National Toxicology Program

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

Names (NTP)

• Dimethylamine
• N-METHYL-METHANAMINE (9CI)

Human Toxicity Excerpts

• Irritation of eyes and throat, sneezing, coughing and dyspnea; pulmonary edema; conjunctivitis; dermatitis; burns of skin and mucous membranes. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 361]**PEER REVIEWED**
  
• ... Vision has become misty and halos have appeared several hr after workmen have been exposed to the vapors of ... amines /incl dimethylamine/ at concn too low to cause discomfort or disability during several hr of exposure. ... The edema of the corneal epithelium, which is principally responsible for the disturbance of vision, clears spontaneously by the next day, but after exceptionally intense exposures the edema and blurring have taken several days to clear and have been accompanied by photophobia and discomfort from roughness of the corneal surface. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 76]**PEER REVIEWED**
  
• Liquid: causes smarting of the skin and first-degree burns on short exposure and may cause secondary burns on long exposure. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5., p. ]**PEER REVIEWED**
  
• Workers in a foundry complaining of breathlessness and choking were found to be exposed to 1-46 mg/cu m dimethylamine in the air. [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. 79]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• ANIMALS EXPOSED TO CONCENTRATED VAPOR SHOW SIGNS OF MUCOUS MEMBRANE AND RESPIRATORY TRACT IRRITATION. EXPOSURES AT SUBLETHAL CONCN MAY RESULT IN TRACHEITIS, BRONCHITIS, PNEUMONITIS AND PULMONARY EDEMA. SKIN CONTACT WITH THE LIQUID CAUSES NECROSIS ... [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 206]**PEER REVIEWED**
  
• ... GROUPS OF 10 RATS, 6 GUINEA PIGS & 1 RABBIT OF EACH SEX PLUS 5 FEMALE MICE & 1 MONKEY WERE GIVEN REPEATED 7-HR DAILY EXPOSURES, 5 DAYS/WK FOR 18-20 WK @ CONCN OF EITHER 183 OR 97 PPM ... CORNEAL INJURY WAS OBSERVED IN GUINEA PIGS & RABBITS AFTER 9 DAYS ... CENTRAL LOBULAR FATTY DEGENERATION & NECROSIS OF PARENCHYMAL CELLS OF THE LIVER ... IN RATS, GUINEA PIGS, RABBITS & MICE. TUBULAR DEGENERATION OF TESTES WAS OBSERVED IN THE MALE RABBIT @ THE HIGHER CONCN & IN THE MALE MONKEY @ THE LOWER CONCN. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 206]**PEER REVIEWED**
  
• ANIMAL TOXICITY HAS BEEN ASCRIBED TO ITS CAUSTIC ACTIONS & TO SYSTEMIC ALKALOSIS. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-106]**PEER REVIEWED**
  
• 5% SOLN DROPPED ONCE ON RABBIT EYE CAUSED HEMORRHAGES IN CONJUNCTIVA, CORNEAL EDEMA, AND SUPERFICIAL OPACITIES. ... A DROP OF UNDILUTED DIMETHYLAMINE PLACED ON RABBIT'S CORNEA, WITH THE LIDS THEN CLOSED AND NO IRRIGATION PERFORMED, CAUSED THE CORNEA TO BECOME WHITISH BLUE & TRANSLUCENT WITHIN FEW SEC, THEN WHITE AS SCLERA IN A MIN ... [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 348]**PEER REVIEWED**
  
• Nitrogenous cmpd were pyrolyzed at 300, 400, 500 and 600 degrees for 3 min, and the mutagenic activities of the pyrolyzates were assayed on Salmonella typhimurium TA98 and TA100 with or without metabolic activation by S9 mix. 14 pyrolyzates, incl dimethylamine, showed mutagenic activity. In the presence of S9 mix, the mutagenic activity began to appear from the pyrolyzate at 400 degrees. The mutagenic pyrolyzates were more active on TA98 than TA100. Some nitrogenous cmpd showed slight mutagenic activity after pyrolysis at 300 degrees for 20 min, although none of the cmpd tested showed any mutagenic activity after pyrolysis at 300 degrees for 3 min. [Ohe T; Mutat Res 101 (3): 175-87 (1982)]**PEER REVIEWED**
  
• Lesions occurring in the respiratory tract of mice after exposure to 10 sensory irritants, at a concn which elicited a respiratory rate decrease of 50% (RD50), were compared with respect to type and severity. The RD50 (ppm) of dimethylamine is 511. After exposure of mice for 6 hr/day for 5 days, the respiratory tract was examined for histopathological changes. All irritants produced lesions in the nasal cavity with a distinct anterior-posterior severity gradient. There was considerable variation in the extent, severity, and nature of the lesions. The lesions ranged from slight epithelial hypertrophy or hyperplasia to epithelial erosion, ulceration, and necrosis with variable inflammation of the subepithelial tissues. [Buckley LA et al; Toxicol Appl Pharmacol 74 (3): 417-29 (1984)]**PEER REVIEWED**
  
• .. Oral admin of sodium nitrite within 1 hr of oral dimethylamine to mice yield a marked dose-dependent inhibition of liver nuclear RNA synthesis. No inhibition of nuclear RNA synthesis was observed when sodium nitrite was given 30 min prior to the dimethylamine. This study suggests the possibility of in vivo biosynthesis of carcinogenic nitrosamines following ingestion of nitrites and secondary amines present in food. ... Animals continuously exposed to as little as 9 mg/cu m of dimethylamine showed mild inflammatory changes, primarily in the lungs. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1096]**PEER REVIEWED**
  
• Exposure to 175 ppm dimethylamine for 6 hr/day for 9 days was shown to inhibit mucociliary function of rats, with mucostasis being more variable in extent than cilia stasis. [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. 78]**PEER REVIEWED**
  
• Histopathologic evaluation of the respiratory tract of rats exposed by inhalation at single concentrations ranging from 600 to 6000 ppm revealed concentration-related changes ranging from ulceration and necrosis to rhinitis, tracheitis, and emphysema. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• ... Mice exposed at 813 to 1626 ppm had ocular and respiratory irritation. Cyanosis, convulsions, and death were observed in mice exposed at concentrations above 5420 ppm. Pathologic evaluation revealed massive hemorrhages near the periphery of the lungs and peripheral emphysema in those mice that died during exposure. Small hemorrhages were found in the lungs of mice killed by design 20 days postexposure. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• In rabbits, a 5% solution administered to the eye caused hemorrhage in the conjunctiva, corneal edema, and superficial opacities. A 6% solution caused marked swelling of the eyelids and serous exudation; undiluted DMA made the cornea translucent almost immediately and produced severe corneal injury. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• A 6% solution of DMA, when applied to the skin of rabbits, caused reddening, then thickening and ulceration after a single treatment. A 3% solution produced similar effects after five treatments. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• DMA was a skin sensitizer in the guinea pig closed epicutaneous test. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• DMA added to the diet (150 mg/kg body weight) for 3.5 months increased liver demethylase activity even in the presence of the enzyme inducer casein. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• DMA is a sensory irritant; the RD50 (the concentrations that produced a mean reduction in respiratory rate of 50% in mice and rats during a 10 minute exposure) were 511 and 573 ppm, respectively. A lower RD50 of 70 ppm (95% confidence limits of 63 ppm to 80 ppm) has also been reported in mice. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• In a repeated exposure study, mice were exposed by inhalation at 511 ppm of DMA 6 hours/day for 5 days. There was a reduction of 10% to 25% of body weight from study initiation in all mice and 3 of 24 mice died during exposure. Nasal lesions were observed in these animals. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• ... Rats were exposed by inhalation 6 hours/day, 5 days/week for 13 weeks at 10, 30, or 100 ppm of DMA. Decreased body weights were observed in the 30 and 100 ppm groups during the first week and in the 100 ppm group in the second week. No body weight effect was observed in rats exposed at 10 ppm. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• In a subchronic study, 15 rats, 15 guinea pigs, 3 rabbits, 2 dogs, and 3 monkeys were exposed continuously by inhalation at approximately 5 ppm of DMA for 90 days. There were no deaths or signs of toxicity and all hematologic values were normal. On histopathologic examination, interstitial inflammatory changes were noted in the lungs of each species. ... The three rabbits and two monkeys showed dilatation of the bronchi. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 480]**PEER REVIEWED**
  
• In a 2 year inhalation study, groups of 95 male and 95 female rats and mice were exposed 6 hours/day, 5 days/week at 10, 50, or 175 ppm of DMA. Concentration dependent toxicity was characterized by decreased body weight (175 ppm only) and progressive inflammatory, degenerative, and hyperplastic lesions of the nasal passages. Nasal toxicity was similar in both rats and mice (no sex differences) affecting respiratory and olfactory epithelia. Lesions were severe at 175 ppm moderate at 50 ppm, and focal and mild at 10 ppm. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 480]**PEER REVIEWED**
  
• ... DMA was evaluated for carcinogenic potential by the inhalation route. Groups of 95 mice and 95 rats were exposed 6 hours/day, 5 days/week for 2 years at 10, 50, or 175 ppm of DMA. Selected animals were killed at 6, 12, 18, and 24 months and subjected to pathological examinations. No increase in tumor incidences were found. No evidence of a carcinogenic response was observed in these animals. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 480]**PEER REVIEWED**
  
• Exposure of rats, mice, guinea pigs and rabbits to 97 or 185 ppm of DMA 7 hr/day, 5 days/week for 18 to 20 weeks revealed corneal injury in eyes of guinea pigs and rabbits as well as central lobular fatty degeneration and necrosis of the liver in all species. However, histopathological examination of rats, guinea pigs, rabbits, monkeys, and dogs exposed to 9 mg/cu m of DMA continuously for 90 days produced only mild inflammatory changes in the lungs of species; dilated bronchi in rabbits and monkeys were noted. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1114]**PEER REVIEWED**
  
• An acute 6 hr whole body exposure of male F344 rats to DMA concn ranging from 600 to 6000 ppm for 6 hr, which produced a spectrum of pathological changes in the nasal passage, including severe congestion, ulcerative rhinitis, and necrosis of the nasal turbinates was reported. Lesions outside the respiratory tract were evident in livers of rats exposed to 2500 to 6000 ppm, and corneal edema was observed in the eyes of rats at 1000 ppm; corneal ulceration, keratitis, edema, and loss of Descement's membrane was present at 2500 to 6000 ppm; in addition, many rats exposed to 4000 or 6000 ppm had necrosis of the iris and severe degeneration of the lens, suggestive of acute cataract formation. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1114]**PEER REVIEWED**
  
• In a one year inhalation study, male and female F344 rats and B6C3F mice were exposed to 0, 10, 15, or 175 ppm DMA for 6 hr/day, 5 days/week for 12 months. The mean body weight gain of rats and mice exposed to 175 ppm was depressed to 90% of control after 3 weeks of exposure. The only other treatment related effects were the dose related lesions confined to the nasal passages, which were very similar in rats and mice; however, after 12 months of exposure, rats had more extensive olfactory lesions. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1114-5]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Rat oral 698 mg/kg [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. 77]**PEER REVIEWED**
  
• LD50 Mouse oral 316 mg/kg [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. 77]**PEER REVIEWED**
  
• LD50 Guinea pig oral 240 mg/kg [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. 77]**PEER REVIEWED**
  
• LC50 Rat inhalation 4700 ppm/4 hour [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 479]**PEER REVIEWED**
  
• LC50 Rat inhalation 4540 ppm/6 hr [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. 77]**PEER REVIEWED**
  
• LC50 Mouse ihl 7650 ppm/ 2 hr [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1275]**PEER REVIEWED**
  
• LD50 Rabbit oral 240 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 1275]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• ... AFTER ORAL ADMIN OF /DIMETHYLAMINE HYDROCHLORIDE/ ... A HIGH PROPORTION OF DIMETHYLAMINE ... WAS RECOVERED /IN URINE/ ... [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1093]**PEER REVIEWED**
  
• Rats were fed a commercial diet containing 23.6 ppm dimethylamine (DMA) or a low-DMA diet containing 1 ppm DMA for 7 days. Excretion of DMA in urine was 432.6 and 272.5 ug/head with the commercial diet and low-DMA diet, respectively. DMA was excreted mostly (approx 95%) in urine. The excess excretion of DMA was probably caused by the formation of DMA by demethylation of trimethylamine in the body. Distribution of DMA in the digestive tract was high in the stomach and small intestine and low in the cecum and large intestine with the commercial diet and was low in the stomach and cecum and high in the small intestine with the low-DMA diet when 1000 ug DMA was force-fed. [Ishiwata H et al; Shokuhin Eiseigaku Zasshi 23 (5): 360-4 (1982)]**PEER REVIEWED**
  
• ... /DIMETHYLAMINE HAS/ BEEN IDENTIFIED AS NORMAL /CONSTITUENT/ OF MAMMALIAN & HUMAN URINE. [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1093]**PEER REVIEWED**
  
• Dimethylamine is normally present in the stomach and urine of animals and humans. The secondary amine is formed from trimethylamine via trimethylamine N-oxide and probably also from dietary lecithin and creatine. The resulting dimethylamine is readily absorbed primarily from the small intestine, and to a much lesser extent, the stomach, and excreted in the urine. Humans consuming a diet high in fish show at least a 4-fold increase in urinary dimethylamine excretion. [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. 76]**PEER REVIEWED**
  
• ...(14)C-Dimethylamine /was/ studied in male Fischer 344 rats following 6 hr inhalation of 10 or 175 ppm of the labeled amine. At 72 hr after exposure, the disposition at both doses was similar with greater than 90% of the radioactivity appearing in the urine and feces, 7-8% in various tissues and 1.5% exhaled as (14)CO2. Over 98% of the urinary radioactivity was the parent (14)C-dimethylamine. [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. 77]**PEER REVIEWED**
  
• It is extensively absorbed (bioavailability 72%); 5% is demethylated to methylene, but 95% is secreted unchanged in the urine. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1427]**PEER REVIEWED**
  

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Metabolism/Metabolites

• The intragastric formation of nitrosodimethylamine (NDA) by bacteria existing in the gastrointestinal tract of monkey was examined by determining the in vitro formation of nitrosodimethylamine from nitrite and dimethylamine in the brain-heart-infusion (BHI) medium, adjusted to pH 6 with gastric juice containing 5000 ppm sodium nitrate and 1000 ppm dimethylamine. Nitrosodimethylamine formation depended on the activity of the nitrate-reducing bacteria in the stomach contents of the monkey, and the concn of nitrite was clearly related to the amount of nitrosodimethylamine. NDA was formed in the brain-heart-infusion medium alone at pH 5 and 6. The addition of gastric juice to the medium increased the formation of nitrosodimethylamine. [Hayashi N et al; Eisei Shikensho Hokoku 100: 72-6 (1982)]**PEER REVIEWED**
  
• The extent of nitrosamine formation and the metabolism of the resultant nitrosamines in vivo were investigated by using (15)N-stable isotope labeling and by the determination of the isotope ratio in the expired N. (15)N-labeled dimethylamine (1.1 mmol/kg) and various doses of nonlabeled nitrile (0.55-2.2 mmol/kg) or labeled nitrile without dimethylamine administered to male rats, which were placed in an enclosed respiratory system. The system was flushed with a mixture containing 80% He and 20% O, and N content of the recirculating atmosphere was determined. When labeled dimethylamine and nonlabeled nitrile were administered, nitrile reacted with secondary amines, followed by enzymic alpha-hydroxylation and decomposition of the ensuing alkyldiazohydroxide to molecular N and an alkyl cation as ultimate carcinogen. When (15)N nitrile was administered, N was released (nitrile reacted with primary amines to release molecular N and formation of the corresponding alcohol or olefin). [Frank H et al; Fresenius Z Anal Chem 317 (6): 660 (1984)]**PEER REVIEWED**
  

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TSCA Test Submissions

• Dimethylamine (CAS# 124-40-3) was tested for chronic toxicity in male and female F-344 rats (95/sex/group) exposed by inhalation to 0, 10, 50, or 175 ppm 6 hours/day, 5 days/week for 24 months. Body weights of mid-concentration rats were higher than those of controls. Effects observed in high-concentration rats included lower body weights and improved mortality compared to controls, increased relative brain weights, receding nasal turbinates, and increased phosphatase and SGOT levels. In low- and mid-concentration rats, relative kidney weights were decreased. Degenerative lesions in the respiratory and olfactory epithelia of the nasal cavity were observed and considered treatment-related. The incidence of uterine stromal polyps was increased in treated rats and considered possibly treatment-related.[Chemical Industry Institute of Toxicology; Letter from Chem. Indust. Inst. of Toxicol. to U.S. EPA Submitting Two Studies on Dimethylamine (1990), EPA Document No. 86-910000024, Fiche No. OTS0530078]**UNREVIEWED**
  

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.