Triphenyltin acetate

   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
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   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
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
   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 by route of exposure
   7.1 Mode of Action
   7.2 Toxicity
      7.2.1 Human data Adults 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
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Biomedical analyses Arterial blood gas analysis Haematological analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
   8.2 Toxicological Analyses and Their Interpretation
      8.2.1 Tests on toxic ingredient(s) of material Simple Qualitative Test(s) Advanced Qualitative Confirmation Test(s) Simple Quantitative Method(s) Advanced Quantitative Method(s)
      8.2.2 Tests for biological specimens Simple Qualitative Test(s) Advanced Qualitative Confirmation Test(s) Simple Quantitative Method(s) Advanced Quantitative Method(s) Other Dedicated Method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis Blood, plasma or serum Urine 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
   8.6 References
   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 CNS Peripheral nervous system Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Others
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ears, nose, throat: local effects
      9.4.10 Hematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid-base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Others
   10.1 General principles
   10.2 Life supportive procedures and symptomatic treatment
   10.3 Decontamination
   10.4 Elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
   11.1 Case reports from literature
   12.1 Specific preventive measures
   12.2 Other

    International Programme on Chemical Safety
    Poisons Information Monograph 589

    1.  NAME

        1.1  Substance

             Triphenyltin acetate

        1.2  Group

             Organotin compound

        1.3  Synonyms

             fentin acetate,
             phentin acetate,
             stannane, (acetyloxy) triphenyl,
             tin triphenyl acetate,
             triphenylaceto stannane,

        1.4  Identification numbers

             1.4.1  CAS number


             1.4.2  Other numbers

                    Hazchem code 2Z
                    NFPA code 2-0-0
                    NIOSH number WH 6650000
                    UN number 2786

        1.5  Main brand names, main trade names

        1.6  Main manufacturers, main importers

    2.  SUMMARY

        2.1  Main risks and target organs

             Triphenyltin has a low toxicity.
             Liver damage (usually fairly slight) is seen in humans, and
             immunotoxicity, fetotoxicity, reproductive toxicity and
             respiratory toxicity have been observed in animals.  Allergic
             reactions are common, especially after dermal exposure.
             Respiratory irritation and irritation of the mucosa have been
             experienced by workers. 

        2.2  Summary of clinical effects

             Malaise,dizziness, vomiting
             Abdominal pain
             Temporary loss of consciousness
             Allergic reactions (irritation of
             Liver enlargement

        2.3  Diagnosis

             The following clinical symptoms are characteristic of
             TPTA poisoning:-
             Malaise, dizziness, vomiting
             Abdominal pain
             Allergic reactions (irritation of
             Liver enlargement
             Laboratory analysis:-
             Obtaining urine or blood samples is of prime importance. 
             Urinary tin levels have been found to peak 5 or 6 days after
             poisoning, and provide a specific diagnosis. A decrease in
             polymorphonuclear leucocyte activity also indicates TPTA
             poisoning, (Colosio et al., 1991). 

        2.4  First-aid measures and management principles

             EYE:  Remove any contact lenses, and wash the eye with
             flowing water for 10 minutes. 

             INHALATION:  Remove the victim from the area of exposure. If
             the victim is conscious make the person lie down quietly and
             give oxygen if available. 
             INGESTION:  Do not induce vomiting. If the victim is
             conscious give 500ml of water to drink. With usual
             precautions and contraindications the use of Ipecac Syrup,
             activated charcoal and a cathartic are indicated in the event
             of ingestion.
             SKIN:  Remove any contaminated clothing immediately. Drench
             the affected area with running water for at least 10
             GENERAL:  The management of triphenyltin poisoning should be
             primarily directed towards decontamination and supportive
             care, as there is no specific antidote. 


        3.1  Origin of the substance

             Organotin compounds have been widely used as pesticides
             over the last 30 years. Triphenyltin acetate was produced in
             1954.  It's comparatively low phytotoxicity meant that as the
             active  principle of Brestanâ it was the first practical
             organotin pesticide.
             Triphenyltin acetate is produced by the following pathway,
             (Bock, 1981). 
             SnCl4 + 4(C6H5)MgCl -> (C6H5)4Sn + 4MgCl2
             (C6H5)4Sn + HCl -> (C6H5)3SnCl + C6H6
             (C6H5)3SnCl + MOH -> (C6H5)3SnOH + MCL
             Heat the triphenyltin hydroxide with glacial acetic

        3.2  Chemical structure


        3.3  Physical properties

             3.3.1  Colour

                    Normal state at room temperature is white
                    odourless crystals.

             3.3.2  State/form

             3.3.3  Description

                    MW = 409.6
                    Solubility @ 20°C: 2.8 mg/100ml in water, (Hayes and
                    Laws, 1991); 0.2% in ethanol, (Bock, 1981); 3.7% in
                    ether, (Bock, 1981). 
                    Melting point:  122-124°C
                    Vapour pressure: 60 torr @ 230°C (Bock, 1981); 1.33 ×
                    10-6 torr @ 30°C, (Hayes and Laws, 1991). 

        3.4  Hazardous characteristics

             Slow decomposition (loss of phenol groups as benzene) of the
             aqueous solution at room temperature and neutral pH. t1/2 @
             30 mins, (Bock, 1981). Lasts indefinitely with dry storage
             and normal temperate. Completely decomposes in sunlight after
             8 hours. Half life on sugar beet leaves is about 3 days,
             (Bock,1981). The half life of TPTA in soil is around 140 days,
             (Duncan, 1980). 
             TPTA produces an acrid smoke and fumes of CO, CO2, tin and
             tin oxides when heated to decomposition.
             Care should be taken to ensure there is no adverse
             phytotoxicity or animal toxicity, especially in aquatic
             environments as aquatic organisms are very susceptible
             (Solomon et al., 1989).  In some aquatic environments it
             seems that TPTA persists for long periods of time, (Duncan,
             TPT has been detected in sediments and bivalves of lake
             Geneva, although tributyltin and dibutyltin were found at
             higher levels, (Becker et al., 1992). 
             Contaminants of technical grade TPTA (containing 0-95% TPTA)
             are approximately 7% tetraphenyltin, 2% diphenyltin and 1%
             volatiles (Bock, 1981).
             The pesticide Brestan 60, in addition to 60% TPTA contains
             15% manganese dithiocarbamate (Maneb), which could confuse
             clinical findings in cases of TPTA poisoning, (NIOSH, 1976).


        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    Fungicide, yeasticide, bacteriacide,
                    molluscicide. Organotin compounds are used as
                    stabilizers in PVC and other plastics.  Antifoulant in
                    ship paint.  200-360 g/ha, 3 to 5 applications per
                    crop is common (Bock, 1981).
                    Kills freshwater snails.
                    Anti-feeding and repellent effects on insects such as

        4.2  High risk circumstance of poisoning

             People involved with spraying the pesticide and
             preparing the aqueous solution are particularly at risk of
             TPTA poisoning.

        4.3  Occupationally exposed populations

             Crop-duster pilots
             Pesticide sprayers
             Factory and agricultural workers


        5.1  Oral

             TPTA may be ingested with vegetable intake.  Risk of
             harmful effects due to normal dietary intake is very low,
             since residues seldom rise above 1 ppm in crops tested. 
             Compulsory waiting periods allow degradation to levels below
             legal limits. 

        5.2  Inhalation

             Poisonings have occurred after respiratory exposure
             during crop spraying and mixing of the powder into water.

        5.3  Dermal

             Cases have been reported in which contact with skin has
             caused poisoning. Workers handling the powder are
             particularly at risk from this type of exposure, (Colosio et
             al., 1991). 

        5.4  Eye

             Airborne TPTA dust irritates the mucous membranes of the

        5.5  Parenteral

             No data available

        5.6  Others

             No data available

    6.  KINETICS

        6.1  Absorption by route of exposure

             Absorption through intact skin is poor, (Stoner, 1966).
             Intraperitoneal absorption is at least 10-fold more efficient
             than oral in laboratory animals, (Stoner, 1966). TPTA given 
             orally is absorbed well in rats and guinea pigs, but not so
             well in sheep, (WHO, 1980). 

        6.2  Distribution by route of exposure

             Triphenyltin is rapidly distributed to all tissues,
             including the brains of rats.
             Oral dosing of sheep produces slight accumulation in liver,
             kidney, lung, pancreas, gall bladder and brain, (Herok and
             Götte, 1963).

        6.3  Biological half-life by route of exposure

             Once absorbed, elimination is slow. One study claims a
             half-life in the rat brain of 3 days, while another study
             indicated a considerably longer half-life in guinea pigs
             (World Health Organization, 1980). 

        6.4  Metabolism

             A large proportion of radioactive Sn is found to be
             converted to inorganic tin in sheep, (Bock, 1981).  Phenyltin
             and diphenyltin are produced in small amounts.  TPTA is
             resistant to biological oxidation by the microsomal
             monooxygenase reaction (Bock, 1981).

             Subacute doses of TPTA to rabbits does not greatly influence
             the level of liver cytochrome P450, but by some unknown
             mechanism there appears to be induction of kidney Cyt P450.
             This induction (2-fold at75 ppm in the diet over a70 day
             period) could have an effect on the metabolism of endogenous
             substrates (Dacasto et al., 1991). 
             The means of metabolism is unknown. Diphenyltin and
             monophenyltin levels in the waste products increase while
             triphenytin levels drop, (Freitag and Bock, 1974).
             Degradation probably occurs as follows: (C6H5)3Sn+ ->
             (C6H5)2Sn2+ -> (C6H5)Sn3+ -> Sn4+ 

        6.5  Elimination by route of exposure

             Rats dosed with low levels of TPT in their diet excrete
             80-90% unchanged in their faeces within7-10 days, (Bock,
             1981; Freitag and Bock, 1974). 
             Sheep given TPTA orally excreted most of it in the faeces
             within a few days, (Herok and Götte, 1963). 


        7.1  Mode of Action

             Low concentrations of triphenyltin and other organotins
             inhibit the H+ translocation of the membrane-bound portion of
             H+ ATPase, (Papa et al., 1982). Some other ATPases and ion
             channels such as the Na+-K+ and the Ca2+ translocating
             ATPases are also affected, (Powers and Beavis, 1991).
             Triphenyltin has been shown to increase the intracellular
             Ca2+ concentration of mouse thymocytes, and the cytotoxicity
             could be caused by the resultant disruption of homeostasis. A
             likely cause for the increase of intracellular Ca2+ is an
             inhibition of the sequestering of Ca2+ by Ca2+ translocating
             ATPases, (Oyama et al., 1992). 
             Organotins may react with thiol groups in proteins, (van der
             Bend et al., 1985; Byington et al., 1974). 
             Anti-inflammatory properties may be caused by the prevention
             of phosphorylation of lipomodulin and the subsequent release
             of arachidonic acid, (Arakawa and Wada, 1984). Triphenyltin
             chloride inhibits histamine release from mast cells, (Nishida
             et al., 1992). 
             Triphenyltin chloride inhibits superoxide production by human
             neutrophils, (Matsui et al., 1983; Miura and Matsui, 1991;
             Matsui et al., 1983).

             The hyperglycaemic action of triphenyltin may be due to the
             inhibition of insulin release, (Manabe and Wada, 1981).

        7.2  Toxicity

             7.2.1  Human data


                             No data available.


                             No data available.

             7.2.2  Relevant animal data

                    The toxicity of organotin compounds increases
                    with the number of alkyl groups attached. Of the
                    trialkyltins, triphenyltin is moderately toxic, but
                    less toxic than trialkyltins with shorter alkyl
                    chains, such as trimethyltin.
                    Acute oral toxicities:
                    LD50 in guinea pigs 10-41 mg/kg, (Bock, 1981).
                    LD50 in rabbits 30-50 mg/kg, (Bock, 1981).
                    LD50 in mice ranges from 81-93 mg/kg, (Bock, 1981).
                    LD50 in rats ranges from 136-491 mg/kg, (Bock, 1981; 
                    Attahiru et al., 1991). 
                    Acute dermal toxicity:
                    Rat dermal LD50 of TPTA in oil is around 450 mg/kg,
                    (Bock, 1981).
                    Dermal LD50 in mice is 350 mg/kg, (Bock, 1981).
                    Dermal LD50 in rabbits is approximately 125 mg/kg,
                    (Bock, 1981). 
                    Chronic oral toxicity:
                    In guinea pigs, the cumulative toxic oral dose appears
                    to be of the same order as the acute toxic dose,
                    (Stoner, 1966). The guinea pig dietary NOEL is no more
                    than 5 ppm, (Verschuuren et al., 1966).  Rats fed TPTA
                    at levels of 300 ppm become ill and die, (Stoner,
                    1966).  NOEL for dogs is less than 5 ppm, (Stoner,

             7.2.3  Relevant in vitro data

                    Haemolysis is caused by TPT chloride at low
                    concentrations in animal blood, but not in human
                    blood, (Byington et al., 1974). 

             7.2.4  Workplace standards

                    In 1965 the ACGIH set the TLV TWA for all
                    organotins at 0.1 mg/m3, (measured as tin). The
                    paucity of both human and animal toxicity data at low
                    organotin concentrations has meant that this TLV was
                    derived by analogy with mercury, selenium and thallium
                    data. There are no specific standards for individual
                    organotin compounds, although the toxicity of
                    different organotin compounds varies greatly, (NIOSH,

             7.2.5  Acceptable daily intake (ADI)

                    The ADI is 0.0005 mg/kg, (FAO/WHO,

        7.3  Carcinogenicity

             Carcinogenicity tests show no carcinogenic effects in
             mice, (Innes et al., 1969). Organotin compounds may actually
             have antitumour activity, (Saxena and Tandon, 1983). 

        7.4  Teratogenicity

             Triphenyltin has no known teratogenic effects.  A study
             by Noda et al., (1991) suggests that TPTA given to maternal
             rats in their days7-17 phase does not induce foetal
             malformations. Embryotoxic effects were, however, seen at
             doses above 3.0 mg/kg maternal body weight. 

        7.5  Mutagenicity

             Results of the dominant lethal assay suggest that TPTA
             is not a mouse mutagen, (Duncan, 1980).

        7.6  Interactions

             No data available


        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

                    Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

                             Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

                             Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

        8.2  Toxicological Analyses and Their Interpretation

             8.2.1  Tests on toxic ingredient(s) of material

            Simple Qualitative Test(s)

            Advanced Qualitative Confirmation Test(s)

            Simple Quantitative Method(s)

            Advanced Quantitative Method(s)

             8.2.2  Tests for biological specimens

            Simple Qualitative Test(s)

            Advanced Qualitative Confirmation Test(s)

            Simple Quantitative Method(s)

            Advanced Quantitative Method(s)

            Other Dedicated Method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

            Blood, plasma or serum


            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

        8.5  Overall Interpretation of all toxicological analyses and
             toxicological investigations

             Sample collection
                    No data available
             Biomedical analysis
                    Allergological investigations should be made, in order
                    to try to confirm TPTA as the toxic agent.  Liver and
                    brain should be tested for signs of damage (Colosio et
                    al., 1991). 

             Toxicological analysis
                    High urinary tin excretion is indicative of recent
                    exposure. The normal value ranges from 10-65 ng Sn/ml
                    urine, (Manzo and Richelmi, 1981). 
                    Tin levels in blood above the average range,
                    (10-20ng/ml) are indicative of tin toxicity, (Manzo
                    and Richelmi, 1981). 
             Other investigations
                    No data available

        8.6  References


        9.1  Acute poisoning

             9.1.1  Ingestion

                    After a lethal dose, death in laboratory
                    animals occurs over several days. Signs and symptoms
                    include weakness, anorexia, watery diarrhoea,
                    staggering, reddish tears, coma and death, (Bock,

             9.1.2  Inhalation

                    Human cases of TPTA inhalation have resulted in
                    malaise, headache, dizziness, loss of consciousness,
                    epigastric pain, dryness of the mouth, photophobia,
                    and liver damage, (Colosio et al., 1991; Manzo and
                    Richelmi, 1981; World Health Organization, 1980). 
                    Animals exposed to TPTA dust showed signs of
                    irritation of mucous membranes, eyes and respiratory
                    tract. Restlessness, grooming and coughing were also
                    seen, but the animals did not die. Post mortem showed
                    respiratory tract irritation, (Bock, 1981). 

             9.1.3  Skin exposure

                    Although it has been claimed that TPTA does not
                    readily penetrate intact skin, (Stoner, 1966)there
                    have been cases of human intoxication.  TPTA
                    poisonings in man have resulted in allergic reactions,
                    liver damage, malaise, metabolic and enzymatic
                    changes, (Colosio et al., 1991), headaches, epigastric
                    pain, and weakness, (World Health Organization,
                    Severe inflammation is produced in rats given TPTA in
                    oil, (Bock, 1981). 
                    Tests of dermal toxicity of triphenyltin fluoride
                    (TPTF) have been conducted on humans, (Andersen and
                    Petri, 1982). In the aromatic solvent it gave rise to
                    burning sensations, erythema and dermal necrosis after
                    30 mins. It should however be noted that TPTA seems to
                    be more acutely dermally toxic than TPTF. 

             9.1.4  Eye contact

                    Triphenyltin is irritating to the eyes, (Bock,
                    1981;  World Health Organization, 1980). 

             9.1.5  Parenteral exposure

                    No data available

             9.1.6  Other

                    No data available

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Reduced immune responses and weight loss
                    (mainly related to reduced food intake) have been
                    observed in rats fed with 15 ppm triphenyltin, (Bock,
                    Decreased levels of peripheral lymphocytes have been
                    observed in rabbits, (Dacasto et al., 1991). 

             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

             Irritation of the eye, respiratory and nasal mucosa are
             experienced before airborne TPTA causes signs of
             Early symptoms of poisoning are malaise, dizziness, vomiting
             and headache, and it can take between a few hours to days for
             them to appear. These symptoms can be found in minor
             poisoning (dermal or inhalation). Allergic symptoms may
             persist for over a week even after slight poisonings.
             Moderately poisoned individuals will often experience
             abdominal pain, with  continued nausea/vomiting for up to
             several days. 
             Severe acute TPTA toxicity has not been well documented in
             the literature. 

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Heart failure is seen in rats given a lethal
                    oral dose, (Attahiru et al., 1991). 

             9.4.2  Respiratory

                    Upper respiratory tract irritation and
                    shortness of breath have been reported in human
                    inhalation cases, (World Health Organization,

                    Rats orally given a high lethal dose of TPTA were
                    found to have severe congestion and haemorrhages of
                    the lungs,(Attahiru et al., 1991).

             9.4.3  Neurological


                             Headache, dizziness, photophobia,
                             and occasionally loss of consciousness and
                             epileptic seizures are seen. Cerebral oedema
                             is seen in rats given lethal oral doses,
                             (Attahiru et al., 1991). 
                             Triphenyltin has an excitotoxic effect on
                             neurons at concentrations ranging from 10-5
                             to 10-7 M, (Oyama and Akaike, 1991; Oyama,
                             Triphenyltin has been shown to increase the
                             severity of maximal electroshock seizures in
                             mice at greater than7.17 mg/kg, (Doctor and
                             Fox, 1982). 

            Peripheral nervous system

                             Spraying with Brestan 60 has been
                             associated with lower limb parasthesia,
                             (Manzo and Richelmi, 1981). 

            Autonomic nervous system

                             Dry mouth and unquenchable thirst
                             have been reported with poisonings involving
                             Brestan 60 containing dithiocarbamate,
                             (National Institute for Occupational Health
                             and Safety, 1976). 

            Skeletal and smooth muscle

                             No data available

             9.4.4  Gastrointestinal

                    Nausea and vomiting occur after poisoning,
                    (Manzo and Richelmi, 1981; Colosio et al., 1991).
                    Heartburn and dryness of the mouth seem to precede the
                    more severe symptoms in the case of Brestan 60
                    poisoning, (National Institute for Occupational Health
                    and Safety, 1976). 

             9.4.5  Hepatic

                    Abdominal pain, liver damage, hepatomegaly, and
                    elevated serum enzyme levels have been reported in
                    poisoning cases. A study on hepatotoxicity in rats
                    showed a decrease in certain hepatic enzyme activities
                    and biliary excretion, (Di Nucci et al., 1986). 
                    High doses given orally to rats cause liver
                    congestion, (Attahiru et al., 1991). 

             9.4.6  Urinary


                             Lethal doses of TPTA given orally to
                             rats cause renal congestion, (Attahiru et
                             al., 1991). 


                             Mild to severe glycosuria has been
                             found in TPTA poisoning cases, (Colosio et
                             al., 1991).

             9.4.7  Endocrine and reproductive systems

                    In female rats, 80 ppm in food caused a slight
                    decrease in litter numbers. 250 ppm caused a distinct
                    reduction of food intake, growth rate and reproductive
                    capability, (Bock, 1981). Female rats fed 20 mg TPTA
                    per kg body weight per day had small ovaries and
                    decreased fertility, (Newton and Hayes, 1968). Male
                    rats fed at 20 mg TPTA/kg body weight per day
                    presented with degenerative changes of the testes,
                    which were shrunken and infertile. It is unknown
                    whether these are primary or secondary effects ofTPTA,
                    (Pate and Hayes, 1968). 

             9.4.8  Dermatological

                    Dermatitis has been seen. Irritation of hands,
                    skin and scrotum were seen in workers spraying 20%
                    TPTA, (WHO,1980). 

             9.4.9  Eye, ears, nose, throat: local effects

                    Irritation of mucous membranes of the eye and
                    respiratory tract have been observed in laboratory
                    animals treated with airborne TPTA dust, (Bock,
                    Identical symptoms were seen in workers spraying 20%
                    TPTA, (WHO, 1980). 

             9.4.10 Hematological

                    Haemolysis is caused by TPT chloride at low
                    concentrations in animal blood, but not in human
                    blood, (Byington et al., 1974). 

             9.4.11 Immunological

                    Subacute administration of dietary TPTA at
                    levels as low as 15 ppm have been shown to have an
                    immunosuppressive effect on rabbits, (Dacasto et al.,
                    Triphenyltin is immunotoxic in rats, but it is thought
                    that the triorganotins with shorter alkyl chain
                    lengths are more immunotoxic, (Snoeij et al., 1985).

             9.4.12 Metabolic

           Acid-base disturbances

                             No data available

           Fluid and electrolyte disturbances

                             No data available


                             Kidney cytochrome P450 levels have
                             become elevated in rabbits treated
                             subchronically with 15 ppm TPTA.
                             Transient hyperglycaemia, glycosuria, and an
                             increase in liver transaminase activity can
                             persist for weeks after poisoning in humans,
                             (Colosio et al., 1991). 

             9.4.13 Allergic reactions

                    Allergic reactions in the form of dermatitis
                    and erythematous eruptions have been reported in
                    humans, (Colosio et al., 1991).

             9.4.14 Other clinical effects

                    No data available

             9.4.15 Special risks

                    Radiolabelled tin in the milk of pregnant
                    sheep fed at 3.2 ppm was detected at a level of 2 mg/L
                    during the 25 days of feeding, and gradually subsided
                    when doses were stopped, (Bock, 1981). 

        9.5  Others

             No data available


        10.1 General principles

             Generally poisonings are not life-threatening, but
             vital signs should be watched in severe cases. Treatment must
             be symptomatic. 

        10.2 Life supportive procedures and symptomatic treatment

             Symptomatic treatment.

        10.3 Decontamination

             Remove and discard contaminated clothing.
             Remove any contact lenses and irrigate exposed eyes with
             copious amounts of water (or saline).
             Induce vomiting, only if the poison does not contain
             hydrocarbon solvents.
             Perform gastric lavage.
             Administer a cathartic. 

        10.4 Elimination

             Not applicable

        10.5 Antidote treatment

             10.5.1 Adults

                    No data available

             10.5.2 Children

                    No data available

        10.6 Management discussion

             No data available


        11.1 Case reports from literature

             Case 1. Adult male, dermal occupational exposure.  A
             case has been reported in which a 36 year old man was exposed
             to an unknown amount of 18.95% TPTA, (Brestan formulation).
             While handling the powder without gloves he accidentally
             spilt some on the exposed cutaneous area of his arms. He
             washed immediately afterwards, but 12 hours later experienced
             bilateral plantar pain, and after 24 hours severe genital
             oedema, followed by an erythematous reaction on his  torso.
             Two days after exposure he was experiencing general  malaise,
             dizziness and abdominal pain. Tests showed an  impairment of
             glucose metabolism, slight glycosuria, liver  enlargement, a
             brief increase in IgE, however patch tests with  Brestan did
             not produce any positive results. Steroid treatment did not
             prevent urticarial recurrences, but antihistamine was found
             to be helpful, (Colosio et al., 1991). 
             Case 2. Adult male, occupational exposure by inhalation. A75
             year old farmer inhaled some Brestan 60 powder (60% TPTA) 
             while preparing the aqueous solution. A few days later he 
             suffered from episodes of sudden malaise, dizziness and 
             temporary loss of consciousness, followed by a severe 
             headache, vomiting and photophobia. Once admitted to hospital 
             he received 10 mg metoclopramide IM twice a day and 6.5 mg
             diethylperazine twice a day as a suppository. Despite the 
             treatment, nausea, vomiting and photophobia persisted for 4 
             days. He underwent a complete recovery in 10 days. All 
             laboratory tests were within normal limit, (Manzo and 
             Richelmi, 1981). 

             Case 3. Adult male epileptic, occupational exposure. A 53
             year old farmer, suffering from primary epilepsy was 
             admitted to hospital 3 hours after spraying Brestan 60 (60% 
             TPTA). He had experienced general malaise, dizziness, 
             headache, asthenia and dryness of the mouth, but the symptoms 
             had mostly disappeared at the time of hospitalization. His 
             liver was slightly enlarged. Symptoms reappeared the next
             day,  and he developed an epileptic seizure which was treated
             with  intravenous diazepam. The following day headache and
             dizziness  were accompanied by lower limb paresthesia. Nine
             days after  admission the patient developed diffuse erythema
             on the face,  which was treated successfully with 25 mg
             promethazine orally  per day, (Manzo and Richelmi, 1981).


        12.1 Specific preventive measures

             Workers exposed to TPTA either in the aqueous form or
             the  powdered form should wear adequate protective clothing. 
             Respirators should be used if there is any chance of 
             inhalation of the powder or the aerosol. Exposed workers
             would  be advised to regularly have their urinary tin levels

        12.2 Other


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        Author:     William R. Norris
                    National Toxicology Group
                    P.O Box 13
                    New Zealand.

        Date:       6 April 1994

    See Also:
       Toxicological Abbreviations