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    UKPID MONOGRAPH




    ANTIMONY (III) TRICHLORIDE




    SM Bradberry BSc MB MRCP
    WN Harrison PhD CChem MRSC
    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 TRICHLORIDE

    Toxbase summary

    Type of product

    Used as a chemical reagent and in veterinary practice.

    Toxicity

    Acute antimony trichloride poisoning is rare.  Exposure may occur in
    industry.  Fatal dose not known.

    Features

    Dermal

         -    Antimony trichloride is irritating to the skin and may cause
              serious burns.

    Ocular

         -    Direct contact may irritate or burn the eye causing pain,
              blepharospasm, lacrimation and photophobia.

    Inhalation

         -    Cough and retrosternal discomfort may be the only early
              features. Following significant exposure hoarseness,
              dyspnoea and stridor (due to laryngeal oedema) may develop.
              In the most severe cases the onset of non-cardiogenic
              pulmonary oedema with increasing breathlessness, wheeze and
              cyanosis may be delayed for up to 36 h.
         -    Systemic features may develop (see antimony Toxbase entry).

    Ingestion

         -    Antimony trichloride ingestion will cause burning of the
              mouth and throat with retrosternal and abdominal pain,
              nausea and vomiting. Severe irritant or corrosive effects
              are likely following substantial ingestion with
              hypersalivation, haematemesis and hypovolaemic shock.
         -    Severe effects may be expected in the mouth and throat where
              contact with saliva will produce hydrochloric acid.
         -    There is a risk of gastric antrum ulceration, haemorrhage
              and perforation.
         -    The larynx may be burned, with oedema causing airway
              obstruction.
         -    Obstructive symptoms due to oesophageal or gastric stricture
              may develop weeks or months later.
         -    Systemic features may develop (see antimony Toxbase entry).

    Management

    Dermal

    1.   Before attempting treatment ensure adequate measures are taken to
         prevent self exposure.
    2.   Wear protective clothing and carry out decontamination in a well
         ventilated area, preferably with its own ventilation system.
    3.   The patient should remove soiled clothing and wash him/herself if
         possible.
    4.   Wash hair and all contaminated skin with copious amounts of
         water.
    5.   Pay special attention to skin folds, fingernails and ears.
    6.   Burns should be treated conventionally as thermal burns. Surgery
         may be required for deep burns.

    Ocular

    1.   Immediately irrigate the affected eye thoroughly with tepid water
         or 0.9 per cent saline.
    2.   Any particles lodged in the conjunctival recesses should be
         removed.
    3.   Continue irrigation with saline infusion (using drip tubing) for
         at least 10-15 minutes.
    4.   Repeated instillation of local anaesthetics (e.g. amethocaine)
         may reduce discomfort and help more thorough decontamination.
    5.   Corneal damage may be detected by instillation of fluorescein.
    6.   Patients with corneal damage, those who have been exposed to
         strong acids and those whose symptoms do not resolve rapidly
         should be referred for ophthalmological assessment.

    Inhalation

    1.   Remove from exposure.
    2.   Give high-flow oxygen by face mask.
    3.   Intubation and assisted ventilation may be necessary.
    4.   Rarely tracheostomy may be required for life-threatening
         laryngeal oedema.
    5.   Corticosteroids in high dosage (prednisolone 60-80 mg/day) may be
         considered for laryngeal and pulmonary oedema but there is no
         confirmed evidence that they improve prognosis. Discuss with an
         NPIS physician.
    6.   If systemic features develop treat as for antimony (see separate
         entry)

    Ingestion

    1.   Secure a clear airway and support respiration as necessary.
    2.   DO NOT attempt gastric lavage.
    3.   There may be some benefit in attempting oral dilution if
         performed immediately, but fluids should not be offered if there
         is inadequate airway protection or severe abdominal pain.

    4.   Morphine may be required for pain,
    5.   Treat shock by replacing lost fluids and blood intravenously.
    6.   Monitor urine output and renal function.
    7.   Early fibreoptic oesophago-gastroscopy (ideally within 24 h) by
         an experienced endoscopist is indicated in symptomatic patients
         to grade the severity of injury and determine prognosis.
    8.   Corticosteroids confer no benefit and may mask abdominal signs of
         perforation.
    9.   An aggressive surgical approach is favoured in those with
         suspected perforation or severe (grade 3) burns.
    10.  In severe cases seek specialist advice from an NPIS physician.
    11.  If systemic features develop treat as for antimony (see separate
         entry).

    References

    Anderson KD, Rouse TM, Randolph JG.
    A controlled trial of corticosteroids in children with corrosive
    injury of the esophagus.
    N Engl J Med 1990; 323: 637-40.

    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.

    Jeng L-BB, Chen H-Y, Chen S-C, Hwang T-L, Jan Y-Y, Wang C-S,
    Chen M-F.
    Upper gastrointestinal tract ablation for patients with extensive
    injury after ingestion of strong acid.
    Arch Surg 1994; 129: 1086-90.

    Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L.
    Oral antimony intoxications in man.
    Crit Care Med 1990; 18: 324-6.

    Miller JM.
    Poisoning by antimony: a case report.
    South Med J 1982; 75: 592.

    Taylor PJ.
    Acute intoxication from antimony trichloride.
    Br J Ind Med 1966; 23: 318-21.

    Winship KA.
    Toxicity of antimony and its compounds.
    Adverse Drug React Acute Poisoning Rev 1987; 2: 67-90.

    Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK.
    Ingestion of corrosive acids. Spectrum of injury to upper
    gastrointestinal tract and natural history.
    Gastroenterology 1989; 97: 702-7.

    Substance name

         Antimony (III) trichloride

    Origin of substance

         Reaction of antimony trisulphide and hydrochloric acid.
                                            (MERCK, 1996)

    Synonyms

         Antimonous chloride
         Antimony chloride
         Antimony butter
         Trichlorostibine
         C.I. 77056                         (MERCK, 1996; RTECS, 1997)

    Chemical group

         A compound of antimony, a group V A element.

    Reference numbers

         CAS       10025-91-9               (DOSE, 1992)
         RTECS     CC4900000                (RTECS, 1997)
         UN        1733                     (DOSE, 1992)
         HAZCHEM   4WE                      (DOSE, 1992)

    Physicochemical properties

    Chemical structure
         SbCl3                              (DOSE, 1992)

    Molecular weight
         228.11                             (DOSE, 1992)

    Physical state at room temperature
         Solid                              (CHRIS, 1997)

    Colour
         White to pale yellow               (OHM/TADS, 1997)

    Odour
         Sharp, unpleasant                  (HSDB, 1997)

    Viscosity
         NIF

    pH
         NIF

    Solubility
         Water: 99 g/L.
         Soluble in benzene, acetone, ethanol, chloroform, hydrochloric
         acid, tartaric acid, dioxane, carbon disulphide, ether and carbon
         tetrachloride.
         Insoluble in pyridine, quinoline and other organic bases.
                                            (MERCK, 1996; HSDB, 1997)

    Autoignition temperature
         NIF

    Chemical interactions
         Trivalent antimony tends to form explosive mixtures with
         perchloric acid when hot.
         Powdered aluminium burns in antimony trichloride vapour.
                                            (HSDB, 1997)

    Major products of combustion
         When heated to decomposition antimony trichloride emits fumes of
         chloride and antimony.             (SAX's, 1996)

    Explosive limits
         NA

    Flammability
         Non flammable                      (OHM/TADS, 1997)

    Boiling point
         283C                              (DOSE, 1992)

    Density
         3.14 at 20C/4C                   (MERCK, 1996)

    Vapour pressure
         133.322 at 49.2C                  (DOSE, 1992)

    Relative vapour density
         NIF

    Flash point
         NA

    Reactivity
         Antimony trichloride reacts vigorously with moisture, generating
         heat and hydrogen chloride gas.
         Corrodes most metals in the presence of moisture.
                                            (CHRIS, 1997; HSDB, 1997)

    Uses

         Mordant for patent leather and for dyeing.
         For bronzing iron.
         Chemical reagent/catalyst.
         Colouring zinc black.
         In the manufacture of other antimony salts.
         Veterinary escharotic and dehorning agent.
                                            (DOSE, 1992; MERCK, 1996)

    Hazard/risk classification

    Index no.  051-001-00-8

    Risk phases
         R34-37 - Causes burns. Irritating to respiratory system.

    Safety phrases
         S(1/2-) 26-45 -Keep locked up and out of the reach of children.
         In case of contact with eyes, rinse immediately with plenty of
         water and seek medical advice. In case of accident or if you feel
         unwell, seek medical advice immediately (show label where
         possible).

    EEC No. 233-047-2                       (CHIP2, 1994)

    INTRODUCTION

    Antimony trichloride is a trivalent antimony compound. It is produced
    commercially by the reaction of antimony trisulphide and hydrochloric
    acid.

    Antimony trichloride is used widely as a chemical reagent and has been
    used in veterinary practice.

    Due to the acidic nature of antimony trichloride exposure may produce
    corrosive injury as well as systemic antimony toxicity.

    EPIDEMIOLOGY

    Antimony trichloride poisoning is rare and is likely only to occur
    occupationally.

    Seven men were exposed to fumes and spray containing antimony
    trichloride following a pump leak during an industrial process. Three
    other men were also exposed on two separate occasions (Taylor, 1966).

    MECHANISM OF TOXICITY

    Antimony trichloride reacts with water to form hydrochloric acid which
    has a direct corrosive effect on mucous membranes.

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

    TOXICOKINETICS

    Absorption

    Antimony trichloride may be absorbed by inhalation. Urine antimony
    concentrations of 1.0 to 5.1 mg/L were measured in workers two days
    after exposure to spray and vapour containing an estimated 73 mg/m3
    antimony (Taylor, 1966).

    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 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). 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).

    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 trichloride is an irritant and concentrated solutions or
    solid material may cause burns.

    Four men were exposed to vapour and spray from a solution containing
    98 per cent antimony trichloride in hydrochloric acid. The most
    severely affected individual suffered a second degree burn to the
    upper chest which healed within 10 days (Taylor, 1966).

    Ocular exposure

    Two men sustained first and second degree burns around both eyes with
    oedema of the lids and conjunctivae following exposure to vapour and
    spray from a 98 per cent solution of antimony trichloride in
    hydrochloric acid. The more severely affected individual suffered a
    small superficial corneal ulcer which cleared within three days. The
    remaining burns cleared within 10 days (Taylor, 1966).

    Contact with solutions of antimony trichloride in hydrochloric acid
    have caused "destruction" of the cornea and conjunctivae (Grant and
    Schuman, 1993).

    Ingestion

    There are no reports of antimony trichloride ingestion although
    corrosive injury may be expected. Systemic antimony toxicity may
    develop also (see antimony monograph).

    Acid ingestions typically produce severe stomach lesions (Hawkins et
    al, 1980) with relative sparing of the oesophagus. However, severe
    caustic effects following antimony trichloride ingestion may be
    expected in the mouth, throat and oesophagus where contact with saliva
    will produce hydrochloric acid locally.

    Gastrointestinal toxicity

    Common early features of corrosive ingestion include immediate pain in
    the mouth, pharynx and abdomen, intense thirst, vomiting, haematemesis
    and diarrhoea. Gastric and oesophageal perforation and chemical
    peritonitis may also occur.

    Late features include antral or pyloric stenosis, jejunal stricture
    formation, achlorhydria, protein-losing gastroenteropathy and gastric
    carcinoma.

    Pulmonary toxicity

    Features associated with corrosive ingestion include hoarseness,
    stridor, respiratory distress and, in severe cases, laryngeal or
    epiglottal oedema. Chemical pneumonitis and adult respiratory distress
    syndrome (ARDS) are recognized.

    Nephrotoxicity

    Renal failure secondary to acute tubular necrosis may complicate
    antimony trichloride ingestion.

    Cardiovascular toxicity

    Circulatory collapse is likely in patients with extensive
    gastrointestinal burns.

    Haemotoxicity

    Disseminated intravascular coagulation and haemolysis may complicate
    concentrated corrosive ingestions.

    Inhalation

    Pulmonary toxicity

    Seven workers suffered irritation of the upper respiratory tract
    following exposure to an estimated 146 mg/m3 hydrochloric acid
    released from a 98 per cent antimony trichloride solution. Two
    individuals showed nasopharyngeal erythema. All the men recovered
    fully within 24 hours (Taylor, 1966).

    Severe laryngeal and pulmonary oedema have been reported following
    inhalation of a corrosive antimony compound (Cordasco and Stone,
    1973).

    Gastrointestinal toxicity

    Seven workers were exposed to vapour containing an estimated 
    73 mg/m3 antimony released from a 98 per cent antimony trichloride
    solution. Two of the men showed no systemic effects. However, four
    individuals developed nausea then abdominal pain some eight hours to
    one day post exposure. The abdominal pain resolved within two to five
    days. The same individuals also reported loss of appetite lasting from
    three to ten days. A fifth person reported loss of appetite on the day
    following exposure only. Three of the workers vomited some hours
    following exposure (Taylor, 1966).

    Urinalysis of samples taken one to two days post exposure showed
    antimony concentrations between 1.0 and 5.1 mg/L (Taylor, 1966).

    Neurotoxicity

    Two of the workers described above developed headaches some hours
    following exposure (Taylor, 1966).

    CLINICAL FEATURES: CHRONIC EXPOSURE

    There are no reports on the chronic toxicity of antimony trichloride
    though the effects of exposure to other antimony compounds have been
    reported.

    Dermal exposure

    Dermatitis following contact with antimony trioxide is well described
    (Oliver, 1933; McCallum, 1989). Typical lesions arise on the arms,
    legs and in the flexures, sparing the face, hands and feet (Renes,
    1953; McCallum, 1989).

    Papules and pustules predominate around sweat and sebaceous glands
    with areas of eczema and lichenification (Paschoud, 1963). These
    so-called "antimony spots" occur mainly in the summer (McCallum,
    1989).

    Skin lesions developed in 23 men employed at an antimony trioxide
    production plant. Most of those affected were furnace workers with
    lesions typically appearing within two weeks of exposure. Itching,
    erythematous papules and pustular eruptions were characteristic,
    usually on dust laden sweaty areas of the skin. The lesions usually
    resolved over two weeks in those removed to cooler parts of the
    factory. Histological examination showed epidermal cellular necrosis
    associated with an acute dermal inflammatory cellular reaction.
    Antimony trioxide patch testing was negative whilst injection of
    methacholine into the affected areas caused enlargement of the
    lesions. The author concluded that antimony trioxide dust initiates an
    irritant reaction when it penetrates sweat ducts (Stevenson, 1965).

    White et al (1993) described three cases of occupational antimony
    dermatitis following several months exposure to antimony dust and
    antimony trioxide fumes. Two of these patients also experienced
    frequent nose bleeds. Both problems resolved when exposure ceased. In
    one patient patch testing for antimony was negative and in another the
    urine antimony concentration was 53.2 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).

    Inhalation

    Pulmonary toxicity

    Chronic occupational exposure to antimony compounds may cause
    "antimony pneumoconiosis" (Cooper et al, 1968; McCallum, 1989).
    Typical radiological findings include diffuse, dense, punctate
    non-confluent opacities predominately in the middle and lower lung
    fields, sometimes associated with pleural adhesions (Potkonjak and
    Pavlovich, 1983).

    These changes developed after at least ten years working in an
    antimony smelting plant where the dust contained nearly 90 per cent
    antimony trioxide with some antimony pentoxide and small amounts (up
    to five per cent) of silica (Potkonjak and Pavlovich, 1983). Cough (in
    31 of 51 subjects) and exertional breathlessness (in 26 cases) were
    the symptoms most frequently reported with wheeze, chest pain or
    generalized weakness in a minority. Nine workers had obstructive lung
    function defects with a combined restrictive/obstructive picture in
    five cases but no isolated restrictive defects or radiological
    evidence of diffuse fibrosis.

    Pneumoconiosis was reported also in workers at an antimony oxide
    production plant. Lung biopsies from two affected individuals revealed
    antimony concentrations of 600-3000 g/g (Le Bouffant et al, 1987).

    Perforation of the nasal septum has been described in antimony workers
    but these cases probably have involved concomitant arsenic exposure
    (McCallum, 1989). There were no cases of nasal perforation in 51
    workers employed at an antimony smelter for 9-31 years (mean 17.9
    years) (Potkonjak and Pavlovich, 1983).

    Cardiovascular toxicity

    ECG changes have been reported in patients treated with antimony
    drugs.

    In the Czechoslovakian literature Klucik and Ulrich (1960) reported
    subjective cardiac complaints and ECG changes in 14 workers
    occupationally exposed to antimony trioxide dust. Significant exposure
    to antimony trisulphide also occurred.

    Brieger et al (1954) attributed ECG T-wave changes and sudden deaths
    to antimony-induced cardiotoxicity following occupational exposure to
    antimony trisulphide although the reliability of this study has been
    criticized (McCallum, 1989).

    An epidemiological study of workers at an antimony processing plant
    showed a decrease in the number of deaths from ischaemic heart disease
    in workers exposed to antimony trioxide compared with other employees
    at the same site (McCallum, 1989).

    Ingestion

    Chronic ingestion is not a recognized toxicological hazard.

    MANAGEMENT

    Dermal exposure

    Ensue 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. Burns should be treated conventionally as for thermal burns
    (e.g. silver sulphadiazine dressing). Surgery may be required for deep
    burns.

    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.

    Inhalation

    Immediate management involves removal from exposure, establishment of
    a clear airway and administration of supplemental oxygen if necessary.
    Mechanical ventilation may be required. Rarely tracheostomy may be
    necessary for life-threatening laryngeal oedema. The administration of
    prednisolone 60-80 mg daily may be considered if laryngeal or
    pulmonary oedema are present but there is no confirmed evidence that
    their use alters prognosis. Discussion of individual cases with an
    NPIS physician is recommended.

    If systemic toxicity is suspected laboratory confirmation of blood and
    urine antimony concentrations should be obtained. Antidotal treatment
    may be considered in confirmed cases (see Antidotes).

    Ingestion

    Decontamination

    Gastric aspiration/lavage is contraindicated. There may be some
    benefit in attempting oral dilution with milk or water, if performed
    immediately, though this is controversial.

    Fluids should not be offered if the patient is not fully conscious, is
    unable to swallow or protect his/her own airway, has respiratory
    difficulty or severe abdominal pain. Possible complications of fluid
    administration include vomiting, aspiration, perforation of the
    gastrointestinal tract and worsening of oesophageal or gastric
    injuries.

    Supportive measures

    Airway support and analgesia should be provided as required. Treat
    shock with intravenous colloid/crystalloid and/or blood. Monitor
    biochemical and haematological profiles and acid/base status.
    Administer antibiotics for established infection only.

    Symptoms and signs are unreliable predictors of the extent of injury
    following acid ingestion (Zargar et al, 1989) and therefore in
    symptomatic patients panendoscopy should be carried out, ideally
    within 12-24 hours to gauge the severity of injury.

    Grade 0:  Normal examination
          1:  Oedema, hyperaemia of mucosa
          2a: Superficial, localized ulcerations, friability, blisters
          2b: Grade 2a findings and circumferential ulceration
          3:  Multiple, deep ulceration, areas of necrosis (Zargar et al,
              1989)

    Following corrosive acid ingestion endoscopic findings within the
    first 36 hours have been successfully used to guide management. In a
    series of 41 patients (Zargar et al, 1989) those with grade 0 and 1
    burns were discharged within one or two days, those with grade 2a
    burns required only supportive care for a little longer, whereas those
    with grade 2b and 3 burns required nutritional support via jejunostomy
    feeding (total parenteral nutrition is an alternative). All patients
    with grade 0, 1 and 2a injury recovered without sequelae. Acute
    complications and death were confined to those with grade 3 burns
    although several patients with grade 2b burns developed oesophageal or
    gastric strictures.

    In view of the high morbidity associated with acid-induced upper
    gastrointestinal perforation and the high incidence of later
    complications requiring surgery, an aggressive surgical approach is
    recommended (Jeng et al, 1994). Surgery should therefore be
    considered:

    1.   If symptoms or signs of gastrointestinal tract perforation are
         evident at initial presentation.
    2.   When endoscopy reveals evidence of grade 3 burns with
         full-thickness necrosis (black, ulcerated mucosa) of the stomach
         or oesophagus.

    Corticosteroids

    In a controlled trial of steroid use among 60 children with
    oesophageal burns following corrosive ingestion (alkalis in the
    majority) the use of steroids (intravenous prednisolone 2 mg/kg within
    24 h and daily until oral intake was resumed then prednisolone
    2.5 mg/kg orally daily for at least three weeks) did not influence
    outcome (Anderson et al, 1990). Smaller case series have also
    concluded that systemic corticosteroids confer no benefit following
    acid ingestion and may exacerbate or mask symptoms of pending
    perforation (Hawkins et al, 1980).

    We do not advocate systemic steroids following antimony trichloride
    ingestion.

    If systemic toxicity is suspected laboratory confirmation of blood and
    urine antimony concentrations should be obtained. Antidotal treatment
    may be considered in confirmed cases (see Antidotes).

    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
         trichloride 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 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 "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

    There are no carcinogenicity data specific to antimony trichloride.

    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 has been implicated also in the aetiology of bladder tumours
    in patients with schistosomiasis who have been treated with antimony
    compounds (Winship, 1987).

    Severe gastric burns following acid ingestion are associated with an
    increased risk of gastric carcinoma.

    Reprotoxicity

    In the Russian literature 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, placentae, amniotic fluid and breast milk
    of these women. Further details were not available in the English
    abstract (Belyaeva, 1967).

    Genotoxicity

    NIF

    Fish Toxicity

    NIF

    EC Directive on Drinking Water Quality 80/778/EEC

    Antimony: Maximum admissible concentration 10 g/L; Chlorides: Guide
    level 25 mg/L, maximum admissible concentration 400 mg/L (DOSE, 1992).

    WHO Guidelines for Drinking Water Quality

    Antimony: Provisional guideline value 0.005 mg/L (WHO, 1993).

    AUTHORS

    SM Bradberry BSc MB MRCP
    WN Harrison PhD CChem MRSC
    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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    See Also:
       Toxicological Abbreviations
       Antimony trichloride (ICSC)