UKPID MONOGRAPH ANTIMONY TRIOXIDE WN Harrison PhD CChem MRSC SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH 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 TRIOXIDE Toxbase summary Type of product Used mainly as a fire retardant in plastics, rubbers, textiles, paper and paints. Toxicity Acute antimony trioxide poisoning is rare. Exposure may occur in industry. Fatal dose not known. Features Topical - Irritant to the skin and eyes. - "Antimony spots" (papules and pustules around sweat and sebaceous glands) may develop after repeated exposure, particularly in warm conditions. Ingestion Moderate ingestions: - Features usually occur within two hours with nausea, vomiting, abdominal pain and diarrhoea. A garlic odour on the breath has been described following ingestion of other antimony salts. 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. A fatality occurred following ingestion of a soluble antimony trioxide derivative (Miller, 1982). Inhalation - Irritant to the respiratory tract and mucous membranes causing conjunctivitis, laryngitis, pharyngitis, tracheitis, rhinitis bronchitis and rarely non-cardiogenic pulmonary oedema. - There may be radiological evidence of pneumonitis. - Chronic occupational inhalation may cause pneumoconiosis with cough, wheeze and diffuse, punctate opacities in the middle and lower zones. Management Dermal 1. If possible the patient should remove soiled clothing and wash him/herself. 2. Wash contaminated hair and skin with soap and copious amounts of water. 3. Pay special attention to skin folds, fingernails and ears. 4. A physician may need to examine the area if irritation or pain persists after washing. Ocular 1. Immediately irrigate the affected eye thoroughly with tepid water or 0.9% saline for at least 10-15 minutes. 2. Any particles lodged in the conjunctival recesses should be removed. 3. Continue irrigation with saline infusion using drip tubing. 4. Repeated instillation of local anaesthetic may reduce discomfort and help more thorough decontamination. 5. Corneal damage may be detected by instillation of fluorescein. 6. Patients with corneal damage and those whose symptoms do not resolve rapidly should be referred for ophthalmological assessment. Ingestion Minor ingestions (very mild or no symptoms): 1. Gastrointestinal decontamination is unnecessary. 2. Symptomatic and supportive measures only. Moderate/substantial ingestions: 1. Gastric lavage should be considered only if the patient presents within one hour; its value is unproven. 2. Symptomatic and supportive measures as dictated by the patient's condition. 3. Monitor the ECG, biochemical and haematological profiles. 4. Collect urine and blood for antimony concentration measurements to confirm diagnosis although these assays are not widely available. Check with NPIS. 5. Chelation therapy with dimercaprol, DMSA or DMPS may be considered; seek specialist advice from an NPIS physician. Inhalation Acute exposure 1. Remove from exposure. 2. Secure cardiorespiratory stability. 3. Perform a chest X-ray in symptomatic patients. 4. Treat symptomatically. 5. If significant respiratory symptoms occur investigate for systemic toxicity: ECG, biochemical and haematological profiles and blood and urine samples for antimony concentration determination. Chronic exposure 1. Investigate as for other causes of pneumoconiosis. 2. Obtain blood and urine for antimony concentration measurements to confirm diagnosis. However, these assays are not widely available. Check with NPIS. 3. Consider the possibility of systemic toxicity. References Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Br J Ind Med 1991;48: 93-7. Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L. Oral antimony intoxications in man. Crit Care Med 1990; 18: 324-6. Miller JM. Poisoning by antimony: a case report. South Med J 1982; 75: 592. 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 trioxide Origin of substance Minerals such as senarmontite and valentinite. (MERCK, 1996) Manufactured by roasting antimony trisulphide ores. (IARC, 1989) Synonyms Diantimony trioxide Antimony white Exitelite Flowers of antimony Valentinite (DOSE, 1992) Chemical group A compound of antimony, a group VA element Reference numbers CAS 1309-64-4 (DOSE, 1992) 1327-33-9 (CSDS, 1989) RTECS CC 5650000 (CSDS, 1989) UN 1549 (CSDS, 1989) HAZCHEM NIF Physicochemical properties Chemical structure Sb2O3 (DOSE, 1992) Molecular weight 291.5 (DOSE, 1992) Physical state at room temperature Crystalline solid (CSDS, 1989) Colour White (CSDS, 1989) Odour None (CHRIS, 1997) Viscosity NA pH NIF Solubility Slightly soluble in water. Soluble in potassium hydroxide, hydrochloric acid. Insoluble in organic solvents. (CSDS, 1989) Autoignition temperature NA Chemical interactions Reacts with organic acids, alcohols, glycols, alpha-hydroxy acids, o-dihydric phenols, sugar alcohols and other polyhydroxy compounds. (OHM/TADS, 1997) Major products of combustion When heated to combustion emits toxic antimony fumes. (HAZARDTEXT, 1997) Explosive limits NIF Flammability Ignites on heating in air. (CSDS, 1989) Boiling point 1550°C (DOSE, 1992) Density 5.2 (DOSE, 1992) Vapour pressure NA Relative vapour density NA Flash Point NA Reactivity Reacts explosively with chlorinated rubber. Forms explosive mixtures with perchloric acid when hot. (CSDS, 1989) Uses Fire retardant in plastics, rubbers, textiles, paper and paints. (IARC, 1989) In enamels and glass. Tartar emetic (antimony potassium tartrate) manufacture. (DOSE, 1992) Hazard/risk classification Index no. 051-005-00-X Risk phases Carc. Cat. 3; R40 - Possible risk of irreversible effects. Xn; R40 - Harmful, possible risk of irreversible effects. S(2-)22-36 - Keep out of reach of children. Do not breathe dust. Wear suitable protective clothing. EEC No. 215-175-0 (CHIP2, 1994) INTRODUCTION Antimony trioxide is a trivalent antimony compound which occurs naturally as the ores valentinite and senarmontite. It is produced commercially by the vapour phase reaction of antimony trisulphide and oxygen. It is used as a fire retardant and as an additive in enamel and glass manufacture. EPIDEMIOLOGY The main route of antimony trioxide exposure is occupational inhalation of dusts. Workers have been exposed in the production of antimony trioxide (Renes, 1953; Schnorr et al, 1995) and from its formation as a by-product of metal smelting (Gerhardsson et al, 1982; Potkonjak and Pavlovich, 1983; Jones, 1994; Schnorr et al, 1995). Other occupational exposure has occurred in the manufacture of ceramics (Motolese et al, 1993), batteries (Kentner et al, 1995) and alloys (White et al, 1993). Accidental intoxication has been reported after leaching of antimony from agate and ceramic containers into acidic beverages (Dunn, 1928; Monier-Williams, 1934; Werrin, 1963). It has been suggested that stibine generated from microbial growth on cot mattresses containing antimony trioxide is a contributing factor in sudden infant death syndrome (SIDS). Although there is some evidence consistent with undue antimony exposure in infants who died of SIDS (Taylor, 1996) other evidence disagrees such that it is most unlikely stibine is the only cause of the syndrome (de Wolff, 1995). A provisional comment by the Chair of the UK Expert Group on Cot Death Theories states so far "there is no evidence of risk to babies" from cot mattress PVC (Bradbury, 1997). Historically, intoxication has resulted from the medical use of antimony trioxide and potassium tartrate as tartar emetic in the treatment of a variety of conditions including malaise, fever, whooping cough and syphilis (Miller, 1982). 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 trioxide may be absorbed by inhalation and ingestion, though gastrointestinal absorption in man is poor. Distribution Absorbed trivalent antimony readily enters red blood cells and accumulates primarily in the spleen, liver and bone (IPCS, 1996). Lauwers et al (1990) estimated that the total body antimony pool in a patient who died following accidental antimony potassium tartrate ingestion was only five per cent of the ingested dose with high antimony concentrations in the liver, gall bladder and gastrointestinal mucosa. This is consistent with antimony undergoing enterohepatic circulation (see below). Excretion Antimony compounds are eliminated mainly in the urine, with small amounts appearing in faeces via bile after conjugation with glutathione. A significant amount of antimony excreted in bile undergoes enterohepatic circulation (Bailly et al, 1991). Some 6-24 months after parenteral antimony therapy, Mansour et al (1967) reported increased urine antimony concentrations (range 5.8-145.3 µg/L) compared to untreated controls (range 2.9-9.1 µg/L). Gerhardsson et al (1982) reported significantly (p<0.001) higher antimony concentrations in the lung tissue of 40 deceased smelter and refinery workers who had been exposed to antimony for some 30 years, compared to 11 unexposed controls. The time from last exposure to death varied from 0-23 years. The antimony concentration in liver and kidney was not significantly different between the two groups, suggesting that following occupational inhalation antimony may be retained in the lung for several years without significant systemic distribution. Kentner et al (1995) estimated a renal elimination half-life of four days following occupational inhalation of antimony trioxide and stibine in 21 employees of a starter battery manufacturing plant. CLINICAL FEATURES: ACUTE EXPOSURE Dermal exposure Antimony trioxide is an irritant although antimony dermatitis typically occurs during chronic occupational exposure. Ocular exposure Antimony trioxide is an eye irritant. Conjunctivitis and blurred vision were reported in workers exposed to antimony trioxide fumes in a smelter plant (Renes, 1953). Ingestion Acute poisoning is rare. Antimony trioxide is poorly soluble and is not readily absorbed from the gastrointestinal tract. Cases have been reported only when the compound has been leached into acidic beverages or has been converted into a more soluble form. Gastrointestinal toxicity Ingestion of a substantial quantity of antimony trioxide may result in nausea, vomiting and diarrhoea. Over fifty people were "very sick" and treated in hospital after drinking lemonade contaminated with 13 mg/L antimony. Antimony trioxide had leached from an enamel container in which the drinks were stored overnight. All the patients recovered completely within several days (Dunn, 1928). Similarly, antimony trioxide leached from enamel or ceramic glaze into acidic beverages caused "a burning sensation in the stomach", colic, nausea, vomiting and "collapse" (Monier-Williams, 1934). One hundred and fifty children developed nausea, vomiting, abdominal pain and diarrhoea some 15 minutes after drinking antimony-contaminated lemonade. The lemonade had a pH of 2.5-3.1 and leached an estimated 30 mg/L antimony into solution from an agate pot in which it was stored for 20-22 hours. Most of the affected children recovered within a few hours, the remainder recovering within a few days (Werrin, 1963). In 1982 Miller recounted the case of the author Oliver Goldsmith who died after ingesting a mixture of antimony trioxide and potassium tartrate. The estimated dose was 132-198 mg antimony. He succumbed after 18 hours severe vomiting and diarrhoea. Cardiovascular and peripheral vascular toxicity Electrocardiographic abnormalities are associated typically with chronic antimony exposure although have not been associated with exposure to antimony trioxide alone. 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 trioxide are irritant to the respiratory tract and mucous membranes and inhalation causes laryngitis (ranging from hoarseness to aphonia), pharyngitis, tracheitis, rhinitis, epistaxis, and bronchitis (Renes, 1953). Metal fume fever has been described (Anonymous, 1984) though less frequently than following exposure to zinc oxide. Radiological evidence of pneumonitis was found in six workers exposed to antimony smelter fumes for 2-12 hours. Inflammatory changes were characteristically peri-hilar with no evidence of peripheral parenchymal damage. Symptoms were alleviated by removal from exposure (and treatment with penicillin aerosols). The average airborne antimony concentration was 10-12 mg/m3 with a maximum measured breathing zone concentration of 70.7 mg/m3 (Renes, 1953). Gastrointestinal toxicity Workers heavily exposed (not specified) to antimony trioxide in a smelter plant developed "gastritis", abdominal pain, diarrhoea and vomiting. Urine antimony concentrations ranged from a trace up to an "exceptionally high" 600 mg/L (Renes, 1953). Neurotoxicity "Neuritis", dizziness and headache were reported amongst workers exposed to antimony trioxide fumes at an antimony smelting plant (Renes, 1953). Nephrotoxicity Albuminuria was reported in a "severely ill" worker with a urine antimony concentration of 600 mg/L after exposure to antimony trioxide in a smelting plant (Renes, 1953). Removal from exposure and symptomatic treatment for several days "provided relief". CLINICAL FEATURES: CHRONIC EXPOSURE The major source of antimony trioxide exposure is as a by-product in the smelting of metal ores (which may also contain arsenic) and in industries such as ceramic, glass and alloy manufacture. Inhalation and dermal contact are the most common routes of exposure. 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, 1962). 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 skin. The lesions usually resolved over two weeks in individuals removed to cooler parts of the factory. Histological examination showed epidermal cellular necrosis associated with an acute dermal inflammatory reaction. Antimony trioxide patch testing was negative whilst injection of methacholine into the affected areas caused enlargement of the lesions. The author concluded that antimony trioxide dust initiated an irritant reaction when it penetrated 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 trioxide has been noted in enamellers and decorators in the ceramics industry (Motolese et al, 1993). Ocular exposure Antimony trioxide is an irritant. Conjunctivitis was reported in 14 of 51 workers exposed to antimony trioxide dust in a smelting plant (Potkonjak and Pavlovich, 1983). Inhalation Pulmonary toxicity Chronic occupational antimony trioxide exposure 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 septum perforation in 51 workers employed at an antimony smelter for 9-31 years (mean 17.9 years) (Potkonjak and Pavlovich, 1983). Cardiovascular toxicity Although ECG changes have been reported in patients treated with antimony drugs there are no reports following exposure to antimony trioxide alone. In the Czechoslovakian literature Klucik and Ulrich (1960) reported subjective cardiac complaints and ECG changes (not specified in English abstract) in 14 workers occupationally exposed to antimony trioxide dust. However, significant antimony trisulphide exposure 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 no excess 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 Ensure adequate self protection before attempting treatment. If possible the patient should remove any contaminated clothing him/herself. Affected areas of skin should be washed with copious quantities of water. Pay special attention to skin folds, fingernails and ears. The most effective treatment for irritant antimony dermatitis is removal from exposure. Ocular exposure Irrigate immediately with lukewarm water or preferably saline for at least 10-15 minutes. A local anaesthetic may be indicated for pain relief and to overcome blepharospasm. The use of fluorescein allows detection of corneal damage. Specialist ophthalmological advice should be sought if any significant abnormality is detected on examination and in those whose symptoms do not resolve rapidly. Ingestion Following substantial ingestion of an antimony compound gastric lavage may be considered if presentation is within the first hour. There are no data to confirm that charcoal adsorbs antimony but the administration to a co-operative patient of 50 g activated charcoal within the first hour following a suspected substantial ingestion is reasonable. Other symptomatic and supportive measures should be dictated by the patient's condition. An ECG should be performed and biochemical and haematological profiles monitored. Blood and urine antimony concentrations are not widely available but may be of interest retrospectively to confirm systemic uptake. Inhalation Removal from exposure and measures to secure cardiorespiratory stability are the priority following acute inhalation of antimony compounds. An ECG should be performed. Respiratory symptoms in those with possible chronic antimony toxicity should be investigated as for other cases of pneumoconiosis. Urine antimony concentrations may be useful to monitor the initial extent of and subsequent reduction in exposure but these assays are not widely available. Antidotes Dimercaprol (British anti-lewisite, BAL) (Thompson and Whittaker, 1947; Braun et al, 1946), dimercaptosuccinic acid (DMSA, Succimer) (Basinger and Jones, 1981) and dimercaptopropane sulphonate (DMPS, Unithiol) (Basinger and Jones, 1981; Hruby and Donner, 1987) have antidotal activity in experimental systemic antimony poisoning (see below). These findings have not been confirmed in controlled studies in man. Dimercaprol In vitro studies Using the pyruvate oxidase system of pigeon brains as a test model, dimercaprol in a molar ratio of 6:1 dimercaprol: antimony was able to protect the enzyme system from inhibition by several antimony salts (Thompson and Whittaker, 1947). Animal studies The LD50 of intramuscular antimony tartrate administered to rabbits was raised from 90 mg Sb/kg in controls to 160 mg Sb/kg in animals treated with intramuscular dimercaprol (30 mg/kg one hour after intoxication followed by 15 mg/kg at six, 24 and 48 hours) (Braun et al, 1946). A total of 45 controls received 50-200 mg/kg antimony tartrate with 56 treated animals receiving 125-200 mg/kg. Clinical studies Four adults with antimony poisoning following the inadvertent consumption of antimony potassium tartrate were treated with intramuscular dimercaprol 200-600 mg daily. Three patients made an uneventful recovery but the fourth, who had a history of cardiorespiratory disease, died on day three. There were no pre-chelation antimony excretion data but in two survivors maximum antimony urine concentrations of 1000 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 trioxide poisoning. The discussion of individual cases with an NPIS physician is recommended. MEDICAL SURVEILLANCE Improved occupational health measures have reduced industrial airborne antimony concentrations significantly but monitoring of ambient air antimony concentrations remains important in some industries (Bailly et al, 1991; Kentner et al, 1995). Routine examination of the skin for "antimony spots" and chest radiography for evidence of pneumoconiosis may also be useful. The potential risk of pulmonary carcinogenicity should be remembered (see below). Although Bailly et al (1991) found that urine antimony excretion among workers exposed to airborne antimony pentoxide and sodium antimoniate correlated to the intensity of exposure, a recent publication from the European Commission concluded "no indicator of effect is available" for biological monitoring of antimony (Apostoli et al, 1994). Normal concentrations in biological fluids "Normal" serum and urine antimony concentrations are quoted as approximately 3 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 is some evidence that occupational antimony exposure is associated with an increased risk of lung cancer although frequent concomitant exposure to arsenic and other heavy metals precludes a definitive conclusion about its carcinogenic potential (Gerhardsson et al, 1982; McCallum, 1989; Gerhardsson and Nordberg, 1993; Jones 1994; Schnorr et al, 1995). Antimony also has been implicated in the aetiology of bladder tumours in patients with schistosomiasis who have been treated with antimony compounds (Winship, 1987). The International Agency for Research on Cancer has concluded antimony trioxide is "possibly carcinogenic to humans" (IARC, 1989). Reprotoxicity In the Russian literature women occupational exposed to antimony aerosols were reported to have a higher incidence of spontaneous abortion, premature births and menstrual disorders. Antimony was present in the blood, urine, placentae, amniotic fluid and breast milk of these women but further details were not available in the English abstract (Belyaeva, 1967). Genotoxicity Bacillus subtilis: produced gene conversion and mitotic recombination (DOSE, 1992). Fish toxicity LC50 (96 hr) bluegill sunfish, fathead minnow 530-833 mg/L (DOSE, 1992). EEC Directive on Drinking Water Quality 80/778/EEC Maximum admissible concentration 10 µg/L, as antimony (DOSE, 1992). WHO Guidelines for Drinking Water Quality Provisional guideline value 5 µg/L, as antimony (WHO, 1993). AUTHORS WN Harrison PhD CChem MRSC SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH UK This monograph was produced by the staff of the Birmingham Centre of the National Poisons Information Service in the United Kingdom. The work was commissioned and funded by the UK Departments of Health, and was designed as a source of detailed information for use by poisons information centres. Date of last revision 28/1/98 REFERENCES Apostoli P, Porru S, Alessio L. Antimony. In: Alessio L, Berlin A. Roi R, van der Venne MT, eds. Biological indicators for the assessment of human exposure to industrial chemicals. Luxembourg: Office for Official Publications of the European Communities, 1994. Anonymous. Metals and the lung. Lancet 1984; 2: 903-4. Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J. 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See Also: Antimony trioxide (ICSC)