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Toxicity Effects

CAS Registry Number: 78-40-0

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 2.

Names 1

  • Phosphoric Acid, Triethyl Ester (9ci)
  • Triethyl phosphate

Human Toxicity Excerpts

  • OTHER TOXICITY INFORMATION: Some ethyl phosphate derivatives (e.g. parathion) are highly toxic cholinesterase inhibitors. Triethyl phosphate is thought to be weak enzyme inhibitor.[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-302] **PEER REVIEWED**

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Non-Human Toxicity Excerpts

  • ALTERNATIVE IN VITRO TESTS: ... /In rats, NADPH-cytochrome c reductase/ triethyl phosphate caused an increase of the reductase activity, but carbon disulfide had no influence on this activity.[Furukawa N et al; Biochem Pharmcol 36 (8): 1291-6 (1987)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE IN VITRO TESTS: ...In vitro inhibition of brain cholinesterase occurs, it appears to have no cumulative action ... .[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1923] **PEER REVIEWED**
  • GENOTOXICITY: Male Q mice received a single i.p. injection of 14 organophosphorus compounds, including 11 insecticides, administered on separate occasions. After a recovery period of 10-15 days, the cytogenetic effects were analyzed in primary spermatocytes at diakinesis-metaphase 1 corresponding to the treatment of A4-B type spermatogonia. At the highest tolerated dose, triethylphosphate (300 mg/kg), did not produce chromosome damage.[Degraeve N et al; Toxicol Lett 21 (3): 315-320 (1984)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Triethyl phosphate (TEP) was tested for mutagenicity in the Salmonella/microsome preincubation assay using a protocol approved by the National Toxicology Program. Triethyl phosphate was tested at doses of 0, 100, 333, 1000, 3333, and 10,000 ug/plate in four Salmonella typhimurium strains (TA 98, TA 100, TA 1535, and TA 1537) in the presence and absence of Aroclor-induced rat or hamster liver S9. Triethyl phosphate was negative in these tests and the highest ineffective dose level tested in any Salmonella tester strain was 10,000 ug/plate.[Zeiger E et al; Environ Mutagen 9: 1-110 (1987)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: ... Triethyl phosphate producing anesthetic like picture with considerable muscle relaxation in relatively high dosages. ...in vitro inhibition of brain cholinesterase occurs, it appears to have no cumulative action ... .[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1923] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Administration of the lethal doses /to rats and mice/ led to excitation with subsequent CNS inhibition, motor coordination disorder, paresis of the hind legs, and respiratory disturbances. Death occurs in 24 hours. Gross pathology examination revealed visceral congestion, particularly in the liver, and hyperemia of the gastric mucosa.[Sheftel, V.O.; Indirect Food Additives and Polymers. Migration and Toxicology. Lewis Publishers, Boca Raton, FL. 2000., p. 227] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: ... We measured fertilization success and percentages of normal, arrested and abnormal embryos exposed to low, medium and high sub-lethal concentrations of inorganic and organic phosphate. Fertilization success was significantly reduced in all phosphate treatments. After attaining the 4-cell stage, embryos exposed to the highest phosphate concentrations displayed arrested development. Percentages of abnormally developing embryos showed a strong concentration dose-response with a significant increase in abnormal embryonic development with increasing phosphate concentration. Overall, these results indicate that the gametes and embryos of L. variegatus may provide a rapid and sensitive model bioassay for the evaluation of phosphate pollutants in marine systems. Our findings also indicate that shallow-water populations of L. variegatus spawning in areas subjected to inorganic and organic phosphate pollutants may suffer detrimental effects on fertilization and embryonic development.[Bottger SA, McClintock JB; Comp Biochem Physiol C Toxicol Pharmacol 129 (4): 307-315 (2001)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Neurotoxicity: Acute neurotoxic effects include: anesthesia, weakness, and brain cholinesterase inhibition (animals) /From table/[O'Donoghue, J.L. (ed.). Neurotoxicity of Industrial and Commercial Chemicals. Volume I. Boca Raton, FL: CRC Press, Inc., 1985., p. 138] **PEER REVIEWED**
  • LABORATORY ANIMALS: Neurotoxicity: Relationships between the anticholinesterase and /CNS depression/-producing action of dimethoate [O,O-dimethyl, S-(N-methylcarbamoyl methyl) phosphorodithioate] and the influence of age, sex, and drug pretreatments on the susceptibility of mice and rats to dimethoate- and triethyl phosphate (TEP)-induced /CNS depression/ were investigated. Although the doses of dimethoate required to produce /CNS depression/ exceeded those that inhibited brain cholinesterase, the onset of /CNS depression/ (loss of righting reflex) occurred before the onset of cholinesterase inhibition. Dose and time response studies indicated that these two effects of dimethoate were independent of each other; however, some evidence was obtained which suggested that the initial /CNS depression/ may delay the lethal cholinergic toxicity. Adult female rats were more susceptible than males to the production of /CNS depression/ by both dimethoate and triethylphosphate, and adults of both sexes were more susceptible to this effect than weanlings. Male mice were more resistant to /CNS depression/ production than rats. Pretreatment of female rats with SKF 525-A 1 hr before dimethoate prolonged the duration of /CNS depression/ and delayed the onset of cholinergic signs. Repeated phenobarbital injections hastened the onset of cholinergic signs, but did not affect the duration of /CNS depression/. SKF 525-A prolonged and phenobarbital shortened triethyl phosphate-induced /CNS depression/ in male mice, but these pretreatments did not significantly affect the duration of TEP /CNS depression/ in adult female rats.[Brown DR, Murphy SD; Toxicol Appl Pharmacol 18 (4): 895-906 (1971)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Central nervous system effects. Rats ip 400 mg/kg for 37 days caused peritoneal irritation; ascites; anesthesia; no paralysis. Inhalation of 28,000 ppm for 6 hours /resulted in/ 3/3 deaths; weakness; gasping respiration. Weak in vitro rat brain /cholinesterase/ inhibition. Slight irritant to guinea pig skin. /from table/[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:953t] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Triethylphosphate (TEP) was fed to rats at dietary levels of 0.1, 0.5, 1.0, 5.0, and 10% for 3 months plus additional time for reproduction studies. Inhibition of growth related to TEP occurred at the 5% level, and reproduction was adversely affected at 1%. Severe anorexia at 10% TEP made it necessary to exclude this group from consideration of TEP toxicity. Liver weight was markedly increased, being detectable in the males at 0.1% TEP or more and in the females at 5% TEP. Adrenal enlargement also occurred at the highest levels, especially in the males. Clinical studies included measurements of blood, brain, and liver acetylcholinesterase, plasma and liver alkaline phosphatase, liver tyrosine transaminase, blood urea nitrogen, liver nitrogen, and hematology. Alterations of these factors were for the most part minimal and would be considered to be within normal ranges. Small, transient elevations of blood cholinesterase were detected at 50 days, followed at 100 days by slight depression in the females receiving 0.5% TEP or more. Brain cholinesterase was also slightly depressed at 5% TEP. Liver alkaline phosphatase was elevated at 5% TEP, while liver tyrosine transaminase became significantly depressed in the males at 0.1% or more and in the females at 5%. Hepatocellular enlargement developed initially in the 1% female rats and appeared in both male and female rats of the 5% group. Minor bile ductule hyperplasia and retention of bile also occurred in the latter group. At levels that would be encountered if used as proposed as a food additive, the daily dosage of TEP would be far below the no-effect level in the rat as related to the present study.[Gumbmann MR et al; Toxicol Appl Pharmacol 12 (3): 360-371 (1968)] **PEER REVIEWED** PubMed Abstract
  • OTHER TOXICITY INFORMATION: Ethyl phosphate is sedating in rats. /Ethyl phosphates/[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-302] **PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LC50 Rat inhalation >8817 mg/cu m/4 hours[OECD; Screening Information Data Set for Triethylphosphate 78-40-0 (October 1998). Available from, as of February 24, 2006: http://www.inchem.org/documents/sids/sids/78400.pdf] **PEER REVIEWED**
  • LD50 Guinea pig dermal >21.4 g/kg[OECD; Screening Information Data Set for Triethylphosphate 78-40-0 (October 1998). Available from, as of February 24, 2006: http://www.inchem.org/documents/sids/sids/78400.pdf] **PEER REVIEWED**
  • LD50 Mouse ip 0.485 g/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 3550] **PEER REVIEWED**
  • LD50 Mouse oral >1.5 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**
  • LD50 Rabbit dermal >20 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**
  • LD50 Rabbit ip 0.8 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**
  • LD50 Rabbit oral 1.6 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**
  • LD50 Rat ip 0.8 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**
  • LD50 Rat oral 1.6 g/kg[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 6:950t] **PEER REVIEWED**

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Absorption, Distribution And Excretion

  • None found

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Metabolism/Metabolites

  • None found

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Tsca Test Submissions

  • The ability of triethyl phosphate to induce morphological transformation in the BALB/3T3 mouse cell line (Cell Transformation Assay) was evaluated. Based on preliminary toxicity determinations, triethyl phosphate was tested at concentrations of 4, 3, 2.5, 1.5 and 0.3 ul/ml in the complete medium, with cell survival ranging from 97.3% to 12.6%. None of the concentrations tested produced a significant increase in the transformation frequencies (p > 0.10) relative to the complete medium control.[Eastman Kodak Company; In Vitro Mammalian Cell Transformation Assay Results. (1983), EPA Document No. FYI-OTS-0884-0328, Fiche No. 0328] **UNREVIEWED**

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Footnotes

1 Source: the NTP's CEBS database.

2 Source: the National Library of Medicine's Hazardous Substance Database, 02/28/2017.

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