National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• Di-n-butyltin dichloride
• DIBUTYLDICHLOROSTANNANE

Human Toxicity Excerpts

• IN WORKERS HANDLING ... /DIBUTYLTIN CHLORIDE/, SKIN LESIONS, EVEN BURNS, HAVE BEEN FOUND. THE IRRITANT EFFECT APPEARED BETWEEN 1 & 8 HR AFTER CONTACT. HEALING WAS RAPID AFTER REMOVAL FROM EXPOSURE. THE EYES CAN ALSO BE AFFECTED ... BUT THE DAMAGE WAS NOT CHRONIC. [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979., p. 621]**PEER REVIEWED**
  
• BLAST TRANSFORMATION OF HUMAN THYMOCYTES WAS INHIBITED AT CONCENTRATIONS AS LOW AS 0.02 UG/ML MEDIUM. [SEINEN W ET AL; IMMUNOPHARMACOLOGY 1 (4): 343 (1979)]**PEER REVIEWED**
  
• One instance of eye injury is reported in a worker who accidentally splashed the liquid in his face and eyes. Despite immediate washing with water, lacrimation and conjunctival hyperemia appeared within minutes and persisted for four days. At the end of a week the skin was still erythematous, but the eyes appeared normal. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 318]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• DIBUTYLTIN CHLORIDE BY INHALATION FOR 1 HR OF RATS AT 1470 MG/CU M, ALTHOUGH PRODUCING HYPOACTIVITY, PTOSIS, & SALIVATION DURING 14 DAYS FOLLOWING, CAUSED NO DEATHS. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1955]**PEER REVIEWED**
  
• ... INDICATIONS OF NONACCUMULATION WERE SEEN IN LONG-TERM (3 MO) ADMINISTRATION OF DIBUTYLTIN CHLORIDE TO RATS AT LEVELS OF 25, 50, & 100 PPM; NO LESIONS RESULTED FROM THIS REGIMEN OTHER THAN THOSE SEEN FROM SINGLE DOSES /HYPOACTIVITY, PTOSIS, SALIVATION/. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1956]**PEER REVIEWED**
  
• ... STUDYING ... ACTION OF SEVERAL DISUBSTITUTED ORGANO TIN CMPD ON THYMUS & THYMUS DEPENDENT LYMPHOID TISSUE, FOUND ... DIBUTYL TIN DICHLORIDE (DBTC) MOST TOXIC OF ORGANOTIN CMPD TESTED, CAUSING MORTALITY IN 6 OF 20 WEANLING RATS AT DIETARY LEVEL OF 150 PPM & SEVERE LIVER & BILIARY CHANGES, AS WELL AS ABDOMINAL EDEMA ... . [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1956]**PEER REVIEWED**
  
• ... DIBUTYL TIN CHLORIDE, A DOSE OF 5 MG/KG BODY WEIGHT DISSOLVED IN TWEEN 80 CAUSED AN ATTACK ON BILE DUCTS WITHIN 1 HR OF /INTRAVENOUS/ INJECTION /TO RATS/. [Lefaux, R. Practical Toxicology of Plastics. Cleveland: CRC Press Inc., 1968., p. 387]**PEER REVIEWED**
  
• IN WEANLING RATS: ... INDUCE/S/ REDUCTION OF THYMUS WT & WT OF PERIPHERAL LYMPHOID TISSUES (POPLITEAL NODES & SPLEEN AT DIETARY LEVELS OF 50 & 150 PPM AFTER 4 & 2 WK). ... WEIGHT REDUCTION /OF THYMUS AND LYMPHOID TISSUE/ WAS DOSE-RELATED ... AT HIGH DOSES ... THYMUS EFFECTS WERE SO SEVERE AS TO PRESENT CHEM THYMECTOMY. EFFECTS WERE COMPLETELY REVERSIBLE. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 2271]**PEER REVIEWED**
  
• ... MALE RATS ... TREATED /DAILY, ORALLY/ WITH DIBUTYL TIN DICHLORIDE SURVIVED 400 MG/KG WITH REVERSIBLE BILE DUCT LESION & NO CEREBRAL EDEMA. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1957]**PEER REVIEWED**
  
• ... DIBUTYLTIN DICHLORIDE APPLIED CUTANEOUSLY TO MALE RATS /PRODUCED/ LITTLE SUPERFICIAL DAMAGE, BUT SOME EDEMA OF SUBCUTANEOUS TISSUES. /FROM TABLE/ [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1961]**PEER REVIEWED**
  
• ... IN WEANLING RATS ... ALLOGRAFT REJECTION WAS SIGNIFICANTLY DELAYED ... IMMUNE RESPONSE VERSUS SHEEP RED CELLS ... DEPRESSED ... HEMAGGLUTINATION & HEMOLYSIS TITERS DECREASED ... INDUCE/S/ IMMUNE SUPPRESSION ... BY SELECTIVE INHIBITION OF T-LYMPHOCYTE ACTIVITY, PARTICULARLY PRONOUNCED DURING DEVELOPMENTAL PHASE OF LYMPHOID SYSTEM. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 2271]**PEER REVIEWED**
  
• ISOLATED THYMOCYTES WERE INCUBATED WITH CARBOHYDRATES IN PRESENCE OF DI-N-BUTYLTIN DICHLORIDE (DBTC). SUBSTRATE CONVERSION, OXYGEN CONSUMPTION & CELL VIABILITY WERE MEASURED. A DOSE-DEPENDENT STIMULATION OF GLUCOSE CONSUMPTION OBSERVED. MOST TOXIC ORGANOTIN COMPOUNDS, DI-N-BUTYLTIN DICHLORIDE & DIETHYLTIN DICHLORIDE, STIMULATED GLUCOSE CONSUMPTION MAXIMALLY AT LEVELS OF 5 & 10 UMOLE, RESPECTIVELY. OXIDATIVE METAB OF GLUCOSE, LACTATE & PYRUVATE BY TRICARBOXYLIC ACID CYCLE WAS INHIBITED BY DIALKYLTIN COMPOUNDS (DOSE-RELATED). DBTC INHIBITED PYRUVATE & ALPHA-KETOGLUTARATE CONVERSION, OXYGEN CONSUMPTION & ATP PRODN OF RAT LIVER MITOCHONDRIA (DOSE-RELATED). IN VIVO DBTC INDUCED THYMUS INVOLUTION. INHIBITION OF ENERGY METABOLISM OF RAT THYMOCYTES BY DIALKYLTINS IS RELATED TO THEIR THYMOLYTIC EFFECTS IN VIVO. [PENNINKS AH, SEINEN W; TOXICOL APPL PHARMACOL 56 (2): 221 (1980)]**PEER REVIEWED**
  
• DI-N-BUTYLTIN DICHLORIDE CAUSED THYMUS ATROPHY IN RAT, WHICH SUPPRESSED IMMUNE REACTIONS. [SEINEN W, PENNINKS A; ANN NY ACAD SCI 320: 499 (1979)]**PEER REVIEWED**
  
• ACUTE ORAL DOSES OF 50 MG/KG DI-N-DIBUTYLTIN DICHLORIDE PRODUCED EDEMA & INFLAMMATION OF THE BILE DUCTS. WHEN FED TO RAT FOR 90 DAYS AT 0, 10, 20, 40, OR 80 PPM, THERE WAS SLIGHT REDUCTION OF GROWTH & FOOD INTAKE AT THE HIGHEST LEVEL. AT 80 PPM ANEMIA WAS REPORTED. TIN WAS NOT FOUND IN ANY OF THE URINE EXAM. THE NO-EFFECT LEVEL ESTABLISHED IN THE DIET OF RATS FOR 90 DAYS WAS 40 PPM, A LEVEL APPROX EQUIVALENT TO AN INTAKE OF 2 MG/KG/DAY. [GAUNT IF ET AL; FOOD COSMET TOXICOL 6 (5): 599 (1968)]**PEER REVIEWED**
  
• DIBUTYLTIN DICHLORIDE AS ADMIN INTRAGASTRICALLY TO RATS (10 & 20 MG/KG DAILY FOR 4 DAYS) CAUSED INFLAMMATION OF PORTAL TRACTS & BILIARY DAMAGE AT END OF THIS PERIOD. PROLYL HYDROXYLASE ACTIVITY WAS INCR OVER CONTROL VALUES IN BOTH GROUPS, & IN VITRO COLLAGEN SYNTH WAS INCR IN HIGHER DOSE GROUP. INTUBATION OF 10 & 20 MG/KG EVERY OTHER DAY FOR 12 DAYS PRODUCED INFLAMMATION IN PORTAL TRACTS, BILIARY DAMAGE, FIBROSIS, NECROSIS, INFARCTED AREAS & GRANULOMATOUS LESIONS. IN HIGHER DOSE GROUP INCR IN HYDROXYPROLINE CONTENT, PROLYL HYDROXYLASE ACTIVITY, & RELATIVE COLLAGEN SYNTH IN VITRO WERE OBSERVED AT END OF 12 DAYS. FIBROGENESIS MAY BE RESULT OF BILIARY DAMAGE &/OR INFLAMMATORY PROCESSES RATHER THAN DIRECT STIMULATION OF FIBROBLASTS. [YERMAKOFF JK ET AL; TOXICOL APPL PHARMACOL 49 (1): 31 (1979)]**PEER REVIEWED**
  
• DIBUTYLTIN DICHLORIDE INDUCED A DOSE-RELATED DECR OF THE THYMUS WT IN YOUNG RATS WHEN GIVEN INTRAGASTRICALLY FOR 10 OR 14 DAYS; IN CHICKEN, A DECR OF BURSA FABRICII WT WAS ALSO OBSERVED. THERE WERE DISTINCT DIFFERENCES IN RESPONSE BETWEEN THE ANIMAL SPECIES. RESPONSE ALSO DEPENDED ON VEHICLE IN WHICH THE AGENT WAS GIVEN. [RENHOF M ET AL; ARCH TOXICOL SUPPL 4: 148 (1980)]**PEER REVIEWED**
  
• DIBUTYLTIN DICHLORIDE WAS APPROX 1000-FOLD HIGHER IN CYTOTOXICITY & GENOTOXICITY THAN DIBUTYLGERMANIUM DICHLORIDE IN VITRO. BOTH DECR ANTIBODY PRODN BY LYMPHOCYTES IN VITRO AT NONCYTOTOXIC DOSES, WHICH MAY EXPLAIN IMMUNOSUPPRESSIVE EFFECT OF THE CMPD IN VIVO. BOTH INDUCED MUTATION IN CHINESE HAMSTER OVARY CELLS, THEREFORE SUGGESTING THAT THEY ARE POTENTIALLY CARCINOGENIC. [LI AP ET AL; TOXICOL APPL PHARMACOL 64 (3): 482 (1982)]**PEER REVIEWED**
  
• Chronic incubation in sublethal concn of ... dibutyltin dichloride incr water and ash contents, and decr solid content in 1 yr old carp. ... Fluctuations in body wt, in weights of the intestine and hepatopancreas, and in the digestive tract amylase activity were observed. [Buzinova NS; Reakts Gidrobiontov Zagryaz 140-5 (1983)]**PEER REVIEWED**
  
• Dibutyltin dichloride ... induced lymphocyte depletion in thymus and thymus dependent areas of spleen and thout signs of myelotoxicity or a generalized toxicity. The numbers and viability of cells isolated from thymus and peripheral cr, whereas the number and viability of bone marrow cells were not reduced. Immunosuppressive properties of dibutyltin this study, a severe decr of the graft versus host response and response to the T-cell mitogens phytohemaglutinin and concanavalin ese cmpd is discussed. In vitro, dibutyltin dichloride ... /is/ extremely cytotoxic. Blast transformation of human as well ibited at concn as low as 0.02 ug dibutyltin dichloride per ml medium. Also the E-rosette formation was inhibited at very low ects upon rat and human lymphocytes suggests that dibutyltin dichloride ... acts in the same manner in rat and man and offers the possibility of a therapeutic use of these cmpd. [Seinen W; Immunopharmacology 1 (4): 343-55 (1979)]**PEER REVIEWED**
  
• To evaluate the functional significance of dibutyltin dichloride ... induced lymphoid depletion, various immune function studies were carried out. Allograft rejection, another cellular immune response, was significantly delayed by dibutyltin chloride. ... The antibody response against Escherichia coli LPS, probably a T (thymus derived) cell independent antigen, was not affected by dibutyltin dichloride. The humoral immune response against sheep red blood cells, which needs the cooperation of T helper cells and B (bone marrow derived) cells, was distinctly depressed by dibutyltin dichloride. Hemaglutination, hemolysin titers and the number of direct plaque forming cells against sheep red blood cells per spleen were decr in a dose related manner by dibutyltin dichloride. Altered immune functions were never found in mice or guinea pigs exposed to dibutyltin dichloride. ... Dibutyltin dichloride ... induces immune suppression in rats by a selective inhibition of T-lymphocyte activity. Immune suppression was most pronounced in animals exposed to the chemicals during the development phase of the lymphoid system. [Seinen W et al; Toxicol Appl Pharmacol 42 (1): 213-24 (1979)]**PEER REVIEWED**
  
• A series of organotin and organolead cmpd were fed to male and female weanling rats for 2 wk at dietary levels of 0, 50, or 150 ppm, in order to evaluate their toxic effects, with special emphasis on the thymus and peripheral lymphoid organs. A dose related reduction in the wt of thymus, spleen, and popliteal lymph node, associated with lymphocyte depletion in the cortex of the thymus and the thymus-dependent areas in the peripheral lymphoid organs, was observed in animals fed ... dibutyltin dichloride. ... These effects were not related to stress. A similar structure-activity relation regarding thymus atrophy by dialkyltin cmpd was observed after iv application. Dibutyltin dichloride ... /was/ effective at a dose of 1 mg/kg. In contrast to rats, lymphoid atrophy did not occur in mice, guinea pigs, or Japanese quail fed ... dibutyltin dichloride. In vitro incubation of thymocytes and bone marrow cells with dibutyltin dichloride ... revealed the same selectivity regarding cell type and species origin of cells as was found in vivo. A dose related decr in the survival of rat thymocytes was observed, whereas rat bone marrow cells were not affected by dibutyltin dichloride ... at levels up to 50 ug/ml. As the survival of human thymocytes was markedly decr by dibutyltin dichloride, it possibly acts in the same manner in man and rat. [Seinen W et al; Toxicol Appl Pharmacol 42 (1): 197-212 (1977)]**PEER REVIEWED**
  
• Morphological studies were performed following acute and chronic poisoning with dibutyltin chloride. ... After ip injection to young adult male rats, the median lethal dose was 5.012 mg/kg for dibutyltin dichloride. ... Major histological findings in animals that died early were generalized circulatory disturbances incl extensive pulmonary hemorrhage and central nervous system edema. The liver, kidney and spleen were the organs demonstrating most extensive morphological alterations after a single LD50 dose. Ultrastructural changes were seen in the capillary walls of liver and kidney, incl glomeruli, and in the liver parenchymal cells (disorganization and vacuolation of the endoplasmic reticulum). Daily oral admin of 20 mg/kg of dibutyltin chloride to the rabbit resulted in slight decr in the peripheral red blood cells and depressed wt gain. There was slight to moderate gastroenteritis and other organ changes. [Wakashin K; Tokyo Ika Daigaku Zasshi 33 (4): 573-96 (1975)]**PEER REVIEWED**
  
• ... In vitro incubation of cerebral cortical tissue with ... dibutyltin dichloride inhibited the reduction of adenine nucleotides. Half-max inhibition occurred with ... 45 uM of dibutyltin. [Bull RJ; Biochem Eff Enviro Pollut p.425-40 (1977)]**PEER REVIEWED**
  
• Dermal application of dibutyltin dichloride at 10 mg/kg body weight per day for a period of 12 days, caused severe local damage and also bile duct injury in rats and mice. [WHO; Environ Health Criteria: Tin and Organotin Cmpds p.69 (1980)]**PEER REVIEWED**
  
• THE TOXICITY OF TRIBUTYLTIN CHLORIDE & DIBUTYLTIN DICHLORIDE ON SERUM ENZYMES & LIPIDS OF RABBITS WERE STUDIED. GELATINE CAPSULES CONTAINING 12, 7, 4 OR 2 MG/KG TRIBUTYLTIN CHLORIDE & 20, 12, 7 OR 4 MG/KG DIBUTYLTIN DICHLORIDE WERE ADMIN ORALLY TO RABBITS 6 TIMES/WK FOR 6 WK. SERUM ENZYMES, LIPIDS, PHOSPHOLIPIDS, BETA-LIPOPROTEINS, TOTAL CHOLESTEROLS, FREE CHOLESTEROLS, FREE FATTY ACIDS WERE DETERMINED IN SERUM ONCE/WK. FATAL TOXICITY OF TRIBUTYLTIN CHLORIDE WAS STRONGER THAN THAT OF DIBUTYLTIN DICHLORIDE. BOTH COMPOUNDS CAUSED ANEMIA. AT LARGER DOSES, DIBUTYLTIN DICHLORIDE EFFECTS WERE STRONGER, ON SMALLER DOSES, TRIBUTYLTIN CHLORIDE WAS STRONGER. ANEMIA BY TRIBUTYLTIN CHLORIDE WAS ACCOMPANIED BY BODY WT LOSS & INCREASED SERUM LIPIDS. ALANINE TRANSAMINASE & LACTATE DEHYDROGENASE INCR MODERATELY FROM 3 WK SUGGESTING LIVER CELL DAMAGE. TRIGLYCERIDES & TOTAL CHOLESTEROLS INCR MORE FROM 1 WK POST-ADMIN OF TRIBUTYLTIN CHLORIDE THAN WITH DIBUTYLTIN DICHLORIDE. BOTH SHOULD BE HANDLED WITH HIGHEST PRECAUTION DURING PREPN, TRANSPORTATION, STORAGE & USE. [MATSUDA H; J TOKYO MED COLL 38 (4): 451-66 (1980, RECD 1981)]**PEER REVIEWED**
  
• The effects of a single intragastric application of dibutyltin dichloride, at a dose of 30 mg/kg body weight, on N-nitrosobis(2-oxopropyl)amine induced pancreatic carcinogenesis were studied in female Syrian golden hamsters. Dibutyltin dichloride, which has been shown to selectively induced bile duct injury, was administered either 1 week before or after N-nitrosobis(2-oxyopropyl)amine initiation. N-nitrosobis(2-oxopropyl)amine was injected sc once a week for 5 weeks at a dose of 10 mg/kg body weight. Controls were injected with N-nitrosobis(2-oxopropyl)amine alone or given dibutyltin dichloride without carcinogen. Animals sacrificed at the end of the 25-week experimental period showed a significant inhibitory effect of dibutyltin dichloride on pancreatic carcinoma induction when dibutyltin dichloride was given before N-nitrosobis(2-oxopropyl)amine treatment, although no such influence was evident with dibutyltin dichloride treatment following N-nitrosobis(2-oxopropyl) amine exposure. These results indicate that the bile duct and more especially common bile-duct injury induced by dibutyltin dichloride may be relevant to the inhibition of the initiation stage of N-nitrosobis(2-oxopropyl)amine induced pancreatic carcinoma development in Syrian hamsters. [Jang JJ et al; Jpn J Cancer Res 77 (11): 1091-4 (1986)]**PEER REVIEWED**
  
• The effects of a single po dose of 0.3-10 mg/kg of organotin compounds such as dibutyltin dichloride and triphenyltin chloride on the development of edema after subplantar injection of 0.5 mg of carrageenan in 0.05 ml of pyrogen-free saline were examined as compared with those of hydrocortisone. Dibutyltin dichloride, triphenyltin chloride and hydrocortisone did not significantly inhibit the development of the first phase of edema at any dose level, but produced more than 90, 70 and 90% inhibition of the second phase, respectively, at a dose of 10 mg/kg 1 hr before the irritant. Moreover, these inhibitions of the second phase were dose-dependent. [Arakawa Y, Wada O; Biochem Biophys Res Commun 125 (1): 59-63 (1984)]**PEER REVIEWED**
  
• Toxicity studies were carried out on the Japanese medaka (Orzyias latipes) with bis(tri-n-butyltin)oxide and di-n-butyltin dichloride, with emphasis on histopathological effects. Freshly fertilized eggs were exposed for 1 and 3 months to a concentration range of 0.1-32 ug bis(tri-n-butyltin)oxide/l in tank water. The range for di-n-butyltin dichloride was 320-3200 ug/l (1 month only). The histopathological effects included vacuolation of hepatocytes, tubulonephrosis and glomerulopathy, vacuolation of the retinal pigment epithelium, keratitis, hyperplasia and inflammation of oral and skin epithelium, hyperplasia and swelling of the gas gland epithelium and thyroid activation. No atrophy of the thymus was found. Except for the retinal and liver lesions, these changes occurred predominantly in the highest concentration with no essential differences in the lesions between 1 and 3 months, or between bis(tri-n-butyltin)oxide and di-n-butyltin dichloride exposure. Liver cell vacuolation was apparently caused by glycogen accumulation, as was confirmed in an additional experiment with guppies, a more expedient species. It is concluded that bis(tri-n-butyltin)oxide and di-n-butyltin dichloride have effects on the liver and gas gland, probably as a result of impaired glycogen breakdown. Effects on superficial epithelia are attributed to the irritative properties of these compounds. In addition, these compounds were toxic to kidney and retina. No observed effect concentrations using histopathology were 0.32 ug/l for bis(tri-n-butyltin)oxide, and lower than 320 ug/l for di-n-butyltin dichloride. Total tin and butyltins were determined by molecular absorption spectrometry, and gas chromatography with flame photometry, respectively, in guppies exposed to bis(tri-n-butyltin)oxide and di-n-butyltindichloride. Considerable amounts of tributyltin were measured in di-n-butyltindichloride exposed fish, and chemical analysis indicated that di-n-butyltindichloride contained tributyltin at a level that may account for the observed toxicity of di-n-butyltindichloride. [Wester PW et al; Aquat Toxicol (AMST) 16 (1): 53-72 (1990)]**PEER REVIEWED**
  
• THE TOXICITY OF TRIBUTYLTIN CHLORIDE & DIBUTYLTIN DICHLORIDE ON SERUM ENZYMES & LIPIDS OF RABBITS WERE STUDIED. GELATINE CAPSULES CONTAINING 12, 7, 4 OR 2 MG/KG TRIBUTYLTIN CHLORIDE & 20, 12, 7 OR 4 MG/KG DIBUTYLTIN DICHLORIDE WERE ADMIN ORALLY TO RABBITS 6 TIMES/WK FOR 6 WK. SERUM ENZYMES, LIPIDS, PHOSPHOLIPIDS, BETA-LIPOPROTEINS, TOTAL CHOLESTEROLS, FREE CHOLESTEROLS, FREE FATTY ACIDS WERE DETERMINED IN SERUM ONCE/WK. FATAL TOXICITY OF TRIBUTYLTIN CHLORIDE WAS STRONGER THAN THAT OF DIBUTYLTIN DICHLORIDE. BOTH COMPOUNDS CAUSED ANEMIA. AT LARGER DOSES, DIBUTYLTIN DICHLORIDE EFFECTS WERE STRONGER, ON SMALLER DOSES, TRIBUTYLTIN CHLORIDE WAS STRONGER. ANEMIA BY TRIBUTYLTIN CHLORIDE WAS ACCOMPANIED BY BODY WT LOSS & INCREASED SERUM LIPIDS. ALANINE TRANSAMINASE & LACTATE DEHYDROGENASE INCR MODERATELY FROM 3 WK SUGGESTING LIVER CELL DAMAGE. TRIGLYCERIDES & TOTAL CHOLESTEROLS INCR MORE FROM 1 WK POST-ADMIN OF TRIBUTYLTIN CHLORIDE THAN WITH DIBUTYLTIN DICHLORIDE. BOTH SHOULD BE HANDLED WITH HIGHEST PRECAUTION DURING PREPN, TRANSPORTATION, STORAGE & USE. /DIBUTYLTIN DICHLORIDE AND TRIBUTYLTIN CHLORIDE/ [MATSUDA H; J TOKYO MED COLL 38 (4): 451-66 (1980, RECD 1981)]**PEER REVIEWED**
  
• THE INHALATION LC50 VALUES FOR VAPORS OF DIMETHYL DICHLORIDE, MONOMETHYLTIN TRICHLORIDE, & DIBUTYLTIN DICHLORIDE WERE 1070, 600.0, & 73.0 MG/L/HR, RESPECTIVELY IN RATS. DIBUTYLTIN-BIS(ISOOCTYLTHIOGLYCOLATE) PRODUCED SEVERE CONJUNCTIVITIS IN THE RABBIT EYE, WHEREAS DIMETHYLTIN-BIS(ISOOCTYLTHIOGLYCOLATE) & MONOMETHYLTIN-TRIS(ISOOCTYLTHIOGLYCOLATE) PRODUCED NO IRRITATION. SKIN IRRITATION IN INCREASING ORDER WAS PRODUCED IN RABBIT BY MONOMETHYLTIN TRIS(ISOOCTYLTHIOGLYCOLATE)
• ... Dibutyl tin cmpd affected mice more than tributyl cmpd or tetrabutyl tin. ... Hemolytic action of tributyltin chloride is much greater than that of dibutyl tin cmpd, while tetrabutyl tin had scarcely any hemolytic action. /Di-, tri-, and tetra-butyl tin/ [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 575]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 RAT INHALATION 73 MG/L/HR [WEISFELD LB; KUNSTSTOFFE 65 (5): 298 (1975)]**PEER REVIEWED**
  
• LD50 White mouse oral 35 mg/kg [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1954]**PEER REVIEWED**
  
• LD50 Rat male oral 100 mg/kg (oil solution) [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1954]**PEER REVIEWED**
  
• LD50 Rat male intraperitoneal 7.5 mg/kg [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 1954]**PEER REVIEWED**
  
• LD50 Mouse oral 70 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1073]**PEER REVIEWED**
  
• LD50 Mouse iv 180 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1073]**PEER REVIEWED**
  
• LD50 Rabbit oral 50 ug/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1073]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• WITHIN 1 HR AFTER IV INJECTION OF 20 UMOL DIBUTYLTIN DICHLORIDE, RATS EXCRETED IN THE BILE 2X10-5 MOL ORGANOTIN/L. THE BILE/PLASMA QUOTIENT WAS 151:1 WHICH INDICATES AN ACTIVE TRANSPORT OF DIBUTYLTIN CHLORIDE FROM LIVER TO THE BILE. BIOTRANSFORMATION WAS NOT INVOLVED IN THE EXCRETION. [MERFKORD J ET AL; PHARMAZIE 37 (2): 146 (1982)]**PEER REVIEWED**
  
• AFTER INJECTION OF DIBUTYL- & DIETHYLTIN COMPOUNDS, HIGHEST CONCENTRATIONS WERE FOUND IN LIVER & KIDNEY OF MICE & RATS. /DIBUTYL- AND DIETHYLTIN COMPOUNDS/ [Friberg, L., G.R. Nordberg, and V.B. Vouk. Handbook on the Toxicology of Metals. New York: Elsevier North Holland, 1979., p. 618]**PEER REVIEWED**
  

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Metabolism/Metabolites

• None found

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TSCA Test Submissions

• None found

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.