Triphenyltin hydroxide

TRIORTHOCRESYL PHOSPHATE TRIPHENYLTIN CHLORIDE TRIPHENYLTIN HYDROXIDE TRIPROPYL ALUHINUH TRIPROPYLAMINE... 

Soderquist, C.J. and D.G. Crosby. 1980. Degradation of triphenyltin hydroxide in water. Jour. Agric. Food Chem. 28 111-117. 

Triphenyltin, as skin irritant, 24 829 Triphenyltin hydroxide, 24 817 as eye irritant, 24 829 Triphenymethane soluble dyes, 7 373t Triphosphorus pentanitride, 79 57 Triple bottom line, 72 807 Triple-bond stretching, 74 235 Triple helices, 77 609 Triple-helix formation, 77 528 Triple-jet crystal growth methods,... 

Kline, E.R., Jarvinen, A.W., andKnuth, M.L. Acutue toxicity of triphenyltin hydroxide to three Cladoceran species, Environ. PoIIut, 56(1) 11-17, 1989. 

One of the largest commercially used Grignard reagents is phenylmagnesium chloride. Millions of kg per year of this Grignard react captively with inorganic halides. Some examples of these products are triphenylphosphine, triphenyltin hydroxide, sodium tetraphenylborate, and triphenyl an tim ony. 

A number of other metals, such as iron and tin. enter into insecticide and peslicide compounds, but as purl of an urganic chemical stniciurc. us exemplified by triphenyltin hydroxide. Such compounds arc sometimes referred lo as organometallics (or, specifically in Ihc case of tin. as orgamilins). Mercury compounds are rapidly being phased out because of their long-term toxic residual effects as pollutants, particularly of fresh and saline waters. Regulations vary I mm one country to another. 

There was an absence of cardiovascular effects in rats, mice and dogs administered triphenyltin hydroxide in the diets for periods of from 4 to 104 weeks (NCI 1978b Sachsse et al. 1987 Tennekes et al. 1989a, 1989b) (see Section 2.2.2.8). 

Triphenyltin hydroxide at a dose of 1.3 mg/kg/day caused a transient decrease in hemoglobin and hematocrit values at 26 and 52 weeks in female rats, but not in the males (Tennekes et al. 1989a). These changes were not apparent at 78 and 104 weeks (Tennekes et al. 1989a), nor were they seen in dogs given the same compound at doses of 0.7 mg/kg/day (Sachsse et al. 1987). 

A dose-related trend towards portal sclerosis and bile duct proliferation was observed in rats given doses of from 0.3 to 6.2 mg/kg/day triphenyltin hydroxide for 52 and 104 weeks there was no corresponding increase in liver weight (Tennekes et al. 1989a). The dose-related trend was stronger in females (p<0.0005) than in males (p<0.005). In mice this same compound was associated with a 35%-40% increase in liver weight and nodular hyperplasia at doses of 15.2 mg/kg/day for males and 20.2 mg/kg/day for females but not at lower doses (Tennekes et al. 1989b). 

In female mice, a dose of 20.2 mg/kg/day triphenyltin hydroxide administered for 80 weeks as associated with dermal sores and burn-like lesions, and was sometimes accompanied by hair loss (Tennekes et al. 1989b). These lesions were present primarily in the back cervical area but were also identified on the head, ears, forelimb and abdomen. Males were affected to a much lesser extent than the females. No skin lesions were associated with the administration of triphenyltin hydroxide to rats or dogs (Sachsse et al. 1987 Tennekes et al. 1989a). 

Triphenyltin hydroxide caused dose-related cystoid changes in the pars intermedia of the pituitary gland for male and female mice administered this compound for 52 or 104 weeks at doses of 0.3-6.2 mg/kg/day (Tennekes et al. 1989a). Up to 40% of the males and 80% of the females were affected at 52 weeks by the highest dose. At the end of 104 weeks, 72.3% of the high dose males and 55.6% of the females exhibited the cystoid changes. The lower incidence in females at 104 weeks related to a high early mortality from fatal pituitary adenomas (see Section 2.2.2.8). 

In mice there were slight to moderate decreases in the levels of IgG, IgA, and IgM in males and females exposed to 15.2 and 20.2 mg/kg/day triphenyltin hydroxide for 80 weeks. Increases in the relative numbers of lymphoid cells, were found in the femoral bone marrow myelograms of all of the exposed animals but there were no observed differences in the peripheral blood lymphocytes and monocytes. It is, accordingly, difficult to evaluate the clinical significance of the bone marrow tests. 

The numbers of males with testicular Leydig cell tumors was increased in animals exposed to 5.2 mg/kg/day triphenyltin hydroxide for 104 weeks (16.7% as opposed to 1.7% in the controls). 

Tumors were also present in mice given diets containing 0.9-20.2 mg/kg/day triphenyltin hydroxide. After sacrifice at 80 weeks, examination of the tissue revealed an increased incidence of hepatocellular adenomas in both sexes. These tumors were consistent with the nodular hyperplasia seen in the livers of the treated animals. As was the case with the rat study, the females appeared to be more sensitive than the males. There was decrease in survival for the females at the highest dose. Only 50% of the females receiving this dose were alive at the termination of the study as opposed to 70% of the males in the same dose group and 74% of the female control animals. 

There is also no conclusive evidence that inorganic tin compounds have carcinogenic properties. However, there are data which indicate that organotin compounds (bis(tributyltin)oxide and triphenyltin hydroxide) may be tumorigenic at low levels of tin. Bis(tributyltin)oxide (2.5 mg/kg/day) and triphenyl tin hydroxide (0.3-6.2 mg/kg/day) were associated with pituitary adenomas in rats of both sexes with exposures of 104-106 weeks. When triphenyltin hydroxide was administered, the pituitary adenomas were present only in the females and contributed to decreased longevity. 

In the studies of long-term exposure of rats to both triphenyltin hydroxide and bis(tributyltin)oxide, most of the tumors were found in endocrine glands. In addition to the pituitary adenomas associated with bis(tributyltin)oxide and triphenyltin hydroxide, there was also an increased incidence of pheochromocytomas of the adrenal gland, parathyroid carcinomas and pancreatic adenocarcinomas in animals from at least one sex. Triphenyltin hydroxide was associated with an increased incidence of testicular Leydig cell tumors in male rats at the highest dose. Hepatic tumors were found in male and female mice following 80 weeks of triphenyltin hydroxide administration. 

The EPA Office of Pesticide Programs reviewed the data for the tumorigenicity of triphenyltin hydroxide and classified it as a possible human carcinogen (Group B2) based on the tumors found in both rats and mice during chronic studies of carcinogenicity. The most appropriate estimate of the unit risk in human equivalents was a q1 of 2.8 (mg/kg/day) from the data on pituitary gland adenomas in female rats. 

Dermal/Ocular Effects. Skin and eye irritations and dermatitis, but not sensitization, have been reported in humans and animals after dermal exposure of acute and intermediate-duration to both inorganic tin and organotin compounds. Mice also experienced a dermatological reaction to triphenyltin hydroxide after oral exposure over a period of 80 weeks. There is a reasonable probability of some skin, eye, and other mucous membrane contact with compounds at hazardous waste sites and the likelihood of irritation and other effects occurring. 

NCI. 1978b. Bioassay of triphenyltin hydroxide for possible carcinogenicity. Bethesda, MD National Cancer Institute, Division of Cancer Cause and Prevention. NCI-CG-TR 139. NTIS No. PB 287399. 

Rodwell DE. 1987. An embryotoxicity study in rabbits with triphenyltin hydroxide. Somerville, NJ American Hoecht Corporation. 

On the other hand, triphenyltin acetate and triphenyltin hydroxide were the first commercial products introduced during the early 1960s followed by triphenyltin chloride, tricyclohexyltin hydroxide, bis(trineophenyltin) oxide, and tricyclohexatin-1,2,4-triazole, respectively. Triphenyltin hydroxide was one of the recommended pesticides for rice and necessary for countries like Thailand where rice is a major component of both domestic and export markets (Visoottiviseth, 2001). 

Triaryltin compounds such as triphenyltin hydroxide (TPTH, Fentin hydroxide, Du-Ter, I), or triphenyltin acetate (TPTOAC, Brestan, II) have been shown to be effective as protectant fungicides. These compounds have demonstrated other activity such as antifoulants, bactericides and algi-cides. Due to their low phytotoxicity they have been developed for plant protection. In several cases they have been reported to exhibit the unusual property of deterring insects from feeding. (2 )... 

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