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.
Zatrucia trójchlorkiem fosforu.
[Phosphorus trichloride poisoning.]
Med Pr 1962; 13: 21-6.
Desai H.
Phosphorus and phosphorus compounds.
In: Sullivan JB, Krieger GR, eds. Hazardous materials toxicology:
Clinical principals of environmental health.
Baltimore, MD: Williams & Wilkins, 1992.
DOSE/Dictionary of substances and their effects. Vol 6.
Cambridge: Royal Society of Chemistry, 1994.
Finnegan MJ, Hodson ME.
Prolonged hypoxaemia following inhalation of hydrogen chloride vapour.
Thorax 1989; 44: 238-9.
Haussler MR, McCain TA.
Basic and clinical concepts related to vitamin D metabolism and
action.
N Engl J Med 1977; 297: 974-83.
Hawkins DB, Demeter MJ, Barnett TE.
Caustic ingestion: Controversies in management. A review of 214 cases.
Laryngoscope 1980; 90: 98-109.
Health and Safety Executive
EH40/97. Occupational exposure limits 1997.
Sudbury: Health and Safety Executive, 1997.
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.
Larson JE, Swigart SA, Angle CR.
Laxative phosphate poisoning: Pharmacokinetics of serum phosphorus.
Hum Toxicol 1986; 5: 45-9.
Lewis RJ.
Sax's Dangerous Properties of Industrial Materials. 9th ed. Vol III.
New York, NY: Van Nostrand Reinhold, 1996.
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 hypocalcemia in children: A case-control study.
J Pediatr 1995; 126: 940-2.
OHM/TADS-Oil and Hazardous Materials/Technial Assistance Data System.
In: Tomes plus. Environmental Health and Safety Series 1. Vol 32.
United States Environmental Protection Agency, 1997.
PATTY/Beliles RP.
Phosphorus, selenium, tellurium, and sulfur.
In: Clayton GD, Clayton FE, eds. Patty's industrial hygiene and
toxicology. Vol 2. 4th ed.
New York: John Wiley & Sons, Inc., 1993.
Payne MP, Shillaker RO, Wilson AJ.
Phosphoric acid, phosphorus pentoxide, phosphorus oxychloride,
phosphorus pentachloride, phosphorus pentasulphide. Toxicity Review
30.
Sudbury: Health and Safety Executive, 1993.
Proctor NH, Hughes JP, Fischman ML.
Chemical Hazards of the Workplace.
Philadelphia, PA: Charles C Thomas, 1988.
Raisz LG.
Physiological and pharmacologic regulation of bone resorption.
N Engl J Med 1970; 282: 909-16.
Reynolds JEF, ed.
Martindale: The Extra Pharmacopoeia.
London: The Pharmaceutical Press, 1993.
Roshchin AV, Molodkina NN.
Chloro compounds of phosphorus as industrial hazards.
J Hyg Epidemiol Microbiol Immunol 1977; 21 : 387-94.
RTECS/Registry of Toxic Effects of Chemical Substances.
In: Tomes plus. Environmental Health and Safety Series 1. Vol 32.
National Institute for Occupational Safety and Health (NIOSH), 1997.
Sassi C.
[Occupational poisoning with phosphorus trichloride].
Med Lav 1952; 43: 298-306.
Waldron HA, Scott A.
Metals - Phosphorus.
In: Hunter's Diseases of Occupations. 8th ed.
London: Edward Arnold, 1994.
Wason S, Gomolin I, Gross P, Mariam S, Lovejoy FH.
Phosphorus trichloride toxicity. Preliminary report.
Am J Med 1984; 77: 1039-42.
WHO.
Guidelines for drinking-water quality. 2nd ed. Vol 1. Recommendations.
Geneva: World Health Organization, 1993.
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.
See Also:
Toxicological Abbreviations
Phosphorus trichloride (ICSC)