Tributyltin 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 circumstances 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 Other |
| 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 Other |
| 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 Others |
| 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/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.6.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESSES |
TRIBUTYLTIN COMPOUNDS
International Programme on Chemical Safety
Group Poisons Information Monograph G018
Chemical
1. NAME
1.1 Substance
Tributyltin compounds
1.2 Group
Tributyltin benzoate;
Tributyltin chloride;
Tributyltin fluoride;
Tributyltin linoleate;
Tributyltin methacrylate;
Tributyltin naphthenate;
Tributyltin oxide.
1.3 Synonyms
Tributyltin benzoate: TBTB; (benzyloxy) tributyl stannane
Tributyltin chloride: TBTCl; Tributyl-chloro stannane
Tributyltin fluoride: TBTF; Tributyl-fluoro stannane
Tributyltin linoleate: TBTL;
Tributyl-(1-oxo-9,12-octadecadienyl)oxy-stannane
Tributyltin methacrylate: TBTM;
Tributyl-(2-methyl-1-oxo-2-propyl)oxy-stannane
Tributyltin naphthenate: TBTN;
Tributyl-mono(naphthenoyloxy) stannane
Tributyltin oxide: TBTO; Hexabutyl distannoxane
1.4 Identification numbers
1.4.1 CAS number
Tributyltin benzoate: 4342-36-3
1.4.2 Other numbers
Tributyltin chloride: 1461-22-9
Tributyltin fluoride: 1983-10-4
Tributyltin linoleate: 24124-25-2
Tributyltin methacrylate: 2155-70-6
Tributyltin naphthenate: 85409-17-2
Tributyltin oxide: 56-35-9
Tributyltin oxide: RTCS: JN8750000
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
Skin and eye iritant.Inhalation of arosols leads to
respiratory irritation. Acute systemic poisoning has never
been reported.
2.2 Summary of clinical effects
Severe dermatitis has been reported after direct contact
with the skin.The potential problem is made worse by the lack
of immediate skin response.
2.3 Diagnosis
Skin and/or eye lesions after exposure of workers during
the manufacturing and formulation of tributyltin (TBT)
compounds, in the application and removal of TBT paints,and
from the use of TBT in wood preservatives.
2.4 First-aid measures and management principles
Removal of contaminted clothes,and leaking gloves,even
if the irritancy of the product is not immediatly apparent.
Washing of the skin (or showering) with water and soap.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Synthetic.
3.2 Chemical structure
Tributyltin benzoate: C19H132O2Sn
Tributyltin chloride: C12H27ClSn
Tributyltin fluoride: C12H27FSn
Tributyltin linoleate: C30H58O2Sn
Tributyltin methacrylate: C16H32O2Sn
Tributyltin oxide: C24H54OSn2
3.3 Physical properties
3.3.1 Colour
3.3.2 State/form
3.3.3 Description
Tributyltin oxide
Relative molecular mass: 596
Boiling point: < -45 °C
Relative density: 1.17 to 1.18
Vapour pressure: 1 x 10 -3
Refractive index: 1.4880 to 1.4895
(IPCS, 1990)
TBTO is flammable but does not form explosive mixtures
with air. It reacts quantitatively at room
temperature with bromide or iodine with cleavage of
the Sn-O bond (a reaction that may be used for
quantitative analysis) (Bahr & Pawlenko, 1978). In
the presence of oxygen, light or heat, slow breakdown
occurs with formation of tetra-n-butyltin,
di-n-butyltin oxide, and eventually tin (IV) oxide by
dealkylation (Evans & Karpel, 1985). TBTO is soluble
in lipids and very soluble in a number of organic
solvents (ethanol, ether, halogenated hydrocarbons
etc.).
3.4 Hazardous characteristics
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Tributyltin compounds have been registered as
molluscicides, as antifoulants on boats, ships, quays,
buoys, crab-pots, fishing nets and cages, as wood
preservatives, as slimicides on masonry, as
disinfectants, and as biocides for cooling systems,
power station cooling towers, pulp and paper mills,
breweries, leather processing and textile
mills.
4.2 High risk circumstances of poisoning
Workers occupationally exposed to dibutyltin and
tributyl tin compounds such as during the manufacture and
formulation of tributyltin compounds, in the application and
removal of TBT paints, and from the use of TBT in wood
preservatives. Exposure of the general public may come from
the contamination of food, particularly fish and shellfish,
and from the domestic application of wood preservatives.
4.3 Occupationally exposed populations
Workers in the manufacture an formulation of tributyltin
compounds, in the application and removal of TBT paints and
from the use of TBT in wood preservatives.
5. ROUTES OF ENTRY
5.1 Oral
There have been no reported cases of poisoning from
ingestion of TBTO or other TBT salts.
5.2 Inhalation
Has been reported in workers in a rubber factory using
TBTO in vulcanizing process (WHO/FAO, 1984).
5.3 Dermal
Skin lesions have been described in workers
occupationally exposed to dibutyltin and tributyltin
compounds.
5.4 Eye
Irritation has been observed in women using a latex
spray containing TBTO as an additive.
5.5 Parenteral
Poisoning has been reported in one publication.
5.6 Other
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Tributyltin is absorbed from the gut (20-50% depending
on the vehicle) and via the skin of mammals (about
10%).
6.2 Distribution by route of exposure
Tributyltin can be transferred across the blood-brain
barrier and from the placenta to the fetus. Absorbed
material is rapidly and widely distributed amongst tissues
principally liver and kidney and, to a lesser extent, in the
spleen, fat, lungs, brain, and muscle.
6.3 Biological half-life by route of exposure
Estimates for biological half-lives range from 23 to
about 30 days.
6.4 Metabolism
Metabolism in mammals is rapid: metabolites are
detectable in blood within 3 hours of TBT administration. TBT
is a substrate for mixed-function oxidases in vitro, but
these enzymes are inhibited by TBT in vitro at very high
concentrations. Metabolism occurs in lower organisms but is
slower, particularly in molluscs. The capacity for
bioaccumulation is therefore much greater than in
mammals.
6.5 Elimination and excretion
Excretion of tributyltin is via the bile rather than the
urine.
7. TOXICOLOGY
7.1 Mode of Action
TBT compounds inhibit oxidative phosphorilation and
alter mitochondrial structure and function.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
No data available.
7.2.1.2 Children
No data available.
7.2.2 Relevant animal data
TBTO oral: LD50 rat 165-277 mg/kg (Elsea &
Paynter, 1958). At dietary doses of 320 mg/kg
(approximately 25 mg/kg bodyweight), high mortality
rates were observed when the exposure time exceeded 4
weeks. TBTO inhalation: exposure to TBTO aerosol at
2.8 mg/m3 produced high mortality, respiratory
distress, inflammatory reaction within the respiratory
tract and histopathological changes of lymphatic
organs. However, exposure to saturated vapour
concentration at room temperature (0.16 mg/m3)
produced no effects.
7.2.3 Relevant in vitro data
No relevant data on humans.
7.2.4 Workplace standards
ACGIH threshold limit value (time-weighed
average) in air was set in the USA in 1979 at 0.1 mg
tin/m3 and a short-term TLV at 0.2 mg tin/m3. The
Federal Republic of Germany recommended, in 1979, to
adopt an occupational exposure standard for organotin
compounds in air of 0.1 mg tin/m3, specified as a
maximum worksite concentration (MAK). The United
Kingdom has also set a recommended occupational
exposure limit of 0.1 mg tin/m3.
7.2.5 Acceptable daily intake (ADI)
A tentative acceptable daily intake of 1.6
µg/kg per day has been adopted in Japan. Many
countries have restricted he use of TBT antifouling
paints as a result of effects on shellfish. The
regulations vary in detail from country to country,
but most ban the use of TBT paints on boats of 25
metres or less. Some countries have exclided boats
with aluminium hulls from this ban. In addition, some
regulations restrict the TBT content of paints or the
leaching rate of TBT from paints to 4 or 5 µg/cm2 per
day, long-term. It would be prudent to base
assessment of the potential hazard to man on data from
the most sensitive species. Effects on host
resistance to T. spiralis have been seen at dietary
levels as low as 5 mg/kg (equivalent to 0.25 mg/kg per
day bodyweight), the NOEL being 0.5 mg/kg (equivalent
to 0.025 mg/kg per day). However the interpretation
of these data for human risk assessment is
controversial. In all other studies a concentration
of 5 mg/kg per day in the diet (equivalent to 0.5
mg/kg body weight, based on short-term studies) was
the NOEL with respect to general, as well as specific,
effects on the immune system. Using fish consumption
figures of 15 and 150 g/day, a value of 1 mg/kg for
residues in fish, and an average human body weight of
60 kg, the following safety margins based on different
immune endpoints are obtained. At a fish consumption
of 15 and 150 g/day, the estimated daily intake of TBT
was 0.25 µg/kg and 2.5 µg/kg respectively (IPCS,
1990).
7.3 Carcinogenicity
One carcinogenicity study on rats has been reported in
which neoplastic changes were observed in endocrine organs at
50 mg/kg diet. The pituitary tumours found at 0.5 mg/kg diet
are considered as having no biological significance since
there was no dose-response relationship. These tumour types
appear usually at high and variable background incidences.
The significance is therefore questionable (IPCS,
1990).
7.4 Teratogenicity
Teratogenic effects have only occurred in experimental
animals that caused overt maternal toxicity. The teratogenic
potential of TBT is therefore, considered to be very low
(IPCS, 1990).
7.5 Mutagenicity
Based on the results of comprehensive mutagenicity
studies, tributyltin compounds are not considered to have
mutagenic potential (IPCS, 1990).
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
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
Acute systemic poisoning has never been reported.
9.1.2 Inhalation
Aerosols leads to respiratory irritation.
9.1.3 Skin exposure
Tributyltin benzoate compounds are irritant to
the skin.
9.1.4 Eye contact
Tributyltin benzoate compounds are irritant to
the eyes.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
Short and long-term effects on experimental
animals have been reported. Owing to wide variation in
the consumption of fish and shellfish and local
differences in residues of TBT in seafood NOEL values
are to be considered.
9.2.2 Inhalation
Irritation of he upper respiratory tract may
occur.
9.2.3 Skin exposure
Skin burns in workers occupationally exposed
have been reported.
9.2.4 Eye contact
Irritation of the eyes may occur.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Course and prognosis are favourable in humans.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
No data available.
9.4.2 Respiratory
Seventy percent of the workers in a rubber
factory using TBTO in the vulcanizing process reported
irritation of the upper respiratory tract. About 20%
also experienced lower chest symptoms (irritation,
tightness and pain), but in all cases the pulmonary
function was unaffected. The extent of the exposure
was not recorded (WHO/FAO, 1984).
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
No data available.
9.4.3.2 Peripheral nervous system
No data available.
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
No data available.
9.4.6 Urinary
9.4.6.1 Renal
No data available.
9.4.6.2 Other
A case of occupational poisoning has
been reported where, along with symptoms of
lassitude, slight occipital headaches and
stiffness in the shoulders, there was a
marked disturbance of the sense of smell
(Akatsuka et al., 1959).
9.4.7 Endocrine and reproductive systems
In animal experiments structural effects on
endocrine organs, mainly the pituitary and thyroid,
have been noted in both short- and long-term studies.
Changes in circulating hormone concentrations and
altered response to physiological stimuli (pituitary
trophic hormones) were observed in short-term tests,
but after long-term exposure most of these changes
appeared to be absent (Funahasi et al., 1980; Krajnc
et al., 1984).
9.4.8 Dermatological
TBTO is a skin irritant and severe dermatitis
has been reported after direct contact with the skin.
The potential problem is made worse by the lack of an
immediate skin response (Lyle, 1958; Baaijens, 1987;
Lewis & Emmett, 1987; Molin & Wahlberg, 1975; Zedler,
1961).
9.4.9 Eye, ears, nose, throat: local effects
TBTO is an eye irritant.
9.4.10 Haematological
In rats decreases in haemoglobin concentration
and erythrocyte volume. resulting from dosing 8 mg/kg,
indicate an effect on haemoglobin synthesis, leading
to microcytic hypochromic anaemia. Anaemia has also
been observed in mice (Krajnc et al., 1984)
9.4.11 Immunological
Effects on experimental animals:
- The characteristic toxic effect of TBTO is on the
immune system Due to effects on the thymus, the
cell-mediated function is impaired. The mechanism
is unknown, but may involve the metabolic
conversion to dimethyltin compounds. Non-specific
resistance is also affected.
- General effects on the immune system (e.g. on the
weight and morphology of lymphoid tissues,
peripheral lymphocyte counts, and total serum
immunoglobin concentrations) have been reported in
several different studies with TBTO using rats and
dogs, but not mice, at overtly toxic dose
levels.
- Only the rat exhibits general effects on the immune
system without other overt signs of toxicity and is
clearly the most sensitive species. TBTO has been
shown to compromise specific immune function in rat
in vivo host resistance studies.
- With present knowledge, the effects on host
resistance are probably of most relevance in
assessing the potential hazard to man, but there is
insufficient experience in these test systems to
fully assess their significance.
- It would be prudent to base assessment of the
potential hazards to humans from the most sensitive
species (Funahashi et al.,1980; Krainc et al.,
1984; Vos et al., 1985; Schering,
1989a-e).
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.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Symptomatic treatment.
10.2 Life supportive procedures and symptomatic/specific
treatment
Not applicable
10.3 Decontamination
After contact with the skin immediately washing with
water and soap, and change of overalls, even if no signs are
present.
10.4 Enhanced elimination
No data available
10.5 Antidote treatment
10.5.1 Adults
Not applicable.
10.6.2 Children
Not applicable.
10.6 Management discussion
Not applicable.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Lewis & Emmet (1987) describe contact dermatitis in a
shipwright resulting from exposure to TBTO-containing
antifouling paint. The man had been spray-painting blocks of
wood and his skin had been exposed to the spray. There was
no immediate sensation, but some irritation was evident
within about an hour. Erythema and ulceration of the exposed
areas were noted on the second day. There were also some
mild pustular lesions on the mucous membrane of the lips,
presumed to be the result of wiping the mouth with
paint-contaminated arms.
Baaijens (1987) described cases of accidental exposure to
TBTO during the manufacture of organotin compounds. Severe
dermatitis developed only where splashes of the material had
been retained on the skin for long periods. In one case, a
worker had been splashed over the face and neck. He left the
work area after the splash and showered. An area behind one
ear had not been washed and the dermatitis had developed in
this one area. Another worker had been splashed on the arm.
He washed his skin but did not change his overalls. Contact
was extended and a large blister developed on his arm.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
12.2 Other
13. REFERENCES
Akatsuka K, Miyazawa J, Igarashi,I, Morishita M, Handa M,
Kawame A, Iwamoto I, Morito F, Murayama K, Nakano S, Yanagibashi
H, Nagasaki T, Kotani Y, Matsutani W, Fukuda I, Iyo T (1959)
[Experimental studies on disturbance of sense of smell due to
butyltin compounds.] J Tokyo Med Coll, 17:1393-1402 (in
Japanese).
Baaijens PA (1987) Health effect screening and biological
monitoring for workers in organotin industries. In: Toxicology and
analytics of the tributyltins: The present status. Proceedings of
an ORTEPA workshop, Berlin, Germany, 15-16 May 1986.
Vlissingen-Oost, The Netherlands, ORTEP-Association,
pp.191-208.
Bahr G & Pawlenko S (1978) Organic tin compounds.In:Bahr G,
Kalinowski H.O, Pawlenko S, ed. Organometallic compounds,
germanium, tin. Stuttgart, Georg Thieme Verlag, pp 512-515
(Methods in Organic Chemistry series).
Elsea JR & Paynter OE (1958) Toxicological studies on
bis(tri-n-butyltin) oxide. Am Med Assoc Arch Ind Health, 18:
214-217.
Evans CJ & Karpel S (1985) Organotin compounds in modern
technology. J organomet Chem Libr, 16: 178-217.
Funahashi N, Iwasaki I, Ide G (1980) Effects of
bis(tri-n-butyltin) oxide on endocrine and lymphoid organs of male
rats. Acta Path Jpn, 30: 955-966.
IPCS (1990) Environmental Health Criteria 116. Tributyl Compounds.
World Health Organization.
Krajnc EI, Wester PW, Loeber JG, Van Leeuwen FXR, Vos JG, Vaessen
HAMG, Van de Heijden CA (1984) Toxicity of
bis(tri-n-butyltin)oxide in the rat. 1. Short-term effects on
general parameters and on the endocrine and lymphoid systems.
Toxocol Appl Pharmacol, 75: 363-386.
Lewis PG & Emmett EA (1987) Irritant dermatitis from tri-butyl tin
oxide and contact allergy from chlorocresol. Contact dermatitis,
17: 129-132.
Lyle WH (1958) Lesions of the skin in process workers caused by
contact withbutyl tin compounds. Br J Ind Med,15: 193-196.
Molin L, Wahlberg JE (1975) Toxic skin reactions caused by
tributyltin oxide (TBTO) in socs. Berufs-dermatosen, 4:
138-142.
Schering (1989a) TBTO-4 week oral (diatary administration)
toxicity study in the rat. Bergkamen, Federal Republic of Germany,
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESSES
Author: A.N.P.van Heijst
Baarnse weg 42A
3735 MJ Bosch en Duin
The Netherlands
Tel: 31-30-287178
Date: January 1994
Peer
Review: Cardiff, United Kingdom, 14-18 February 1994
(N.Besbelli, O.Kasilo, L.Lefebvre, J.Szajewski,
W.Temple, A.N.P.van Heijst)
Editor: Mrs J. Duménil
International Programme on Chemical Safety
Date: May 1999