N-ニトロソモルホリン

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": ... Incineration may be only feasible method for disposal of contaminated laboratory waste from biological expt. However, not all incinerators are suitable for this purpose. The most efficient type ... is probably the gas-fired type, in which a first-stage combustion with a less than stoichiometric air:fuel ratio is followed by a second stage with excess air. Some ... are designed to accept ... aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb soln onto suitable combustible material, such as sawdust. Alternatively, chem destruction may be used, esp when small quantities ... are to be destroyed in laboratory. /Chemical Carcinogens/

For more Disposal Methods (Complete) data for N-NITROSOMORPHOLINE (8 total), please visit the HSDB record page.

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of food & beverage containers or utensils, & the application of cosmetics should be prohibited in any laboratory. All personnel should remove gloves, if worn, after completion of procedures in which carcinogens have been used. They should ... wash ... hands, preferably using dispensers of liq detergent, & rinse ... thoroughly. Consideration should be given to appropriate methods for cleaning the skin, depending on nature of the contaminant. No standard procedure can be recommended, but the use of organic solvents should be avoided. Safety pipettes should be used for all pipetting. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their outdoor clothes & wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... clothing should be changed daily but ... discarded immediately if obvious contamination occurs ... /also,/ workers should shower immediately. In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. If gowns are of distinctive color, this is a reminder that they should not be worn outside of lab. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": ... Operations connected with synth & purification ... should be carried out under well-ventilated hood. Analytical procedures ... should be carried out with care & vapors evolved during ... procedures should be removed. ... Expert advice should be obtained before existing fume cupboards are used ... & when new fume cupboards are installed. It is desirable that there be means for decreasing the rate of air extraction, so that carcinogenic powders can be handled without ... powder being blown around the hood. Glove boxes should be kept under negative air pressure. Air changes should be adequate, so that concn of vapors of volatile carcinogens will not occur. /Chemical Carcinogens/

For more Preventive Measures (Complete) data for N-NITROSOMORPHOLINE (10 total), please visit the HSDB record page.

0.85 [mg/m3]

9.3 [mg/m3]

56 [mg/m3]

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves.

PRECAUTIONS FOR "CARCINOGENS": ... Dispensers of liq detergent /should be available./ ... Safety pipettes should be used for all pipetting. ... In animal laboratory, personnel should ... wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. ... gowns ... /should be/ of distinctive color, this is a reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/

Wear nitrile rubber gloves, protective laboratory coat, self-contained breathing apparatus, eye protection and protective shoes. /Nitrosamines/

A NIOSH survey of a rubber vehicle sealing plant in May 1994 revealed N-nitrosomorpholine concentrations in personal breathing zone samples of 0.04 to 0.18, 0.03 to 0.26, and 0.01 to 2.42 ug/cu m of salt bath line operators, salt bath line feeders and assistants and molding/finishing operators, respectively(1).

Female Sprague-Dawley rats were randomly divided into four groups (Group 1: Control, Group 2: Sham-operated, Group 3: Ovariectomy, Group 4: ovariectomy+estrogen) with treatment of a single i.p. injection of diethylnitrosamine (100mg/ kg body weight) followed by N-nitrosomorpholine (100ppm) in drinking water for 20 weeks for the established rat HCC model. Physiological estrogen was administered by 17alpha-Ethynylestradiol at a dose of 30ug/ kg body weight while rats in the sham-operated group were treated with saline after initiation of liver carcinogenesis. Treatment of ovariectomized animals with 17alpha-Ethynylestradiol (30ug/kg body weight/ day) resulted in a significant decrease in the initiation, development and metastasis of HCC and an increase in the survival time of animals dead before the termination of experiment as compared with rats treated with ovariectomy only (p<0.05); whereas this difference disappeared when compared with the other three groups.

The effect of cysteamine (2-aminoethanethiol hydrochloride) on hepatocarcinogenesis induced by N-nitrosomorpholine was investigated in male Sprague-Dawley rats. 20 rats received alternate day sc injections of cysteamine, and beginning in exptl wk 3 were given drinking water containing 250 mg/l NMOR for 8 wk. Controls (n= 20) received saline sc. By wk 18, all rats that had received cysteamine had body and liver wt that were slightly increased over those of sodium chloride treated rats. Pre-neoplastic and neoplastic lesions staining positive for gamma-glutamyl transpeptidase or glucose-6-phosphate dehydrogenase were examined by histochemical techniques. In wk 18, quantitative histological analysis showed that prolonged administration /of/ cysteamine resulted in a significant reduction in the number of gamma-glutamyl transpeptidase-positive and glucose-6-phosphate dehydrog enase-positive hepatic lesions (from 31.4/sq cm for saline controls to 3 to 15.9/sq cm, respectively). Histologically, hepatocellular carcinomas were significantly fewer and smaller in gamma-glutamyl transpeptidase-positive and glucose-6-phosphate dehydrogenase-positive lesions in rats treated with cysteamine than in untreated rats. Admin of cysteamine also caused a significant decr in the liver norepinephrine concn and in the labeling indices of pre-neoplastic lesions and the surrounding liver.

Effects of 3,4,3',4'-tetrachlorobiphenyl on glucose-6-phosphatase (G6Pase)-altered hepatic foci of N-nitrosomorpholine treated B6C3F1 mice were investigated. 3,4,3',4'-Tetrachlorobiphenyl was chosen as a selective 3-methylcholanthrene-type inducer and tumor promoter. To initiate hepatocarcinogenesis, mice were treated with N-nitrosomorpholine (160 mg/L, in drinking water for 7 weeks), as in previous studies with the rat model. After a treatment-free interval of 22 weeks, 3,4,3'-4'-tetrachlorobiphenyl was administered (5 x 50 mg/kg, every 3 days), and liver foci were analysed 10 weeks after the start of 3,4,3',4'-tetrachlorobiphenyl treatment. The number of G6Pase-negative and -positive foci per liver was markedly diminished following 3,4,3',4'-tetrachlorobiphenyl treatment (to 32% and 57%, respectively). On the other hand, the mean volume of the remaining G6Pase-altered foci was enhanced, owing to an increase in the percentage of foci of large size (greater than 0.5 sq mm). Throughout the experimental period of 39 weeks prolonged liver injury due to N-nitrosomorpholine and 3,4,3',4'-tetrachlorobiphenyl treatment was demonstrated by histology and by elevated serum levels of glutamate-oxaloacetate transaminase. In contrast to the rat system, 3,4,3',4'-tetrachlorobiphenyl exhibited opposing effects on liver foci in the mouse model: (a) moderate tumor-promoting effects and (b) cytotoxic effects in N-nitrosomorpholine injured liver, leading to decreased numbers of liver foci.

The effects of oral fructose on hepatocarcinogenesis were investigated. Carcinogenesis was induced in male Sprague-Dawley rats by application of N-nitrosomorpholine for 7 weeks. Afterwards, the animals received fructose in the drinking water (120 g/L) and food ad libitum (group I) or tap water and food ad libitum (group II). The incidence of hepatocellular carcinoma in rats treated with N-nitrosomorpholine plus fructose was 46% as compared to 24% in animals receiving N-nitrosomorpholine alone (P < 0.05). There was no difference in the incidences of other malignancies between the groups (group I: 32.1%, group II: 32.0%). Morphometric evaluation of preneoplastic liver lesions indicated the enhancing effect of the fructose treatment several months before malignant tumors appeared. As early as 6 weeks after treatment the hepatic parenchyma occupied by focal lesions was increased from 6.7% in the animals which had received N-nitrosomorpholine alone to 8.5% (P < 0.05) in animals having received N-nitrosomorpholine plus fructose. This increase was predominantly caused by an increase in glycogen storing foci (P < 0.0005). In addition, the fructose treatment caused a histochemically detectable increase in the activity of glucose-6-phosphatase and glucose-6-phosphate dehydrogenase in both the hepatocytes of the focal lesions and the surrounding parenchyma. In the N-nitrosomorpholine plus fructose group the activity of the glucose-6-phosphatase in the foci was frequently approximately equal to the activity in the parenchyma of untreated controls.

For more Interactions (Complete) data for N-NITROSOMORPHOLINE (15 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), estimated Koc values of 22 and 4(SRC), determined respectively from a structure estimation method(2) and using a log Kow of -0.44(3) and a regression-derived equation(2), indicates that N-nitrosomorpholine is expected to have very high mobility in soil(SRC). Although N-nitrosomorpholine's estimated vapor pressure of 0.036 mm Hg at 20 °C(4) and measured Henry's Law constant of 2.45X10-8 atm-cu m/mole(5) suggest that volatilization from dry and moist soil is not expected to occur(SRC), inhalation toxicity studies found that N-nitrosomorpholine was volatile at room temperatures with inhalation exposure possible(6). N-Nitrosomorpholine absorbs UV light strongly above 290 nm(7,8) and is expected to photolyze on the soil surface exposed to sunlight, a reaction which would be more rapid in the presence of radical scavengers or at lower pH(7).

AQUATIC FATE: Based on a classification scheme(1), estimated Koc values of 22 and 6(SRC), determined respectively from a structure estimation method(2) and using a log Kow of -0.44(3) and a regression-derived equation(2), indicate that N-nitrosomorpholine is not expected to adsorb to suspended solids and sediment(SRC). N-Nitrosomorpholine is not expected to volatilize from water surfaces(4) based on a measured Henry's Law constant of 2.45X10-8 atm-cu m/mole(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from a its log Kow and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low. Nitrosamines photolyze rapidly in sunlight in aqueous solution forming an amino radical and NO(7,8). Under neutral conditions or in the absence of radical scavengers, rapid recombination of the radicals and nitric oxide formed during photolysis may occur(7,8). In the presence of radical scavengers decay is rapid(7,8). The rate of photo-induced degradation also increases at lower pH(7,8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), N-nitrosomorpholine, which has an estimated vapor pressure of 0.036 mm Hg at 20 °C(2) will exist solely as a vapor in the ambient atmosphere. Vapor-phase N-nitrosomorpholine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 5 hours(SRC), calculated from its rate constant of 7.48X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). In air, N-nitrosomorpholine is expected to photolyze rapidly in sunlight; the half-life is expected to be similar to dimethylnitrosamine, 30 minutes in full sunlight(4).

None of the 11 types of cheese (9 Italian, 2 Dutch) analyzed for volatile nitrosamines contained N- nitrosomorpholine (detection limit 5.0 ug/kg)(1). In a preliminary survey of the Italian market, N-nitrosomorpholine was not detected in samples of canned luncheon meat and cured meat products (detection limit 0.3 ppb)(2). None of the 63 samples of various fish and seafoods analyzed for volatile nitrosamines contained N-nitrosomorpholine (detection limit approx 0.3-0.5 ppb)(3).

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of June 21, 2012: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=59-89-2]

N-Nitrosomorpholine was identified in the effluent from the manufacture of 2,4,6-trinitrotoluene (TNT); 1 year sampling period, 54 samples, 54.1% positive, concentration range 0.1-0.3 mg/L(1). A 1978 wastewater sample from a tire chemical factory in Ohio contained 0.003 ug/g of N-nitrosomorpholine(2). Utility steam condensate from the tire chemical factory contained 0.002 ug/g, possibly due to the use of morpholine as a corrosion inhibitor in the steam processing unit(2).

Aqueous samples were taken from inlets and outlets of 3 sewage treatment works and from cutting-fluid recovery plant whose contents are periodically discharged into a water system of one of the three sewage works. All samples contained N-nitrosomorpholine.

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/

Using a structure estimation method based on molecular connectivity indices(1), the Koc of N-nitrosomorpholine can be estimated to be 22(SRC). The Koc of N-nitrosomorpholine can be estimated as 4(SRC), using a log Kow of -0.44(2) and a regression-derived equation(1). According to a classification scheme(3), these estimated Koc values suggest that N-nitrosodiethylamine is expected to have very high mobility in soil.

The ability of N-nitrosomorpholine to induce morphological transformation in the BALB/3T3 mouse cell line (Cell Transformation Assay) was evaluated. Based on preliminary clonal toxicity determinations (exposure time=3 days), N-nitrosomorpholine, in 0.5% aqueous DMSO, was tested at 0, 0.03, 0.1, 0.3, 1.0 and 3.0 mg/mL, with cell survival ranging from 109.5% to 89.0% relative to the solvent control. None of the tested concentrations produced significantly greater transformation frequencies relative to the solvent controls.

The ability of N-nitrosomorpholine (NM) to induce specific locus mutations at the TK locus in cultured L5178Y mouse lymphoma cells (Mouse Lymphoma Mutagenesis Assay) was evaluated in the presence and absence of Aroclor-induced rat liver S9 metabolic activation. Based on preliminary toxicity tests, 10 cultures treated with 31.3 uL/mL to 1000 uL/mL NM were cloned, producing a range of total growth for the nonactivated and activated cultures of 30.4-44.3% and 26.1-74.7%, respectively. None of the nonactivated cultures produced mutant frequencies significantly greater than the solvent controls (acetone) over the concentration range tested. All of the activated cultures produced mutant frequencies significantly greater than the solvent controls, ranging from 2.3-fold above background at 125 ug/mL to 4.4-fold above background at 1000 ug/mL. A dose-dependent response was observed.

The mutagenicity of N-nitrosomorpholine (NM) was evaluated in Salmonella tester strains TA98, TA100, TA1535, TA1537 and TA1538 (Ames Test), both in the presence and absence of added metabolic activation by Aroclor-induced rat liver S9 fraction. Based on the results of preliminary bacterial toxicity determinations, NM, diluted with DMSO, was tested for mutagenicity at concentrations up to 1 mg/plate using a 20 minute preincubation technique. NM caused a positive response in strains TA1535, and TA100 following metabolic activation.

The effects of N-nitrosomorpholine (NNM) were examined in the DNA repair test in E. coli strains W3110 (DNA repair proficient) and P3478 (DNA repair deficient). Based on preliminary toxicity tests, NNM was tested at seven concentrations ranging from 0 to 2500 ug/tube (mixture volume in tube 0.65-0.75 mL) both in the presence and absence of Aroclor-induced rat liver S9 metabolic activation using the 2 hr preincubation method. The test material (dissolved in DMSO) forms a precipitate at dose levels of 500 ug/tube and above. NNM exhibited genetic activity in the activated system as evidenced by the reduction in the survival index (the ratio of % deficient survivors to % proficient survivors was 0.51). There were no differences observed between treated and control nonactivated organisms with respect to the survival index.

N-Nitrosomorpholine was detected in the air inside 16 out of 38 new (1979) cars, concn range trace-2.5 ug/cu m, average concentration 0.65 ug/cu m(1,3). For control purposes, ambient air samples taken at the new car dealers where the cars were obtained, contained no N-nitrosamines(3). In 1978, N-nitrosomorpholine was analyzed for but not found in air outside a tire chemical factory and an aircraft tire factory located in Ohio, detection limit 0.05 ug/cu m(2). As part of an EPA study of air quality in public buildings, six buildings, a new hospital, office and nursing home and another office, office/school, and nursing home, a screening analysis of nitrosamines was performed at each location for all monitoring trips (10 in all)(4). During this screening, only N-nitrosomorpholine was found in any of the samples, and only in samples from the old office building. Concentrations did not appear to vary between sampling locations and daytime and nighttime means (standard deviation) were 0.17 (0.09) and 0.36 (0.13) ng/cu m. The building contained a fast food restaurant on the ground floor and a cooking odor could be detected throughout the building. It is thought that cooking at the restaurant could be the source of N-nitrosomorpholine thoughout the building(4).

/GENOTOXICITY/ N-nitrosomorpholine (NMOR) belongs to the group of N-nitrosamines and represents a known hepatocarcinogen. Exposure to this compound is considered to be a potential health hazard to humans. There is, however, considerable evidence that the effect of many carcinogenic agents can be markedly influenced or altered by various natural substances. The objective of this study was to assess the DNA-protective and anticlastogenic effects of the derivative of a natural compound, carboxymethyl chitin-glucan (CM-CG), against genotoxicity of N-nitrosomorpholine (NMOR) in human hepatoma cells HepG2 and hamster lung cells V79 cultured in vitro. The exponentially growing cells were pre-treated during 24 h with three different concentrations of CM-CG (150, 750 and 1500 mg/mL) and then treated with different concentrations of NMOR. DNAprotective effects of CM-CG were evaluated by single-cell gel electrophoresis (SCGE, comet assay) and anticlastogenic effects by chromosomal aberration assay. At the SCGE assay a short-term (30 min) and at the chromosomal aberration assay a continuous treatment with NMOR was used. In both HepG2 and V79 cells pre-treated with CM-CG, a significant decrease of the percentage of DNA lesions induced by NMOR was observed along with a reduction of NMOR-induced chromosomal aberrations. We did not find any substantial differences between the genotoxic effects of NMOR on HepG2 and V79 cells, which have different histopathological origins and different levels of metabolizing enzymes. Three different concentrations of CM-CG exerted a similar protective effect against NMOR-induced DNA lesions and chromosomal aberrations in both HepG2 and V79 cells.

/GENOTOXICITY/ ... N-nitroso compounds (NOC), known to induce kidney tumors in rats, were assayed for DNA-damaging activity in primary cultures of human and rat kidney cells. DNA fragmentation was measured by the alkaline elution technique. ... N-nitrosomorpholine was inactive at the highest concentration tested (32 mM). ...

/OTHER TOXICITY INFORMATION/ ... Health hazards ... related to the consumption of water containing large concentrations of nitrate (or nitrite) ... /include/ potential formation of carcinogenic nitrosamines. /Nitrosamines/

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. N-Nitrisomorpholine is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Nitrosamines/

The levels for nitrosamines through ingestion of contaminated water and contaminated aquatic organisms ... which may result in incremental increase of cancer risk over the lifetime are estimated at 1X10-5, 1X10-6, and 1X10-7. The corresponding criteria are 8.0 ng/l, 0.8 ng/L, and 0.08 ng/L, respectively. For consumption of aquatic organisms only, excluding consumption of water, the levels are 12,400 ng/L, 1,240 ng/L, and 124 ng/L, respectively. /Nitrosamines/

N-Nitrosomorpholine is not used commercially in the United States.

Used as a solvent for polyacrylonitrile and to synthesize n-aminomorpholine; Not commercially used in the US; [HSDB]

N-Nitrosomorpholine is used as a research chemical.

Patents have been issued for the use of NMOR as a solvent for polyacrylonitrile ... and as a chemical intermediate in synthesis of N-aminomorpholine. It has also been found to be effective against microbial infections. No evidence was found that it has been used commercially for these purposes.

(1977) NOT PRODUCED COMMERCIALLY IN USA

(1979) NOT PRODUCED COMMERCIALLY IN USA