Reports
available from The National Technical Information Service
(NTIS)
- see http://www.ntis.gov/ |
| Order
No. |
Title |
Keywords |
CAS
No. |
NTIS/OTS0509273
EPA/OTS;
Doc #40+7863021 |
2000
(?)
- DISSIPATION AND DETOXIFICATION OF ORGANOTINS IN THE
ENVIRONMENT
M
& T CHEM INC |
M
& T CHEM INC
ALKYLTINS
ENVIRONMENTAL FATE
BIODEGRADATION |
56-35-9
379-52-2
1983-10-4 |
NTIS/OTS0509272
EPA/OTS;
Doc #40+7863020 |
2000
(?)
- THE ENVIRONMENTAL CHEMISTRY OF THREE ORGANOTIN CHEMICALS
M
& T CHEM INC |
M
& T CHEM INC
ALKYLTINS
ENVIRONMENTAL FATE
PHYSICAL/CHEMICAL PROPERTIES
PARTITION COEFFICIENT
PHOTOLYSIS
HYDROLYSIS
BIODEGRADATION |
56-35-9
379-52-2
1983-10-4 |
NTIS/OTS0509271
EPA/OTS;
Doc #40+7763019 |
2000
(?)
- THE SAFE DISPOSAL OF ORGANOTINS IN SOIL
M
& T CHEM INC |
M
& T CHEM INC
ALKYLTINS
ENVIRONMENTAL FATE
TRANSPORT PROCESSES
PHOTOLYSIS
BIODEGRADATION |
56-35-9
379-52-2
1983-10-4 |
NTIS/OTS0555205
EPA/OTS;
Doc #88-920008707 |
1992
-
INITIAL SUBMISSION: ACUTE TOXICITY STUDY OF TRIPHENYLTIN
FLUORIDE IN EMBRYOS OF CRASSOSTREA VIRGINICA WITH COVER
LETTER DATED 07/24/92
EG&G
BIONOMICS |
ATOCHEM
NORTH AMERICA INC
TRIPHENYLTIN FLUORIDE
ENVIRONMENTAL EFFECTS
ACUTE TOXICITY
MOLLUSKS |
379-52-2
|
From
Toxline at Toxnet
NIOSH/00059851
Source:
M and T Chemicals, Inc. (Unpublished report submitted
to NIOSH), Rahway, N. J., IBT No. N1632, 14 pages, 1
reference, 1972
Acute
Dust Inhalation Toxicity Study with Triphenyltin Fluoride
in Albino Rats
Elliott CB
An acute dust inhalation toxicity study using albino
rats as experimental animals was performed for the compound
triphenyltin-fluoride. The acute dust inhalation median
lethal concentration of the test compound is 0.29 milligrams
per liter of air based on a four hour exposure period.
Untoward behavioral reactions
exhibited by the animals included gasping, bloody nasal
discharge, bloody ocular discharge, and weakness. Body
weight gains of the survivors of the 14 day observation
period were less than normal. Gross
pathologic observation revealed mild to severe focal
discoloration of the lungs in all test animals.
Keywords:
DCN-174112
Organo tin compounds
Respiratory system disorders
Growth
Eye disorders
Neuromotor disorders
Lung disorders
Toxic substances
Nasal disorders
Organo metallic compounds
Eyes
Pathology
Dusts
|
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12353640&dopt=Abstract
Biosci Biotechnol
Biochem 2002 Aug;66(8):1748-50
Shogaols
from Zingiber officinale as promising antifouling agents.
Etoh H, Kondoh T, Noda R, Singh
IP, Sekiwa Y, Morimitsu K, Kubota K.
Faculty of Agriculture, Shizuoka University, Japan. acheto@agr.shizuoka.ac.jp
We isolated the highly potent attachment-inhibitors (three times
more active than standard CuSO4 in the blue mussel assay), trans-6-,
8-, and 10-shogaols, from a hexane extract of the roots of ginger,
Zingiber officinale Roscoe. Trans-8-shogaol showed the highest
antifouling activity comparable with that of tributyltin fluoride
(TBTF), which is recognized as one of the most effective antifouling
agents, in the conventional submerged assay.
PMID: 12353640 [PubMed - in process]
From Toxline at Toxnet
ANALYTICA CHIMICA ACTA; 340 (1-3). 1997.
5-20.
A study of the applicability of various
ionization methods and tandem mass spectrometry in the analyses
of triphenyltin compounds.
MIERMANS C JH, FOKKENS RH, NIBBERING N
MM
Inst. Inland Water Management, Waste Water Treatment, P.O.
Box 17, 8200 AA Lelystad, Netherlands.
BIOSIS COPYRIGHT: BIOL ABS. Triphenyltin
compounds are widely introduced into the Dutch aquatic environment.
To be able to detect them in environmental samples, the ionization
methods of electron ionization, chemical ionization, fast atom
bombardment, field desorption, thermospray and electrospray
have been applied to triphenyltin acetate, chloride, fluoride
and hydroxide to find out which of these methods is best suited
to obtain molecular weight information on the intact molecules.
For this purpose, field desorption is shown to be the most appropriate
method giving, without fragmentation, molecular ion peaks, with
the exception of triphenyltin hydroxide. The latter compound
gives rise to the base peak at m/z 716, due to the formation
of bis(triphenyltin)oxide. Field desorption tandem mass spectrometry,
applied to the molecular ions, has shown that the main decomposition
pathway corresponds to the loss of a phenyl radical. Subsequently,
sediment and surface water samples from the Dutch inland wat
CAS Registry Numbers:
1262-21-1
1262-21-1
900-95-8
892-20-6
639-58-7
379-52-2
76-87-9
From Toxline at Toxnet
APPLIED ORGANOMETALLIC CHEMISTRY; 10 (5). 1996.
317-337.
Analytical methods for speciation of
organotins in the environment.
ATTAR KM
Cent. Anal. Mater. Charact. Lab., King Fahd Univ. Pet. Miner.,
Dhahran 31261, Saudi Arabia.
BIOSIS COPYRIGHT: BIOL ABS. The growing awareness over the environmental
fate of organotin compound is reflected in the large number
of analytical methods developed for their speciation. Organotin
compounds have varying degrees of toxicological properties,
depending on the nature and number of alkyl groups bonded to
the tin atom. Most of the analytical speciation methods applied
to actual environmental media have involved prior derivatization
to transform organotin compounds into volatile hydrophobic analytes
amenable to separation and Identification by gas chromatography
coupled to a sensitive and selective tin detector. Evidence
exists that members of the same homologous series are related
by environmental degradation pathways. Chemical treatment prior
to analysis, or high temperatures associated with gas chromatography
separation, may alter the relative amounts of organotins in
samples and blur the true environment picture. To avoid species
redistribution that may occur during derivatization or [abstract
truncated]
CAS Registry Numbers:
39858-44-1
39858-44-1
15231-44-4
7529-52-4
6056-50-4
2406-68-0
2406-65-7
2406-60-2
2155-70-6
2067-76-7
1983-10-4
1631-78-3
1631-73-8
1011-95-6
1002-53-5
997-50-2
892-20-6
761-44-4
688-73-3
660-74-2
597-64-8
594-27-4
379-52-2
56-35-9
From Toxline at Toxnet
APPL ORGANOMET CHEM; 7 (3). 1993.
219-222.
The effects of salinity and pH on the
speciation of some triphenyltin compounds in estuarine sediments
using Moessbauer spectroscopy.
WHALEN D, LUCERO R, MAY L, ENG G
Dep. Chem., Univ. D.C., 4200 Connecticut Ave. NW, Washington,
DC 20008, USA.
BIOSIS COPYRIGHT: BIOL ABS. The speciation of some triphenyltin
compounds i.e. triphenyltin hydroxide, triphenyltin chloride,
triphenyltin fluoride, under varying
salinity and pH conditions, was studied by Mossbauer spectroscopy
in both anoxic and oxic estuarine sediments. The results indicate
that altering the pH or salinity of the sediment environment
does not apparently affect the speciation of these compounds.
CAS Registry Numbers:
900-95-8
900-95-8
892-20-6
688-73-3
639-58-7
379-52-2
76-87-9
From Toxline at Toxnet
APPL ORGANOMET CHEM; 6 (3). 1992.
273-278.
Speciation of some triphenyltin compounds
in estuarine sediments using Moessbauer spectroscopy.
LUCERO RA, OTIENO MA, MAY L, ENG G
Dep. Chem., Univ. District Columbia, 4200 Connecticut Ave.
NW, Washington, D.C. 20008.
BIOSIS COPYRIGHT: BIOL ABS. The speciation of several triphenyltin
compounds, i.e. triphenyltin hydroxide, acetate, chloride and
fluoride, was studied by Mossbauer spectroscopy in both anaerobic
and aerobic estuarine sediments. The results indicated that
triphenyltin hydroxide and acetate were converted to the triphenyltin
cation, the species that interacts with the sediments. However,
both triphenyltin fluoride and chloride
remained in their molecular form in their interaction with the
sediments.
CAS Registry Numbers:
892-20-6
892-20-6
639-58-7
379-52-2
76-87-9
From Toxline at Toxnet
HOUGHTON, D. R., R. N. SMITH AND H. O. W. EGGINS (ED.). BIODETERIORATION,
7; SEVENTH INTERNATIONAL BIODETERIORATION SYMPOSIUM, CAMBRIDGE,
ENGLAND, UK, SEPTEMBER 6-11, 1987. XVI+843P. ELSEVIER APPLIED
SCIENCE PUBLISHERS: LONDON, ENGLAND, UK; NEW YORK, NEW YORK,
USA. ILLUS. MAPS. ISBN 1-85166-221-9.; 0 (0). 1988.
305-308.
THE MINIMUM LEACHING RATE OF SOME TOXINS
FROM ANTIFOULING PAINTS REQUIRED TO PREVENT SETTLEMENT OF FOULING
ORGANISMS
DE LA COURT FH
BIOSIS COPYRIGHT: BIOL ABS. RRM ALGAE BARNACLE CUPROUS OXIDE
TRIPHENYLTIN FLUORIDE
CAS Registry Numbers:
1317-39-1
1317-39-1
379-52-2
From Toxline at Toxnet
J CHEM TECHNOL BIOTECHNOL A CHEM TECHNOL; 37 (8). 1985
(RECD. 1986). 387-394.
BIOACTIVITY OF ANTIFOULING PAINTS BASED
ON ORGANOTIN TOXICANTS
BENITEZ JC, GIUDICE CA, RASCIO V JD
BIOSIS COPYRIGHT: BIOL ABS. RRM TRIBUTYLTIN FLUORIDE TRIPHENYLTIN
FLUORIDE SEAWATER
Keywords:
Mathematical Biology and Statistical Methods
Ecology
Biochemical Studies-General
Biophysics-Bioengineering
Toxicology-General
CAS Registry Numbers:
1983-10-4
1983-10-4
379-52-2
From Toxline at Toxnet
Source: BOWEN, H. J. M. A SPECIALIST PERIODICAL REPORT ENVIRONMENTAL
CHEMISTRY, VOL. 3. A REVIEW OF THE LITERATURE PUBLISHED UP TO
END 1982. IX+144P. ROYAL SOCIETY OF CHEMISTRY: LONDON, ENGLAND.
ILLUS. MAPS. ISBN 0-85186-775-8.; 0 (0). 1984.
49-77.
THE ENVIRONMENTAL CHEMISTRY OF ORGANOTIN
COMPOUNDS
BLUNDEN SJ, HOBBS LA, SMITH PJ
HEEP COPYRIGHT: BIOL ABS. RRM FISH PLANT SOIL POLLUTION METAL
POLLUTION
CAS Registry Numbers:
41083-11-8
41083-11-8
13121-70-5
1983-10-4
1461-25-2
1118-46-3
1067-33-0
900-95-8
688-73-3
683-18-1
379-52-2
76-87-9
56-36-0
56-35-9
From Toxline at Toxnet
BULL ENVIRON CONTAM TOXICOL 33:460-467,1984
DIFFERENTIAL RESPONSE OF MARINE ORGANISMS
TO CERTAIN METAL AND AGRICHEMICAL POLLUTANTS
LEE HH, XU CH
Name of Agent (CAS RN):
TRIPHENYLTIN ACETATE ( 900-95-8 )
TRIPHENYLTIN FLUORIDE ( 379-52-2 )
SODIUM PENTACHLOROPHENATE ( 131-52-2 )
CADMIUM ( 7440-43-9 )
CHROMIUM ( 7440-47-3 )
COPPER ( 7440-50-8 )
LEAD ( 7439-92-1 )
MAGNESIUM ( 7439-95-4 )
MERCURY ( 7439-97-6 )
NICKEL ( 7440-02-0 )
ZINC ( 7440-66-6 )
From Toxline at Toxnet
1984 Veiligheid Dec. 1984, Vol.60,
No.12, p.629-638. Illus.
Antifouling paints
Doorgeest T
Contents of this survey: plant fouling and mineral incrustations,
their effect on underwater metal structures and preventive measures;
types of antifouling paint; active substances (copper (I) oxide,
copper or bronze powders; tributyltin oxide, tributyltin
fluoride, triphenyltin fluoride,
etc. and their properties); solvents; cleaning methods (hazards
from detergents, high-pressure sprays and shotblasting) and
application of paints; health hazards; preventive measures,
personal protection and work clothes; welding and cutting of
structures covered by antifouling paint; safety labelling; decontamination
of clothes; personal hygiene; waste disposal; TLVs; first aid;
medical supervision; regulations in the Netherlands.
CAS Registry Numbers:
7440-50-8
1317-39-1
56-35-9
379-52-2
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6305366&dopt=Abstract
Biochem Pharmacol
1983 May 15;32(10):1627-34
Triphenyltin
fluoride in vitro inhibition of rabbit platelet collagen-induced
aggregation and ATP secretion and blockade of arachidonic acid
mobilization from membrane phospholipids.
Manabe S, Wada O, Matsui H, Takada
M, Kobayashi N, Maekawa T.
Recent studies have demonstrated that triphenyltin
fluoride (TPTF) inhibits collagen-induced aggregation
and ATP secretion of rabbit platelets in vivo [S. Manabe and
O. Wada, J. Toxic. Sci. 6, 236 (1981)]. The aim of the present
investigation was to test the effects in vitro of TPTF on platelet
aggregation and to elucidate the mechanism of the inhibitory
action by studying the release and metabolism of arachidonic
acid and the cyclic AMP contents of rabbit platelets treated
in vitro with TPTF. Although no inhibitory effect of TPTF was
found on sodium arachidonate-induced platelet aggregation and
ATP secretion, TPTF inhibited both reactions induced by collagen.
Triphenylarsine and triphenylantimony did not inhibit, even
at a concentration of 10(-3) M. The anti-aggregating concentration
(IC50) of TPTF was 6.0 x 10(-6) M against collagen. TPTF had
no inhibitory effect on the conversion of exogenous arachidonic
acid to malondialdehyde (MDA) by platelets, while the collagen-induced
production of arachidonate metabolites [MDA, 12-L-hydroxy-5,8,10-heptadecatrienoic
acid (HHT) and thromboxane B2] was remarkably inhibited by TPTF.
Furthermore, TPTF apparently inhibited the collagen-induced
release of arachidonic acid from platelets, although the formation
of phosphatidic acid was not inhibited. Total cyclic AMP content
after TPTF exposure was not changed significantly. These
results indicate that TPTF inhibited the collagen-induced arachidonic
acid release from platelet phospholipids, presumably by acting
on phospholipase A2. Furthermore, it seems unlikely that the
inhibition of arachidonic acid release by TPTF can be explained
by the level of cyclic AMP in platelets.
PMID: 6305366 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6865093&dopt=Abstract
Sangyo Igaku 1983
Jan;25(1):15-22
[The
effect of triphenyltin fluoride on aggregation, ATP secretion
and malondialdehyde formation of rabbit platelets in vitro]
[Article in Japanese]
Manabe S, Wada O, Matsui H, Ono
T, Arakawa Y, Iwai H.
Recent studies have demonstrated that triphenyltin fluoride
(TPTF), widely used as an agricultural chemical and a marine
antifoulant, inhibits collagen-induced platelet aggregation
and ATP secretion in rabbits ex vivo. The aim of the present
investigation was to elucidate the mechanism of the inhibitory
action of TPTF by investigating platelet malondialdehyde (MDA)
formation, aggregation and ATP secretion following the stimulation
by various stimuli of rabbit platelets treated in vitro with
TPTF, other triphenyl metals and aspirin. Although no inhibitory
effect of TPTF was found on sodium arachidonate-induced platelet
aggregation and ATP secretion, TPTF inhibited dose-dependently
both platelet aggregation and ATP secretion induced by collagen.
The antiaggregating (IC50) concentration of TPTF was 6.0 X 10(-6)
M against collagen. In addition, TPTF prevented the collagen-,
and thrombin-induced formation of MDA, but had little inhibitory
effect on the conversion of exogenous arachidonic acid to MDA
in platelets. In contrast, aspirin (10(-3) M) inhibited platelet
aggregation, ATP secretion and MDA formation induced by all
the stimuli tested. Other triphenyl metals did not any inhibitory
effect on collagen-, and sodium arachidonate-induced platelet
aggregation and ATP secretion even at a final concentration
at 10(-3) M. These results suggest that
TPTF has a specific inhibitory effect on platelet aggregation
and ATP secretion by acting at some step(s) of platelet membrane
between the binding site of collagen and thrombin and the release
of arachidonic acid.
PMID: 6865093 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
Contact Dermatitis May 1982, Vol.8,
No.3, p.173-177. Illus. 14 ref.
Occupational irritant contact folliculitis
associated with triphenyl tin fluoride (TPTF) exposure
Andersen KE, Petri M
Report of a case of occupational irritant contact folliculitis
due to triphenyl tin fluoride (TPTF) in a worker manufacturing
antifouling paint. Contact allergy was excluded by patch testing
with TPTF. An attempt to reproduce the follicular reaction in
man, rabbit and guinea pig proved unsuccessful. The follicular
reaction pattern may be dependent not only on the substance
but also on the subject and the exposure circumstances.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6752493&dopt=Abstract
Sangyo Igaku 1982
Jan;24(1):24-54
[Recent
progress in the study of analytical methods, toxicity, metabolism
and health effects of organotin compounds]
[Article in Japanese]
Wada O, Manabe S, Iwai H, Arakawa Y.
Over the years, a variety of uses has been found of organic
tin compounds as fungicides, as stabilizers in plastics and
for other industrial uses. The purpose of this article is to
summarize and review the results so far obtained as to the analytical
method for organotins in biological samples, the toxicity, metabolism,
and biochemical and health effects of organotin compounds.
1) Many methods have been developed for analysis of organotin
compounds by spectrophotometry, polarography, gas- or liquid-chromatography,
etc. These methods, however, are mainly for analysis of organotins
in standard solutions or in water, and
are not suitable for organotin compounds in biological samples.
Recently, we have developed several methods for analysis of
various kinds of organotin compounds in biological samples.
These methods are able simultaneously to separate and determine
trace amounts (at nanogram order) of organotin compounds and
their metabolites in the same biological samples.
2) Acute toxicity of organotin compounds which appeared on the
literature are summarized. Trialkyl and triaryl compounds seem
to be more toxic than the tetra-, di-, or mono-compounds of
the same chain length. With an increase in the number of C atoms
the toxicity of alkyl compounds decreases. Aryltin compounds
are less toxic than alkyltin compounds.
3) Intestinal absorption sites for tetra-alkyltins are jejunum
and duodenum, and those for trialkyltins are ileum and jejunum.
A considerable amount of orally administered tetra- and trialkyltins
of low molecular weights are absorbed, but only very little
of the other organotin compounds seems to be absorbed from the
gastrointestinal tract. Absorbed organotin compounds rapidly
undergo dealkylation by the microsomal mono-oxygenase system
dependent on cytochrome P-450 in the liver, brain or other organs,
and the compounds and their metabolites distribute to the whole
body, ultimately being excreted into urine, bile and faeces.
The biological half life of organotin compounds in mammals is
usually short, a half of the amount of tributyl- and triphenyl-tins
deposited in the body disappearing in several days. A part of
organotin compounds excreted into bile is demonstrated to have
been absorbed from the intestine and to circulate in the body
via enterohepatic circulation.
4) Specific effects of organotin compounds on the biological
systems and health include disturbance of the structure and
function of the central nervous system (interstitial edema of
white matter), inhibited oxidative phosphorylation in mitochondria
of cells, atrophy of the thymus and thymus dependent lymphoid
tissues resulting in the dysfunction of T cells for immunity,
inhibited enzyme activity, lesions in the liver and bile ducts
etc., although some specificity is observed among species of
animals and organotin compounds. Recently
we found that a single oral administration of triphenyltin fluoride
to rabbits induces transient diabetes and diabetic lipemia by
inhibiting insulin secretion from morphologically normal pancreatic
B-cells...
Publication Types: Review
PMID: 6752493
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7030827&dopt=Abstract
Diabetes 1981
Dec;30(12):1013-21
Triphenyltin
fluoride (TPTF) as a diabetogenic agent. TPTF induces diabetic
lipemia by inhibiting insulin secretion
from morphologically intact rabbit B-cell.
Manabe S, Wada O.
Recent work in our laboratory has shown that oral administration
of triphenyltin fluoride (TPTF)
evokes hypertriglyceridemia in rabbits.
The present experiments were conducted to elucidate the
mechanism of TPTF-induced hypertriglyceridemia in rabbits by
a combined biochemical and ultrastructural approach. After a
single TPTF administration, fasting blood glucose and plasma
triglyceride levels increased significantly (P less than 0.02)
for about 20 days. On the other hand, both plasma and adipose
tissue lipoprotein lipase (LPL) activity was markedly decreased
(P less than 0.001) during this period, and triglyceride production
rates on day 2 after TPTF administration was significantly decreased
(P less than 0.01). Density-gradient ultracentrifugation showed
a remarkable accumulation of chylomicron and VLDL in the composition
of plasma lipoproteins. Insulin injection to the hypertriglyceridemic
rabbits induced a significant recovery of the decreased plasma
LPL activity with a concomitant decrease of plasma triglyceride
levels, while abeyance of insulin injection resulted in a decrease
of LPL activity again. A significant inhibition of insulin release
in response to the loading of glucose, glucagon, or arginine
was observed in the TPTF rabbits (P less than 0.02). Inhibition
of glucagon release was also observed in the arginine-loading
test (P less than 0.01). Electron microscopic studies showed
small abnormalities in the pancreatic islets of TPTF-treated
rabbits. These findings suggest that TPTF
inhibits insulin release from rabbit islets, subsequently inducing
diabetic lipemia due to the insulin deficiency. Furthermore,
it is possible to provide a new animal model for diabetes and
diabetic lipemia by administration of TPTF to rabbits.
PMID: 7030827 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7334675&dopt=Abstract
No
abstract available
Nippon Eiseigaku
Zasshi 1981 Oct;36(4):687-93
[Triphenyltin
fluoride-induced hypertriglyceridemia in rabbits (author's transl)]
[Article in Japanese]
Manabe M, Wada O, Manabe S.
PMID: 7334675 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
Proc. Annu. Mar. Coat. Conf. 18: 1-18 1978
Dissipation and detoxification of organotins
in the environment.
Sheldon AW
M&T Chem. Inc., Rahway, NJ
PESTAB. The dissipation of 3 commonly used organotins in soil
environments was studied. These test materials were: tributyltin
oxide (TBTO), tributyltin fluoride (TBTF), and triphenyltin
fluoride (TPhTF). The soil employed in these studies
was sandy loam obtained from South Carolina. Soil samples were
treated with about 2.5 ppm of 1 of the 3 test compounds. After
182 days all 3 test compounds showed substantial degradation,
especially in those samples kept under aerobic conditions. Degradation
under anaerobic conditions was not as consistent as that under
aerobic conditions. In the aerobic tests the TPhTF had released
37.2% of the applied radioactivity as CO2; the TBTF had evolved
11.6% and the TBTP, 14.2%. It is suggested
from these studies that the organotins used in antifouling coatings
are not persistent pesticides and do not present the hazards
usually associated with persistent materials.
From Toxline at Toxnet
1975
Journal of Paint Technology, Vol. 47, No. 600, pages 54-58
Effects
Of Organotin Anti-Fouling Coatings On Man And His Environment
Sheldon
AW
Abstract:
The acute and chronic toxicities of anti fouling coatings were
studied in animals. The acute oral median lethal dose (LD50)
was determined for bis(tri-n-butyltin)oxide (56359),
tributyltin-fluoride (1983104) and
triphenyltin-fluoride (379-52-2) for rats and rabbits.
The acute dermal LD50 was also determined. Primary skin and
eye irritation were assessed for these compounds. A subacute
dermal toxicity study was performed using albino-rabbits exposed
to 14.0, 27.2 or 68.0 milligrams per kilogram (mg/kg) applied
to the skin of the back each day. Mortality, reactions, body
weight, hematologic and clinical blood chemistry, urine and
gross microscopic pathology were studied. An assessment of the
carcinogenicity of tributyltin-fluoride was made in male Swiss-white-mice.
Animals received a dermal application of 15mg of 5 or 10 percent
tributyltin-fluoride solution 3 times a week for 6 months. The
acute oral LD50 of bis(tri-n-butyltin)oxide was 234mg/kg and
its acute dermal toxicity was 11,700mg/kg as a powder. The
acute oral LD50 of tributyltin-fluoride was 200mg/kg and the
dermal LD50 was 680mg/kg. The acute oral LD50 of triphenyltin-fluoride
was 1,170mg/kg. All were severe or extreme
eye irritants and most were moderate to severe skin irritants.
In the 90 day study, no effects were seen at 14mg/kg. A
dose of 68mg/kg was toxic, with increases in total and differential
leukocyte counts and decreases in body weight. Skin lesions
were seen. At 27.2mg/kg effects were less pronounced. No carcinogenic
effects were seen from the dermal application of either concentration
of tributyltin-fluoride to mice. The author concludes that skin
and eye irritation are the major hazards from these organotin
anti fouling coating when used by humans.
From Science Direct
Spectrochimica Acta; Volume 21, Issue 5 , May 1965,
Pages 1013-1014
Research note
The infrared spectra of triphenyltin
fluoride, tris(pentafluorophenyl)-tin fluoride, tri-n-butyltin
fluoride, and di-n-propyltin fluoride
D. H. Brown, Ali Mohammed and D. W. A.
Sharp
Chemistry Department University of Strathclyde Glasgow C.1,
Scotland
From Toxline at Toxnet
Nucleonics, Vol. 9, No. 2, pages 51-58, 153 references, 1951
Methods of Fluorine and Fluoride Analysis-III
McKenna FE
Methods of fluorine (7782414) and fluoride determination are
reviewed. The pertitanic-acid and fluosilicic-acid methods are
discussed, and analysis of fluorocarbons, volatile fluorides,
and elementary fluorine are described. Methods discussed include:
reactions of fluoride with peroxide treated titanium solutions;
spectrochemical determination; determination as bismuth-fluoride
(7787613); and antimony-fluoride (7783702); determination as
boron-trifluoride (7637072); determination as
triphenyl-tin-fluoride (379-52-2); determination with
benzidine (92875); determination as a complex uranium-fluoride
(11133714); determination as a complex molybdenum-fluoride (7783779);
colorimetric determination as lead-sulfide (1314870); colorimetric
determination with methemoglobin; acidimetric alkalimetric titrations;
determination by the enzymatic inhibition due to fluorides;
determination of the wettability of glass; determination of
fluorine in organic fluoro compounds; and determination of fluorine
or fluorides in specific materials. The author concludes that
such factors as the amount of fluoride, the type of matrix,
and the proficiency of the analyst with the various methods
must determine the analytical methods to be considered.
CAS Registry Numbers:
7782-41-4
7782-41-4
7787-61-3
7783-70-2
7637-07-2
379-52-2
92-87-5
11133-71-4
7783-77-9
1314-87-0
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