor necessitating parenteral
    administration of antimony pharmaceuticals.


    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).


    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.


    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).


    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,


    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.



    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).


    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,


    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).


    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,

    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).


    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).


    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).


    Rai et al (1994b) described combined ninth and tenth cranial nerve
    palsies in a patient with kala-azar treated with parenteral


    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,

    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).




    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.


    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.


    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.


    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,

    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.


    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 exposure standard

    Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3
    (Health and Safety Executive, 1995).



    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).


    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,



    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).


    SM Bradberry BSc MB MRCP
    ST Beer BSc

    National Poisons Information Service (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    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


    Apostoli P, Porru S, Alessio L.
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    Luxembourg: Office for Official Publications of the European
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    for the biological monitoring of workers exposed to inorganic
    Br J Ind Med 1991;48: 93-7.

    Balzan M, Fenech F.
    Acute renal failure in visceral leishmaniasis treated with sodium
    Trans R Soc Trop Med Hyg 1992; 86: 515-6.

    Basinger MA, Jones MM.
    Structural requirements for chelate antidotal efficacy in acute
    antimony(III) intoxication.
    Res Commun Chem Pathol Pharmacol 1981; 32: 355-63.

    Belyaeva AP.
    The effect produced by antimony on the generative function.
    Gig Tr Prof Zabol 1967; 11: 32-7.

    Braconier JH, Miörner H.
    Recurrent episodes of thrombocytopenia during treatment with sodium
    stibogluconate (letter).
    J Antimicrob Chemother 1993; 31: 187-8.

    Braun HA, Lusky LM, Calvery HO.
    The efficacy of 2,3-dimercaptopropanol (BAL) in the therapy of
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    J Pharmacol Exp Ther 1946; 87: 119-25.

    Brieger H, Semisch CW, Stasney J, Piatnek DA.
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