UKPID MONOGRAPH
ANTIMONY PENTACHLORIDE
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.
ANTIMONY PENTACHLORIDE
Toxbase summary
Type of product
Used as a chemical reagent.
Toxicity
Acute antimony pentachloride poisoning is rare. Exposure may occur in
industry. Fatal dose not known.
Features
Dermal
- Antimony pentachloride 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.
- Systemic features may develop (see antimony Toxbase entry).
Ingestion
- Antimony pentachloride 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 acid.
- 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.
- Systemic features may develop (see antimony Toxbase entry).
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. Discussion with
an NPIS physician is recommended.
6. If systemic features develop treat as for antimony (see separate
entry)
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.
11. If systemic features develop treat as for antimony (see separate
entry).
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.
Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J.
Experimental and human studies on antimony metabolism: their relevance
for the biological monitoring of workers exposed to inorganic
antimony.
Br J Ind Med 1991;48: 93-7.
Cordasco EM.
Newer concepts in the management of environmental pulmonary edema.
Angiology 1974; 25: 590-601.
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.
Lauwers LF, Roelants A, Rosseel M, Heyndrickx B, Baute L.
Oral antimony intoxications in man.
Crit Care Med 1990; 18: 324-6.
Miller JM.
Poisoning by antimony: a case report.
South Med J 1982; 75: 592.
Winship KA.
Toxicity of antimony and its compounds.
Adverse Drug React Acute Poisoning Rev 1987; 2: 67-90.
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
Antimony pentachloride
Origin of substance
NIF
Synonyms
Antimony (V) chloride
Antimony perchloride
Pentachloroantimony
Antimonic chloride
Antimony chloride
Butter of antimony (DOSE, 1992; RTECS, 1997)
Chemical group
A compound of antimony, a group V A element.
Reference numbers
CAS 7647-18-9 (DOSE, 1992)
RTECS CC5075000 (RTECS, 1997)
UN 1730 (liquid); 1731 (solution) (DOSE, 1992)
HAZCHEM 4X (liquid); 2X (solution) (DOSE, 1992)
Physicochemical properties
Chemical structure
SbCl5 (DOSE, 1992)
Molecular weight
299.02 (DOSE, 1992)
Physical state at room temperature
Oily liquid (MERCK, 1996)
Colour
Colourless to yellow (MERCK, 1996)
Odour
Pungent (HSDB, 1997)
Viscosity
2.034 CP at 29.4°C (HSDB, 1997)
pH
NIF
Solubility
Water: Decomposes.
Soluble in carbon disulphide, chloroform, carbon tetrachloride,
hydrochloric acid and tartaric acid. (DOSE, 1992; HSDB, 1997)
Autoignition temperature
NIF
Chemical interactions
Corrodes metal. (CHRIS, 1997)
Major products of combustion
Decomposes to give antimony and hydrogen chloride.
(HSDB, 1997)
Explosive limits
NIF
Flammability
Non flammable (OHM/TADS, 1997)
Boiling point
79°C at 22 mm Hg (DOSE, 1992)
Density
2.336 at 20°C/4°C (DOSE, 1992)
Vapour pressure
133.322 Pa at 22.7°C (DOSE, 1992)
Relative vapour density
NA
Flash point
NA
Reactivity
Mono- and tetrahydrates are formed in the presence of small
amounts of water.
Large amounts of water cause hydrolysis to Sb2O5.
(MERCK, 1996)
Uses
A chemical reagent.
As a catalyst when replacing a fluorine substituent with chlorine
in organic compounds. (MERCK, 1996; DOSE, 1992)
Hazard/risk classification
Index no. 051-002-00-3
Risk phases
C;R34 - Xi;R37 Causes burns. Irritating to respiratory system.
Safety phrases
S(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. 231-601-8 (CHIP2, 1994)
INTRODUCTION
Antimony pentachloride is a pentavalent antimony compound. It is used
as a chemical reagent.
Due to the acidic nature of antimony pentachloride exposure may
produce corrosive injury as well as systemic antimony toxicity.
EPIDEMIOLOGY
Antimony pentachloride poisoning is rare and is likely only to occur
occupationally.
Cordasco (1974) reported 59 cases of pulmonary oedema, of which three
were ascribed to antimony pentachloride exposure. Two deaths resulted.
MECHANISM OF TOXICITY
Antimony pentachloride reacts with water to form hydrochloric acid
which has a direct corrosive effect on mucous membranes (Cordasco,
1974).
The mechanism of systemic toxicity of antimony compounds is unclear
but may involve disruption of thiol proteins via binding to sulphydryl
groups (de Wolff, 1995).
TOXICOKINETICS
Absorption
Antimony compounds may be absorbed by inhalation. Urine antimony
concentrations of 1.0 to 5.1 mg/L were measured in workers two days
after exposure to spray and vapour containing an estimated 73 mg/m3
antimony.
Gastrointestinal absorption in man is poor.
Distribution
Absorbed pentavalent antimony accumulates primarily in the spleen,
liver and bone (IPCS, 1996).
Lauwers et al (1990) estimated that the total body pool of antimony in
a patient who died following accidental antimony potassium tartrate
ingestion was only five per cent of the ingested dose with high
antimony concentrations in the liver, gall bladder and
gastrointestinal mucosa. This is consistent with antimony undergoing
enterohepatic circulation (see below).
Excretion
Antimony compounds are eliminated mainly in the urine, with small
amounts appearing in faeces via bile after conjugation with
glutathione. A significant amount of antimony excreted in bile
undergoes enterohepatic circulation (Bailly et al, 1991). Some 6-24
months after parenteral antimony therapy, Mansour et al (1967)
reported increased urine antimony concentrations (range 5.8-145.3
µg/L) compared to untreated controls (range 2.9-9.1 µg/L).
Kentner et al (1995) estimated a renal elimination half-life of four
days following occupational inhalation of antimony trioxide and
stibine in 21 employees of a starter battery manufacturing plant.
CLINICAL FEATURES: ACUTE EXPOSURE
Dermal exposure
Antimony pentachloride is an irritant and concentrated solutions or
liquid material may cause burns.
A 39 year-old worker was admitted to hospital with second and third
degree burns over most of his body following accidental release of
antimony pentachloride vapour. He developed severe respiratory
features also (see below) but recovered after 95 days (Cordasco,
1974).
Ocular exposure
Antimony pentachloride is corrosive and direct contact may irritate or
burn the eye causing pain, blepharospasm and photophobia.
Ingestion
There are no reports of antimony pentachloride ingestion although
corrosive injury may be expected. Systemic antimony toxicity may
develop also (see antimony monograph).
Acid ingestions typically produce severe stomach lesions (Hawkins et
al, 1980) with relative sparing of the oesophagus. However, severe
caustic effects following antimony pentachloride ingestion may be
expected in the mouth, throat and oesophagus where contact with saliva
will produce hydrochloric acid locally.
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
corrosive ingestion.
Cardiovascular toxicity
Circulatory collapse is likely in patients with extensive
gastrointestinal burns.
Haemotoxicity
Disseminated intravascular coagulation and haemolysis may complicate
concentrated corrosive ingestions.
Inhalation
Pulmonary toxicity
A 39 year-old man developed a severe cough, wheeze, dyspnoea and chest
tightness immediately following exposure to antimony pentachloride
vapour. Examination revealed crackles in both lung fields. Pulmonary
oedema developed some 12 hours after admission. Arterial blood gas
analysis revealed profound hypoxia (pO2 = 4.0 kPa) with bilateral
pulmonary vascular congestion on X-ray. Constant positive pressure
ventilation was commenced and "massive doses of corticosteroid"
administered. His condition improved somewhat although recovery was
complicated by the development of a laryngeal stricture requiring a
tracheostomy. The patient was discharged 95 days after admission
(Cordasco, 1974).
Gastrointestinal toxicity
Nausea, vomiting, abdominal pain and anorexia have accompanied
laboratory confirmation of systemic antimony poisoning following
inhalation of a corrosive trivalent antimony compound (Taylor, 1966).
CLINICAL FEATURES: CHRONIC EXPOSURE
There are no reports regarding chronic antimony pentachloride toxicity
though the effects of exposure to other antimony compounds have been
reported.
Dermal exposure
Dermatitis following contact with antimony trioxide is well described
(Oliver, 1933; McCallum, 1989). Typical lesions arise on the arms,
legs and in the flexures, sparing the face, hands and feet (Renes,
1953; McCallum, 1989).
Papules and pustules predominate around sweat and sebaceous glands
with areas of eczema and lichenification (Paschoud, 1963). These
so-called "antimony spots" occur mainly in the summer (McCallum,
1989).
Skin lesions developed in 23 men employed at an antimony trioxide
production plant. Most of those affected were furnace workers with
lesions typically appearing within two weeks of exposure. Itching,
erythematous papules and pustular eruptions were characteristic,
usually on dust laden sweaty areas of the skin. The lesions usually
resolved over two weeks in those removed to cooler parts of the
factory. Histological examination showed epidermal cellular necrosis
associated with an acute dermal inflammatory cellular reaction.
Antimony trioxide patch testing was negative whilst injection of
methacholine into the affected areas caused enlargement of the
lesions. The author concluded that antimony trioxide dust initiates an
irritant reaction when it penetrates sweat ducts (Stevenson, 1965).
White et al (1993) described three cases of occupational antimony
dermatitis following several months exposure to antimony dust and
antimony trioxide fumes. Two of these patients also experienced
frequent nose bleeds. Both problems resolved when exposure ceased. In
one patient patch testing for antimony was negative and in another the
urine antimony concentration was 53.2 µg/L ("normal" < 1.0 µg/L).
Positive patch testing to antimony has been noted in enamellers and
decorators in the ceramics industry (Motolese et al, 1993).
Inhalation
Pulmonary toxicity
Chronic occupational exposure to antimony compounds may cause
"antimony pneumoconiosis" (Cooper et al, 1968; McCallum, 1989).
Typical radiological findings include diffuse, dense, punctate
non-confluent opacities predominately in the middle and lower lung
fields, sometimes associated with pleural adhesions (Potkonjak and
Pavlovich, 1983).
These changes developed after at least ten years working in an
antimony smelting plant where the dust contained nearly 90 per cent
antimony trioxide with some antimony pentoxide and small amounts (up
to five per cent) of silica (Potkonjak and Pavlovich, 1983). Cough (in
31 of 51 subjects) and exertional breathlessness (in 26 cases) were
the symptoms most frequently reported with wheeze, chest pain or
generalized weakness in a minority. Nine workers had obstructive lung
function defects with a combined restrictive/obstructive picture in
five cases but no isolated restrictive defects or radiological
evidence of diffuse fibrosis.
Pneumoconiosis was reported also in workers at an antimony oxide
production plant. Lung biopsies from two affected individuals revealed
antimony concentrations of 600-3000 µg/g (Le Bouffant et al, 1987).
Perforation of the nasal septum has been described in antimony workers
but these cases probably have involved concomitant arsenic exposure
(McCallum, 1989). There were no cases of nasal perforation in 51
workers employed at an antimony smelter for 9-31 years (mean 17.9
years) (Potkonjak and Pavlovich, 1983).
Cardiovascular toxicity
ECG changes have been reported in patients treated with antimony
drugs.
In the Czechoslovakian literature Klucik and Ulrich (1960) reported
subjective cardiac complaints and ECG changes in 14 workers
occupationally exposed to antimony trioxide dust. Significant exposure
to antimony trisulphide also occurred.
Brieger et al (1954) attributed ECG T-wave changes and sudden deaths
to antimony-induced cardiotoxicity following occupational exposure to
antimony trisulphide although the reliability of this study has been
criticized (McCallum, 1989).
An epidemiological study of workers at an antimony processing plant
showed a decrease in the number of deaths from ischaemic heart disease
in workers exposed to antimony trioxide compared with other employees
at the same site (McCallum, 1989).
Ingestion
Chronic ingestion is not a recognized toxicological hazard.
MANAGEMENT
Dermal exposure
Ensue 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. The use of fluorescein allows
detection of corneal damage. Specialist ophthalmological advice should
be sought if any significant abnormality is detected 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. Discussion of individual cases with an
NPIS physician is recommended.
If systemic toxicity is suspected laboratory confirmation of blood and
urine antimony concentrations should be obtained. Antidotal treatment
may be considered in confirmed cases (see Antidotes).
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
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).
We do not advocate systemic steroids following antimony pentachloride
ingestion.
If systemic toxicity is suspected laboratory confirmation of blood and
urine antimony concentrations should be obtained. Antidotal treatment
may be considered in confirmed cases (see Antidotes).
Antidotes
Dimercaprol (British anti-Lewisite, BAL) (Braun et al, 1946; Thompson
and Whittaker, 1947), dimercaptosuccinic acid (DMSA, Succimer)
(Basinger and Jones, 1981) and dimercaptopropane sulphonate (DMPS,
Unithiol) (Basinger and Jones, 1981; Hruby and Donner, 1987) have
antidotal activity in experimental systemic antimony poisoning (see
below). These findings have not been confirmed in controlled studies
in man.
Dimercaprol
In vitro studies
Using the pyruvate oxidase system of pigeon brains as a test model,
dimercaprol in a molar ratio of 6:1 dimercaprol: antimony was able to
protect the enzyme system from inhibition by several antimony salts
(Thompson and Whittaker, 1947).
Animal studies
The LD50 of intramuscular antimony tartrate administered to rabbits
was raised from 90 mg Sb/kg in controls to 160 mg Sb/kg in animals
treated with intramuscular dimercaprol (30 mg/kg one hour after
intoxication followed by 15 mg/kg at six, 24 and 48 hours) (Braun et
al, 1946). A total of 45 controls received 50-200 mg/kg antimony
tartrate with 56 treated animals receiving 125-200 mg/kg.
Clinical studies
Four adults with antimony poisoning following the inadvertent
consumption of antimony potassium tartrate were treated with
intramuscular dimercaprol 200-600 mg daily. Three patients made an
uneventful recovery but the fourth, who had a history of
cardiorespiratory disease, died on day three. There were no
pre-chelation antimony excretion data but in two survivors maximum
antimony urine concentrations of 1000 µg/L and 1500 µg/L were reported
some 36 and 72 hours after poisoning respectively. Urine volumes were
not stated (Lauwers et al, 1990).
Bailly et al (1991) reported a 24 year-old woman who made an
uneventful recovery after ingesting an undetermined amount of antimony
trisulphide. She was treated with dimercaprol 200 mg tds for five days
but there was no evidence of enhanced urinary antimony elimination
with therapy.
DMSA
Animal studies
DMSA was given intraperitoneally to mice at a molar ratio of 10:1
DMSA: antimony twenty minutes after administration of potassium
antimonyl tartrate (120 mg/kg; twice the LD50). The survival ratio
was 28/30 (Basinger and Jones, 1981).
Clinical studies
There are no human data.
DMPS
Animal studies
DMPS has been shown to be an effective chelating agent in mice
following intraperitoneal administration of potassium antimonyl
tartrate (120 mg/kg; twice the LD50). The survival rate was 19/30
when intraperitoneal DMPS was given twenty minutes after intoxication
at a molar ratio of 10:1 DMPS: antimony. However, DMSA was
significantly more effective under these conditions (see above)
(Basinger and Jones, 1981).
Clinical studies
There are no human data.
Antidotes: Conclusions and recommendations
1. Clinical data regarding antimony chelation are scarce.
2. Dimercaprol effectively chelates antimony but has been superseded
by the less toxic thiol antidotes DMPS and DMSA.
3. In limited animal studies DMSA is a more effective antimony
chelator than DMPS.
4. Parenteral or oral DMSA therapy may be considered in antimony
pentachloride poisoning. The discussion of individual cases with
an NPIS physician is recommended.
MEDICAL SURVEILLANCE
Improved occupational health measures have reduced industrial airborne
antimony concentrations significantly but monitoring of ambient air
antimony concentrations remains important in some industries (Bailly
et al, 1991; Kentner et al, 1995).
Routine examination of the skin for "antimony spots" and chest
radiography for evidence of pneumoconiosis may also be useful. The
potential risk of pulmonary carcinogenicity should be remembered (see
below).
Although Bailly et al (1991) found that the urinary antimony excretion
of workers exposed to airborne antimony pentoxide and sodium
antimoniate correlated to the intensity of exposure, a recent
publication from the European Commission concluded "no indicator of
effect is available" for biological monitoring of antimony (Apostoli
et al, 1994).
Normal concentrations in biological fluids
"Normal" serum and urine antimony concentrations are quoted as
approximately 3 µg/L and 0.8 µg/L respectively (Poisindex, 1997).
OCCUPATIONAL DATA
Maximum exposure limit
Long-term exposure limit (8 hour TWA reference period) 0.5 mg/m3
(Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There are no carcinogenicity data specific to antimony pentachloride.
There is some evidence that occupational antimony exposure is
associated with an increased risk of lung cancer although frequent
concomitant exposure to arsenic and other heavy metals precludes a
definitive conclusion about is carcinogenic potential (Gerhardsson et
al, 1982; McCallum, 1989; Gerhardsson and Nordberg, 1993; Jones, 1994;
Schnorr et al, 1995).
Antimony has been implicated also in the aetiology of bladder tumours
in patients with schistosomiasis who have been treated with antimony
compounds (Winship, 1987).
Severe gastric burns following acid ingestion are associated with an
increased risk of gastric carcinoma.
Reprotoxicity
In the Russian literature women occupationally exposed to antimony
aerosols were reported to have a higher incidence of spontaneous
abortion, premature births and menstrual disorders. Antimony was
present in the blood, urine, placentae, amniotic fluid and breast milk
of these women. Further details were not available in the English
abstract (Belyaeva, 1967).
Genotoxicity
Bacillus subtilis rec assay positive (DOSE, 1992).
Fish Toxicity
NIF
EC Directive on Drinking Water Quality 80/778/EEC
Antimony: Maximum admissible concentration 10 µg/L. Chlorides: Guide
level 25 mg/L, maximum admissible concentration 400 mg/L (DOSE, 1992).
WHO Guidelines for Drinking Water Quality
Antimony: Provisional guideline value 0.005 mg/L (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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A controlled trial of corticosteroids in children with corrosive
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N Engl J Med 1990; 323: 637-40.
Bailly R, Lauwerys R, Buchet JP, Mahieu P, Konings J.
Experimental and human studies on antimony metabolism: their relevance
for the biological monitoring of workers exposed to inorganic
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Br J Ind Med 1991;48: 93-7.
Basinger MA, Jones MM.
Structural requirements for chelate antidotal efficacy in acute
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See Also:
Toxicological Abbreviations