UKPID MONOGRAPH PHOSPHORUS TRICHLORIDE 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 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. PHOSPHORUS TRICHLORIDE Toxbase summary Type of product A common industrial chemical used in chemical synthesis. Toxicity Phosphorus trichloride is corrosive. Skin exposure, inhalation or ingestion of a significant quantity of phosphorus trichloride or its hydration products can be dangerous. Features Dermal - Phosphorus 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. Ingestion - Phosphorus 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 and phosphoric acids. - 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. 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. Discuss with an NPIS physician. 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. Management of ingestion of an aqueous phosphorus trichloride solution is as for phosphoric acid (see separate monograph). 5. Morphine may be required for pain, 6. Treat shock by replacing lost fluids and blood intravenously. 7. Monitor urine output and renal function. 8. 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. 9. Corticosteroids confer no benefit and may mask abdominal signs of perforation. 10. An aggressive surgical approach is favoured in those with suspected perforation or severe (grade 3) burns. 11. In severe cases seek specialist advice from an NPIS physician. References Caravati EM. Metabolic abnormalities associated with phosphoric acid ingestion. Ann Emerg Med 1987; 16: 904-6. Cello JP, Fogel RP, Boland CR. Liquid caustic ingestion. Spectrum of injury. Arch Intern Med 1980; 140: 501-4. Hawkins DB, Demeter MJ, Barnett TE. Caustic ingestion: Controversies in management. A review of 214 cases. Laryngoscope 1980; 90: 98-109. 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. Mazariegos-Ramos E, Guerrero-Romero F, Rodríguez-Morán M, Lazcano-Burciaga G, Paniagua R, Amato D. Consumption of soft drinks with phosphoric acid as a risk factor for the development of hypocalcaemia in children: A case-control study. J Pediatr 1995; 126: 940-2. von Muhlendahl KE, Oberdisse U, Krienko EG. Local injuries by accidental ingestion of corrosive substances by children. Arch Toxicol 1978; 39: 299-314. Wason S, Gomolin I, Gross P, Mariam S, Lovejoy FH. Phosphorus trichloride toxicity: Preliminary report. Am J Med 1984; 77: 1039-42. 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 Phosphorus trichloride Origin of substance Manufactured by reacting yellow phosphorus with chlorine. (PATTY, 1993) Synonyms Phosphorus chloride Trichlorophosphine (DOSE, 1994) Chemical group A compound of phosphorus, a group VA element. Reference numbers CAS 7719-12-2 (DOSE, 1994) RTECS TH3675000 (RTECS, 1997) UN 1809 (DOSE, 1994) HAZCHEM 4WE (DOSE, 1994) Physicochemical properties Chemical structure PCl3 (DOSE, 1994) Molecular weight 137.33 (DOSE, 1994) Physical state at room temperature Liquid (OHM/TADS, 1997) Colour Colourless (OHM/TADS, 1997) Odour Pungent, irritating odour, similar to HCI. (OHM/TADS, 1997) Viscosity NIF pH Forms acids in water. (DOSE, 1994) Solubility Decomposes in water. (DOSE, 1994) Autoignition temperature NIF Chemical interactions Reacts with water and acids. Can react with oxidizing materials, organic matter and metals. Reacts with carboxylic acids to form violently unstable products. (LEWIS, 1996) Major products of combustion Generates toxic irritating fumes of hydrogen chloride and phosphorus oxides. (CHRIS, 1997) Explosive limits Violent reaction with water evolves hydrogen chloride and diphosphane gas which may then ignite. (LEWIS, 1996) Flammability Not flammable (CHRIS, 1997) Boiling point 76°C (DOSE, 1994) Density 1.574 at 21°C (DOSE, 1994) Vapour pressure 13332 Pa at 21°C (DOSE, 1994) Relative vapour density 4.7 (CHRIS, 1997) Flash point > 66°C (DOSE, 1994) Reactivity Rapidly hydrolyzed in the presence of water to form hydrogen chloride, phosphoric acid and phosphorous acid. (PAYNE et al, 1993) Uses Catalyst, chlorinating agent, etchant, phosphinylation agent and used in organic synthesis. (DOSE, 1994) Hazard/risk classification Index no. 015-007-00-4 C; R34 - Corrosive, causes burns. Xi; R37 - Irritating to the respiratory system. S(1/2)7/8-26-45 - Keep locked up and out of the reach of children. Keep container tightly closed and dry. 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. 231-749-3 (CHIP2, 1994) INTRODUCTION Phosphorus trichloride is the most commonly used of the phosphorus halide compounds. The primary sites of toxicity are the skin, mucous membranes, eyes and respiratory tract where contact with water forms phosphoric and hydrochloric acids. There is no evidence that phosphorus poisoning occurs from phosphorus trichloride exposure. EPIDEMIOLOGY Phosphorus trichloride reacts extremely violently with water and as such is unstable in the environment. The main sources of exposure are occupational (Sassi, 1952; Roshchin and Molodkina, 1977) or as the result of an accidental spillage (Dadej, 1962; Wason et al, 1984; Finnegan and Hodson, 1989). Approximately 450 patients required hospital examination following exposure to phosphorus trichloride released after a railroad accident (Wason et al, 1984). MECHANISM OF TOXICITY Phosphorus trichloride produces fumes and vapours which are toxic by inhalation (Desai, 1992). Irritant effects primarily result from the action of the hydrochloric and phosphoric acids formed in contact with water (Proctor et al, 1988) including tissue fluids of the upper respiratory tract and eyes (Waldon and Scott, 1994). Increased blood phosphate concentrations following phosphoric acid ingestion have been associated with hypocalcaemia, hypotension and acidosis (Caravati, 1987). Hypocalcaemia occurs via inhibition of 1-hydroxylase, with diminished 1,25-dihydroxyvitamin D3 formation (Haussler and McCain, 1977). Increased serum phosphate concentrations also inhibit bone resorption with reduced calcium release (Raisz, 1970). Hydrogen ion loads produce a metabolic acidosis which further exacerbates hypocalcaemia (Mazariegos-Ramos et al, 1995). TOXICOKINETICS Absorption Phosphorus trichloride rapidly decomposes to phosphoric and hydrochloric acids which are absorbed by ingestion, inhalation and dermal contact. Distribution Phosphoric acid is distributed widely in the body as phosphate. Increased serum phosphate concentrations have been reported rarely after phosphoric acid ingestion (Caravati, 1987). Excretion Absorbed phosphate is filtered at the glomerulus and partially reabsorbed with phosphate clearance 80 per cent of creatinine clearance. A small amount of phosphate is excreted in faeces (Larson et al, 1986; Reynolds, 1993). In infants with normal renal function the half-life of serum phosphate following single oral or rectal overdose is 5-11 hours (Larson et al, 1986). CLINICAL FEATURES: ACUTE EXPOSURE Dermal exposure Phosphorus trichloride is a skin irritant and corrosive which may cause severe burns (Proctor et al, 1988; Lewis, 1996). Skin irritation was experienced by 12 per cent of 450 individuals exposed to unknown concentrations of phosphorus trichloride and its hydration products released after a railroad accident (Wason et al, 1984). Four workers were exposed to an estimated 36800 mg/m3 phosphorus trichloride, 116300 mg/m3 hydrochloric acid and 62500 mg/m3 phosphorous acid for periods of a few to tens of seconds following an explosion. "Severe skin irritation" was reported as well as serious pulmonary and ocular effects (Dadej, 1962, cited by Payne et al, 1993). Ocular exposure The major symptoms reported after exposure to a spillage of phosphorus trichloride and its subsequent hydration products were eye irritation, lacrimation and blurred vision. Initial physical examination showed mild to moderate conjunctivitis (Wason et al, 1984). These features plus photophobia were reported in workers exposed occupationally to phosphorus trichloride concentrations greater than 10 mg/m3 (Sassi, 1952; Roshchin and Molodkina, 1977). Eye irritation and "corrosion" were reported when four workers were exposed to 36800 mg/m3 phosphorus trichloride, 116300 mg/m3 hydrochloric acid and 62500 mg/m3 phosphorous acid for a few to tens of seconds (Dadej, 1962, cited by Payne et al, 1993). Inhalation Pulmonary toxicity Early features following corrosive inhalation include cough and retrosternal discomfort. Hoarseness, dyspnoea and, in severe cases, stridor due to laryngeal oedema may follow. Following significant exposure there is a risk of delayed onset non-cardiogenic pulmonary oedema (with increasing breathlessness, wheeze and cyanosis) which may take up to 36 hours to develop. Exposure to a spillage of phosphorus trichloride and its subsequent hydration products caused nausea, dyspnoea and cough. Throat irritation, headache, sputum production, chest pain, rash, wheezing and abdominal pain were also reported. Of 450 patients seen in hospital all were discharged within two days without evidence of residual effects. Seventeen patients returned for assessment. Pulmonary function tests showed impaired large and small airways resistance inversely correlating with distance from the spill (Wason et al, 1984). There was a significant improvement to near normal lung function among seven individuals who attended a follow-up study one month later (pre-exposure lung function was not known). Following an explosion involving phosphorus trichloride and its hydration products (Dadej, 1962, cited by Payne et al, 1993) four workers were exposed for periods of a few to tens of seconds to an estimated 36800 mg/m3 phosphorus trichloride, 116300 mg/m3 hydrochloric acid and 62500 mg/m3 phosphorous acid. Three sustained severe irritant or corrosive effects to the skin and eye plus "bronchial inflammation" and pulmonary oedema; they died within 24 hours from cardiopulmonary failure. The fourth person, who was exposed for several seconds, suffered irritant effects to the eyes, skin and respiratory tract but recovered completely after three weeks. In the Italian literature Sassi (1952) studied a group of 23 chemical workers exposed acutely and subacutely to 10-150 mg/m3 phosphorus trichloride. Cases of acute poisoning occurred two to six hours after exposure. Features included burning eyes and throat, irritation of the pharyngeal mucous membranes, "bronchitis", fever and leucocytosis. The effects were reported to resolve in three to six days. Similar effects were described by Roshchin and Molodkina (1977) who reviewed the health of Russian workers exposed to phosphorus trichloride. These authors emphasised how features of eye and upper respiratory tract irritation typically preceded effects on the lower airways. Thus initial eye irritation, photophobia, lacrimation, rhinitis, tracheitis, laryngitis, and a dry cough usually occurred before dyspnoea, bronchitis and chest pain. Some acute intoxications resulted in chronically increased bronchial sensitivity. The most severe effects occurred following exposure to 10-20 mg/m3 phosphorus trichloride. A single exposure of a patient to hydrogen chloride vapour and a small amount of phosphorus trichloride caused prolonged hypoxaemia and delayed persistent asthma (Finnegan and Hodson, 1989). In the French literature Boutoux et al (1995) reported a patient who developed asthma associated with chemical pneumonitis after accidental exposure to phosphoric acid. Evidence of airways hyperresponsiveness persisted one year later. Haemotoxicity Moderate leucocytosis, neutrophilia and an increased erythrocyte sedimentation rate frequently accompany features of pulmonary toxicity (Sassi, 1952; Roshchin and Molodkina, 1977). Hepatotoxicity Transiently elevated lactate dehydrogenase activity was reported in six of 17 patients exposed to phosphorus trichloride and its hydration products. However, it was not confirmed that this was the hepatic iso-enzyme (Wason et al, 1984). Ingestion There are no reports of phosphorus trichloride ingestion over at least the last 30 years. The effects of ingestion are due to the corrosive nature of phosphorus trichloride and its hydration products, phosphoric and hydrochloric acid. Acid ingestions typically produce severe stomach lesions (Hawkins et al, 1980) with relative sparing of the oesophagus. However, severe caustic effects following phosphorus trichloride ingestion may be expected in the mouth, throat and oesophagus where contact with saliva will produce hydrochloric and phosphoric acids locally. Phosphoric acid ingestion is considered in a separate monograph. Systemic effects have been reported following phosphoric acid ingestion due to increased serum phosphate concentrations (Caravati, 1987). 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 phosphorus trichloride ingestion. Cardiovascular toxicity Circulatory collapse is likely in patients with extensive gastrointestinal burns. Hypotension, non-specific T wave flattening in the limb leads and inverted T waves in leads V4-6 have been reported in a patient who ingested 90-120 mL of a solution containing 20 per cent "hydrogen phosphate". These abnormalities resolved within 24 hours (Caravati, 1987). Haemotoxicity Disseminated intravascular coagulation and haemolysis may complicate concentrated corrosive ingestions. Metabolic disturbances A patient developed hyperphosphataemia, hypocalcaemia and a metabolic acidosis after ingesting 90-120 mL 20 per cent "hydrogen phosphate" (Caravati, 1987). Serum concentrations of calcium and phosphate were 2.05 mmol/L and 2.3 mmol/L respectively. Arterial blood gas analysis showed pH 7.19, HCO3- 6 mmol/L and an anion gap of 23 mmol/L. These abnormalities resolved within 36 hours following intravenous fluid and sodium bicarbonate plus oral aluminium hydroxide (as a phosphate binder). Injection There are no reports of phosphorus trichloride injection although excessive intravenous administration of phosphoric acid salts has been reported to cause hyperphosphataemia, hypocalcaemic tetany, hypotension, oedema and acute renal failure (Reynolds, 1993). CLINICAL FEATURES: CHRONIC EXPOSURE Inhalation Pulmonary toxicity In the Italian literature 23 chemical workers developed pharyngeal irritation, dyspnoea and asthma one to eight weeks after exposure to 10-150 mg/m3 phosphorus trichloride. Emphysema was described in workers exposed for at least one year (Sassi, 1952). Roshchin and Molodkina (1977) described a characteristic progression of respiratory features among workers exposed to phosphorus trichloride with initial upper respiratory tract irritation progressing to bronchopneumonia in those with persistent exposure. Chronic cough and wheeze may result from prolonged repeated exposure to "low concentrations" of phosphorus trichloride. The chronic pulmonary changes are reported to be "non-fibrotic and non-progressive", though there are no confirming data (Proctor et al, 1988). Haemotoxicity The pulmonary features among 23 chemical workers (described above) exposed to phosphorus trichloride 10-150 mg/m3 (Sassi, 1952) were accompanied frequently by fever and a neutrophil leucocytosis. Gastrointestinal toxicity Inhaled phosphorus trichloride has been reported to damage the teeth of exposed workers by reacting with saliva to form corrosive acids (Roshchin and Molodkina, 1977). 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. 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. Specialist ophthalmic advice should be sought if any abnormality is detected or suspected 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. Discuss with an NPIS physician. 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. Dilution may dissipate heat produced during hydration to concentrated phosphoric and hydrochloric acids which are themselves highly corrosive. 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). A 42 year-old man who sustained moderate distal oesophagitis and severe proximal gastritis after ingesting 240 mL phosphoric acid (concentration unknown) fully recovered without steroid therapy. Steroids were also not used in the treatment of a 64 year-old man who ingested 90-120 mL 20 per cent phosphoric acid (Caravati, 1987). Management details were not given of a patient who suffered fatal gastric perforation after ingesting an unstated amount of phosphoric acid (Hawkins et al, 1980). We do not advocate systemic steroids following phosphorus trichloride ingestion. Enhancing elimination Hyperphosphataemia following phosphoric acid ingestion is rare and can be managed effectively with fluid diuresis and, if severe, the use of oral phosphate binders such as aluminium hydroxide. Haemodialysis enhances phosphate elimination but is likely to be indicated only in the presence of renal failure (Caravati, 1987). MEDICAL SURVEILLANCE Ensure adequate ventilation and air concentrations below the occupational exposure standard. Appropriate protective equipment should be available when using concentrated solutions. People with a history of asthma should be identified prior to employment if inhalational exposure is likely. OCCUPATIONAL DATA Occupational exposure standard Short-term exposure limit (15 minute reference period) 3.8 mg/m3. Long term exposure limit 1.3 mg/m3 (8 hour TWA reference period) (Health and Safety Executive, 1997). OTHER TOXICOLOGICAL DATA Carcinogenicity There is an increased risk of gastric carcinoma following severe mucosal damage after corrosive ingestion but no documented cases involving phosphorus trichloride. Reprotoxicity There are no data regarding the reprotoxicity of phosphorus trichloride. Genotoxicity In in vivo rat bone marrow and in human and mouse peripheral lymphocytes chromosomal aberrations and induction of micronuclei were negative (DOSE, 1994). Fish toxicity (phosphoric acid) LC50 (96 hr) "aquatic life" 100-1000 ppm (DOSE, 1994). EC Directive on Drinking Water Quality 80/778/EEC Guideline level 400 µg/L; maximum admissible concentration 5000 µg/L, as P2O5 (DOSE, 1994). WHO Guidelines for Drinking Water Quality NIF (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. Date of last revision 28/1/98 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. Boutoux M, Leroyer C, Bernard R, Dewitte JD. [Reactive airways dysfunction syndrome after exposure to phosphoric acid vapours]. Arch Mal Prof Med Trav 1995; 56: 45-7. Caravati EM. 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