Triethyltin
1. NAME
1.1 Substance
Triethyltin
1.2 Group
Organotin compounds
1.3 Synonyms
Iodotriethylstannane
Triethyliodostannane
Triethylstannyl iodide
1.4 Identification numbers
1.4.1 CAS number
2943-86-4
1.4.2 Other numbers
Not available.
2. SUMMARY
2.1 Main risks and target organs
Cerebral oedema of the white matter.
2.2 Summary of clinical effects
Severe headache, nausea and vomiting, visual and
psychological disturbances, and sometimes loss of
consciousness.
2.3 Diagnosis
Intolerable severe diffuse headache and signs of
cerebral oedema 24 to 48 days after exposure to organotin
compounds is indicative of poisoning.
2.4 First-aid measures and management principles
Steroid therapy may diminish the severity of brain
oedema. Surgical decompression has been considered to be the
only effective treatment that offered any benefit in human
cases.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
No data available.
3.2 Chemical structure
(C2H5)3Sn
Molecular weight: 205.88
3.3 Physical properties
3.3.1 Colour
Colourless.
3.3.2 State/form
Liquid
3.3.3 Description
Melting point: 75°C
Boiling point: 161°C
Solubility:
insoluble in cold water
insoluble in hot water
soluble in alcohol and organic solvents
(Weast, 1967)
3.4 Other characteristics
No data available.
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
4.1.2 Description
Monosubstituted organotin compounds (RSnX3) are
used as stabilisers in polyvinyl chloride films.
Disubstituted organotin compounds (R2SnX2) are mainly
used in the plastics industry, particularly as
stabilisers in polyvinyl chloride. They are also used
as catalysts in the production of polyurethane foams
and silicones at room-temperature vulcanization.
Trisubstituted organotin compounds (R3SnX) have
biocidal properties. The most important of these
compounds are the tributyl-, triphenyl-,and
tricyclohexyltin compounds, which are used as
agricultural and general fungicides,bactericides,
antihelminthics, miticides, herbicides,molluscides,
insecticides, nematocides, ovicides, rodent
repellents, and antifoulants in boat paints. The
tetrasubstituted organotin compounds (R4Sn) are mainly
used as intermediates in the preparation of other
organotin compounds(WHO, 1980).
The hazard associated with the use of organotin
compounds was unmasked by an incident in 1954
involving over 200 cases of poisoning, of which 100
were fatal. The cause was the ingestion of an oral
preparation containing diethyltin diiodide at 15
mg/capsule. It was suggested, however, that ethyl
triiodide, triethyltin iodide and tetraethyltin were
present as impurities (WHO, 1980).
4.2 High risk circumstance of poisoning
Workers involved in the processing of trisubstituted
compounds may be subject to excessive exposure. Workers
spraying fields or treating plants with trialkyl compounds
may also run the risk of exposure to these compounds (WHO,
1980).
4.3 Occupationally exposed populations
No data available.
5. ROUTES OF ENTRY
5.1 Oral
Main circumstance of poisoning in literature.
5.2 Inhalation
Four cases of acute poisoning due to exposure to
organotin vapours have been reported (Prüll and Rompel,
1976).
5.3 Dermal
Trialkyltin compounds are well absorbed on contact with
the skin. Application of a 20% fat solution of various
triethyltin derivates was applied to the skin of rats and
mice for 10 minutes is fatal for all animals within 20 to 30
minutes (Ignatjeva et al., 1968).
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Tin compounds with a short alkyl chain are readily
absorbed from the intestinal tract.
6.2 Distribution by route of exposure
Following intravenous administration of triethyltin, a
large quantity of triethyltin was found in the liver, with
smaller quantities in the kidney, brain, and whole blood in
the rabbit, 2 hours after administration (Cremer 1957,
1958).
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Tri-substituted organotin compounds are dealkylated in
the liver.
6.5 Elimination by route of exposure
Rats fed a diet containing triethyltin accumulated 0.7
mg triethyltin in their tissues; when a normal diet was then
substituted no triethyltin could be detected in the tissues
after 12 days (Cremer 1957). The route of excretion was not
known.
7. TOXICOLOGY
7.1 Mode of Action
Triethyltin is a powerful metabolic inhibitor. Three
interactions with mitochondrial respiration occur. In
halide-containing media, the triorganotin compounds mediate
an exchange of halide for hydroxyl ions across the
mitochondrial membrane, resulting in a disturbance of the
existing proton gradient. The triorganotins also bind to a
component of the ATP-synthetase complex, leading to direct
inhibition of ATP production. Finally, gross mitochondrial
swelling occurs after incubation, particularly with the more
lipophilic triorganotin compounds. As a result the
triorganotins are effective inhibitors of mitochondrial ATP
synthesis (Aldridge and Cremer 1955; Aldridge 1958,1976;
Aldridge and Street 1964; Selwyn et al., 1970; Selwyn
1976).
The toxic action of triethyltin on the central nervous system
of rodents was first described by Stoner et al., (1955). In
more detailed studies in the rat, Magee et al.,(1979)
reported that dietary concentrations of 20 mg/triethyltin/kg
feed induced interstitial oedema of the white matter of the
brain and spinal cord without obvious neuronal damage. Oedema
due to a progressive increase in water, sodium, and chloride
in the central nervous system caused increased cerebral fluid
pressure (Magee et al., 1957; Leow et al, 1979).Vascular
permeability to molecules larger than 3000 D was not altered
significantly. It was concluded that the basic pathologic
lesion was limited to myelin. Lesser changes in the
peripheral nervous system have also been observed (Gerren et
al., 1976; Graham et al., 1976).
Triethyltin has been shown to reduce concentrations of
various neurotransmitters, including norepinephrine,
serotonin, and dopamine in adult rat brain (Moore and Brody
1961, Bentue-Ferrer et al., 1985). As a consequence of these
lesions, electrophysiological alterations (Gerren et al.,
1976; Dyer et al., 1981) and behavioural abnormalities
(Squibb et al., 1980) have been demonstrated in rodents
exposed to triethyltin.
In the rat intraperitoneal administered triethyltin is
associated with a decrease of 30 to 40% in cerebral blood
flow was observed. After 48 hours an increase of cerebral
blood flow increased by 13 to 24% above control values. These
changes were accompanied by macroscopic features of brain
oedema and changes in the cerebral vascular network. Cerebral
oxygen consumption was decreased (Pluta and Ostrowska,
1987).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
The estimated toxic dose for an
adult is reported to be approximately 70 mg
of triethyltin over 8 days (Barnes and
Stoner, 1959).
7.2.1.2 Children
Ingestion of 3 capsules of
Stalinon(R) was sufficient to cause
intoxication in a 9-year-old child (Fontan et
al., 1955). Stalinon(R),an oral preparation
of 15 mg of diethyltin diiodide and 100 mg
vitamin F per capsule, was dispensed as a
treatment for staphylococcal skin infections.
However it contained also impurities such as
monomethyltin triiodide and also triethyltin
iodide 1.5 mg in each capsule, what is
believed to be the primary agent of
intoxication.
7.2.2 Relevant animal data
LD50 intraperitoneal rat triethyltin sulfate:
5.7 mg/kg (Stoner, 1966). Triethyltin sulfate was
equally toxic to the rat after intravenous,
intraperitoneal, and oral administration. The lethal
dose was 10 mg/kg, causing death within 4 to 5 days
(Stoner et al., 1955). LD50 intraperitoneal rat
triethyltin chloride: 5 mg/kg (Robinson,
1969).
7.2.3 Relevant in vitro data
Not relevant.
7.2.4 Workplace standards
No data available.
7.2.5 Acceptable daily intake (ADI) and other guideline
levels
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
The physico-chemical characteristics of triethyltin
indicate that it is likely to cross the placenta, but its
distribution in the placental-fetal unit is unknown. The
relative lack of formed myelin in fetal brain may prevent
cerebral oedema and redistribute the triethyltin to other
neural elements. No data are available on the possible
teratogenicity of triethyltin (Reuhl and Cranmer,
1984).
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemcial analysis
8.3.1.1 Blood, plasma or serum
Fatal doses of triethyltin in the
rat are associated with moderate
hyperglycaemia secondary to the release of
adrenaline from the adrenal medulla. An
increase in blood non-protein nitrogen may
be secondary to the reduced renal function
(Stoner et al, 1955).
8.3.1.2 Urine
No data available.
8.3.1.3 Other biological specimens
The cerebrospinal fluid is usually
normal.
8.3.2 Arterial blood gas analyses
No data available.
8.3.3 Haematological analyses
No data available.
8.3.4 Interpretation of biomedical investigations
No data available.
8.4 Other biomedical (diagnostic) investigations and their
interpretation
CAUTION: ophthalmoscopy may be completely normal even
in case of very severe cerebral oedema (Alajouanine, 1958).
The cerebrospinal fluid is usually normal but pressure is
raised. Alajouanine (1958) reported normal lumbar puncture
even in patients with severe cerebral oedema.
The electroencephalogram may be randomly altered and the
changes do not suggest any localised lesion (Barnes and
Stoner 1959).
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
201 case reports, including 98 deaths, have
been reviewed by Alajouanine et al., (1958). The
predominant symptom, occurring in 98% of cases, was a
diffuse headache, sometimes intolerably severe, which
appeared a few days after exposure. Nausea and
vomiting occurred in 73%; visual disturbances (mainly
photophobia, but also double vision), colour-vision
disturbances, and blindness occurred in 33%. Frequent
symptoms and signs were urinary incontinence, vertigo,
loss of weight, and abdominal pains. Absence of fever
and a tendency towards hypothermia were also noted.
Psychological disturbances were reported in 70% of the
cases. Other findings were meningeal irritation,
somnolence, insomnia, convulsions, constipation, and
bradycardia.
The electrocardiogram was abnormal in some cases but
did not suggest any localised lesion. Death was due to
respiratory or cardiac changes occurring during
convulsive episodes. It is probable that most of the
symptoms and signs were attributable to cerebral
oedema, the occurrence of which was established at
autopsies and at decompressive surgery (Cossa et al,
1958; Fontan et al., 1958).
It has been reported that only 10 of the 103 subjects
who survived recovered completely: in the remainder,
symptoms such as headache and asthenia persisted for
at least 4 years (Barnes and Stoner 1959).
9.1.2 Inhalation
In four cases of acute poisoning due to
exposure to organotin vapours, symptoms included
vertigo, headaches, nausea and vomiting and visual
disturbances. Clinically, papilloedema was evident and
all patients displayed pathological abnormalities on
the electroencephalograms. These abnormalities were
reversible in 7 to 25 days, and all patients recovered
clinically. The organotin compound or compounds
involved were not identified (Pruel and Rompel,
1976).
9.1.3 Skin exposure
No data available.
9.1.4 Eye contact
No data available.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Muscular weakness, at least partly due to
neurological effects and often resulting in partial or
total paralysis, has been frequently observed in
chronically intoxicated animals (Graham et al, 1976a;
Bierkamper and Bassett, 1984). In man, cerebral oedema
is the most pronounced finding but muscular weakness
and paralysis have also been observed (Alajouanine et
al., 1958).
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
It has been reported that only 10 of the 103 subjects
who survived severe poisoning recovered completely; in the
remainder, symptoms such as headache and asthenia persisted
for at least 4 years (Barnes and Stoner 1959).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
No data available.
9.4.2 Respiratory
No data available.
9.4.3 Neurological
9.4.3.1 CNS
Symptoms and signs attributed to
cerebral oedema include (Alajouanine et al.,
1958):
- diffuse headache, sometimes intolerably
severe, and appearing a few days after
ingestion of Stalinon(R);
- nausea and vomiting;
- visual disturbances: mainly photophobia but
also double vision, abnormal colour-vision
and blindness;
- stupor;
- meningeal irritation, somnolence, insomnia,
convulsions, constipation, and
bradycardia.
9.4.3.2 Peripheral nervous system
Transitory paralysis lasting 5 to 6
hours, and even persisting paresis, were
common in patients poisoned by contaminated
Stalinon(R) (Alajouanine 1958).
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
No data available.
9.4.4 Gastrointestinal
Nausea and vomiting was observed in 146
patients and abdominal pain was reported by 19 of the
201 persons involved in the Stalinon case.
Constipation occurred in 31 patients and diarrhoea in
8 (Alajouanine et al., 1958).
9.4.5 Hepatic
No data available.
9.4.6 Urinary
9.4.6.1 Renal
Transitory or prolonged urine
retention occurred in patients with
paraplegia.
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Various di- and triorganotin compounds are
irritant to the skin or eyes in rodents and man, but
no data are available on triethyltin.
9.4.9 Eye, ears, nose, throat: local effects
EYE: The commonest effect is photophobia seen
in 67 of the 201 patients in the Stalinon poisoning in
France. Other visual disturbances include: diplopia
due to paralysis of the oculomotor nerve; amblyopia;
and transitory or definitive amaurosis within 24 hours
of exposure (Alajouanine, 1958).
EARS: Hearing may be impaired. Triethyltin and
trimethyltin initially disrupt the functional
integrity of either inner hair cells or spinal
ganglion cells within the cochlea such that
depolarisation occurs only following a significant
increase in stimulus intensity (Clerici et al,
1991).
9.4.10 Hematological
In vitro the most haemolytic organotin
compounds are the alkyltin derivatives with alkyl
groups of 3 to 6 carbon atoms (Byington et al.,
1974).
9.4.11 Immunological
Some of the triorganotin compounds are
immunotoxic. Thymus weight reduction, associated with
a depletion of cortical lymphocytes, occurs in rats
fed with tripropyltin, tributyltin, and triphenyltin
compounds at dietary levels as low as 15 to 25 mg/kg
(Vos et al., 1984; Krajnc et al., 1984; Snoey et al.,
1985). However, these effects may be less apparent
than neurotoxicity (Snoey et al., 1985).
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available.
9.4.12.2 Fluid and electrolyte disturbances
No data available.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
No data available.
9.5 Others
No data available.
10. MANAGEMENT
10.1 General principles
Monitor vital signs and initiate life-supportive measures.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
10.2.2 Biomedical analysis
10.2.3 Toxicological analysis
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic treatment
Studer et al., (1973) reported that steroid therapy
appeared to diminish the severity of brain oedema and
mortality in rats.
Surgical decompression has been considered the only effective
treatment clinically (Alajouanine et al., 1958).
10.4 Decontamination
Effective methods are not available.
10.5 Elimination
All known methods, even exchange transfusion, have
proved ineffective.
10.6 Antidote treatment
10.6.1 Adults
No data available.
10.6.2 Children
Not applicable.
10.7 Management discussion
Dimercaprol may be an effective antidote in dialkyl
poisoning but has no effect in cases of trialkyl
poisoning.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Acute toxicity of an ingested alkyltin compound has
been observed in man as a result of the Stalinon incident in
France in 1954.
Stalinon was an oral preparation containing 15 mg of
diethyltin diiodide for the treatment of boils and other
staphylococcal skin infections, osteomyelitis, anthrax and
acne. The main impurities in Stalinon were monoethyltin
triiodide and triethyltin iodide. Triethyltin iodide,
approximately 1.5 mg per capsule, is believed to be the
primary cause of poisoning. The striking interstitial oedema
of the cerebral white matter which occurred in these victims
was later reproduced by administration of triethyltin to
laboratory animals.
Over 100 of the 217 known cases of Stalinon poisoning died
after exposure to an estimated dose of 3 g of triethyltin
iodide over the course of 6 to 8 weeks. As little as 70 mg of
triethyltin iodide ingested over an 8-day period appeared to
be toxic in adults. The signs and symptoms occurred after a
latent period of about 4 days, with extremely severe,
persistent headache, often associated with vomiting, vertigo,
urine retention, photophobia and other signs of visual
disturbance. Also noted were anorexia, hypothermia, increased
tendency to sleep and psychiatric disturbances. Severe cases
were characterised by impaired consciousness followed by
coma. Death occurred in coma or during convulsions, or from
respiratory or cardiac failure. Ten of the victims who
survived appeared to recover completely. The remainder
experienced attacks of headache and asthenia which persisted
for more than 4 years. In 4 cases, paraplegia, incontinence
and loss of sensation appeared to be irreversible (Boyer,
1989).
11.2 Internally extracted data on cases
11.3 Internal cases
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes
Not available.
12.2 Specific preventive measures
Not known.
12.3 Other
While recent studies suggest that the highly toxic
alkyltins might be formed by microbial metabolism in the
environment (Hodge et al., 1979; Hallas et al., 1982) the
extent to which this occurs naturally and the significance to
health has not been determined. Detailed studies of
environmental transformation and bio-accumulation of
organotins are needed to determine environmental risks (Reuhl
and Cranmer, 1984).
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES),
COMPLETE ADDRESSES
Author: Prof.Dr.A.N.P.van Heijst
Baarnse weg 42A
3735 MJ Bosch en Duin
The Netherlands
Telephone -30-287178
28-07-1993
Peer Review Group: Cardiff 14-18 February 1994:
N.Besbelli, O.Kasilo, L.Levebvre,
J.Szajewski, Temple, A.N.P.van Heijst.
Editor: M.Ruse
Finalised: IPCS, April 1997