Trimethyltin compounds
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/form |
| 3.3.3 Description |
| 3.4 Hazardous characteristics |
| 4. USES |
| 4.1 Uses |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstance of poisoning |
| 4.3 Occupationally exposed populations |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination and excretion |
| 7. TOXICOLOGY |
| 7.1 Mode of Action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Relevant animal data |
| 7.2.3 Relevant in vitro data |
| 7.2.4 Workplace standards |
| 7.2.5 Acceptable daily intake (ADI) |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 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) |
| 8.2.2.5 Other dedicated method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central Nervous System (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid-base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Other |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.3 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES |
TRIMETHYLTIN COMPOUNDS
International Programme on Chemical Safety
Group Poisons Information Monograph G019
Chemical
1. NAME
1.1 Substance
Trimethyltin compounds
1.2 Group
Trimethyltin acetate;
Trimethyltin chloride;
Trimethyltin cyanate;
Trimethyltin hydroxide;
Trimethyltin iodide;
Trimethyltin isothiocyanate;
Trimethyltin sulphate;
Trimethyltin thiocyanate.
1.3 Synonyms
1.4 Identification numbers
1.4.1 CAS number
Trimethyltin acetate: 1118-14-5
1.4.2 Other numbers
Trimethyltin chloride: 1066-45-1
Trimethyltin cyanate: 73940-86-0
Trimethyltin hydroxide: 56-24-6
Trimethyltin iodide: 811-73-4
Trimethyltin isothiocyanate: 15597-43-0
Trimethyltin sulphate: 63869-87-4
Trimethyltin thiocyanate: 4638-25-9
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Trimethyltin (TMT) is a neurotoxin which damages areas
of the limbic system, cerebral cortex, and the
brainstem.
2.2 Summary of clinical effects
Depending on the dose, the symptoms may appear from a
few hours up to 3 days. Signs and symptoms: headache,
tinnitus, deafness, visual disturbances, impaired memory,
disorientation, attacks of rage, bouts of depression,
psychotic behaviour, syncope, coma and, in the most severe
cases, respiratory depression requiring artificial.
2.3 Diagnosis
Specific symptoms such as memory defects, bouts of
depression alternating with attacks of rage lasting for hours
to days after an accident with organotin compounds, should be
an indication to test urine on tin concentrations.
2.4 First-aid measures and management principles
Because there is no effective therapy, only pure
symptomatic therapy can be given.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
The origin is only accidental in manufacturing processes
of organotin compounds. Because of the toxicity of TMT its
use should be practically excluded.
3.2 Chemical structure
General structure: (CH3)3 Sn
3.3 Physical properties
3.3.1 Colour
Colourless liquid
3.3.2 State/form
3.3.3 Description
Mol.wt.163.80
Sp.gr.1.570
Melting Point 23°C
Boiling point 18°C
Soluble in org.solv.
(Weast & Selby 1967)
3.4 Hazardous characteristics
No data available.
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Alkyltin compounds are used for production of
plastics in the chemical industry. They inhibit the
dissociation of hydrochloric acid from
polyvinylchloride (PVC) and in combination with PVC
they are not toxic. However, as free molecules
organic tin compounds are highly toxic.
4.2 High risk circumstance of poisoning
Synthesis of dimethyltin (used in the manufacturing of
plastics) from inorganic tin and methyl chloride under 4
athmosphere of pressure, results in 80% dimethyltin, 8%
trimethyltin and 4% monomethyltin. Trimethyltin chloride
vaporizes readily, augmenting its potential as inhalant
toxicant.
4.3 Occupationally exposed populations
Workers in the manufacturing of plastics.
5. ROUTES OF ENTRY
5.1 Oral
Intake of an unknown amount of TMT in wine by a
48-year-old woman caused death after six days (Kreyberg et
al., 1992).
5.2 Inhalation
Inhalation of trimethyltin chloride is a common form of
occupational exposure (Fortemps et al., 1978, Ross et al.,
1981; Rey et al., 1984; Besser et al., 1987; Yanofsky et al.,
1991).
5.3 Dermal
Trimethyltin is well absorbed on contact with the skin.
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
Trialkyltin compounds are well absorbed through the skin
and are readily absorbed from the lungs and intestinal
tract.
6.2 Distribution by route of exposure
Trisubstituted organotin compounds have been found in
the brain of various animal species.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Trisubstituted organotin compounds are dealkylated in
the liver.
6.5 Elimination and excretion
No data available.
7. TOXICOLOGY
7.1 Mode of Action
TMT causes a disturbance of brain glutamate metabolism
and GABAergic system (Chang & Dyer, 1983; Naalsund et al.,
1985; Hikal et al., 1988). The reduction in glutamate uptake
and synthesis will deplete the neuronal glutamate, which
together with a reduction in brain taurine, probably produced
the tremor as seen in animals. A reduced GABA synthesis was
also reported. This reduction of GABA synthesis in the
GABAergic neurons (inhibitory), together with an increased
release of glutamate under the influence of TMT, will promote
the situation of "hyperexcitation".
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
LD(est)50 man 3.0 mg/kg (Aldridge et
al., 1981). Neuronal necrosis in the fascia
dentata of the hippocampus, and in the spinal
ganglia, pyramidal hippocampus, cerebral
cortex and Purkinje cell layer of the
cerebellum (Besser et al., 1987).
Electronmicroscopy: accumulation of lysosomal
dense bodies and disorganization of the
granular endoplasmatic reticulum in the
neurons same as in experimental TMT
intoxication (Boulding et al., 1981; Brown et
al., 1979; Nolan et al., 1990; Kreyberg et
al., 1992).
7.2.1.2 Children
No data available.
7.2.2 Relevant animal data
LD50 rat oral trimethyltin chloride 12.6 mg/kg
(Brown et al., 1979).
LD50 rat oral trimethyltin chloride 9.2 mg/kg (Reuhl &
Cranmer, 1984).
In experimental TMT intoxications in rats neuronal
necrosis in the limbic system structures, especially
in the hippocampal formation and pyriform cortex. In
addition necrosis occurred in the neurons of the
neocortex, basal ganglia, Purkinje cells, brainstem,
spinal cord, and dorsal ganglia (Brown et al., 1979;
Bouldin et al., 1981; Aldridge et al., 1981; Dyer et
al., 1982).
7.2.3 Relevant in vitro data
No relevant data
7.2.4 Workplace standards
No data available.
7.2.5 Acceptable daily intake (ADI)
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
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)
8.2.2.5 Other dedicated method(s)
8.2.3 Interpretation of toxicological analyses
The excretion rate of tin in urine correlated
with severity of tin intoxication. Above 1000 ppb in
urine, respiratory insufficiency was observed (Rey et
al., 1984). Serum level of 13 µg/dL TMT and a urine
level of 52 µg/dL has been measured in an acute
intoxication (Yanofski et al., 1991). Normal mean of
organotin in urine is 0.1 µg/dL.
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
Hypokalaemia has been reported
(Kreyberg et al., 1992).
8.3.1.2 Urine
No data available.
8.3.1.3 Other fluids
No data available.
8.3.2 Arterial blood gas analyses
Metabolic acidosis has been reported (Kreyberg
et al., 1992).
8.3.3 Haematological analyses
Disseminated intravascular coagulation has been
reported in a severe poisoning (Kreyberg et al.,
1992).
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
EEG shows focal temporal spikes and rythmic temporal
discharge and delta waves (Yanofski et al., 1991).
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
After a latent period of 1-3 days: tinnitus,
deafness, lightheadedness, vertigo, impaired memory,
aggressiveness and episodes of unresponsiveness,
respiratory depression, coma (Kreyberg et al.,
1992)
9.1.2 Inhalation
Disorientation, confabulation, retrograde and
anterograde amnesia, disturbances in sexual behaviour,
complex partial seizures, ataxia, hearing loss,
paresthesias in the legs, and mild slowing sensory
nerve conduction without reflex changes or sensory
loss (Besser et al.,1987).
9.1.3 Skin exposure
No data available in literature, but symptoms
may be identical to those in exposure by inhalation.
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
No data available.
9.2.2 Inhalation
Workers whose histories suggested extensive
exposure demonstrated non-specific symptoms such as
forgetfulness, fatigue, loss of libido, loss of
motivation, headache, and sleep disturbances, as well
as specific symptoms such as bouts of depression
alternating with attacks of rage lasting for hours to
days (Ross et al., 1981).
9.2.3 Skin exposure
No data available in literature, but signs and
symptoms may be identical to those in poisoning by
inhalation.
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
Prognosis:
The long term prognosis of severely intoxicated persons is
poor (Rey et al., 1984). Neurological sequelae are observed:
extrapyramidal, hyperkinesia, severe cortical defects, severe
memory deficits and aggressiveness. Complete recovery is
possible but persistent memory loss for 6 months has been
observed (Yanofski et al., 1991).
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 Central Nervous System (CNS)
Signs of the limbic system:
Disorientation, confabulation, retrograde and
anterograde amnesia, aggressiveness, hyperphagia,
disturbances in sexual behaviour, complex partial
seizures and intermittent rhythmic delta activity of
spikes arising from one or both temporal lobes.
Cerebellar dysfunction:
Ranged from mild gaze-evoked nystagmus to severe
ataxia in severe poisoning (Besser et al., 1987).
9.4.3.2 Peripheral nervous system
Sensory disturbances:
Hearing loss (15 to 30 dB), paresthesias in
the legs and mild sensory nerve conduction
without reflex changes or sensory loss
(Besser et al., 1987).
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
No data available.
9.4.5 Hepatic
Massive fatty degeneration has been reported in
a fatal poisoning (Yanofski et al., 1991).
9.4.6 Urinary
9.4.6.1 Renal
Acute tubular necrosis has been
reported in a fatal poisoning (Yanofsky et
al., 1991).
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
No data available.
9.4.9 Eye, ears, nose, throat: local effects
Tinnitis and deafness have been observed
(Yanofsky et al., 1991). Acute effects on cochlear
functions in guinea pigs demonstrated compound action
potential sensitivity impairment in pure tone stimuli
at a broad range of frequencies (Yanofsky et al.,
1991; Kreyberg et al., 1992).
9.4.10 Haematological
Disseminated intravascular coagulation has
been observed (Kreyberg, 1992).
9.4.11 Immunological
Possible immunotoxic properties of TMT may be
overshadowed by the neurotoxicity (Snoey, 1987; Snoey
et al., 1985).
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Metabolic acidosis has been
reported in a fatal poisoning (Kreyberg et
al., 1992).
9.4.12.2 Fluid and electrolyte disturbances
Hypokalaemia has been reported
(Kreyberg et al., 1992).
9.4.12.3 Other
No data vailable.
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.
9.6 Summary
10. MANAGEMENT
10.1 General principles
There is no effective therapy (Besser et al., 1987)
10.2 Life supportive procedures and symptomatic treatment
Symptomatic treatment
10.3 Decontamination
No data available.
10.4 Enhanced elimination
Plasmapheresis proved to be unsuccessful in 5 patients
(Yanofski, 1991).
10.5 Antidote treatment
10.5.1 Adults
Although there is a high protein binding of
tin there was no measurable effect of plasma
separation. d-Penicillamine therapy has no effect on
tin excretion (Rey et al., 1984).
10.5.2 Children
No data available.
10.6 Management discussion
There are currently no guidelines for the management of
the acute poisoning or neurological sequelae of trimethyl
exposure. Neither dimercaprol nor penicillamine are thought
to be effective (Barnes & Stoner, 1959; Yanofski et al.,
1991). Treatment of organotin toxicity is supportive,
although experience with human exposure to this substance is
limited.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A 48-year-old woman and her friend drank some wine that
was later shown to be contaminated with TMT. Ten minutes
after the first mouthfuls they both noticed tinnitus and felt
"strange". Her friend only drank one or two mouthfuls but
her symptoms continued and she was hospitalized because of
tinnitis and vertigo a few days later. She suffered from
loss of memory for several months but she is now back to work
without sequellae. The other subject drank one glass or more
and became gradually restless with episodes of
unresponsiveness. After three hours she became agitated and
started to yell and scream. She also lost control of her
bowels. She remained restless and agitated when she was
admitted to the hospital the next morning. She presented
with hypokalaemia and leucocytosis. Her condition
deteriorated rapidly with development of metabolic acidosis
and liver derangement. She was given sedatives and treated
with a respirator until she died five days later.
A 23-year-old male chemistry student presented to the
emergency department with burns of the face, hand and chest.
He had been working in the laboratory with
bis-trimethyl-stannyl acetylene and ether when a flash fire
occurred, igniting the substance. He immediately washed
under the laboratory shower. The patient did well until 48
hours later when a friend noticed that he was not acting like
himself, repeating himself frequently and not able to
remember events in the past. Over the course of the next two
days, he exhibited memory problems and confusion. The patient
had a gradual improvement over the next several
months.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Warning for riks and danger of working with organotin
compounds is a necessity. The effectiveness of protective
clothes and masks should be checked. In exposed workers
regular testing of tin concentration in urine is
advised.
12.3 Other
No data available.
13. REFERENCES
Aldridge WN, Brown AW, Brierley JB, Verschoyle RD, Street BW
(1981) Brain damage due to trimethyltin compounds. Lancet ii:
692-693.
Barnes JM & Stoner HB (1959) The toxicology of tin compounds.
Pharmacol Rev 11: 211-232.
Besser R, Kraemer G, Thuembler T, Bohl J, Gutman L, Hopf HC
(1987) Acute trimethyltin limbic-cerebellar syndrome. Neurology
37: 945-950
Bouldin TW, Goines ND, Bagnell CR, Krigman MR (1981) Pathogenesis
of trimethyltin neuronal toxicity. Am J Pathol 104:237-249.
Brown AW, Aldridge WN, Street BW, Verschoyle RD (1979) The
behavioral and neuropathologic sequellae of intoxication by
trimethyltin compounds in the rat. Am J Pathol 97: 59-82.
Chang LW & Dyer RS (1983) A time-course study of trimetyltin
induced neuropathology in rats. Neurobeh Teratol 5: 443-459.
Dyer RS, Walsh TJ, Wonderlin WF (1982) Trimethyltin-induced
changes in gross morphology of the hippocampus. Neurobeh Toxicol
Teratol 4: 141-147.
Fortemps E, Amand G, Bomboir A, Lauwerys R, Laterre EC (1978)
Trimethyltin Poisoning-Report of Two Cases. Int Arch Occup Environ
Hlth 41:1
Hikal AH, Light GW, Slikker W, Scarlet A, Ali AF (1988)
Determination of aminoacid in different regions of rat brain
application to acute effects of TMT. Life Sci 42: 2029-2035.
Kreyberg S, Torvik A, Bjorneboe A, Wiik-Larsen W, Jacobsen D
(1992) Trimethyltin poisoning:report of a case with postmortem
examination. Clin Neuropath 11: 256-259.
Naalsund LV, Selen CN, Fonnum F (1985) Changes in neurobiological
parameters in the hippocampus after exposure to TMT.
Neurotoxicology 6: 145-158.
Nolan CC, Brown AW, Cavanagh JB (1990) Regional variations in
nerve cell responses to trimethyltin intoxication in Mongolian
gerbils and rats:Futher evidence for involvement of the Golgi
apparatus. Acta Neuropathol (Berl) 81: 204-212.
Rey Ch, Reinecke HJ, Besser R (1984) Methyltin intoxication in six
men: toxicologic and clinical aspects. Vet Hum Toxicol 26:
121-122.
Ross WD, Emmerett EA, Steiner J, Tureen R (1981) Neurotoxic
effects of occupational exposure to organotins. Am J Psychiat 138:
1092-1094.
Snoey NJ (1987) "Triorganotin compounds in Immunotoxicology and
Biochemistry". PhD thesis, University of Utrecht.
Snoey NJ, Van Iersel AAJ, Penninks AH, Seinen W (1985) Toxicity of
organotin compounds: Comparative in vivo studies with a series of
trialkyltin compounds and triphenyl chloride in male rats. Toxicol
Appl Pharmacol 81: 274-286.
Weast RC & Selby SM eds (1967) CRC Handbook of Chemistry and
Physics 48th ed. The chemical Rubber Co. Cleveland, Ohio.
Yanofsky NN, Nierenberg D, Turco JH (1991) Acute short term memory
loss from trimethyltin exposure.J Emerg Med 9:137-139.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESSES
Author: Dr A.N.P. van Heijst.
Baarnse weg 42 A
3735 MJ Bosch en Duin
The Netherlands
Tel: 31-30-287178
Date: July 1993
Peer
review: Quebec, Canada, September 1993
(Dr E. Wickstrom, Dr A.Wong, Dr A.N.P. van Heijst)
Editor: Mrs J. Duménil
International Programme on Chemical Safety
Date: May 1999