UKPID MONOGRAPH ANTIMONY PENTACHLORIDE SM Bradberry BSc MB MRCP 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 PENTACHLORIDE Toxbase summary Type of product Used as a chemical reagent. Toxicity Acute antimony pentachloride poisoning is rare. Exposure may occur in industry. Fatal dose not known. Features Dermal - Antimony pentachloride 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 pentachloride 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% 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. Discussion with an NPIS physician is recommended. 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. Cordasco EM. Newer concepts in the management of environmental pulmonary edema. Angiology 1974; 25: 590-601. 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. 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 pentachloride Origin of substance NIF Synonyms Antimony (V) chloride Antimony perchloride Pentachloroantimony Antimonic chloride Antimony chloride Butter of antimony (DOSE, 1992; RTECS, 1997) Chemical group A compound of antimony, a group V A element. Reference numbers CAS 7647-18-9 (DOSE, 1992) RTECS CC5075000 (RTECS, 1997) UN 1730 (liquid); 1731 (solution) (DOSE, 1992) HAZCHEM 4X (liquid); 2X (solution) (DOSE, 1992) Physicochemical properties Chemical structure SbCl5 (DOSE, 1992) Molecular weight 299.02 (DOSE, 1992) Physical state at room temperature Oily liquid (MERCK, 1996) Colour Colourless to yellow (MERCK, 1996) Odour Pungent (HSDB, 1997) Viscosity 2.034 CP at 29.4°C (HSDB, 1997) pH NIF Solubility Water: Decomposes. Soluble in carbon disulphide, chloroform, carbon tetrachloride, hydrochloric acid and tartaric acid. (DOSE, 1992; HSDB, 1997) Autoignition temperature NIF Chemical interactions Corrodes metal. (CHRIS, 1997) Major products of combustion Decomposes to give antimony and hydrogen chloride. (HSDB, 1997) Explosive limits NIF Flammability Non flammable (OHM/TADS, 1997) Boiling point 79°C at 22 mm Hg (DOSE, 1992) Density 2.336 at 20°C/4°C (DOSE, 1992) Vapour pressure 133.322 Pa at 22.7°C (DOSE, 1992) Relative vapour density NA Flash point NA Reactivity Mono- and tetrahydrates are formed in the presence of small amounts of water. Large amounts of water cause hydrolysis to Sb2O5. (MERCK, 1996) Uses A chemical reagent. As a catalyst when replacing a fluorine substituent with chlorine in organic compounds. (MERCK, 1996; DOSE, 1992) Hazard/risk classification Index no. 051-002-00-3 Risk phases C;R34 - Xi;R37 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. 231-601-8 (CHIP2, 1994) INTRODUCTION Antimony pentachloride is a pentavalent antimony compound. It is used as a chemical reagent. Due to the acidic nature of antimony pentachloride exposure may produce corrosive injury as well as systemic antimony toxicity. EPIDEMIOLOGY Antimony pentachloride poisoning is rare and is likely only to occur occupationally. Cordasco (1974) reported 59 cases of pulmonary oedema, of which three were ascribed to antimony pentachloride exposure. Two deaths resulted. MECHANISM OF TOXICITY Antimony pentachloride reacts with water to form hydrochloric acid which has a direct corrosive effect on mucous membranes (Cordasco, 1974). 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 compounds 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. Gastrointestinal absorption in man is poor. Distribution Absorbed pentavalent antimony 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 µg/L) compared to untreated controls (range 2.9-9.1 µg/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 pentachloride is an irritant and concentrated solutions or liquid material may cause burns. A 39 year-old worker was admitted to hospital with second and third degree burns over most of his body following accidental release of antimony pentachloride vapour. He developed severe respiratory features also (see below) but recovered after 95 days (Cordasco, 1974). Ocular exposure Antimony pentachloride is corrosive and direct contact may irritate or burn the eye causing pain, blepharospasm and photophobia. Ingestion There are no reports of antimony pentachloride 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 pentachloride 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 corrosive 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 A 39 year-old man developed a severe cough, wheeze, dyspnoea and chest tightness immediately following exposure to antimony pentachloride vapour. Examination revealed crackles in both lung fields. Pulmonary oedema developed some 12 hours after admission. Arterial blood gas analysis revealed profound hypoxia (pO2 = 4.0 kPa) with bilateral pulmonary vascular congestion on X-ray. Constant positive pressure ventilation was commenced and "massive doses of corticosteroid" administered. His condition improved somewhat although recovery was complicated by the development of a laryngeal stricture requiring a tracheostomy. The patient was discharged 95 days after admission (Cordasco, 1974). Gastrointestinal toxicity Nausea, vomiting, abdominal pain and anorexia have accompanied laboratory confirmation of systemic antimony poisoning following inhalation of a corrosive trivalent antimony compound (Taylor, 1966). CLINICAL FEATURES: CHRONIC EXPOSURE There are no reports regarding chronic antimony pentachloride toxicity 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 µg/L ("normal" < 1.0 µg/L). Positive patch testing to antimony 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 µg/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 pentachloride 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) (Braun et al, 1946; Thompson and Whittaker, 1947), dimercaptosuccinic acid (DMSA, Succimer) (Basinger and Jones, 1981) and dimercaptopropane sulphonate (DMPS, Unithiol) (Basinger and Jones, 1981; Hruby and Donner, 1987) have antidotal activity in experimental systemic antimony poisoning (see below). These findings have not been confirmed in controlled studies in man. Dimercaprol In vitro studies Using the pyruvate oxidase system of pigeon brains as a test model, dimercaprol in a molar ratio of 6:1 dimercaprol: antimony was able to protect the enzyme system from inhibition by several antimony salts (Thompson and Whittaker, 1947). Animal studies The LD50 of intramuscular antimony tartrate administered to rabbits was raised from 90 mg Sb/kg in controls to 160 mg Sb/kg in animals treated with intramuscular dimercaprol (30 mg/kg one hour after intoxication followed by 15 mg/kg at six, 24 and 48 hours) (Braun et al, 1946). A total of 45 controls received 50-200 mg/kg antimony tartrate with 56 treated animals receiving 125-200 mg/kg. Clinical studies Four adults with antimony poisoning following the inadvertent consumption of antimony potassium tartrate were treated with intramuscular dimercaprol 200-600 mg daily. Three patients made an uneventful recovery but the fourth, who had a history of cardiorespiratory disease, died on day three. There were no pre-chelation antimony excretion data but in two survivors maximum antimony urine concentrations of 1000 µg/L and 1500 µg/L were reported some 36 and 72 hours after poisoning respectively. Urine volumes were not stated (Lauwers et al, 1990). Bailly et al (1991) reported a 24 year-old woman who made an uneventful recovery after ingesting an undetermined amount of antimony trisulphide. She was treated with dimercaprol 200 mg tds for five days but there was no evidence of enhanced urinary antimony elimination with therapy. DMSA Animal studies DMSA was given intraperitoneally to mice at a molar ratio of 10:1 DMSA: antimony twenty minutes after administration of potassium antimonyl tartrate (120 mg/kg; twice the LD50). The survival ratio was 28/30 (Basinger and Jones, 1981). Clinical studies There are no human data. DMPS Animal studies DMPS has been shown to be an effective chelating agent in mice following intraperitoneal administration of potassium antimonyl tartrate (120 mg/kg; twice the LD50). The survival rate was 19/30 when intraperitoneal DMPS was given twenty minutes after intoxication at a molar ratio of 10:1 DMPS: antimony. However, DMSA was significantly more effective under these conditions (see above) (Basinger and Jones, 1981). Clinical studies There are no human data. Antidotes: Conclusions and recommendations 1. Clinical data regarding antimony chelation are scarce. 2. Dimercaprol effectively chelates antimony but has been superseded by the less toxic thiol antidotes DMPS and DMSA. 3. In limited animal studies DMSA is a more effective antimony chelator than DMPS. 4. Parenteral or oral DMSA therapy may be considered in antimony pentachloride 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 µg/L and 0.8 µg/L respectively (Poisindex, 1997). OCCUPATIONAL DATA Maximum exposure limit Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3 (Health and Safety Executive, 1997). OTHER TOXICOLOGICAL DATA Carcinogenicity There are no carcinogenicity data specific to antimony pentachloride. 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 is 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 Bacillus subtilis rec assay positive (DOSE, 1992). Fish Toxicity NIF EC Directive on Drinking Water Quality 80/778/EEC Antimony: Maximum admissible concentration 10 µg/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 WN Harrison PhD CChem MRSC SM Bradberry BSc MB MRCP 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. 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