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Di-2-ethyl hexyl phthalate

Diethylene glycol Diethylene glycol ether Di-(2 ethyl hexyl) phthalate Diethylenetriamine Difluorodibromomethane Difluorodichloromethane Diglycidyl ether of Bisphenol A Dihydrocapsaicin... [Pg.367]

Biodegradation of Di-n-Butyl Phthalate and Di-2-Ethyl-hexyl Phthalate in Freshwater Hydrosoil, 333-339. [Pg.93]

Koch HM, Preuss R, Angerer J (2006) Di(2-ethyl-hexyl)phthalate (DEHP) human metabolism and internal exposure - an update and latest results. Int J Androl 29 155-165... [Pg.295]

Rowland IR (1974) Metabolism of di-(2-ethyl-hexyl) phthalate by the contents of the alimentary tract of rat. Food Cosmetic Toxicol 12 293-303... [Pg.329]

A poly (vinylchloride) membrane electrode was described for local anesthetics, based on dibenzo-24-crown-8 as the electroactive material, and di(2-ethyl)hexyl phthalate as the plasticizer [74]. It was reported that the electrode exhibited a Nemstian response to procaine, and other electrode properties were also presented. The analysis was performed at pH 6 to 6.5 vs. S.C.E., with a 0.2 M lithium acetate agar bridge. Less efficient crown ethers studied at this time were benzo-15-crown-5, dibenzo-18-crown-6, and dibenzo-30-crown-10. [Pg.423]

Urinary system-. Groups of 20 male Fischer 344 rats were given 0.05%7V-ethyl-jV-hydroxyethylnitrosamine (EHEN) for two weeks in the diet followed by di(2-ethyl-hexyl) phthalate [purity unspecified] at a concentration of 0 or 1.2% in the diet for 24 weeks. Rats were killed at 27 weeks. Di(2-ethylhexyl) phthalate increased the numbers of rats with renal (tubular) cell tumours (EHEN + di(2-ethylhexyl) phthalate 65% versus 20% for EHEN alone p < 0.01) and the mean number of tumours per kidney (EHEN + di(2-ethylhexyl) phthalate 1.1 versus EHEN alone 0.2,< 0.01) (Kurokawa etal., 1988). [Pg.70]

Male Fischer 344 rats (body weight, 100-150 g) were fed 0.5-4% di(2-ethyl-hexyl) phthalate in the diet for one or four weeks and male Swiss Webster mice (20-30 g) were fed 2 or 4% di(2-ethylhexyl) phthalate in the diet for one or four weeks (Reddy etal., 1976). Di(2-ethylhexyl) phthalate increased relative liver weights and markedly induced hepatic carnitine acetyltransferase activity in both species (up to 25-fold in rats and 10-fold in mice). Some increase in hepatic catalase activity (approximately two-fold) was observed and subjective (non-morphometric) ultra-structural examination revealed marked peroxisome proliferation. This study also demonstrated that di(2-ethylhexyl) phthalate was a hypolipidaemic agent, as serum triglyceride levels were reduced to one seventh of control values in rats and one third of control values in mice. [Pg.81]

The involvement of testosterone in the testicular atrophy caused by di(2-ethyl-hexyl) phthalate was examined by co-administration of testosterone (1 mg/kg bw) subcutaneously with 2000 mg/kg bw di(2-ethylhexyl) phthalate [purity not specified] in groundnut oil to adult male Wistar rats for 15 days (Parmar et al., 1987). Administration of di(2-ethylhexyl) phthalate reduced the sperm count and also significantly increased the activity of y-GT, lactate dehydrogenase and P-glucuronidase and decreased the activity of sorbitol dehydrogenase and acid phosphatase. Co-adminis-tration of testosterone seemed to normalize the sperm count and the activity of testicular enz5mies. The role of testosterone in the testicular toxicity of di(2-ethylhexyl) phthalate has not been fully elucidated. Several reports refer to increased or decreased testosterone levels in plasma and testicular tissue. [Pg.101]

RLV/Fischer rat assay without the addition of an exogenous metabolic activation system. In a single study, mouse JB6 epidermal cells were transformed by di(2-ethyl-hexyl) phthalate without activation and in one of two studies a weak response was reported in the CSHIOT A cell transformation assay with di(2-ethylhexyl) phthalate in either the absence or presence of exogenous metabolic activation. BALB/c-3T3 cells were not transformed by di(2-ethylhexyl) phthalate with or without metabolic activation. Di(2-ethylhexyl) phthalate inhibited gap-junctional intercellular communication in Chinese hamster V79 cells in six of seven studies, but not in one study of liver cells of cynomolgus monkeys in vivo. Di(2-ethylhexyl) phthalate treatment of Syrian hamster embryo cells in a two-stage exposure with 12-O-tetradecanoylphorbol 13-acetate resulted in superinduction of ornithine decarboxylase, an early event in morphological transformation no effect was seen after a one-stage treatment with di(2-ethylhexyl) phthalate alone. [Pg.115]

Significant species differences have been observed in the absorption and disposition of di(2-ethylhexyl) phthalate. The peroxisome-proliferating effect of di(2-ethyl-hexyl) phthalate has been related most specifically in susceptible species to metabolites VI, IX and mono(2-ethylhexyl) phthalate however, analysis of the disposition data does not provide an explanation for the observed species differences in di(2-ethylhexyl) phthalate-induced hepatic peroxisome proliferation. [Pg.116]

Di(2-ethylhexyl) phthalate is ubiquitous in the general environment as a result of its widespread use in poly(vinyl chloride) products. It is found in ambient air at levels usually below 100 ng/m. The highest levels of di(2-ethylhexyl) phthalate in foods are found in milk products, meat and fish and in other products with a high fat content, where concentrations up to 10 mg/kg have been reported. The leaching of di(2-ethyl-hexyl) phthalate Ifom flexible plastics used in medical devices, such as during dialysis and transfusion, can result in large direct exposures. [Pg.121]

There is inadequate evidence in humans for the carcinogenicity of di(2-ethyl-hexyl) phthalate. [Pg.124]

In making its overall evaluation of the carcinogenicity to humans of di(2-ethyl-hexyl) phthalate, the Working Group took into consideration that (a) di(2-ethylhexyl) phthalate produces liver tumours in rats and mice by a non-DNA-reactive mechanism involving peroxisome proliferation h) peroxisome proliferation and hepatocellular proliferation have been demonstrated under the conditions of the carcinogenicity studies of di(2-ethylhexyl) phthalate in rats and mice and (c) peroxisome proliferation has not been documented in human hepatocyte cultures exposed to di(2-ethylhexyl) phthalate nor in the liver of exposed non-human primates. Therefore, the mechanism by which di(2-ethylhexyl) phthalate increases the incidence of hepatocellular tumours in rats and mice is not relevant to humans. [Pg.124]

Agency for Toxic Substances and Disease Registry (1993) Toxicological Profile Di(2-ethyl-hexyl) Phthalate, Atlanta, GA, Department of Health and Human Services Albro, P.W. (1986) Absorption, metabolism and excretion of di(2-ethylhexyl) phthalate by rats and mice. Environ. Health Perspect, 65, 293-298 Albro, P.W. Lavenhar, S.R. (1989) Metabolism of di(2-ethylhexyl)phthalate. Drug Metab. Rev., 21, 13-34... [Pg.125]

Jain, G.C. Joshi, S.C. (1991) Effects of plasticizer di-(2-ethyl hexyl) phthalate (DEHP) on reproductive function of mice. Z. Angew. ZooL, 4, 465 70... [Pg.135]

Mizuguchi, H., Kudo, N., Ohya, T. Kawashima, Y. (1999) Effects of tiadenol and di-(2-ethyl-hexyl)phthalate on the metabolism of phosphatidylcholine and phosphatidylethanolamine in the liver of rats comparison with clofibric acid. Biochem. Pharmacol, 57, 869-876 Mocchiutti, N.O. Bernal, C.A. (1997) Effects of chronic di(2-ethylhexyl) phthalate intake on the secretion and removal rate of triglyceride-rich lipoproteins in rats. Food chem. Toxicol, 35, 1017-1021... [Pg.139]

Dabholkar AS. 198 8. Peroxisomes in the rat brain and the effects of di-(2-ethyl)hexyl phthalate during postnatal development An electron-microscopic study. Acta Anat 131 218-221. [Pg.254]

The opposite behavior as sketched before was detected for solutions of PS in DOP [112], Again, the critical temperature (an UCST at Tc = 12 °C in the quiescent state) turned out to be a function of the shear rate to which the solution is subjected. But, in contrast to solutions of PS and PB in DOP, here enhancements of the UCST as large as 28 °C were recorded at a shear rate of 220 s-1. Similar results have been found for PS solutions in di(2-ethyl hexyl)phthalate or in a mixture of cis- and frans-decalin [113], The solutions demixed in a converging flow from a reservoir into a capillary tube. It has been observed that an increase in the deformation rate raised the UCST or reduced the region of miscibility. In both of these studies an increase of the cloud point temperature of the polymer solutions was used as an indication of phase separation. [Pg.73]

The main phthalates under investigation are butyl benzyl phthalate (BBP), dibutyl phthalate (DBP), di-2-ethyl hexyl phthalate (DEHP), diisononyl phthalate (DINP) and diisodecyl phthalate (DIDP). These investigations include EU risk assessments based on sound science but the political positions on flexible PVC and phthalates cannot be ignored. [Pg.10]

For many years, di-2-ethyl hexyl phthalate has been the primary plasticiser for medical devices made of PVC, but there are concerns regarding its toxicity. The potential of a lesser used plasticiser, tributyl citrate, is examined. The properties of plasticised vinyl compositions were compared, including extraction, volatility, thermal stability, low temperature flexibility and mechanical properties. 12 refs. [Pg.126]

Degussa AG Di 2 ethyl hexyl phthalate (DOP) 2-Ethylhexanol, phthalic anhydride Catalytic esterification, low alpha number NA NA... [Pg.140]

Plasticizers—small organic molecules that act as lubricants between chains—are usually added to thermoplastics to keep them from becoming brittle at room temperature. A good example is polyCvinyl chloride), which is brittle when pure but becomes supple and pliable when a plasticizer is added. In fact, the drip bags used in hospitals to deliver intravenous solutions are made of poly vinyl chloride). Dialkyl phthalates such as di(2-ethyl-hexyl) phthalate are commonly used for this purpose, although questions about their safety have recently been raised. [Pg.1275]

Itsuki-Yoneda A, Kimoto M, Tsuji H, et al. Effect of a hypolipidemic drug, Di (2-ethyl-hexyl) phthalate, on mRNA-expression associated fatty acid and acetate metabolism in rat tissues. Biosci Biotechnol Biochem. 2007 71(2) 414-420. [Pg.241]

Willhite CC (2001) Weight-of-evidence versus strength-of-evidence in toxicologic hazard identification Di(2-ethyl-hexyl) phthalate (DEHP). Toxicology 160(1-3) 219-226. [Pg.734]


See other pages where Di-2-ethyl hexyl phthalate is mentioned: [Pg.228]    [Pg.71]    [Pg.73]    [Pg.75]    [Pg.78]    [Pg.80]    [Pg.85]    [Pg.89]    [Pg.90]    [Pg.91]    [Pg.95]    [Pg.97]    [Pg.97]    [Pg.99]    [Pg.102]    [Pg.116]    [Pg.125]    [Pg.127]    [Pg.128]    [Pg.139]    [Pg.141]    [Pg.41]   
See also in sourсe #XX -- [ Pg.206 ]

See also in sourсe #XX -- [ Pg.52 ]

See also in sourсe #XX -- [ Pg.686 ]

See also in sourсe #XX -- [ Pg.686 ]

See also in sourсe #XX -- [ Pg.686 ]




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Di- -ethyl phthalate

Ethyl 3,3-di

Ethyl Phthalate

Ethyl-hexyl

Hexyl

Phthalates

Phthalation

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