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8
Monoethanolamine

This chapter summarizes the relevant toxicologic studies on monoethanolamine (MEA). Selected chemical and physical properties, toxicokinetic and mechanistic data, and inhalation exposure levels from the National Research Council (NRC) and other agencies are also presented. The subcommittee considered all of that information in its evaluation of the Navy’s current and proposed 1-hour (h), 24-h, and 90-day exposure guidance levels for MEA. The subcommittee’s recommendations for MEA exposure levels are provided at the conclusion of this chapter along with a discussion of the adequacy of the data for defining those levels and the research needed to fill the remaining data gaps.

PHYSICAL AND CHEMICAL PROPERTIES

MEA is a viscous, hygroscopic liquid (Budavari et al. 1989). Selected physical and chemical properties are summarized in Table 8-1.

OCCURRENCE AND USE

MEA has a variety of uses. It is used as a scrubbing agent to remove carbon dioxide and hydrogen sulfide from gases; as a reagent in the synthesis of surface active agents and antibiotics; as a component in polishes and emulsifiers; as a softening agent in the tanning industry; and as an agent to disperse agricultural chemicals (Budavari et al. 1989). MEA is used along with diethanolamine in cosmetic products as an emulsifier, thickener, wetting agent, detergent, and alkalizing agent (CIR 1983). Ethanolamines, including MEA, are used in synthetic and semisynthetic machining and



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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants 8 Monoethanolamine This chapter summarizes the relevant toxicologic studies on monoethanolamine (MEA). Selected chemical and physical properties, toxicokinetic and mechanistic data, and inhalation exposure levels from the National Research Council (NRC) and other agencies are also presented. The subcommittee considered all of that information in its evaluation of the Navy’s current and proposed 1-hour (h), 24-h, and 90-day exposure guidance levels for MEA. The subcommittee’s recommendations for MEA exposure levels are provided at the conclusion of this chapter along with a discussion of the adequacy of the data for defining those levels and the research needed to fill the remaining data gaps. PHYSICAL AND CHEMICAL PROPERTIES MEA is a viscous, hygroscopic liquid (Budavari et al. 1989). Selected physical and chemical properties are summarized in Table 8-1. OCCURRENCE AND USE MEA has a variety of uses. It is used as a scrubbing agent to remove carbon dioxide and hydrogen sulfide from gases; as a reagent in the synthesis of surface active agents and antibiotics; as a component in polishes and emulsifiers; as a softening agent in the tanning industry; and as an agent to disperse agricultural chemicals (Budavari et al. 1989). MEA is used along with diethanolamine in cosmetic products as an emulsifier, thickener, wetting agent, detergent, and alkalizing agent (CIR 1983). Ethanolamines, including MEA, are used in synthetic and semisynthetic machining and

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants TABLE 8-1 Physical and Chemical Data on Monoethanolaminea Synonyms Aminoethanol, β-aminoethanol, 2-amino-1-ethanol, β-aminoethyl alcohol, 1-amino-2-hydroxyethane, ethanolamine, colamine, β-ethanolamine, ethylolamine, glycinol, 2-hydroxyethanamine, β-hydroxyethylamine, 2-hydroxyethylamine, olamine CAS registry number 141-43-5 Molecular formula HOCH2CH2NH2 Molecular weight 61.08 Boiling point 170.8°C Melting point 10.3°C Flash point 195°C Explosive limits 5.5% to 17% Specific gravity 1.0117 at 25°C/4°C Vapor pressure 0.404 mmHg at 25°C Solubility Soluble in water, methanol, and acetone Conversion factors 1 ppm = 2.5 mg/m3; 1 mg/m3 = 0.4 ppm aData on explosive limits and vapor pressure were taken from HSDB (2003); all other data were taken from Budavari et al. (1989). Abbreviations: mg/m3, milligrams per cubic meter; mmHg, millimeters of mercury; ppm, parts per million. grinding fluids as corrosion inhibitors or to adjust pH (Kenyon et al. 1993). Analysis of a selection of machining and grinding fluids identified MEA at concentrations generally less than the detection limit (0.2 micrograms per milliliter [μg/mL]) to 2%; one product contained 11% MEA (Kenyon et al. 1993). On board submarines, MEA is used in the ventilation system scrubbers to remove carbon dioxide from the air. No atmospheric measurements of MEA on board submarines have been reported. SUMMARY OF TOXICITY At high concentrations, airborne MEA is an irritant to the skin, eyes, and respiratory tract of laboratory animals. Continuous exposure to high concentrations of MEA for long periods of time has been reported to pro-

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants duce lethargy in laboratory animals. High oral doses of MEA have been reported to result in organ weight and histopathologic changes in the liver and kidneys of laboratory animals; the effects observed suggest that MEA may interfere with lipid metabolism. The liver is the primary site of metabolism for MEA, and metabolites of MEA are found in the urine of laboratory animals. MEA is an intermediate in the formation of phospholipids and choline, and it is formed endogenously from serine. MEA is excreted in the urine of unexposed humans and animals. Genotoxicity studies with MEA have been largely negative for mutagenic and clastogenic effects. Unlike diethanolamine, MEA has not been found to form a stable nitrosamine. No medical case reports or epidemiologic studies were identified during this review of MEA. Data are lacking for several toxicity end points, including chronic exposure effects, carcinogenicity, and male reproductive effects. Effects in Humans Accidental Exposures No relevant information was identified. Experimental Studies Weeks et al. (1960) reported that volunteers who smelled MEA vapor described the odor as ammoniacal, musty, or foreign; some volunteers were unable to characterize the odor. The MEA concentration detectable for 50% of a group of human volunteers (n = 12) was 2.6 parts per million (ppm) (95% confidence interval [CI] = 2-3.3 ppm) (Weeks et al. 1960). Volunteers detected the MEA by means of sensation rather than odor; a describable odor was noted at about 25 ppm (Weeks et al. 1960). Occupational and Epidemiologic Studies In a National Institute for Occupational Safety and Health (NIOSH) health hazard evaluation report (NIOSH 1993), the authors noted in a summary paragraph about MEA that “no systemic effects from industrial exposure have been reported.” A similar observation was made by Beard and Noe (1981). No other relevant information was identified.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants Effects in Animals Acute Toxicity The LC50 (concentration lethal to 50% of subjects) of MEA is estimated to be greater than its theoretical saturated vapor concentration (520 ppm) on the basis that no mortality was found in rats exposed to saturated MEA vapor for 6 h (Knaak et al. 1997). The acute oral toxicity (LD50) of MEA in rats is in the range of 1,720-2,740 milligrams per kilogram (mg/kg) (Smyth et al. 1951; CIR 1983). The Cosmetic Ingredient Review (CIR 1983) provided the following oral LD50 values for other species: mouse, 700-1,500 mg/kg; rabbit, 1,000-2,900 mg/kg; and guinea pig, 600 mg/kg. The dermal LD50 for MEA in rabbits was reported to be 1 g/kg (ACGIH 2001). MEA at concentrations of 1%, 5%, and 10% was tested in vivo and in vitro for histopathologic evidence of irritation using the skin of C3H mice (Helman et al. 1986). Although no skin lesions were observed, lactate dehydrogenase (LDH) values were elevated in the culture medium for skin discs exposed to MEA at 5% or 10% in vitro. Leakage of LDH from the skin discs was interpreted by the authors to suggest mild toxicity to mouse skin (Helman et al. 1986). Aqueous solutions at 25% were corrosive to rabbit skin in vivo (Knaak et al. 1997). Undiluted MEA is considered severely irritating to the eye (Knaak et al. 1997). No animal studies for skin sensitization or allergenicity have been reported. Repeated Exposures and Subchronic Toxicity Treon et al. (1957) exposed dogs, cats, guinea pigs, mice, and rats to MEA vapor and aerosol using a number of exposure scenarios that included 793 mg per cubic meter (m3) (primarily as an aerosol) for 7 h per day for 5 days or 126 mg/m3 (primarily as a vapor) for 7 h per day for 25 days over a 30-day period. The authors noted that the only effect observed was difficult breathing in guinea pigs exposed at 260 mg/m3 or greater. Timofievskaya (1962) exposed rats to MEA at 80-160 ppm via inhalation for 5 h per day for up to 6 months. Decreased body weights, altered hematology, altered urine chemistries, and altered hippuric acid synthesis were observed. The authors concluded that the liver and kidneys were target organs.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants Continuous inhalation exposure studies (24 h per day, 7 days per week) were conducted with MEA using dogs, guinea pigs, and rats (Weeks et al. 1960). Groups of three male beagle dogs were continuously exposed to MEA at 6, 12, 26, or 102 ppm for 60, 90, 90, or 30 days, respectively (Weeks et al. 1960). Because no attempt was made to prevent carbon dioxide (CO2) in the exposure chambers from binding to MEA, CO2 concentrations in the test chambers were slightly lower than in the control chambers. At 102 ppm, clinical signs were marked and included evidence of skin irritation, rales, and tremors; MEA condensed on all surfaces, causing the haircoats of the dogs to become wet, matted, and greasy. On the first day of MEA exposure, the dogs showed their immediate discomfort through behaviors, including an uneasy demeanor, scratching at the chamber door, panting, muzzle licking, and vigorous head shaking, which were followed by salivation and vomiting within a few hours. Within 24 h of initiation of exposure, the dogs responded poorly to attempts to attract their attention, and they were lethargic by 48 h. Head shaking during the first 4 days of exposure resulted in hematomas at the base of the ears. Skin irritation involving the scrotum and sternum was observed by the fourth day of exposure and became more generalized and more severe as the exposure period progressed. One of the dogs in the treatment group died after 25 days of exposure. At necropsy, skin irritation was the only consistent change. Microscopic examination of various tissues showed cloudy swelling of hepatocytes, increased Kupffer cell pigmentation, and vascular congestion in the liver. Kidney tubules also showed evidence of cloudy swelling and hyaline droplet formation. The nasal turbinate mucosa was eroded in some areas, and plasma cell infiltrates were present in other areas. The lungs of the dog that died had small foci of hemorrhage and pneumonitis. Clinical chemistry changes included decreases in albumin and increases in globulin in the three exposed dogs. Hematologic changes included increases in white blood cell count, changes in white blood cell ratios, and decreases in hemoglobin and hematocrit values in the three exposed dogs. At 26 ppm, dogs showed immediate signs of restlessness and discomfort. They were more irritable than the controls, and after a few days they were less alert and appeared lethargic. Their haircoats became wet, greasy, and matted. The dogs’ skin became irritated and developed small ulcers at floor contact points in less than a week’s time. At 12 ppm, there were no behavioral effects observed immediately at the beginning of the exposure period or after 1 h or 24 h of exposure to MEA. However, skin irritation was observed, and animals became lethargic after 3 weeks of exposure. At 6 ppm,

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants there were slight decreases in alertness and activity, and there was some skin irritation after 2-3 weeks of exposure. No significant pathology, clinical chemistry, or hematology changes were seen at exposure levels below 102 ppm. A group of 22 male guinea pigs was exposed to MEA at 75 ppm continuously for 24 days, and a group of 30 male guinea pigs was exposed at 15 ppm continuously for 90 days (Weeks et al. 1960). At 75 ppm, the animals were restless, irritable, and obviously uncomfortable. They initially showed increased activity, but as the exposure period lengthened, they showed decreased activity and increased water consumption. Evidence of skin irritation was observed. An unstated level of mortality was seen. Microscopic examination of tissues showed fatty changes in the liver, slight cloudy swelling in the liver and kidneys, increased lymphocyte infiltration in the lungs, and decreased spermatogenesis. At 15 ppm, animals became less active after about 3 days of exposure and were definitely lethargic after 10 days. Weight gain was decreased about 10%, and water consumption increased 40%. No other changes were reported for animals in the 15-ppm group. A group of 45 female rats was continuously exposed to MEA at 66 ppm for 30 days, a second group of 45 female rats was continuously exposed at 12 ppm for 90 days, and a third group of 20 male and female rats was continuously exposed at 5 ppm for 40 days (Weeks et al. 1960). The effects observed in rats exposed at the high and intermediate exposure concentrations were similar to those observed in guinea pigs similarly exposed. Microscopic examination of the tissues of rats exposed to MEA at 66 ppm showed fatty changes in the liver, slight cloudy swelling in the liver and kidneys, increased lymphocyte infiltration of the lungs, and patchy pneumonitis. At 5 ppm, all rats showed pelt discoloration after 12 days and transitory hair loss over the head and back after 3 weeks. Slowness in movement also was observed after 3 weeks of exposure at 5 ppm. The body-weight gains of the rats exposed at 5 ppm were not different from those of the control group. No gross or microscopic changes were observed in the organs of rats exposed at 5 or 12 ppm. In a study reported by Smyth et al. (1951), rats were not affected by MEA in their diets when fed 320 mg/kg per day for 90 days. However, liver and kidney weights were increased at 640 mg/kg per day, and mortality was observed in animals that consumed 1,280 mg/kg per day.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants Chronic Toxicity No relevant studies were identified. Reproductive Toxicity in Males The testes of two dogs that survived exposure to MEA at 102 ppm for 30 days showed decreased spermatogenesis on histologic examination (Weeks et al. 1960). The testes of a third dog that died after exposure at 102 ppm also showed decreased sperm formation (Weeks et al. 1960). Spermatogenesis appeared to be decreased in an unspecified number of guinea pigs exposed to MEA at 75 ppm (Weeks et al. 1960). Due to the limited amount of information available, the significance of the findings is uncertain. Immunotoxicity Repeated-insult skin patch tests for allergenicity in human volunteers have shown negative results (Knaak et al. 1997). The results provided no evidence of hypersensitivity to MEA. No other immunotoxicity studies were identified in the literature. Genotoxicity MEA provided no evidence of mutagenicity when tested with strains TA98, TA100, TA1535, TA1537 of Salmonella typhimurium with or without activation by Aroclor 1254 stimulated rat or hamster S9 liver fractions (Mortelsmans et al. 1986). The Hazardous Substances Data Bank (HSDB 2003) cites a Russian study indicating that MEA is a weak inducer of chromosome breaks in cultured human lymphocytes. Dean et al. (1985) found no mutagenic or clastogenic effects in studies of MEA in Escherichia coli WP2 tyr, Sacchraromyces cerevisiae, and a rat liver cell chromosomal aberration assay. Inoue et al. (1982) found no evidence of genotoxicity in an in vitro hamster embryo transformation assay.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants Carcinogenicity No relevant studies were identified. TOXICOKINETIC AND MECHANISTIC CONSIDERATIONS MEA is the only endogenously occurring ethanolamine formed by mammalian metabolic systems. MEA is formed from serine and is an intermediate in the formation of phospholipids and choline. MEA is naturally excreted in the urine of unexposed humans (Dent and Walshe 1953; HSDB 2003). The average urinary excretion rates in men and women are 0.162 mg/kg per day and 0.492 mg/kg per day, respectively (HSDB 2003). The systemic distribution and metabolism of [14C]-labeled MEA was studied in athymic nude mice following application to their skin or application to human skin grafted onto the mice (Klain et al. 1985). Extensive metabolism of the MEA that penetrated the skin was observed; 24% of the applied radioactive dose was found in the liver, which was a major site of metabolism. Radiolabel was found in all organs examined, including the kidneys (2.53% of dose), lungs (0.55% of dose), brain (0.27% of dose), and heart (0.15% of dose). Hepatic ethanolamine, choline, and serine were highly radioactive, as were hepatic proteins. Of the topical radioactive dose, 18% was metabolized to 14CO2, and 4.6% was excreted in the urine over 24 h. Urinary metabolites included glycine, serine, choline, and uric acid. Radiolabel was found in expired air 5 minutes after intraperitoneal injection of [14C]-labeled MEA (Klain et al. 1985). The distribution and metabolism of MEA following intraperitan eal injection was similar to that seen following dermal application (Taylor and Richardson 1967). INHALATION EXPOSURE LEVELS FROM THE NRC AND OTHER ORGANIZATIONS Several organizations have established or proposed inhalation exposure limits or guidelines for MEA. Selected values are summarized in Table 8-2.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants TABLE 8-2 Selected Inhalation Exposure Levels for Monoethanolamine from NRC and Other Agenciesa Organization Type of Level Exposure Level (ppm) Reference Occupational       ACGIH TLV-TWA 3 ACGIH 2002   TLV-STEL 6   NIOSH REL-TWA 3 NIOSH 2004   REL-STEL 6   OSHA PEL-TWA 3 29 CFR       1910.1000 Submarine       NRC EEGL   NRC 1984   1 h 50     24 h 3     CEGL       90 days 0.5   aThe comparability of EEGLs and CEGLs with occupational and public health standards or guidance levels is discussed in Chapter 1, section “Comparison to Other Regulatory Standards or Guidance Levels.” Abbreviations: ACGIH, American Conference of Governmental Industrial Hygienists; CEGL, continuous exposure guidance levels; EEGL, emergency exposure guidance level; h, hour; NIOSH, National Institute for Occupational Safety and Health; NRC, National Research Council; OSHA, Occupational Safety and Health Administration; PEL, permissible exposure limit; ppm, parts per million; REL, recommended exposure limit; STEL, short-term exposure limit; TLV, Threshold Limit Value; TWA, time-weighted average. SUBCOMMITTEE RECOMMENDATIONS The subcommittee’s recommendations for EEGL and CEGL values for MEA are summarized in Table 8-3. The U.S. Navy values are provided for comparison. 1-Hour EEGL In recommending exposure guidance levels for MEA, the subcommittee considered several issues. There is a limited amount of information about the effects associated with the inhalation of MEA. The information

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants TABLE 8-3 Emergency and Continuous Exposure Guidance Levels for Monoethanolamine (ppm) Exposure Level U.S. Navy Values NRC Recommended Current Proposed Values EEGL           1 h 50 6 4   24 h 3 3 4 CEGL           90 days 0.5 0.5 0.5 Abbreviations: CEGL, continuous exposure guidance level; EEGL, emergency exposure guidance level; h, hour; NRC, National Research Council; ppm, parts per million. that is available is incomplete when compared with modern protocols used for inhalation toxicity studies. Because MEA was deposited on the skin of test animals during inhalation exposures, absorption of MEA through the skin or ingestion of MEA due to grooming might have contributed to the systemic effects observed in some of the studies. Data on MEA exposures in humans via inhalation are not available for use in determining exposure guidance levels. Consequently, there is a significant amount of uncertainty in identifying exposure guidance levels for MEA in submarine atmospheres. Uncertainty in interpreting clinical sign information provided in the critical study further complicates the extrapolation of animal data for developing exposure levels. The only study that provides relevant information for extrapolation is Weeks et al. (1960). In that study, MEA vapor apparently condensed on the inside of the inhalation chamber walls and other surfaces and was deposited in sufficient concentration on the haircoats of the test animals to make the hair and skin wet, greasy to the touch, and matted. The deposition of MEA on the test animals was associated with skin irritation affecting dogs, rats, and guinea pigs. As the test concentrations of MEA decreased, the onset time to grossly observable deposition and skin irritation increased. At 26 ppm, dogs showed immediate skin and behavioral changes. At 12 ppm, dogs and rats showed no effects at 1 and 24 h, but showed skin and behavioral changes similar to those seen at 26 ppm after 2-3 weeks of continuous exposure. It is unlikely that surface deposition of MEA would occur in the submarine environment or that submarine crew would tolerate the accumulation of MEA on their skin. The clothing worn by the crew would most likely protect the skin from significant MEA

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants deposition, and the crew would most likely remove MEA deposited on their skin by washing. Along with the reported deposition of MEA on the skin and the signs of skin irritation, test animals were observed to be less alert and to have reduced activity levels. Because the test animals were exposed nearly continuously, observations of behavioral effects were presumably made through the windows in the inhalation chamber walls. It is difficult to know precisely how to interpret the results reported by Weeks et al. (1960), because no follow-up behavioral examinations were conducted. The behavioral effects may have been a secondary consequence of the skin irritation observed; affected animals might have reduced their activity levels because of fatigue associated with chronic dermal irritation. Alternatively, the behavioral changes might have been primary effects. The subcommittee made the conservative assumption that reduced alertness and reduced activity levels were primary effects that could be used for determining exposure guidance levels. To determine the 1-h EEGL for MEA, the 12-ppm continuous exposure in dogs conducted by Weeks et al. (1960) was chosen as the most appropriate exposure scenario for extrapolation. Although the mode of action of MEA is unknown, no effects were observed after exposure at 12 ppm for 1 or 24 h. At 12 ppm, effects associated with MEA were observed after 3 weeks of continuous exposure. Because there was little variation in the responses of dogs, rats, and guinea pigs at similar MEA exposure levels, an interspecies uncertainty factor of 3 was applied. No intraspecies uncertainty factor was applied, because little variability is expected in the responses of submarine crew members to deposition of MEA on the skin. Also, dermal allergenicity studies in human volunteers did not result in sensitization (Knaak et al. 1997), indicating that the effects of skin contact with MEA are unlikely to vary among humans. Application of the uncertainty factor of 3 to the no-effect concentration of 12 ppm results in a 1-h EEGL for MEA vapor of 4 ppm. 24-Hour EEGL Because the 12-ppm continuous-exposure study in dogs did not result in effects until after 2-3 weeks of exposure (Weeks et al. 1960), there should not be any differences in the toxicologic results of exposures to MEA lasting 1 or 24 h. Therefore, extrapolating for the 24-h EEGL results in the same concentration (4 ppm) as was recommended above for the 1-h EEGL.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants 90-Day CEGL Weeks et al. (1960) did not provide a no-effect level for repeated inhalation exposures of greater than 2-3 weeks duration. To determine a 90-day CEGL, the exposure scenario that resulted in the lowest-effect level was chosen for extrapolation. Rats exposed to MEA at 5 ppm via inhalation for 40 days showed pelt discoloration after 12 days of exposure. Transitory hair loss over the head and back and slowness in movement were observed after 3 weeks of exposure. The interspecies uncertainty factor was set at 3. Because exposure at 5 ppm resulted in minimally adverse effects, a LOAEL-to-NOAEL uncertainty factor of 3 was used for calculating the CEGL. The 90-day CEGL resulting from the application of a total uncertainty factor of 10 to the rat low-effect level of 5 ppm is 0.5 ppm. That value is an approximate order of magnitude less than that associated with behavioral changes in rats and dogs and is thus considered protective. DATA ADEQUACY AND RESEARCH NEEDS There is a paucity of data available for determining the effects of MEA following inhalation exposure. The available studies are considered incomplete because little information is provided about histologic, hematologic, and enzymatic changes that might be produced systemically or in the nasal turbinates following repeated or long-term exposure to MEA. None of the inhalation studies provide a no-effect level useful for direct extrapolation to human exposure conditions. Although MEA does not appear to be genotoxic, no data on carcinogenicity are available for review. Additional short-term studies would be helpful for developing 1- and 24-h exposure limits with greater confidence, because there is insufficient resolution within the available data set to support the development of different values for those time points. Well-designed continuous 90-day and lifetime studies would provide information for developing 90-day exposure limits and for determining the carcinogenic potential of MEA. REFERENCES ACGIH (American Conference of Governmental Industrial Hygienists). 2001. Documentation of the Threshold Limit Values and Biological Exposure Indices, 7th Ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists.

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants ACGIH (American Conference of Governmental Industrial Hygienists). 2002. TLVs & BEIs: Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices-2002. Cincinnati, OH: American Conference of Governmental Industrial Hygienists. Beard, R.R., and J.T. Noe. 1981. Aliphatic and alicyclic amines: Ethanolamine (2-Aminoethanol). Pp. 3168 in Patty's Industrial Hygiene and Toxicology, Vol. 2B. Toxicology, 3rd Rev. Ed., G.D. Clayton, and F.E. Clayton, eds. New York: John Wiley & Sons. Budavari, S., M.J. O’Neil, A. Smith, and P.E. Heckelman, eds. 1989. Pp. 588 in the Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals, 11th Ed. Rahway, NJ: Merck and Co., Inc. CIR (Cosmetic Ingredient Review). 1983. Final Report on the safety assessment of triethanolamine, diethanolamine, and monoethanolamine. J. Am. Coll. Toxicol. 2(7):183-235. Dean, D.J., T.M. Brooks, G. Hodson-Walker, and D.H. Hutson. 1985. Genetic toxicology testing of 41 industrial chemicals. Mutat. Res. 153(1-2):57-77. Dent, C.E., and J.M. Walshe. 1953. Primary carcinoma of the liver: Description of a case with ethanolaminuria, a new and obscure metabolic defect. Br. J. Cancer 7(2):166-180. Helman, R.G., J.W. Hall, and J.Y. Kao. 1986. Acute dermal toxicity: in vivo and in vitro comparisons in mice. Fundam. Appl. Toxicol. 7(1):94-100. HSDB (Hazardous Substances Data Bank). 2003. 2-Aminoethanol CASRN 141-43-5. TOXNET, Specialized Information Services, U.S. National Library of Medicine, Bethesda, MD. [Online]. Available: http://toxnet.nlm.nih.gov/cgibin/sis/htmlgen?HSDB [accessed 2003]. Inoue, K., T. Sunakawa, K. Okamoto, and Y. Tanaka. 1982. Mutagenicity test and in vitro transformation assays on triethanolamine. Mutat. Res. 101(4):305-314. Knaak, J.B., H.W. Leung, W.T. Stott, J. Busch, and J. Bilsky. 1997. Toxicology of mono-, di-, and triethanolamine. Rev. Environ. Contam. Toxicol. 149:1-86. Klain, G.J., W.G. Reifenrath, and K.E. Black. 1985. Distribution and metabolism of topically applied ethanolamine. Fundam. Appl. Toxicol. 5(6):S127-S133. Kenyon, E.M., S.K. Hammond, J. Shatkin, S.R. Woskie, M.F. Hallock, and T.J. Smith. 1993. Ethanolamine exposures of workers using machining fluids in the automotive parts manufacturing industry. Appl. Occup. Environ. Hyg. 8(7):655-661. Mortelsmans, K., S. Haworth, T. Lawlor, W. Speck, B. Tainer, and E. Zeiger. 1986. Salmonella mutagenicity tests: II. Results from testing 270 chemicals. Environ. Mutagen. 8(Suppl. 7):1-119. NIOSH (National Institute for Occupational Safety and Health). 1993. Health Hazard Evaluation Report: Fairchild Fashion & Merchandising Group, New York. HETA 93-367-2321. [Online]. Available: http://www.cdc.gov/niosh/hhe/reports/pdfs/1993-0367-2321.pdf [accessed March 31, 2004].

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Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants NIOSH (National Institute for Occupational Safety and Health). 2004. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) 2004-103. National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, Cincinnati, OH. NRC (National Research Council). 1984. Pp. 17-25 in Emergency and Continuous Exposure Guidance Levels for Selected Airborne Contaminants, Vol. 2. Washington, DC: National Academy Press. Smyth, H.F., Jr., C.P. Carpenter, and C.S. Weil. 1951. Range finding toxicity data: List IV. AMA Arch. Ind. Hyg. Occup. Med. 4(2):119-122. Taylor, R.J., and K.E. Richardson. 1967. Ethanolamine metabolism in the rat. Proc. Soc. Exp. Biol. Med. 124(1):247-252. Timofievskaya, L.A. 1962. Toxicologic characteristics of aminoethanol [in Russian]. Toksikol. Nov. Prom. Khim. Vesh. 4:81-91 (as cited by Knaak et al. 1997). Treon, J.F., F.P. Cleveland, K.L. Stemmer, J. Cappel, F. Shaffer, and E.E. Larson. 1957. Toxicity of Monoethanolamine in Air. Kettering Laboratory, University of Cincinnati, Cincinnati, OH (as cited by Knaak et al. 1997). Weeks, M.H., T.O. Downing, N.P. Musselman, T.R. Carson, and W.A. Groff. 1960. The effects of continuous exposure of animals to ethanolamine vapor. Am. Ind. Hyg. Assoc. J. 21:374-381.