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National Research Council (US) Committee on Toxicology. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2. Washington (DC): National Academies Press (US); 1984.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2.

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Chemical formula:C2H7NO
Molecular weight:61.08
Chemical Names:2-Aminoethanol, ethylolamine, ß-aminoethyl alcohol, glycinol, 2-hydroxyethylamine, ß-hydroxyethylamine, monoethylamine
Synonyms:Olamine, colamine
CAS number:141-43-5
Melting point:10.5°C
Boiling point:170.5°C (760 mm Hg)
Flash point (open cup):200°F
Specific gravity:1.0179
Vapor pressure:0.4 mm Hg (20°C)
Vapor density:2.1 (air = 1)
Solubility in water:Complete
Odor threshold (sensation):2.6 ppm (Weeks et al., 1960)
Odor threshold (describable):25 ppm (Weeks et al., 1960)
General characteristics:Colorless liquid with mildly ammoniacal odor and relatively strong base
Conversion factors:1 ppm = 2.5 mg/m3
1 mg/m3 = 0.4 ppm


Ethanolamine is used to remove carbon dioxide from submarines. It is also used to scrub natural gas; as a dispersant for agricultural products; as a softening agent for hides; as an accelerator (after reaction with other substances) in the production of antibiotics, polishes, and waving solutions for hair; as a corrosion inhibitor; as a rubber accelerator; an intermediate in the production of emulsifiers, soaps, and detergents; and in some hair-care products. Dow, Olin, Texaco, and Union Carbide are the primary producers in the United States. Ethanolamine may contain isopropylamine, diethanolamine, triethanolamine, water, and ammonia.



The I.G. Elberfeld Toxicology Index of 1931, as quoted by Browning (1953), stated that pure ethanolamine produced marked redness and infiltration when it was applied to human skin on gauze and allowed to remain for 1.5 h. There is little other information on the effects of ethanolamine in man. An anonymous report in Bioenvironmental Safety News Letter (1972) described a case in which “a drop of amine fell” into the right eye of a sailor aboard a submarine. Within a minute, he was able to get to an eye bath, and he flushed his eye for 30 min. He had prompt medical attention, but vision in his right eye deteriorated from 20/20 to 20/200. The report stated that “he will have partial permanent disability.” The same report referred to an earlier, similar incident.

Paustovskaia et al. (1977) stated that “persons working in conditions of increased concentrations of derivatives of cyclo- and dicyclohexylamine and MEA inhibitors of atmospheric corrosion of metals frequently showed changes of the central nervous system, myocardium and hepatobiliary system. Changes in the heart and liver result from the toxic effect of amine derivations on the tissues and also of indirect influence via the central nervous system. Estimation of lactic dehydrogenase isoenzymes is a valuable differential-diagnostic index of myocardial and hepatic pathology due to the effect of amines of the polymethylene series.”*

The maximal permissible concentration of ethanolamine suggested by Sidorov and imofeevskaya (1979) was 0.5 mg/m3 (approximately 0.2 ppm). They stated that workers exposed to ethanolamine at concentrations of greater than 1 mg/m3 suffer from chronic bronchitis, disorders of the liver, asthenic syndrome, and dystonia.

No controlled-exposure or epidemiologic studies with ethanolamine have been reported.


LD50 values are given in Table 4. Grant (1962) referred to Carpenter and Smyth (1946) and stated that a drop of ethanolamine applied to rabbit eyes causes injury similar to that caused by ammonia, but slightly less severe (graded 9 on a scale of 1-10 after 24 h). Union Carbide Corporation (1970) reported that the dermal LD50 of ethanolamine in rabbits is 1.00 ml/kg (24-h covered exposure). It was judged a moderate primary skin irritant, on the basis of the response to application of 0.01-ml amounts to uncovered rabbit skin 24 h later. Hinglais (1947) reported that ethanolamine had considerable necrotic action on the skin.

TABLE 4. LD50 Values of Ethanolamine.


LD50 Values of Ethanolamine.

In a study of inhalation toxicity, Sidorov et al. (1968) exposed mice and cats to vapors of ethanolamine (heated to 80°C) for 2 h. The maximal vapor and condensation aerosol concentration achieved was 970 ppm. The cats “displayed vomiting tendencies.”* No other signs were noted. A single 8-h exposure to “concentrated vapors” did not kill any of six rats (Union Carbide Corporation, 1970). Guinea pigs survived a 15-min exposure to ethanolamine at 193 ppm, but four of six died after 1-h exposure at 233 ppm (Treon et al., 1957).

Smyth et al. (1951) obtained the following results in a 90-d dietary feeding study in rats in which the minimal daily dose was 160 mg/kg and the maximal, 2,670 mg/kg:

Maximal daily dose with no effect:320 mg/kg
Minimal daily dose that produced altered liver or kidney weight:640 mg/kg
Minimal daily dose that produced histopathologic lesions and deaths:1,280 mg/kg

Investigators at the Kettering Laboratory (Treon et al., 1957) conducted a series of animal inhalation exposures to ethanolamine. The exact amount of free ethanolamine delivered to the animals is unknown, because carbon dioxide in the stream of dried air converted some of the ethanolamine to a carbonate. Dogs and cats survived concentrations of 990 ppm for 7 h on each of four consecutive days. Rats, rabbits, and mice were less susceptible than guinea pigs, but more suspectible than cats or dogs. Of 61 animals, 60 survived exposure at either 104 or 108 ppm for 7 h on each of five consecutive days. All but one of 26 mice survived exposure at 51 ppm for 7 h on each of 25 d over 5 wk. At autopsy, the dogs and cats appeared normal. Animals of the other species that died showed acute pulmonary irritation. The survivors had acute bronchitis and pneumonia superimposed on the pulmonary lesions.

Rats, guinea pigs, and dogs were exposed to ethanolamine for 24 h/d for 1-90 d at mean concentrations of 5-102 ppm (Weeks et al., 1960). High concentrations (66-102 ppm in dogs, 66-75 ppm in rodents) for 30 d caused extensive damage (to skin, liver, and kidney) and some deaths. Dogs exposed at 102 ppm showed some biochemical and hematologic changes; these changes were not seen in the other animals. Intermediate concentrations (12-26 ppm) for 90 d caused no fatalities during the 90-d study. Dogs exposed at 12 or 26 ppm and rodents exposed at 12-15 ppm became lethargic early in the study; the dogs recovered, but the rodents did not. The skin of all animals became irritated. Male dogs and immature rats of both sexes were exposed at 5 or 6 ppm for 40 d (rats) or 60 d (dogs). Some decrease in activity was observed. Skin irritation was also noted, although much less than in the animals exposed at high concentrations.

No data were found on chronic, carcinogenic, teratogenic, or reproductive effects of exposure to ethanolamine. This compound does not appear to be mutagenic in the Salmonella typhimurium reverse-mutation bioassay with and without S-9 using strains TA 1535 and TA 100 (Hedenstedt, 1978). Inoue et al. (1982) reported that ethanolamine was very toxic at 500 μg/ml in a cell-transformation assay; it did not produce any morphologic transformation at 25-500 μg/L.


Ethanolamine is a normal constituent of mammalian urine (Table 5), and 6-48% of ethanolamine given to rats orally is recovered in the urine (Luck and Wilcox, 1953). In rats, 8 h after an intraperitoneal injection of 14C-labeled ethanolamine, 54% of the 14C was found in the liver, spleen, kidneys, brain, and diaphragm, and 11.5% was accounted for as expired 14CO2. The liver contained approximately 50% of the 14C, nearly all in the lipid fraction. The main metabolic pathway is incorporation into the phospholipid fraction. The maximal rate of respiratory excretion of14CO2 was observed between 1 and 2 h after administration; that indicates rapid oxidation of ethanolamine. The rate of excretion then dropped rapidly, and that suggests either dilution of the compound by endogenous ethanolamine or conversion of ethanolamine into compounds not readily catabolized (Taylor and Richardson, 1967).

TABLE 5. Urinary Excretion of Ethanolamine .


Urinary Excretion of Ethanolamine .

Weeks et al. (1960) cited unpublished data from the Mellon Institute that showed that, in dogs treated with Nembutal (sodium pentobarbital), ethanolamine either stimulated (at low doses) or depressed (at lethal doses) the central nervous system.


The ACGIH (1983) recommended an 8-h TLV-TWA of 3 ppm and a 15-min TLV-STEL of 6 ppm. The OSHA (1983) standard is an 8-h PEL (permissible exposure limit) of 3 ppm. Sidorov and Timofeevskaya (1979) suggested an occupational exposure limit of 0.2 ppm.


The toxicity of ethanolamine was studied by the Committee on Toxicology in 1967. The study of Weeks et al. (1960) indicated that skin and eye irritation and immediate signs of irritability and restlessness followed by central nervous system depression are the major adverse effects seen in unanesthetized experimental animals exposed to ethanolamine at 12-26 ppm for 24 h. Continuous exposure at 5-6 ppm produced some behavioral changes in animals, but only after 2-3 wk of exposure. On the basis of these data, the commitee believes that the previous recommendations are adequate. However, we note that additional data could help to refine these exposure limits. For example, reports concerning dose- and time-dependent central nervous system changes after ethanolamine exposure need to be confirmed and elaborated. It would be desirable to have better quantitative data on these changes. Although behavioral-toxicology studies are relatively new and their results are difficult to interpret, some of them might be incorporated into the studies suggested above or run separately. It would be most useful if more data on accidental exposure to humans or 40-h/wk occupational exposure could be gathered, including estimated concentrations, symptoms (if any), clinical findings, and sequelae.

The present Committee's recommended EELs and CEL for ethanolamine and the limits proposed in 1967 are shown below.

60-min EEL50 ppm50 ppm
24-h EEL3 ppm3 ppm
90-d CEL0.5 ppm0.5 ppm


  • American Conference of Governmental Industrial Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances and Physical Agents in the Work Environment with Intended Changes for 1983-1984. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. 93 p.
  • Bioenvironmental Safety News Letter. 1972. Second monoethanolamine injury reported. p.40 (April).
  • Browning, E. 1953. Toxicity of Industrial Organic Solvents. New York: Chemical Publishing Co. 411 p.
  • Carpenter, C.P., and Smyth, H.F., Jr. 1946. Chemical burns of the rabbit-cornea. Am. J. Ophthalmol. 29:1363-1372. [PubMed: 20276971]
  • Grant, W.M. 1962. Toxicology of the Eye. Springfield, Ill.: Charles C Thomas. 641 p.
  • Hartung, R., and Cornish, H.H. 1968. Cholinesterase inhibition in the acute toxicity of alkyl-substituted 2-aminoethanols. Toxicol. Appl. Pharmacol. 12:486-494.
  • Hedenstedt, A. 1978. Mutagenicity screening of industrial chemicals: Seven aliphatic amines and one amide tested in the Salmonella/ microsomal assay. Mutat. Res. 53:198-199 , abstr. no. 90.
  • Hinglais, H. 1947. Method of measuring irritation and necrosis produced by chemical derivatives [amino alcohols] on the skin and mucous membranes. Produits Pharm. 2:445-449.
  • Inoue, K., Sunakawa, T., Okamoto, K., and Tanaka, Y. 1982. Mutagenicity tests and in vitro transformation assays on triethanolamine. Mutat. Res. 101:305-313. [PubMed: 6810163]
  • Luck, J.M., and Wilcox, A. 1953. On determination of ethanolamine in urine and factors affecting its daily output. J. Biol. Chem. 205:859-866. [PubMed: 13129264]
  • Occupational Safety and Health Administration. 1983. Toxic and Hazardous Substances. Air contaminants. 29CFR 1910.1000.
  • Paustovskaia, V.V., Krashniuk, E.P., Onikienko, F.A., and Vasiliuk, L.M. 1977. Effect of working conditions on health of persons working with inhibitors of atmospheric corrosion of metals. Vrach Delo. Number 4: 121-124. [PubMed: 860484]
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  • Sidorov, K.K., and Timofeevskaya, L.A. 1979. Data for substantiation of the maximum permissible concentration of monoethanolamine in the working environment. Gig. Tr. Prof. Zabol. No. 9:55.
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  • Sutton, W.L. 1963. Aliphatic and alicyclic amines: Ethanolamine (2-aminoethanol). In Patty, F.A., editor; , ed. Industrial Hygiene and Toxicology. Vol. II. Toxicology, Fassett, D.W., editor; , and Irish, D.D., editor. , eds. 2nd rev. ed. New York: Interscience Publishers. p.2064-2066.
  • Taylor, R.J., Jr., and Richardson, K.E. 1967. Ethanolamine metabolism in the rat. Proc. Soc. Exp. Biol. Med. 124:247-252. [PubMed: 6017778]
  • Treon, J.F., Cleveland, F.P., Stemmer, K.L., Cappel, J., Larson, E.E., and Shaffer, F. 1957. Toxicity of monoethanolamine in air. Cincinnati: Kettering Laboratory.
  • Union Carbide Corporation. 1970. Ethanolamines. [Technical booklet] New York: Union Carbide Corporation, Chemicals and Plastics. p. 30.
  • Vernot, E.H., MacEwen, J.D., Haun, C.C., and Kinkead, E.R. 1977. Acute toxicity and skin corrosion data for some organic and inorganic compounds and aqueous solutions. Toxicol. Appl. Pharmacol. 42:417-423. [PubMed: 595018]
  • Weeks, M.H., Downing, T.O., Musselman, N.P., Carson, T.R., and Groff, W.A., 1960. The effects of continuous exposure of animals to ethanolamine vapor. Am. Ind. Hyg. Assoc. J. 21:374-381. [PubMed: 13783714]




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Bookshelf ID: NBK208294


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