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    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.
    Metabolic abnormalities associated with phosphoric acid ingestion
    Ann Emerg Med 1987; 16: 904-6.

    CHIP2/Chemicals (Hazard Information and Packaging for Supply)
    Regulations 1994.
    Health and Safety Commission.
    Sudbury: Health and Safety Executive, 1994.

    CHRIS/Chemical Hazard Response Information System.
    In: Tomes plus. Environmental Health and Safety Series 1. Vol 32.
    United States Coast Guard, 1997.

    Dadej B.
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