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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
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    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