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    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.

    Date of last revision
    28/1/98

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See Also:
        Phosphoric acid solutions (CHEMINFO)