UKPID MONOGRAPH ANTIMONY SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH This monograph has been produced by staff of a National Poisons Information Service Centre in the United Kingdom. The work was commissioned and funded by the UK Departments of Health, and was designed as a source of detailed information for use by poisons information centres. Peer review group: Directors of the UK National Poisons Information Service. ANTIMONY Toxbase summary Type of product Used in alloys, textiles, catalysts, enamels, ceramics, fireworks and pigments. Antimony salts are used in the treatment of leishmaniasis and schistosomiasis. Toxicity A fatality has occurred following the mistaken ingestion of tartar emetic (antimony potassium tartrate). Antimony toxicity more typically follows the parenteral administration of antimony pharmaceuticals in the treatment of schistosomiasis and leishmaniasis. Features Topical - Irritant to the skin and eyes. - Ocular exposure to antimony pentachloride or antimony trichloride fumes have produced corneal burns. - "Antimony spots" (papules and pustules around sweat and sebaceous glands) may develop after repeated exposure. Ingestion Moderate ingestions: - Features usually start within 30 minutes to 2 hours with a metallic taste, nausea, vomiting, abdominal pain and diarrhoea. There may be a garlic odour on the breath. Substantial ingestions: - Severe vomiting and diarrhoea (which may contain blood) and haemorrhagic gastritis may ensue. Myocardial depression, vasodilation and fluid loss may cause shock with hypotension, electrolyte disturbances and acute renal failure. Cerebral oedema, coma and convulsions are possible. Death may occur from ventricular fibrillation. - Chronic ingestion may result in anorexia, weight loss, diarrhoea, peripheral neuropathy, palmar keratosis and skin rash. Inhalation - Irritant to the respiratory tract and mucous membranes: Conjunctivitis, laryngitis, pharyngitis, tracheitis, rhinitis and bronchitis, rarely pulmonary oedema. - There may be radiological evidence of pneumonitis. - Chronic occupational inhalation may cause pneumoconiosis with cough, wheeze and diffuse, punctate opacities in the middle and lower zones. Injection - The treatment of leishmaniasis and schistosomiasis has been associated with anorexia, nausea, vomiting, abdominal pain, a metallic taste, diarrhoea, pancreatitis, reversible elevations of liver enzyme activities, myalgia, arthralgia, proteinuria, ECG changes (T wave inversion, Q-T interval prolongation, S-T segment abnormalities), phlebitis, uveitis, optic atrophy and rarely anaphylactic shock, acute renal failure, hepatic necrosis and bone marrow hypoplasia. Management Topical - Surface decontamination with soap and water where appropriate. Ingestion Minor ingestions (very mild or no symptoms): 1. Gastrointestinal decontamination is unnecessary. 2. Symptomatic and supportive measures only. Moderate/substantial ingestions: 1. Gastric lavage should be considered only if the patient presents within one hour; its value is unproven. 2. Symptomatic and supportive measures as dictated by the patient's condition. 3. Monitor the ECG, biochemical and haematological profiles. 4. Collect urine and blood for antimony concentration measurements. 5. Chelation therapy with dimercaprol, DMSA or DMPS may be considered, but only after specialist advice from the NPIS. Inhalation Acute exposure 1. Remove from exposure. 2. Secure cardiorespiratory stability. 3. Perform a chest X-ray in symptomatic patients. 4. Treat symptomatically. 5. If significant respiratory symptoms occur investigate for systemic toxicity: ECG, biochemical and haematological profiles and blood and urine samples for antimony concentration determination. Chronic exposure 1. Investigate as for other causes of pneumoconiosis. 2. Obtain blood and urine for antimony concentration measurements. 3. Consider the possibility of systemic toxicity. Injection - Discontinue therapy if adverse effects occur and monitor as above. References Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Br J Ind Med 1991;48: 93-7. Hepburn NC, Siddique I, Howie AF, Beckett GJ, Hayes PC. Hepatotoxicity of sodium stibogluconate in leishmaniasis. Lancet 1993; 342: 238-9. Hepburn NC, Nolan J, Fenn L, Herd RM, Neilson JM, Sutherland GR, Fox KA. Cardiac effects of sodium stibogluconate: myocardial, electrophysiological and biochemical studies. QJM 1994; 87: 465-72. Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L. Oral antimony intoxications in man. Crit Care Med 1990; 18: 324-6. Renes LE. Antimony poisoning in industry. Arch Ind Hyg Occup Med 1953; 7: 99-108. Werrin M. Chemical food poisoning. Q Bull Assoc Food Drug Offic 1963; 27: 38-45. White Jr GP, Mathias CGT, Davin JS. Dermatitis in workers exposed to antimony in a melting process. J Occup Med 1993; 35: 392-5. Winship KA. Toxicity of antimony and its compounds. Adverse Drug React Acute Poisoning Rev 1987; 2: 67-90. Substance name Antimony Origin of substance Found in many naturally occuring minerals, stibnite (SbS3) is the major source of the metal. Synonyms Antimony black Antimony black Stibium (CSDS, 1989) Chemical group A group V element Reference Numbers CAS 7440-36-0 (CSDS, 1989) RTECS CC4025000 (RTECS, 1996) UN 2871 (CSDS, 1989) HAZCHEM CODE 2Z (CSDS, 1989) Physico-chemical properties Chemical structure Antimony, Sb (DOSE, 1992) Molecular weight 121.75 (DOSE, 1992) Physical state at room temperature Solid Colour Silvery white (CSDS, 1989) Odour NIF Viscosity NA pH NA Solubility Insoluble in hot or cold water. (HSDB, 1996) Soluble in hot concentrated sulphuric acid. (CSDS, 1989) Autoignition temperature NIF Chemical interactions Finally divided antimony will react violently with nitric acid, and ammonium nitrate. (NFPA, 1986) Fumes of antimony hydride may be released on contact with acids. (Sax, 1984) Explosive reactions will follow contact of bromoazide with antimony. (NFPA, 1986) Antimony will burn spontaneously in gaseous chlorine, fluorine or bromine. (NFPA, 1986) Nascent hydrogen will react with antimony to form toxic stibine. (DOSE, 1992) Major products of combustion NIF Explosive limits NIF Flammability May burn, but will not ignite readily. (HSDB, 1996) Boiling point 1635°C (CSDS, 1989) Density 6.684 at 25°C (CSDS, 1989) Vapour pressure 133.3 Pa at 886°C (CSDS, 1989) Relative vapour density NA Flash Point NA Reactivity NIF Uses The most important use of antimony is as an alloying ingredient with metals such as lead, tin and copper. Antimony trioxide is used as a flame retardant in textiles, as a catalyst, and as an opacifier in glass, enamels and ceramics. Antimony tetroxide is used as an oxidation catalyst. Antimony trisulphide is used in fireworks, matches, as a pigment, and in the manufacture of ruby glass. Antimony pentasulphide is used in vulcanization processes. Pentavalent antimony preparations (including sodium stibogluconate) are still used in the treatment of leishmaniasis. Trivalent compounds (especially antimony potassium tartrate) inactivate schistosomes by inhibiting the activity of phosphofructokinase. (Bueding and Fisher, 1966; PATTY, 1994) Hazard/risk classification NIF INTRODUCTION Antimony is a metalloid since it has properties of both metals and non-metals. It exists in a trivalent and pentavalent state and forms inorganic and organic compounds. Examples of trivalent antimony compounds are antimony trioxide, antimony trisulphide, antimony trichloride, antimony potassium tartrate (tartar emetic) and stibine (SbH3). Pentavalent antimony compounds include antimony pentasulphide and antimony pentoxide. Sodium stibogluconate (sodium antimony gluconate) exists with antimony in both the trivalent and pentavalent forms. Elemental antimony oxidises slowly in moist air to form a mixture of antimony and antimony oxide and burns in air to form antimony trioxide vapour. Pentavalent antimony is an oxidising agent. Historically, the systemic administration of antimony compounds has been used in the treatment of many conditions including syphilis, whooping cough and gout and topical antimony compounds were believed to improve herpetic lesions, leprosy, mania and epilepsy. Antimony has been used also as an emetic, a decongestant and a sedative and still has a role in the treatment of tropical infections. Industrial exposure to antimony occurs mainly by inhalation of dust or fumes during the processing or packaging of antimony compounds. Antimony poisoning also has occurred following the misuse of pharmaceuticals. MECHANISM OF TOXICITY The mechanism of toxicity of antimony compounds is unclear but may involve disruption of thiol proteins via binding to sulphydryl groups (de Wolff, 1995). TOXICOKINETICS Absorption Antimony compounds may be absorbed by inhalation and ingestion, though gastrointestinal absorption in man is poor necessitating parenteral administration of antimony pharmaceuticals. Distribution Absorbed trivalent and pentavalent antimony compounds differ significantly in their distribution; trivalent compounds have an affinity for red blood cells whereas pentavalent antimony is found in the plasma. Following injection or oral administration significant antimony concentrations can be found in the liver, kidney, thyroid, adrenals and bone (Winship, 1987). Some pentavalent antimony is reduced to the trivalent form in the liver (Winship, 1987). Lauwers et al (1990) estimated that the total body pool of antimony in a patient who died following accidental antimony potassium tartrate ingestion was only five per cent of the ingested dose with high antimony concentrations in the liver, gall bladder and gastrointestinal mucosa. This is consistent with antimony undergoing enterohepatic circulation (see below). Excretion Antimony compounds are eliminated mainly in the urine, with small amounts appearing in faeces via bile after conjugation with glutathione. A significant amount of antimony excreted in bile undergoes enterohepatic circulation (Bailly et al, 1991). Rees et al (1980) demonstrated that some 80-90 per cent of an intramuscular dose of sodium stibogluconate was recovered in the urine within six hours of administration. However, even some 6-24 months after parenteral antimony therapy, Mansour et al (1967) reported increased urine antimony concentrations (range 5.8-145.3 µg/L) compared to untreated controls (range 2.9-9.1 µg/L). Gerhardsson et al (1982) reported significantly higher antimony (p<0.001) concentrations in 40 deceased smelter and refinery workers who had been exposed to antimony for some 30 years, compared to 11 unexposed controls. The time from last exposure to death varied from 0-23 years. The antimony concentration in liver and kidney was not significantly different between the two groups, suggesting that following occupational inhalation antimony may be retained in the lung for several years without significant systemic distribution. Kentner et al (1995) estimated a renal elimination half-life of four days following occupational inhalation of antimony trioxide and stibine in 21 employees of a starter battery manufacturing plant. CLINICAL FEATURES: ACUTE EXPOSURE Dermal exposure Antimony and its compounds are skin irritants although antimony dermatitis typically occurs during chronic occupational exposure (see below) (Poisindex, 1996). Ocular exposure Exposure to high concentrations of antimony pentachloride or antimony trichloride fumes produces severe eye irritation and sometimes corneal burns (Grant and Schuman, 1993). Ingestion Gastrointestinal toxicity One hundred and fifty children who drank lemon which had been refrigerated for 20 hours in a large agate pot experienced nausea, vomiting and diarrhoea which was found to be due to the leaching of antimony from the agate lining (Werrin, 1963). In 1982 Miller recounted the death of the author Oliver Goldsmith, who committed suicide in 1774 by ingesting a mixture of antimony oxide (antimony trioxide) and potassium tartrate and succumbed after 18 hours from severe vomiting and diarrhoea. More recently, Lauwers et al (1990) reported four adults who presented with similar gastrointestinal features having mistaken "tartar emetic" (antimony potassium tartrate) for "cream of tartar". Three of them made an uneventful recovery but the fourth died from haemorrhagic gastritis complicated by cardiorespiratory failure. A 24 year-old woman who attempted suicide by ingesting an unknown quantity of antimony trisulphide presented within one hour complaining of a metallic taste, epigastric pain and dysphagia. She made an uneventful recovery (Bailly et al, 1991). Cardiovascular and peripheral vascular toxicity Electrocardiographic abnormalities are associated typically with chronic antimony exposure. Following acute antimony ingestion two patients had "moderate bradyrhythmic dysfunctions" at presentation (Lauwers et al, 1990). Phlebitis occurred in four patients who accidentally ingested antimony potassium tartrate (Lauwers et al, 1990). Inhalation Pulmonary toxicity Dusts and fumes of antimony and its compounds are irritant to the respiratory tract and mucous membranes and inhalation causes conjunctivitis, laryngitis, pharyngitis, tracheitis, rhinitis and bronchitis (Renes, 1953; Taylor, 1966). Metal fume fever has been described (Anonymous, 1984) though less frequently than following exposure to zinc oxide. There may be radiological evidence of pneumonitis which resolves upon removal from exposure (Renes, 1953). Inhalation of antimony pentachloride has resulted in pulmonary oedema (Cordasco, 1974). Gastrointestinal toxicity In addition to respiratory tract irritation, seven men exposed to antimony trichloride fumes also experienced abdominal pain, anorexia, and vomiting (Taylor, 1966) . Renes (1953) reported similar symptoms in association with diarrhoea, headache and dizziness, in smelter workers exposed to antimony fumes. Injection Hepatotoxicity A 27 year-old woman with cutaneous leishmaniasis developed a transient rise in alaninine aminotransferase activity (to 2.4 times the upper limit of normal) when she was inadvertently given ten times the intended dose of parenteral pentavalent sodium stibogluconate (Herwaldt et al, 1992) but hepatotoxicity is more typically observed during prolonged therapy with antimony pharmaceuticals. Cardiovascular toxicity No cardiovascular complications arose in a patient who accidentally was given ten times the intended intravenous dose of sodium stibogluconate (Herwaldt et al, 1992). CLINICAL FEATURES: CHRONIC EXPOSURE Dermal exposure Dermatitis following contact with antimony compounds is well described although this is not usually a problem after contact with the metal (McCallum, 1989). Typical lesions arise on the arms, legs and in the flexures, sparing the face, hands and feet (Renes, 1953; McCallum, 1989). Papules and pustules predominate around sweat and sebaceous glands with areas of eczema and lichenification. These so-called "antimony spots" occur mainly in the summer (McCallum, 1989). White et al (1993) described three cases of occupational antimony dermatitis following several months exposure to antimony dust and antimony trioxide fumes. Two of these patients also experienced frequent nose bleeds. Both problems resolved when exposure ceased. In one patient patch testing for antimony was negative and in another the urine antimony concentration was 53.2 µg/L ('normal' < 1.0 µg/L). Positive patch testing to antimony trioxide has been noted in enamellers and decorators in the ceramics industry (Motolese et al, 1993). Inhalation Pulmonary toxicity Chronic occupational exposure to antimony and its compounds may cause "antimony pneumoconiosis" (McCallum, 1989). Typical radiological findings include diffuse, dense, punctate non-confluent opacities predominately in the middle and lower lung fields, sometimes associated with pleural adhesions (Potkonjak and Pavlovich, 1983). These changes developed after at least ten years working in an antimony smelting plant where the dust contained nearly 90 per cent antimony trioxide with some antimony pentoxide and small amounts (up to five per cent) of silica (Potkonjak and Pavlovich, 1983). Cough (in 31 of 51 subjects) and exertional breathlessness (in 26 cases) were the symptoms most frequently reported with wheeze, chest pain, generalised weakness or conjunctivitis in a minority. Nine workers had obstructive lung function defects with a combined restrictive/obstructive picture in five cases but no isolated restrictive defects or radiological evidence of diffuse fibrosis. Perforation of the nasal septum has been described in antimony workers but these cases probably have involved concomitant exposure to arsenic (McCallum, 1989). There were no cases of nasal perforation in 51 workers employed at an antimony smelter for 9-31 years (mean 17.9 years) (Potkonjak and Pavlovich, 1983). Brieger et al (1954) attributed ECG T-wave changes and sudden deaths to antimony-induced cardiotoxicity following occupational exposure to antimony trisulphide (Sb2S3) although the reliability of this study has been criticised (McCallum, 1989). Injection Dermal toxicity Davis (1968) reported antimony dermatitis in some four per cent of 160 patients treated with antimonial drugs. Gastrointestinal toxicity Patients treated for some one to two weeks with parenteral antimony compounds frequently reported anorexia, nausea and vomiting with some complaints of abdominal pain, a metallic taste and diarrhoea (Davis, 1968). Pancreatitis also has been reported as a complication of parenteral therapy with stibogluconate or meglumine antimonate (McCarthy et al, 1993; de Lalla et al, 1993; Gasser et al, 1994). Hepatotoxicity Parenteral treatment with antimony compounds has caused hepatic necrosis although reversible elevations of liver enzyme activities are more typical (Winship, 1987; Saenz et al, 1991; Hepburn et al, 1993). Nephrotoxicity In a review of 92 patients with visceral leishmaniasis (kala-azar) treated with sodium stibogluconate, two developed renal toxicity manifest as renal casts, proteinuria and an increased serum urea concentration although these patients were also receiving intramuscular pentamidine which is recognised renal toxin (Chunge et al, 1984). Other patients treated with sodium stibogluconate have developed acute renal failure (Balzan and Fenech, 1992; Rai et al, 1994b). Renal tubular acidosis and tubular necrosis have also been described (Horber et al, 1991; Rai et al, 1994a). Cardiovascular and peripheral vascular toxicity ECG changes following exposure to antimony compounds are seen typically in patients with leishmaniasis or schistosomiasis who have been treated with parenteral antimony compounds. Typical features include T wave inversion or amplitude reduction, Q-T interval prolongation and S-T segment abnormalities (Davis, 1968; Chulay et al, 1985; Henderson and Jolliffe, 1985). These effects usually reverse when treatment is discontinued. In 12 soldiers with cutaneous leishmaniasis treated with sodium stibogluconate Hepburn et al (1994) found that although a reversible decrease in T-wave amplitude occurred during treatment there were no significant changes in echocardiographic induces of left ventricular function, arrhythmia frequency or heart-rate variability. The authors concluded that 20 mg/kg/day sodium stibogluconate for 20 days had no cardiac side-effects in most fit, young patients. Gupta (1990) similarly noted that T-wave changes induced by antimony therapy were not associated with a deterioration in cardiac function. In a review of 160 patients with schistosomiasis treated with antimonal drugs (Davis, 1968) retrosternal chest pain was reported by 27 individuals. In three cases this was associated with acute vascular collapse immediately after intravenous drug administration (after the first dose in one case) suggesting an anaphylactic-type response. Phlebitis occurred in 31 patients receiving intravenous sodium stibogluconate in the treatment of visceral leishmaniasis (Chunge et al, 1984) and in one patient administered antimony sodium tartrate in the treatment of urinary schistosomiasis (Davis, 1968). Neurotoxicity Rai et al (1994b) described combined ninth and tenth cranial nerve palsies in a patient with kala-azar treated with parenteral stibogluconate. Haemotoxicity Mallick (1990) described bone marrow hypoplasia as a complication of sodium stibogluconate administration and other authors have described leucopenia (Hiēsönmez et al, 1988; Saenz et al, 1991) or recurrent episodes of thrombocytopenia (Braconier and Miörner, 1993) during parenteral antimonial therapy. Chunge et al (1984) also reported epistaxis in 13 patients, in three cases associated with pancytopenia. Musculoskeletal toxicity Myalgia and arthralgia are reported frequently by patients with leishmaniasis or schistosomiasis treated with parenteral antimony compounds (Davis, 1968; Winship, 1987; Castro et al, 1990; Saenz et al, 1991). Ocular toxicity Parenteral treatment with antimony potassium tartrate (tartar emetic) in the treatment of leishmaniasis has resulted in bilateral blindness with dilated unreactive pupils and optic atrophy (Grant and Schuman, 1993). In a review of 92 patients with visceral leishmaniasis treated with parenteral stibogluconate, eight developed eye disease (after completion of treatment and apparent cure) including uveitis and retinal haemorrhages (Chunge et al, 1984). Forsyth (1958) reported one patient who developed transient retinal haemorrhages and exudates and another in whom the fundus was described as 'granular' following parenteral sodium antimony tartrate therapy for schistosomiasis. Visual acuity was diminished in both cases but returned to normal within six months. Three children who received repeated courses of parenteral tartar emetic in the treatment of schistosomiasis developed irreversible optic atrophy (Kassem et al, 1976). MANAGEMENT Ingestion Decontamination Following ingestion of an antimony compound gastric lavage may be considered if presentation is within the first hour. There are no data to confirm that charcoal adsorbs antimony but the administration to a cooperative patient of 50 g activated charcoal within the first hour following a suspected substantial ingestion is reasonable. Other symptomatic and supportive measures should be dictated by the patient's condition. An ECG should be performed and biochemical and haematological profiles monitored. Inhalation Removal from exposure and measures to secure cardiorespiratory stability are the priority following acute inhalation of antimony compounds. Respiratory symptoms in those with possible chronic antimony toxicity should be investigated as for other cases of pneumoconiosis. Urine antimony concentrations may be useful to monitor the initial extent of and subsequent reduction in exposure. Antidotes Dimercaprol (Thompson and Whittaker, 1947; Braun et al, 1946), DMSA (Basinger and Jones, 1981) and DMPS (Basinger and Jones, 1981; Hruby and Donner, 1987) have antidotal activity in experimental systemic antimony poisoning (see below) but these findings have not been confirmed in controlled studies in man. Dimercaprol Using the pyruvate oxidase system of pigeon brains as a test model, dimercaprol was able to protect the enzyme system from inhibition by several antimony salts (Thompson and Whittaker, 1947). Four adults with antimony poisoning following the inadvertent consumption of antimony potassium tartrate were treated with intramuscular dimercaprol 200-600 mg daily. Three patients made an uneventful recovery but the fourth, who had a history of cardiorespiratory disease died on day three. In two survivors treatment was associated with an apparent increased urine antimony excretion (Lauwers et al, 1990). Bailly et al, (1991) reported a 24 year-old woman who made an uneventful recovery after ingesting an undetermined amount of antimony trisulphide. She was treated with dimercaprol for five days (200 mg tds) but there was no evidence of enhanced urinary antimony elimination with therapy. DMSA and DMPS The antidotal efficacy of thiol chelating agents was examined in animal survival experiments. Twenty minutes following intraperitoneal administration to mice of potassium antimonyl tartrate at twice the LD50 (120 mg/kg), DMSA or DMPS were given intraperitoneally at a molar ratio of 10:1 chelating agent: antimony. The overall survival rates were 28/30 and 19/30 respectively, indicating that both chelating agents were effective, with DMSA superior in the conditions of this study (Basinger and Jones, 1981). There are no human data. MEDICAL SURVEILLANCE Improved occupational health measures have reduced industrial airborne antimony concentrations significantly but monitoring of ambient air antimony concentrations remains important in some industries (Bailly et al, 1991; Kentner et al, 1995). Routine examination of the skin for "antimony spots" and chest radiography for evidence of pneumoconiosis may also be useful. The potential risk of pulmonary carcinogenicity should be remembered. Although Bailly et al, (1991) found that the urinary antimony excretion of workers exposed to airborne antimony pentoxide and sodium antimoniate correlated to the intensity of exposure, a recent publication from the European Commission concluded there is "no indicator of effect is available" for biological monitoring of antimony (Alessio et al, 1994). 'Normal' serum and urine antimony concentrations are approximately 3 µg/L and 0.8 µg/L respectively (Poisindex, 1996). OCCUPATIONAL DATA Occupational exposure standard Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3 (Health and Safety Executive, 1995). OTHER TOXICOLOGICAL DATA Carcinogenicity There is some evidence that occupational antimony exposure is associated with an increased risk of lung cancer although frequent concomitant exposure to arsenic and other heavy metals precludes a definitive conclusion about its carcinogenic potential (Gerhardsson et al, 1982; McCallum, 1989; Gerhardsson and Nordberg, 1993; Jones, 1994; Schnorr et al, 1995). Antimony also has been implicated in the aetiology of the bladder tumours in patients with schistosomiasis who have been treated with antimony compounds (Winship, 1987). Reprotoxicity Women occupationally exposed to antimony aerosols were reported to have a higher incidence of spontaneous abortion, premature births and menstrual disorders. Antimony was present in the blood, urine, placenta, amniotic fluid and breast milk of these women (Belyaeva, 1967). Genotoxicity NIF Fish toxicity LC50 (28 day) rainbow trout 0.66 mg/L (DOSE, 1992). EEC Directive on Drinking Water Quality 80/778/EEC Maximum admissible concentration 10 µg/L (DOSE, 1992). AUTHORS SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH UK This monograph was produced by the staff of the Birmingham Centre of the National Poisons Information Service in the United Kingdom. The work was commissioned and funded by the UK Departments of Health, and was designed as a source of detailed information for use by poisons information centres. Date of last revision 16/7/96 REFERENCES Apostoli P, Porru S, Alessio L. Antimony. In: Alessio L, Berlin A. Roi R, van der Venne MT, eds. 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See Also: Antimony (ICSC)