Testing Information

Testing Status of Agents at NTP

CAS Registry Number: 141-43-5 Toxicity Effects

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

Names (NTP)

  • Ethanolamine
  • 2-AMINOETHANOL (9CI)
  • MONOETHANOLAMINE
  • BETA-AMINOETHYL ALCOHOL
  • 2-HYDROXYETHYLAMINE

Human Toxicity Excerpts

  • SIGNS AND SYMPTOMS: ... When undiluted monoethanolamine is applied to human skin on gauze for 1 1/2 hr, only marked redness and infiltration of the skin result. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:783]**PEER REVIEWED**
  • SIGNS AND SYMPTOMS: ... A concentration of 5.9% ethanolamine is irritating to human skin. [Gillner M et al; Nord 29: 49-73 (1993) ]**PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Symptoms associated with /CNS depression/ of the ethanolamines /in humans/ include increased blood pressure, diuresis, salivation, and pupillary dilation. Large doses produce sedation, coma, and death following depression of blood pressure and cardiac collapse. /Ethanolamines/ [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 428]**PEER REVIEWED**
  • SIGNS AND SYMPTOMS: MEA inhalation by humans has been reported to cause immediate allergic responses of dyspnea and asthma and clinical symptoms of acute liver damage and chronic hepatitis. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Corrosive. Causes severe eye and skin burns. May be harmful if absorbed through skin or inhaled. Irritating to skin, eyes, respiratory system. [Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 49-70]**PEER REVIEWED**

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Non-Human Toxicity Excerpts

  • LABORATORY ANIMALS: Acute Exposure: ... Administration of monoethanolamine by the intravenous route in dogs produced increased blood pressure, diuresis, salivation, and pupillary dilation ... [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:782]**PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /Investigators/ exposed laboratory animals to ethanolamine vapor and to mist. Rats, mice, rabbits, and guinea pigs exposed at high concentrations developed pulmonary, hepatic, and renal lesions. /Investigators/ found no difference in mortality as a result of physical state of the air-borne compound, i.e. vapor or mist. [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 1]**PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Drop of ethanolamine applied to rabbit eyes causes injury similar to that caused by ammonia, but less severe, graded 9 on a scale of 10. [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 1]**PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /Investigators/ injected ip approximately 168 mg/kg of MEA into male albino mice every day for 4 days. Mice were sacrificed at 6, 12, 24, 48, and 96 hrs. At all times from12 to 96 hr, the liver ethanol kinase levels of the treated mice were significantly higher than control mouse liver levels. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: /Investigators/ found that the intravenous administration of MEA to rabbits for seven days increased the level of aspartate and glutamate in the kidneys and decreased the levels in the brain. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ... In a 90-day subacute oral toxicity study of unneutralized ethanolamine in rats that a maximum daily dose of 0.32 g/kg resulted in no effect; 0.64 g/kg/day resulted in altered liver or kidney wt; and at 1.28 g/kg death occurred. Ethanolamine is considered to be liver toxin. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:782]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ...Dogs, guinea pigs, and rats /were exposed/ continuously to ethanolamine vapors (24 hr/day, 7 days.wk, except for 15 min each day when chambers were cleaned) for 24-90 days. Exposure to 66-102 ppm of ethanolamine caused deaths and lesions in the skin (vacuolated epithelial cells and ulceration), lungs (inflammation), liver (cloudy swelling), and kidney (cloudy swelling in the tubular epithelium), and testis (reduced spermatogenesis). The major effects in animals exposed to 12-26 ppm ethanolamine were skin irritation and lethargy. Skin irritation was also observed in animals exposed to 5-6 ppm ethanolamine for 40-60 days. There was a decrease in the albumin-globulin ratio and a decrease in hemoglobin and hematocrit values in dogs exposed to 102 ppm ethanolamine. These findings correlate with the kidney and liver damage caused by ethanolamine and indicate that red blood cell formation may also have been suppressed. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 427]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ... Rats, mice, and rabbits exposed to ethanolamine by daily inhalation of 0.26 mg/L for five weeks exhibited respiratory tract irritation; histopathological examinations also showed some non specific mild degenerative changes of the liver and kidneys. A subchronic oral toxicity study in rats indicated a no observed effect level (NOEL) of 320 mg/kg body weight. Higher doses caused hepatic and renal damage; deaths occurred at 1280 mg/kg/day. Repeated inhalation of low doses (0.029 mg/L) of ethanolamine caused behavioral effects in dogs (progressive stages of excitation followed by depression). There are very limited data available on long term toxicology; in one oral study low doses of ethanolamine caused no adverse effects in dogs. [Gillner M et al; Nord 29: 49-73 (1993) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ...Repeated applications of ethanolamine are irritant to rabbit skin in low concentrations (<1%), severely irritant in higher concentrations, and corrosive both at a 30% concentration level in a single patch application and at > or =10% concentration over a period of 14 days. The level of severe injury to the rabbit eye is as low as 5%. [Gillner M et al; Nord 29: 49-73 (1993) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Pregnant Sprague-Dawley rats and New Zealand White rabbits were exposed dermally to 0, 10, 25, and 75 mg/kg/day of monoethanolamine (MEA) for approximately 6 hr/day on Days 6 through 15 (rats) or 6 through 18 (rabbits) of gestation. A fifth dose group of 225 mg MEA/kg/day was evaluated in rats only. Dermal exposure of pregnant rats to 225 mg/kg/day and rabbits to 75 mg/kg/day resulted in significant increases in the incidence of skin irritation/lesions and maternal body weight effects. In general, the dermal irritation observed at the high dose was progressive, beginning with erythema and leading to necrosis, scabs, and scar formation. Doses of 25 mg/kg/day to rabbits produced only minor irritation. Despite maternal effects observed in rats and rabbits, no evidence of developmental or fetal toxicity was observed at any dose level tested. Thus, it was concluded that MEA was not developmentally toxic following dermal application at exposure levels up to and including 225 mg/kg/day for rats and 75 mg/kg/day for rabbits. [Liberacki AB et al; Fundam Appl Toxicol 31 (1): 117-123 (1996) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: /Investigators/ administered ethanolamine to rats by oral feeding (0.5% ethanolamine in food, or 320 mg/kg/day) for 90 days. The rats were not affected; however, at a higher dose (1.28 g/kg/day), deaths occurred. [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 2]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: The administration of MEA at a dose of 60 mg/kg/day for 30 days to albino rats with experimentally-induced coarction of the aorta resulted in elevated levels of phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine in the rat myocardium. Metabolic changes produced by MEA action may have inhibited the development of cardiac insufficiency in these animals. [Christian M, ed; J American College of Toxicology 2 (7): 183- 226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Pregnant Wistar rats (40/group) were administered monoethanolamine (MEA) as an aqueous solution by gavage at dose levels of 0, 40, 120, and 450 mg/kg/day on days 6 through 15 of gestation. On day 20 of gestation, 25 dams/group were euthanized and the fetuses were delivered by cesarean section, weighted, sexed, and examined for external, visceral, and skeletal alterations. The remaining dams (15/group) were allowed to litter and rear their pups to day 21 postpartum. The dams and pups were then euthanized and examined for gross pathologic changes. Gavage administration of 450 mg MEA/kg/day to pregnant rats resulted in maternal toxicity as evidenced by statistically significant (alpha = 0.05) decreases in feed consumption on gestation days 6-8 and 17-20 and on postpartum days 0-4. Additionally, statistically significant decreases in mean maternal body weights were observed on gestation days 15, 17, and 20 and on lactation days 0, 4, 7, and 21. Body weight gains of the 450 mg/kg/day dams were also significantly decreased (13% relative to controls) on gestation days 15-20. There was no evidence of maternal toxicity at 40 or 120 mg/kg/day of MEA. Despite the maternal effects observed at 450 mg/kg/day, no significant fetal effects were observed at this or any dose level tested, nor were there any indications of a treatment-related effect on postnatal growth or on the viability of offspring. Thus, it was concluded that MEA was not developmentally toxic to Wistar rats following repeated oral administration, even at maternally toxic dose levels as high as 450 mg/kg/day. [Hellwig J, Liberacki AB; Fundam Appl Toxicol 40 (1): 158-162 (1997) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Maternal toxicity /of New Zealand white rabbits/ was seen at the two higher dose levels /(25, 75 mg/kg body weight)/ as skin irritation and at the highest dose level as reduced weight gain. ... There was no treatment related effect on the incidence of any fetal variation or malformation or on the number of malformed fetuses. [European Chemicals Bureau; IUCLID Dataset, 2-Aminoethanol (141-43-5) (2000 CD-ROM edition). Available from the database query page: http://ecb.jrc.it/esis/esis.php as of February 13, 2006. ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The incubation of chicken eggs with 0.03% MEA for 18 hr increases the number of eggs with visible blastodisks, increased the synthesis of proteins, fats and carbohydrates, and increased the number of hatching chicks. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: A composite hair dye and base containing 22% MEA was given to 60 female rats at concentrations of 0 to 7800 ppm in the diet from Day 6 to 15 of gestation. The rats were sacrificed at day 19 and there was no evidence of any adverse effects on the rats or their pups. No differences were observed in the average number of implantation sites, live pups, early or late resorptions per litter, or females with one or more resorption sites. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: A composite hair dye and base was also administered at a dose of 0-19.5 mg/kg/day by gavage to 48 artificially inseminated rabbits from day 6 to 18 of gestation. The rabbits were sacrificed at day 30. There was no evidence of any teratologic effect. Fetal survival was not adversely affected and no grossly abnormal fetuses or soft tissue defects were seen. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The embryopathic effects of high doses of ethanolamine were evaluated in pregnant Long-Evans rats during oranogenesis. Ethanolamine was given by gavage at levels of 0, 500, 300, or 50 mg/kg/day (24%, 14.4%, or 2.4% of the LD50 value). Ethanolamine caused dose-dependent increases in intrauterine deaths, malformations, and intrauterine growth retardation. Embryolethality caused by 50 mg/kg of ethanolamine was not random: male pups contiguous to two male siblings (designated mMm) were almost quantitatively replaced by resorptions that were contiguous to two male pups (designated mRm) (mMm pups constituted 6.7% of control implants and decreased to only 0.9% of group II implants while mRm resorptions increased from 0.3% in controls to 5.6% in group II dams). Intrauterine growth retardation and increases in gross structural anomalies (considered indicative of depressed fetal growth) more severely affected male than female offspring at all dose levels. Pups of either sex who were contiguous to male siblings were more adversely affected than those offspring contiguous to one or more female siblings. [Mankes RF; Teratogenesis Carcinog Mutagen 6 (5): 403-17 (1986) ]**PEER REVIEWED**
  • GENOTOXICITY: Monoethanolamine was found to be negative when tested for mutagenicity using the Salmonella/microsome preincubation assay, using the standard protocol approved by the National Toxicology Program (NTP). Monoethanolamine was tested in as many as 5 Salmonella typhimurium strains (TA 1535, TA 1537, TA 97, TA 98, and TA 100) in the presence and absence of rat and hamster liver S-9, at doses of 0.01, 0.033, 0.10, 0.33, 1.0, 3.3, and 10.0 mg/plate. The highest ineffective dose tested in any Salmonella typhimurium strain was 10.000 mg/plate. [Mortelmans K et al; Environ Mutagen 8: 1-119 (1986) ]**PEER REVIEWED**
  • GENOTOXICITY: It is shown that monoethanolamine and triethanolamine are weak inducers of chromosome breaks in Crepis capillaris seeds, and induce low levels of gene mutations in the Ames systems. [Arutiunian RM et al; Tsitol Genet 21 (6): 450-4 (1987) ]**PEER REVIEWED**
  • GENOTOXICITY: It is shown that monoethanolamine and triethanolamine are weak inducers of chromosome breaks in cultures of human lymphocytes. [Arutiunian RM et al; Tsitol Genet 21 (6): 450-4 (1987) ]**PEER REVIEWED**
  • GENOTOXICITY: Monoethanolamine has been demonstrated to be non mutagenic in the Ames Salmonella typhimurium assay, with and without S9 metabolic activation, using TA 1535, TA 1537, TA 1538, TA 98, and TA 100; and also negative in the Escherichia coli assay, Saccharomyces gene conversion assay, and rat liver chromosome assay. /It was suggested/ that the lack of mutagenic activity was in accord with the absence of electrophilic reactivity. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:783]**PEER REVIEWED**
  • GENOTOXICITY: Ethanolamine did not induce transformation of hamster embryo cells at concentrations between 25 and 500 mg/mL. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 428]**PEER REVIEWED**
  • ALTERNATIVE IN VITRO TESTS: MEA bleached the visual pigment, rhodopsin, from water washed bovine retinal rod chromophores, which are responsible for vision in dim light. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: At higher doses, one sees sedation, coma, and death from hypotension, and cardiovascular collapse /in animals/. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 707]**PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LD50 Guinea pig oral 620 mg/kg body weight [European Chemicals Bureau; IUCLID Dataset, 2-Aminoethanol (141-43-5) (2000 CD-ROM edition). Available from the database query page: http://ecb.jrc.it/esis/esis.php as of February 14, 2006. ]**PEER REVIEWED**
  • LD50 Rats oral 10.2 g/kg [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 664]**PEER REVIEWED**
  • LD50 Rabbit dermal 1025 mg/kg body weight [European Chemicals Bureau; IUCLID Dataset, 2-Aminoethanol (141-43-5) (2000 CD-ROM edition). Available from the database query page: http://ecb.jrc.it/esis/esis.php as of February 13, 2006. ]**PEER REVIEWED**
  • LD50 Rat ip 67 mg/kg [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1607]**PEER REVIEWED**
  • LD50 Rat iv 225 mg/kg [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1607]**PEER REVIEWED**
  • LD50 Rat im 1750 mg/kg [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1607]**PEER REVIEWED**
  • LD50 Mouse oral 700 mg/kg [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1608]**PEER REVIEWED**
  • LD50 Mouse ip 50 mg/kg [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 1608]**PEER REVIEWED**

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Absorption, Distribution and Excretion

  • The excretion rate in men was found to vary between 4.8 and 22.9 mg/day with a mean of 0.162 mg/kg /body weight/. 11 women were observed to excrete larger amounts, varying between 7.7 and 34.9 mg/day with a mean excretion rate of 0.492 mg/kg/day. The excretion rates in animals were approximately, for cats, 0.47 mg/kg/day; for rats, 1.46 mg/kg/day; and for rabbits, 1.0 mg/kg/day. From 6-47% of monoethanolamine administered to rats can be recovered in the urine. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V4 p.782]**PEER REVIEWED**
  • Persistence of low levels of radioactivity in dog whole blood was obtained after admin of (14)C-labeled ethanolamine. Excretion of radioactivity as % of dose in dog urine was 11. After 24 hr total blood radioactivity as % of dose was 1.69. [Rhodes C, Case DE; Xenobiotica 7 (1-2): 112 (1977) ]**PEER REVIEWED**
  • Ethanolamine: is a normal urine constituent in man, excreted at a rate of 5-23 mg/day ... 40 percent of an administered dose is deaminated and excreted as urea. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 707]**PEER REVIEWED**
  • The skin penetration of 2-aminoethanol was tested in an in vitro model with full thickness skin prepaeations from mice, rats, humans and rabbits. Within 6 hours the following amounts penetrated through whole skin: rat skin 5.98%, mouse skin 16.92%, rabbit skin 8.66%, human skin 0.61%. [European Chemicals Bureau; IUCLID Dataset, 2-Aminoethanol (141-43-5) (2000 CD-ROM edition). Available from the database query page: http://ecb.jrc.it/esis/esis.php as of February 13, 2006. ]**PEER REVIEWED**
  • Eight hr after ip injection of 0.52 umoles of 14C-ethanolamine in Wistar rats, 11.5% of the injected dose was recovered as 14CO2. At that time, about 50% of the injected radioactivity was found in the liver, and significant amounts (>2% 14C/g tissue) were detected in the spleen and brain. In the liver, >90% of the radioactivity was found in the lipid fraction; in the kidney, spleen and brain, the percent in the lipid fraction was about 60, 30, and 54%, respectively. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 425]**PEER REVIEWED**
  • Twenty-four hr after dermal application of 14C-ethanolamine to athymic nude mice (4 ug to 1.45 sq cm), 19% of the applied dose was recovered in expired CO2; this value was similar to that obtained after ip injection of ethanolamine. Radioactivity from 14C-ethanolamine was widely distributed in the body, with the highest levels found in the liver (26%) and kidneys (2.2%). Radioactivity was observed in hepatic phospholipids as the ethanolamine, serine, and choline bases, and in proteins and amino acids isolated from liver and skin sections. Urinary excretion included radioactive ethanolamine, urea, glycine, serine, uric acid, and choline. Thus, ethanolamine penetrates mouse skin and may be oxidized to CO2, incorporated into hepatic phospholipids, or metabolized to amino acids. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 425]**PEER REVIEWED**
  • Twenty-four hr after administration of 14C-ethanolamine to dogs, total radioactivity in the blood was 1.69% of the administered dose. 11% of the dose was excreted in the urine. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 426]**PEER REVIEWED**
  • The normal excretion rate, determined in 24-hour urine specimens from eight young adult male students, varied between 4.8 and 22.9 mg ethanolamine/day (mean of 0.162 mg/kg body weight/day); females excreted larger amounts, 12.9 to 57 mg/day (mean of 0.492 mg/kg/day). [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 2]**PEER REVIEWED**
  • From 6% to 48% of orally administered ethanolamine was recovered in rat urine in 24 hours on dosages of 3.33 and 53 mg/100 grams body weight, respectively. [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 2]**PEER REVIEWED**

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Metabolism/Metabolites

  • 40 percent of (15)N-labeled ethanolamine appears as urea within 24 hr when it is given to rabbits, suggesting that it is deaminated. In rat liver homogenates, ethanolamine undergoes demethylation yielding formaldehyde. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:782]**PEER REVIEWED**
  • Ethanolamine (monoethanolamine) is a normal intermediate in the metabolism of some animal species, having a part in the formation of phospholipids ... . [American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2005., p. 2]**PEER REVIEWED**
  • The distribution and metabolism of topical (14)C ethanolamine was studied in vivo, using athymic nude mice, human skin grafted onto athymic nude mice, and in vitro, using excised pig skin. Ethanolamine was the only radioactive phospholipid base detected in the human skin grafts, in the mouse skin, and in the pig skin. Ethanolamine that penetrated human skin grafts or mouse skin was extensively metabolized in the animal. The liver is a major site for metabolism of ethanolamine, containing over 24% of the applied radioactive dose. The kidneys, lungs, brain, and the heart contained 2.53, 0.55, 0.27, and 0.15% of the dose, respectively. Hepatic, human skin graft, and mouse skin proteins were also highly radioactive. Over 18% of the topical radioactive dose oxidized to (14)CO2 and 4.6% was excreted in the urine over 24 hr. Urea, glycine, serine, choline, and uric acid were the urinary metabolites of ethanolamine. [Klain GJ et al; Fundam Appl Toxicol 5 (6 Pt 2): S127-33 (1985)]**PEER REVIEWED**
  • In liver tissue, ethanolamine has also been demonstrated to be converted into amino acids, which in turn were incorporated into hepatic proteins. Hepatic ethanolamine was methylated to choline and converted to serine. All 3 compounds were incorporated into hepatic phospholipids. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 4:783]**PEER REVIEWED**
  • 2-Aminoethanol metabolism occurs via partial deamination in the body to form ethylene glycol, which is then partially oxidized to oxalic acid. [Sheftel, V.O.; Indirect Food Additives and Polymers. Migration and Toxicology. Lewis Publishers, Boca Raton, FL. 2000., p. 661]**PEER REVIEWED**
  • It was suggested that the main metabolic pathway for ethanolamine in rats involves its incorporation into phospholipids, presumably via exchange with serine in phosphatidylserine, resulting in the formation of phosphatidylethanolamine. The incorporation of 14C-ethanolamine into ethanolamine phosphoglycerides in liver, heart and brain has been extensively studied and is thought to occur via the CDP-ethanolamine pathway or by a base exchange reaction. [Snyder, R. (ed.). Ethyl Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 425]**PEER REVIEWED**
  • Labeled MEA was administered ip to adult female rats, the rats were sacrificed, and incorporation of MEA into phopholipids was traced in the liver, the blood, and the brain. /Investigators discovered that MEA was converted to phosphatidylethanolamine in all the tissues. However, the step-wise methylation of phosphatidylethanolamine that converts it to phosphatidylcholine, which occurs rapidly in the liver and less rapidly in extrahepatic tissues, did not occur at all in the brain. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • Labeled purified MEA from an unspecified source and demosrated a coenzyme-B12-dependent ethanolamine deaminase mediated conversion of MEA to acetaldehyde and ammonia. /Investigators/ administered MEA intraperitoneally to rats and observed an increase in blood urea and brain glutamine. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**
  • Investigators: labeled MEA and administered it in feed to rats. They detected labeled acetate in the urine of rats. They suggested that MEA is phosphorylated by ATP in vivo, converted to acetaldehyde, ammonia, and inorganic phosphate and then the acetaldehyde is oxidized to acetate. [Christian M, ed; J American College of Toxicology 2 (7): 183-226 (1983) ]**PEER REVIEWED**

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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.

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Web page last updated on May 14, 2008