UKPID MONOGRAPH PHOSPHORIC ACID 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. PHOSPHORIC ACID Toxbase summary Type of product A common industrial chemical used in the manufacture of fertilizers, detergents, soft drinks and in water treatment. Toxicity Ten to 25 per cent phosphoric acid solutions are irritant and more concentrated solutions corrosive. Skin exposure, inhalation or ingestion of any quantity of a concentrated solution can be dangerous. 5 mL of a 1.0 per cent solution was not caustic to the oral mucosa (von Muhlendahl et al, 1978). A patient has survived ingestion of 90-120 mL of a metal cleaner containing 20 per cent "hydrogen phosphate" (Caravati, 1987). Features Dermal - Solutions greater than 10 per cent are irritating to the skin and higher concentrations may cause burns. Ocular - Direct contact may irritate or burn the eye causing pain, blepharospasm, lacrimation and/or 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 - Ingestion of greater than 10 per cent solutions will cause immediate burning of the mouth and throat possibly with retrosternal and abdominal pain, nausea and vomiting. - Severe irritant or corrosive effects are likely following ingestion of greater than 20 per cent solutions with hypersalivation, haematemesis and hypovolaemic shock. - 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. - There is a single report of hyperphosphataemia, hypocalcaemia and metabolic acidosis occurring after acute ingestion of 90-120 mL of 20 per cent phosphoric acid (Caravati, 1987). 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 luke- warm 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. Continue irrigation with saline infusion (using drip tubing) for at least 10-15 minutes. 3. Repeated instillation of local anaesthetic may reduce discomfort and help more thorough decontamination. 4. Corneal damage may be detected by instillation of fluorescein. 5. 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. High dose corticosteroids (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. 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. 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. Shuster J, Jenkins A, Logan C, Barnett T, Riehle R, Zackson D, Wolfe H, Dale R, Daley M, Malik I, Schnarch S. Soft drink consumption and urinary stone recurrence: A randomized prevention trial. J Clin Epidemiol 1992: 45: 911-6. von Muhlendahl KE, Oberdisse U, Krienke 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 Phosphoric acid Origin of substance Obtained commercially from phosphate rock deposits. (CSDS, 1990) Synonyms Orthophosphoric acid (CSDS, 1990) Chemical group A compound of phosphorus, a group VA element. Reference numbers CAS 7664-38-2 RTECS TB 63 00000 UN 1805 HAZCHEM CODE 2 R (CSDS, 1990) Physicochemical properties Chemical structure H3PO4 (CSDS, 1990) Molecular weight 98.00 (DOSE, 1994) Physical state at room temperature Viscous liquid or rhombic crystals (CSDS, 1990) Colour Colourless (CSDS, 1990) Odour Odourless (HSDB, 1997) Viscosity NIF pH 1.5 (0.1 N aqueous solution) (HSDB, 1997) Solubility Very soluble in water (CSDS, 1990) Autoignition temperature NA Chemical interactions Contact with common metals produces hydrogen which may form flammable mixtures in air. When used for metal cleaning may react with impurities in the metal to release phosphine gas. (HAZARDTEXT, 1997) Major products of combustion Phosphorus oxides are released when heated to decomposition. (HAZARDTEXT, 1997) Explosive limits NA Flammability Not combustible (HAZARDTEXT, 1997) Boiling point 213°C (OHM/TADS, 1997) Density 1.864 at 20°C (CSDS, 1990) Vapour pressure 3.8 Pa at 20°C (DOSE, 1994) Relative vapour density 3.4 (HSDB, 1997) Flash point NA Reactivity Reacts exothermically with water. (HAZARDTEXT, 1997) Uses In manufacture of superphosphates for fertilizers, phosphate salts, polyphosphates and detergents. Catalyst in ethylene manufacture and hydrogen peroxide purification. Flavour, acidulant, synergistic antioxidant and sequestrant in food. Pharmaceutic acid. In dental cements. In process engraving, metal rustproofing, latex coagulation, analytical reagent. As a veterinary product in the treatment of lead poisoning. (DOSE, 1994) Hazard/risk classification Index no. 015-011-00-6 Risk phrases 25% Conc C; R34. Corrosive. Causes burns. 10% Conc 25% Xi; R36/38. Irritant. Irritating to eyes and skin. Safety phrases 5(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. 231-633-2 (CHIP2, 1994) INTRODUCTION Phosphoric acid is a strong acid and common industrial chemical used in the manufacture of a wide number of products, notably porcelain and metal cleaners, detergents and fertilizers. It is also used as a food additive and is a major constituent of many soft drinks. Low phosphate concentrations are found in drinking water to which it is added in some areas in order to reduce lead solubility. There is no evidence that phosphorus poisoning occurs from phosphoric acid exposure (Desai, 1992). EPIDEMIOLOGY The widespread use of phosphoric acid in industry has been the source of both chronic (Fabbri et al, 1977) and acute exposure following spillage, fire or explosion. Of 100, mainly occupational, cases of chemical burns admitted to a regional burns unit over an eight year period, two were due to phosphoric acid (Herbert and Lawrence, 1989). Phosphoric acid in household cleaning products has been the source of suicidal and accidental ingestion (Cello et al, 1980; Hawkins et al, 1980; Caravati, 1987). Excessive consumption of phosphoric acid-containing soft drinks has been associated with hypocalcaemia in children (Mazariegos-Ramos et al, 1995) and increased recurrence of urinary stones in adults (Shuster et al, 1992). Historically, industrial phosphine exposure has been reported from the use of phosphoric acid baths when elevated temperatures and the presence of metal produced sufficient nascent hydrogen to reduce the acid to phosphine (Anonymous, 1955). MECHANISM OF TOXICITY Phosphoric acid is caustic to the eyes, skin and mucous membranes of the respiratory and gastrointestinal tracts (Hawkins et al, 1980; Caravati, 1987; Desai, 1992). 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 Phosphoric acid can be absorbed by ingestion, inhalation and dermal contact. Distribution Absorbed 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 serum half-life of phosphate following single oral or rectal overdose is 5-11 hours (Larson et al, 1986). CLINICAL FEATURES: ACUTE EXPOSURE The Health and Safety Executive has classed phosphoric acid solutions between 10 and 25 per cent as irritant with more concentrated solutions corrosive (CHIP2, 1994). By contrast, the US Consumer Product Safety Commission has suggested concentrations of 15-35 per cent should be considered weak irritants, 35-60 per cent strong irritants and greater than 60 per cent solutions corrosive (Meditext, 1997). Dermal exposure Concentrated solutions are irritating to the skin. A 75 per cent solution will cause serious skin burns. The dust is particularly irritating to the skin in the presence of water (CSDS, 1990). Ocular exposure Direct contact may irritate or burn the eye depending on the concentration. Tested on human eyes, 0.16 M phosphoric acid buffered to pH 2.5 caused moderate brief stinging but no injury when applied as a single drop. The same solution adjusted to pH 3.4 caused no discomfort. Phosphoric acid has been held responsible for burns of the eye from superphosphate fertilizers (Grant and Schuman, 1993). Conjunctivitis, lacrimation and blurred vision were reported after exposure to phosphorus trichloride and its hydration products following a spillage (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). Inhalation Phosphoric acid has a low vapour pressure at room temperature so significant exposure is unlikely unless it is in the form of a mist or spray. Pulmonary toxicity Phosphoric acid is a respiratory tract irritant with the severity of symptoms increasing with acid concentration. Early features 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 which may take up to 36 hours to develop. In the French literature a patient with no previous history of asthma developed wheeze associated with chemical pneumonitis after accidental phosphoric acid inhalation (Boutoux et al, 1995). Evidence of airways hyperresponsiveness persisted one year later. A Russian study cited by Payne et al (1993) described the response of 15 non-smoking adults aged 18-36 years exposed to phosphoric acid aerosols. No airways irritation was reported at a concentration of 1.6 mg/m3. Eighteen per cent of subjects reported airways irritation at 7.2 mg/m3 and 82 per cent at 11.0 mg/m3. Several studies have reported the effects of exposure to phosphorus trichloride and its hydration products. Phosphorus trichloride is rapidly hydrolyzed to phosphoric and hydrochloric acids on contact with water, including moisture in the upper respiratory tract. Exposure to a spillage of phosphorus trichloride and its hydration products primarily caused nausea, dyspnoea and cough. Throat irritation, headache, sputum production, chest pain, wheeze and abdominal pain were also reported. Of 450 patients seen in hospital 15 were admitted and all discharged within two days without residual effects. Pulmonary function tests in 17 patients showed impaired large and small airway 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). In a review of the health of Russian workers exposed to phosphorus trichloride Roshchin and Molodkina (1977) emphasized that 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 acute exposure to phosphorus trichloride concentrations of 10-20 mg/m3. Haemotoxicity Moderate neutrophilia and an increased erythrocyte sedimentation rate are associated frequently with pulmonary features of phosphorus trichloride exposure (Sassi, 1952; Roshchin and Molodkina, 1977). Hepatotoxicity Transiently increased lactate dehydrogenase activity was reported in six of 17 patients exposed to phosphorus trichloride and its hydration products. It was not confirmed, however, that this was the hepatic iso-enzyme (Wason et al, 1984). Ingestion The effects of acute phosphoric acid ingestion are due to its corrosive nature, the severity of symptoms reflecting the concentration of the solution rather than the amount taken. Where severe gastrointestinal burns ensue there is a high risk of multi-organ damage. Five millilitres of a one per cent solution was "not caustic" when held in the mouth for five seconds (von Muhlendahl et al, 1978). By contrast, exposure of the soft tissue of the mouth to 50 per cent phosphoric acid for more than five minutes will burn (Payne et al, 1993). Ingestion of as little as 8 mL phosphoric acid (presumably neat) has been reported to be the "minimum lethal dose" for a 68 kg man. However, the original source of this information is not referenced and its reliability is unclear (Payne et al, 1993). A patient survived ingestion of 90-120 mL of a metal cleaner containing 20 per cent "hydrogen phosphate" (Caravati, 1987). Another patient survived ingestion of 240 mL of an unknown concentration of phosphoric acid (Cello et al, 1980). Gastrointestinal toxicity Although there is often relative sparing of the oesophagus following acid ingestion, with more severe stomach lesions (Hawkins et al, 1980), this is not universally true (Zarger et al, 1989). The suggested mechanism is rapid transit to the stomach with pooling at the pylorus due to pyloric spasm. The same mechanism, plus an alkaline milieu, spares the duodenum where acid burns are less frequent and less severe. Concentrated phosphoric acid ingestion produces local caustic effects on the mucosa of the oropharynx, oesophagus and stomach analogous to other strong acids (Hawkins et al, 1980; Caravati, 1987). Common early features include immediate pain in the mouth, pharynx and abdomen, intense thirst, dysphagia, vomiting, haematemesis and diarrhoea. Gastric and oesophageal perforation and chemical peritonitis may ensue. Late features include antral or pyloric stenosis, jejunal stricture formation, achlorhydria, protein-losing gastroenteropathy and gastric carcinoma. Caravati (1987) reported a 64 year-old man who ingested 90-120 mL 20 per cent "hydrogen phosphate" in attempted suicide. On admission one hour later he complained of a burning throat, hoarseness, mild abdominal pain and nausea. He had watery stools and vomited approximately 100 mL blood-stained liquid. The posterior pharynx was inflamed with discrete patches of mucosal pallor, the abdomen tender and the stool contained blood. "Prompt" endoscopy revealed partial thickness burns of the posterior oropharynx, distal oesophagus and a pre-existing Billroth II anastomosis. The patient recovered fully. A patient who ingested an unstated amount of phosphoric acid sustained extensive oesophageal burns and necrosis of the stomach, duodenum, jejunum, and pancreas complicated by spontaneous gastric perforation (Hawkins et al, 1980). He required four laparotomies for recurrent abdominal haemorrhage but died 19 days after admission. A 42 year-old man presented with oropharyngeal burns and haematemesis one hour after ingesting 240 mL phosphoric acid (concentration unknown) (Cello et al, 1980). Endoscopy (time post ingestion not stated) revealed moderate distal oesophagitis and severe proximal gastritis. The duodenum was normal. The gastric injuries healed completely. Steroids were not employed. 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). Pulmonary toxicity Features associated with corrosive acid 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 phosphoric acid ingestion although there are no reported cases. 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 developed hyperphosphataemia and hypocalcaemia after ingesting 90-120 mL of a solution containing "hydrogen phosphate" 20 per cent, isopropanol 9 per cent, non-ionic dispersants 32 per cent and inert ingredients 68 per cent. The abnormalities resolved within 24 hours (Caravati, 1987). Haemotoxicity Disseminated intravascular coagulation and haemolysis may complicate concentrated acid ingestion. Injection There are no reports of phosphoric acid injection although excess intravenous administration of phosphoric acid salts has been reported to cause hyperphosphataemia, hypocalcaemic tetany, hypotension, and acute renal failure (Reynolds, 1993). CLINICAL FEATURES: CHRONIC EXPOSURE Inhalation The main source of exposure to phosphoric acid mists and sprays is occupational. In the Italian literature chronic bronchitis was reported in 46 per cent and an obstructive lung function defect in 37 per cent of 35 workers at a phosphoric acid production plant. However, concomitant exposure to volatile fluorides was considered to be aetiologically significant (Fabbri et al, 1977). Respiratory complications have been reported also in workers exposed to phosphorus trichloride which is hydrolyzed to phosphoric acid and hydrochloric acid on contact with water, including moisture in the upper respiratory tract. In the Italian literature twenty three chemical workers developed pharyngeal irritation, dyspnoea and asthma one to eight weeks after exposure. Emphysema was described in workers exposed for at least one year. Poisoning was frequently accompanied by fever and a moderate leucocytosis (Sassi, 1952). Roshchin and Molodkina (1977) described a characteristic progression of respiratory features among industrial workers exposed to phosphorus trichloride with initial upper respiratory tract irritation progressing to bronchopneumonia in those with persistent exposure. Gastrointestinal toxicity Inhaled phosphorus trichloride reacts with saliva to form corrosive acids which damage the teeth (Roshchin and Molodkina, 1977). Ingestion The main source is phosphoric acid-containing soft drinks such as cola. Mazariegos-Ramos et al (1995) suggested a relationship between ingestion of phosphoric acid-containing soft drinks and hypocalcaemia in children. Fifty-seven children with no previously identified chronic medical problem and serum calcium concentrations less than 2.2 mmol/L were significantly more likely (p<0.001) to consume at least 1.5 L phosphoric acid-containing drinks (Coca-Cola or Pepsi-Cola) weekly and to be more prone to seizures (p<0.02) and cramps (p<0.001) than 171 controls (with normal serum calcium concentrations). The mean (± SD) serum phosphate concentrations in the hypocalcaemic and control groups were 1.7 ± 0.4 mmol/L and 1.6 ± 0.3 mmol/L respectively. In the above study the hypocalcaemic children (mean age 67 months) consumed an average 2.25 L Coca-Cola or Pepsi-Cola weekly (approximately 360-440 mg phosphate). By contrast, ingestion of up to 3000 mg phosphoric acid daily for four weeks did not have any significant effect on the calcium balance of six adults (Payne et al, 1993). Nephrotoxicity Consumption of soft drinks containing phosphoric acid has been linked to the recurrence of urinary stones in adult men (Shuster et al, 1992). The mechanism is unclear but is likely to involve increased calcium phosphate precipitation. 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 luke-warm 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. 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 hypovolaemic 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 phosphoric 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 used successfully 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 phosphoric acid ingestion. Enhancing elimination Hyperphosphataemia following phosphoric acid ingestion is rare and has been managed effectively with fluid diuresis and 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 working with 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) 2 mg/m3 (Health and Safety Executive, 1997). OTHER TOXICOLOGICAL DATA Carcinogenicity There is no reliable information on the carcinogenic potential of phosphoric acid (Payne et al, 1993). Severe gastric burns following acid ingestion are associated with an increased risk of gastric carcinoma. Reprotoxicity There are no data regarding the reprotoxicity of phosphoric acid. Genotoxicity Salmonella typhimurium TA97, TA98, TA100, TA104 with and without metabolic activation negative. Escherichia coli without metabolic activation negative (DOSE, 1994). Fish toxicity 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. 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See Also: Phosphoric acid solutions (CHEMINFO)