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DIMETHYLACETAMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dimethylacetamide is an excellent dipolar solvent, with a high dielectric constant, that readily dissolves gases and numerous organic and inorganic substances. It is a clear, colorless to pale yellow liquid with a faint odor of ammonia. It is most commonly used in the acrylic fiber, polyester films and pharmaceutical industries, with occupational exposures via the dermal and inhalation routes being most common. Due to its vapor pressure, inhalation exposures with toxicity can occur. On heating, it decomposes to produce toxic fumes of nitrogen oxides.

Specific Substances

    1) Acetic acid, dimethylamide
    2) Acetyldimethylamine
    3) Dimethylacetone amide
    4) Dimethylamide acetate
    5) DMA
    6) DMAC
    7) NN-Dimethylacetamide
    8) Molecular Formula: C4-H9-N-O
    9) CAS 127-19-5
    10) ACETDIMETHYLAMIDE
    11) DMA (DIEMTHYLACETAMIDE)
    12) U-5954
    1.2.1) MOLECULAR FORMULA
    1) C4-H9-N-O

Available Forms Sources

    A) FORMS
    1) Dimethylacetamide is a clear, colorless to pale yellow, oily liquid with a faint odor of ammonia. It is a high-boiling, polar solvent that readily dissolves gases and numerous organic and inorganic substances. It is miscible with water and all common organic solvents (Anon, 2000; Budavari, 1996; HSDB , 2000). This chemical is a combustible liquid and vapor. Because of its vapor pressure (theoretical saturation of approximately 2600 ppm), inhalation exposures must be controlled. Due to its dermal absorption, skin contact must also be controlled (Clayton & Clayton, 1994).
    B) SOURCES
    1) Dimethylacetamide (DMAC) is not known to occur naturally. DMAC is prepared by the reaction of N,N-dimethylamine and acetic anhydride or methyl acetate (Fairhurst et al, 1992). It has also been prepared from the reaction of acetic anhydride and dimethylformamide (HSDB , 2001).
    C) USES
    1) This chemical is primarily used as a polar solvent in the acrylic fiber industry in the manufacture of acrylic fibers. In the polyester film industry it is used as a solvent for the manufacture of polyester films. Dimethylacetamide is used as a paint stripper because of its very rapid removal action. It is a booster solvent in coating and adhesive formulations (Bingham et al, 2001; HSDB , 2001; Fairhurst et al, 1992).
    2) In the pharmaceutical industry this chemical is used both as a solvent and as a reactant. It is a commercial solvent used as a parenteral drug vehicle for some antineoplastic agents. Also, it is used as a reaction medium for the manufacture of agricultural products, wetting agents and plasticizers. It is an extraction agent for gases and oils (HSDB , 2001; Clayton & Clayton, 1994; JEF Reynolds , 2000).
    3) Dimethylacetamide is a purification and crystallization solvent for aromatic dicarboxylic acids (Clayton & Clayton, 1994).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Human data on dimethylacetamide (DMAC) toxicity is limited. In human clinical trials, toxic effects of intravenous DMAC included dose-related gastrointestinal (vomiting) and central nervous system toxicity (CNS depression followed by mental excitation with delusions and hallucinations), and hypotension. Acute toxic dermal and inhalation exposure has resulted in severe hepatitis, rhabdomyolyses, hallucinations, and coagulopathy. Dermal irritation with burns has been reported following liquid exposure.
    B) In animal studies, target organs for toxicity are the liver, central nervous system, and skin. Liver damage appears to be produced most consistently in animal studies.
    C) Systemic effects in humans can occur through oral, dermal and inhalational absorption.
    0.2.5) CARDIOVASCULAR
    A) Acute toxic exposures may result in hypotension.
    0.2.7) NEUROLOGIC
    A) Acute toxic exposures have resulted in initial CNS depression followed by stimulation, with hallucinations, delusions, and agitation.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur after toxic exposures.
    B) Esophagitis has been reported following unintentional ingestions.
    0.2.9) HEPATIC
    A) Liver toxicity (elevated liver enzymes, jaundice, hepatomegaly) is a primary clinical effect of dimethylacetamide toxicity. Hepatic necrosis and liver failure may occur in extreme cases.
    0.2.14) DERMATOLOGIC
    A) DMAC is a skin irritant. Prolonged dermal exposures have resulted in second-degree burns.
    0.2.20) REPRODUCTIVE
    A) DMAC does not appear to be teratogenic in animal studies. Embryotoxicity in animals has been reported.

Laboratory Monitoring

    A) Serum dimethylacetamide levels are not clinically useful nor readily available.
    B) The relationship between airborne inhaled dimethylacetamide and urinary monomethylacetamide has been used to suggest biologic monitoring in the workplace.
    C) Monitor for CNS depression, liver toxicity and rhabdomyolysis following an acute exposure.
    D) Monitor fluid and electrolyte status following significant vomiting or diarrhea.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no antidote for dimethylacetamide (DMAC) poisoning. Treatment is symptomatic and supportive.
    B) DMAC is an irritant and potentially corrosive agent at high concentrations; when ingested it can cause esophageal or gastric burns or erosions. Endoscopy may be necessary in the unlikely event of a substantial ingestion.
    C) MUCOSAL DECONTAMINATION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    D) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    E) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    0.4.3) INHALATION EXPOSURE
    A) Dimethylacetamide is absorbed following inhalation of toxic concentrations.
    B) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    C) Control severe agitation/hallucinations with intravenous benzodiazepines.
    D) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    E) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Dimethylacetamide is well absorbed following dermal exposure of toxic vapor or liquid concentrations.
    2) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    3) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    4) Control severe agitation/hallucinations with intravenous benzodiazepines.

Range Of Toxicity

    A) Dimethylacetamide (DMAC) has a relatively low order of acute toxicity. Between 28 and 287 grams of DMAC were given intravenously to humans over a 5 day period with dose-related toxic effects of CNS depression followed by mental excitatory states, hypotension, nausea and vomiting, and elevations of hepatic transaminase levels.

Clinical Effects

Summary Of Exposure

    A) Human data on dimethylacetamide (DMAC) toxicity is limited. In human clinical trials, toxic effects of intravenous DMAC included dose-related gastrointestinal (vomiting) and central nervous system toxicity (CNS depression followed by mental excitation with delusions and hallucinations), and hypotension. Acute toxic dermal and inhalation exposure has resulted in severe hepatitis, rhabdomyolyses, hallucinations, and coagulopathy. Dermal irritation with burns has been reported following liquid exposure.
    B) In animal studies, target organs for toxicity are the liver, central nervous system, and skin. Liver damage appears to be produced most consistently in animal studies.
    C) Systemic effects in humans can occur through oral, dermal and inhalational absorption.

Vital Signs

    3.3.3) TEMPERATURE
    A) Toxic exposures may result in spiking fevers (Kim, 1988; Marino et al, 1994).
    1) Following exposure to very high levels of dimethylacetamide (DMAC) (cumulative dose of 140 grams in one adult) high fever developed (Kim, 1988).
    2) Marino et al (1994) reported a high fever (102.2) during the first day of hospitalization in a patient who had fallen into a solution of 65% DMAC and 0.5% unreacted 1,2-ethanediamine.

Heent

    3.4.3) EYES
    A) CONJUNCTIVITIS - Ocular exposure to prolonged, high concentrations of fumes has resulted in conjunctival injection in humans (Marino et al, 1994; Su et al, 2000).
    B) CORNEAL irritation is produced in rabbits, mice, and dogs when exposed to dimethylacetamide in high concentrations (Kim, 1988). Direct application of liquid to animal eyes has produced mild to moderate eye irritation (Fairhurst et al, 1992). Conjunctival irritation in animal studies was quickly reversible (Kennedy & Sherman, 1986).
    3.4.6) THROAT
    A) Accidental exposure to a concentrated solution has resulted in throat pain and dysphagia, resulting in esophagitis with focal ulcerations (Marino et al, 1994; Su et al, 2000).

Cardiovascular

    3.5.1) SUMMARY
    A) Acute toxic exposures may result in hypotension.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) High acute doses, or prolonged high doses may result in hypotension. Three patients receiving 100 to 600 mg/kg/day for 2 to 5 days consecutively, in a study for treatment of various malignancies, became hypotensive approximately 6 days after therapy began. Hypotension was dose-related (Kim, 1988).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPERTENSION
    a) RATS receiving intravenous doses of 708 to 1480 mg/kg experienced a brief period of hypotension followed by a marked, prolonged period of hypertension (Kim, 1988).
    2) HYPOTENSION
    a) DOGS/CATS - Transient hypotension was noted in dogs and cats receiving single intravenous doses of 236 mg/kg (Kim, 1988).
    b) GUINEA PIGS - A marked positive dose-related inotropic response was seen in an electric driven guinea pig left atrial preparations; a decline in tension at concentrations above those causing maximum contractility was reported during dimethylacetamide toxicity studies (Kim, 1988).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) BRONCHITIS
    1) Bronchitis has been associated with dimethylacetamide (DMAC) exposures.
    B) ACUTE LUNG INJURY
    1) Non-cardiogenic pulmonary edema was reported in an adult following a mixed exposure to DMAC, ethylenediamine, and diphenylmethane di-isocyanate (the latter two agents are known respiratory sensitizers); however, pneumonitis with pulmonary edema has not been reported after pure DMAC exposures in humans (Su et al, 2000).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Repeated inhalation exposure at 100 ppm and above has produced nasal and upper respiratory tract irritation, which increased in severity with increasing exposure levels (Fairhurst et al, 1992).

Neurologic

    3.7.1) SUMMARY
    A) Acute toxic exposures have resulted in initial CNS depression followed by stimulation, with hallucinations, delusions, and agitation.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) The most frequent clinical sign of acute toxicity in humans is central nervous system (CNS) depression, which appears to be dose-related, and which is followed by a mental excitatory state (vivid hallucinations, delusions, agitation) (Kim, 1988).
    2) CASE SERIES - Fifteen patients receiving 100 to 610 mg/kg/day intravenously for 2 to 5 consecutive days in a clinical trial for treatment of malignancies all developed a distinctly abnormal mental state when the drug dosage reached a critical level of 400 mg/kg/day for 3 days or more (equivalent to a total dose greater than 84 grams).
    a) Signs of toxicity included depression, lethargy, confusion and disorientation. By the fourth or fifth dose of dimethylacetamide (DMAC), striking hallucinations, perceptual distortions, and delusions were noted in 9 patients. EEG studies in 5 of these patients noted changes which paralleled the CNS alterations. CNS changes returned to normal following discontinuation of DMAC (Kim, 1988).
    3) CASE REPORT - Following a 90 minute accidental submersion in a vat containing a solution of 65% dimethylacetamide and 0.5% unreacted 1,2-ethanediamine, a 32-year-old male was confused, agitated, and delirious. He became combative and was hallucinating upon examination. Disorientation and irrational behavior required the use of restraints. Active hallucinations were apparent during the first 48 hours after hospital admission, which gradually subsided (Marino et al, 1994).
    4) CASE REPORT - Hallucinations, delusions and later impaired consciousness were noted at admission in a 27-year-old male following inhalational exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days. An EEG showed diffuse moderate cortical dysfunction and slow waves at 4-7 Hz, 20-80 mcV. Serial urinary monomethylacetamide and EEG correlated with his clinical condition (Su et al, 2000).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur after toxic exposures.
    B) Esophagitis has been reported following unintentional ingestions.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Gastrointestinal toxicity has been reported following exposures in humans, with nausea and vomiting, often accompanied by anorexia. Several episodes of vomiting may occur within 1 to 2 hours. Gastrointestinal toxicity appears to be a dose-related effect, with vomiting occurring within 14 hours after DMAC exposure (Kim, 1988).
    B) ESOPHAGITIS
    1) Unintentional ingestion has resulted in erosions, erythema, and focal ulcerations in the upper one-third of the esophagus, visible on endoscopy (grade 2 severity) (Marino et al, 1994). Treatment included demulcents and cimetidine. In another case of primarily inhalation exposure, upper GI bleeding, oral mucositis, esophagitis, and gastric erosion were reported (Su et al, 2000).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DIARRHEA
    a) Following repeated dermal applications or single or repeated intravenous dimethylacetamide doses in dogs, diarrhea was a common toxic effect (Kim, 1988).

Hepatic

    3.9.1) SUMMARY
    A) Liver toxicity (elevated liver enzymes, jaundice, hepatomegaly) is a primary clinical effect of dimethylacetamide toxicity. Hepatic necrosis and liver failure may occur in extreme cases.
    3.9.2) CLINICAL EFFECTS
    A) TOXIC HEPATITIS
    1) Repeated exposures or very high acute exposures can produce signs of liver toxicity, with the first being increases in serum clinical enzymes followed by histopathological changes in hepatocytes. Extreme exposures can produce hepatic necrosis and possibly liver failure (Clayton & Clayton, 1994; Marino et al, 1994).
    2) Hepatotoxicity, with elevations in serum hepatic transaminase levels, has been reported in 7 patients receiving 400 mg/kg/day intravenously of dimethylacetamide for at least 3 days (Kim, 1988). Peak elevations of the transaminases occurred between 5 and 7 days after initiation of therapy and returned to normal within 2 to 5 days after reaching a peak.
    3) Jaundice has been observed in workers exposed to 20 or 25 ppm, with dermal exposure contributing to this effect (Marino et al, 1994).
    4) Primary adverse findings of 41 workers exposed (mostly dermally) for 2 to 10 years were liver abnormalities, with hepatomegaly reported in 14 of the workers (Bingham et al, 2001).
    5) Chemical hepatitis, with mild elevations of liver enzymes, was reported in a worker following exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days (Su et al, 2000).
    6) Spies et al (1995a) reported on workers exposed to airborne dimethylacetamide. They found that brief threshold limit value-level exposure and chronic low-level exposure (estimated maximum of 3.0 ppm 12-hour time-weighted average) do not cause hepatotoxic clinical chemistry changes.
    7) CASE REPORT - A 32-year-old male was reported to develop severe hepatitis (peak AST 2065 IU/L, ALT 3661 IU/L, LDH 2250 IU/L, bilirubin 5.1 mg/dL, PT 22.3 sec) and secondary coagulopathy following prolonged (90 minute) accidental occupational inhalational and dermal exposure to a solution containing 65% dimethylacetamide and 0.5% unreacted 1,2-ethanediamine. The worker had fallen into a vat of the solution and was removed 90 minutes later. The patient improved with symptomatic therapy over the following 7 days (no signs of encephalopathy) (Marino et al, 1994).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) In animal studies, liver damage is consistently produced by high-level exposure (Kim, 1988; Kennedy & Sherman, 1986). In dogs exposed repeatedly to dermal applications of dimethylacetamide (DMAC) or by single or repeated intravenous doses, elevation of liver transaminases and alkaline phosphatase levels were noted, as well as microscopic evidence of hepatocellular damage with jaundice and diarrhea. Kennedy & Sherman (1986) reported hepatic necrosis (cause of death) in rabbits following 4 consecutive daily doses of 2000 mg/kg applied dermally.
    b) Mice surviving near lethal doses of DMAC showed necrosis of hepatocytes, splenic lymphocytes, and necrotic pancreatitis (Marino et al, 1994).
    c) Liver necrosis and hypertrophy were the predominant findings in animals following repeated inhalation exposures to 100 ppm and above. Marked, but reversible, liver damage was noted in rats receiving oral dosing of 450 mg/kg/day. In another animal study, repeated dermal application (94 to 289 mg/kg/day) resulted in liver damage, which increased in severity with increasing dose (Fairhurst et al, 1992).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MARROW DEPRESSION
    a) Hypocellularity in the bone marrow has been reported following toxic inhalation exposures (622 ppm for 4 consecutive days) in rat studies. Lymphocyte depletion in the thymus and spleen were also noted (Fairhurst et al, 1992).

Dermatologic

    3.14.1) SUMMARY
    A) DMAC is a skin irritant. Prolonged dermal exposures have resulted in second-degree burns.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Dimethylacetamide is a mild to moderate dermal irritant at high concentration exposures (Kim, 1988).
    2) CASE REPORT - Following a 90 minute accidental dermal exposure to a solution containing 65% dimethylacetamide and 0.5% unreacted 1,2-ethanediamine, a 32-year-old worker developed second-degree burns and cellulitis to areas where he had laid in the chemical mixture. The skin burns responded to topical therapy (Marino et al, 1994). It is likely that ethanediamine contributed to the dermal lesions since it is a corrosive.
    3) CASE REPORT - Skin burns were reported in a 27-year-old worker following exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days (Su et al, 2000).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) CASE REPORT - Following an accidental dermal and inhalation exposure to a solution of 65% dimethylacetamide and 0.5% unreacted 1,2-ethanediamine, a 32-year-old worker was reported to have an elevated CPK (3816 IU/L), with normal urinary function (Marino et al, 1994). The rhabdomyolysis may have been a secondary effect of this patient's extreme agitation and hours of physical restraint.
    2) CASE REPORT - Rhabdomyolysis, with a CPK of 7049 IU/L, was reported in a worker following exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days (Su et al, 2000).

Reproductive

    3.20.1) SUMMARY
    A) DMAC does not appear to be teratogenic in animal studies. Embryotoxicity in animals has been reported.
    3.20.2) TERATOGENICITY
    A) EMBRYOTOXICITY
    1) RATS/RABBITS - Dimethylacetamide (DMAC) has been shown to be primarily embryotoxic when pregnant females were administered DMAC during gestation periods, often at maternally toxic doses (Kim, 1988). Weak teratogenic effects were seen following toxic doses given to the mother.
    2) In a developmental toxicity study, by inhalation in rats, both fetal and maternal toxicity were reported at 282 ppm, with a no-observed adverse-effect level of 100 ppm for both dam and conceptus. NO malformations were noted in the rat fetus, even at dimethylacetamide levels that were toxic to the dam (Solomon et al, 1991).
    3) In rats, dimethylacetamide 400 mg/kg/day, administered by gavage, caused malformations of the fetal heart, major vessels, and oral cavity. Significant maternal toxicity was also observed (Hathaway et al, 1996).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS127-19-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Dimethylacetamide has NOT been shown to be carcinogenic in animal studies (Kim, 1988; Clayton & Clayton, 1994).
    2) Chronic toxicity studies in rats and mice, following inhalation exposures up to 18 months in mice and 2 years in rats, demonstrated NO oncogenicity. No increase in hepatic cell proliferation was noted in either animal species (Malley et al, 1995).

Genotoxicity

    A) DNA inhibition was observed in mice and sister chromatid exchange in hamster ovary cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Serum dimethylacetamide levels are not clinically useful nor readily available.
    B) The relationship between airborne inhaled dimethylacetamide and urinary monomethylacetamide has been used to suggest biologic monitoring in the workplace.
    C) Monitor for CNS depression, liver toxicity and rhabdomyolysis following an acute exposure.
    D) Monitor fluid and electrolyte status following significant vomiting or diarrhea.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Following a toxic exposure, monitor serum hepatic enzyme levels. In cases of hepatic dysfunction, follow coagulation studies.
    2) Monitor serum and electrolyte levels in patients with excessive vomiting and/or diarrhea.
    3) Monitor CPK, especially in cases of extreme agitation.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Biological monitoring by measuring urinary N-methylacetamide (or monomethylacetamide) is a useful means of assessing total body exposure to dimethylacetamide (HSDB , 2001; Marino et al, 1994). Biologic surveillance in industries with dimethylacetamide inhalation exposure often includes urinary monomethylacetamide concentrations for workers, which appears to correlate most strongly with dimethylacetamide air levels (Borm et al, 1987; Spies et al, 1995).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Following a highly toxic exposure, monitor for CNS effects of confusion, delirium, agitation, and hallucinations.

Methods

    A) CHROMATOGRAPHY
    1) Gas chromatography equipped with a flame ionization detector has been used to determine the presence and quantity of monomethylacetamide and acetamide (dimethylacetamide metabolites) in the urine, which can then be used to predict exposure to dimethylacetamide (HSDB , 2000; Marino et al, 1994). The same method has been used to quantify dimethylacetamide in rat and mouse plasma (Hundley et al, 1994).
    2) Infrared spectroscopy and thin-layer chromatographic techniques have also been used to measure the urinary metabolites (Kim, 1988).
    3) Gas chromatography techniques are used for workplace airborne analysis of dimethylacetamide, with a working range of 10 to 80 mg/m(3) with a 50-L air sample (Bingham et al, 2001).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Serum dimethylacetamide levels are not clinically useful nor readily available.
    B) The relationship between airborne inhaled dimethylacetamide and urinary monomethylacetamide has been used to suggest biologic monitoring in the workplace.
    C) Monitor for CNS depression, liver toxicity and rhabdomyolysis following an acute exposure.
    D) Monitor fluid and electrolyte status following significant vomiting or diarrhea.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    B) GASTRIC ASPIRATION
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    C) ACTIVATED CHARCOAL
    1) It is unknown if activated charcoal adsorbs dimethylacetamide, and its use may obscure endoscopy findings.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive; there is no specific antidote.
    B) ENDOSCOPIC PROCEDURE
    1) Occupational exposures are generally through dermal and inhalational routes. However, in the unlikely event of an ingestion, endoscopy may be required if esophageal or gastric burns or erosions are suspected, due to the acidic corrosive nature of dimethylacetamide. It has been suggested that inhalation of high concentrations of DMAC may result in esophageal burns.
    C) MONITORING OF PATIENT
    1) CNS depression may occur. Monitor for clinical signs and treat symptomatically.
    2) LIVER FUNCTION - This agent is an hepatotoxin, with the liver being a primary target organ of toxic exposures. Monitor serum hepatic enzymes.
    D) FLUID/ELECTROLYTE BALANCE REGULATION
    1) FLUID LOSS may occur if vomiting and/or diarrhea is extensive. Monitor and replace as appropriate.
    E) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive; there is no specific antidote.
    B) MONITORING OF PATIENT
    1) CNS depression may occur. Monitor for clinical signs and treat symptomatically.
    2) LIVER FUNCTION - This agent is an hepatotoxin, with the liver being a primary target organ of toxic exposures. Monitor serum hepatic enzymes.
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) FLUID LOSS may occur if vomiting and/or diarrhea is extensive. Monitor and replace as appropriate.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) PULMONARY EDEMA
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    F) PSYCHOMOTOR AGITATION
    1) INDICATION
    a) If patient is severely agitated, sedate with IV benzodiazepines.
    2) DIAZEPAM DOSE
    a) ADULT: 5 to 10 mg IV initially, repeat every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    3) LORAZEPAM DOSE
    a) ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed (Manno, 2003).
    b) CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    4) Extremely large doses of benzodiazepines may be required in patients with severe intoxication in order to obtain adequate sedation. Titrate dose to clinical response and monitor for hypotension, CNS and respiratory depression, and the need for endotracheal intubation.
    G) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive; there is no specific antidote.
    B) MONITORING OF PATIENT
    1) CNS depression may occur. Monitor for clinical signs and treat symptomatically.
    2) LIVER FUNCTION - This agent is an hepatotoxin, with the liver being a primary target organ of toxic exposures. Monitor serum hepatic enzymes.
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) FLUID LOSS may occur if vomiting and/or diarrhea is extensive. Monitor and replace as appropriate.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    E) PSYCHOMOTOR AGITATION
    1) INDICATION
    a) If patient is severely agitated, sedate with IV benzodiazepines.
    2) DIAZEPAM DOSE
    a) ADULT: 5 to 10 mg IV initially, repeat every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    3) LORAZEPAM DOSE
    a) ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed (Manno, 2003).
    b) CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    4) Extremely large doses of benzodiazepines may be required in patients with severe intoxication in order to obtain adequate sedation. Titrate dose to clinical response and monitor for hypotension, CNS and respiratory depression, and the need for endotracheal intubation.
    F) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    G) HEMODIALYSIS
    1) There is no data concerning the use of hemodialysis following dimethylacetamide intoxications. However, due to its low tissue distribution and its extensive renal clearance, it may be prudent to attempt hemodialysis in severe cases or in cases of renal compromise following poisonings.
    H) HEMOPERFUSION
    1) Hemoperfusion with activated charcoal was performed for 5 hours per day for 3 days in a worker following exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days (Su et al, 2000). A decrease in urine monomethylacetamide from 3265 mg/g to 4 mg/g creatinine over 4 days was noted, but hemoperfusion clearance was not calculated. Serial urinary monomethylacetamide correlated with the clinical condition.
    I) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) There is no data concerning the use of hemodialysis following dimethylacetamide intoxications. However, due to its low tissue distribution and its extensive renal clearance, it may be prudent to attempt hemodialysis in severe cases or in cases of renal compromise following poisonings.
    B) HEMOPERFUSION
    1) Hemoperfusion with activated charcoal was performed for 5 hours per day for 3 days in a worker following exposure to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days (Su et al, 2000). A decrease in urine monomethylacetamide from 3265 mg/g to 4 mg/g creatinine over 4 days was noted, but hemoperfusion clearance was not calculated. Serial urinary monomethylacetamide correlated with the clinical condition.

Range Of Toxicity

Summary

    A) Dimethylacetamide (DMAC) has a relatively low order of acute toxicity. Between 28 and 287 grams of DMAC were given intravenously to humans over a 5 day period with dose-related toxic effects of CNS depression followed by mental excitatory states, hypotension, nausea and vomiting, and elevations of hepatic transaminase levels.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) MICE: A median lethal dose ranging from 2.2 to 4.9 grams/kilogram, depending on route of exposure, is reported for mice (Kim, 1988).
    2) RATS: A median lethal dose ranging from 2.0 to 7.5 grams/kilogram, depending on route of exposure, is reported for rats (Kim, 1988).
    3) The lethal dose for skin absorption of dimethylacetamide by pregnant rats and rabbits was approximately 7.5 g/kg and 5.0 g/kg, respectively (ACGIH, 1991).
    4) One male rat exposed to 300 ppm dimethylacetamide for 12 hours/day in a protocol totaling 10 exposures (5 exposures, 2 rest days, 5 exposures) died following the seventh exposure (Kinney et al, 1993).

Maximum Tolerated Exposure

    A) ADULT
    1) In a clinical malignancy trial, adults receiving 400 milligrams/kilogram/day of intravenous dimethylacetamide for 4 to 5 days (cumulative doses ranging from 28 to 287 grams) experienced numerous toxic effects. Symptoms included: CNS depression followed by mental excitation, nausea and vomiting, hypotension, and elevations of hepatic transaminase levels (Kim, 1988). Effects were reversible upon discontinuation of the drug.
    B) OCCUPATIONAL
    1) Workers repeatedly exposed to 20 to 25 ppm dimethylacetamide developed jaundice. Appreciable skin absorption was thought to have occurred (Hathaway et al, 1991) Marino et al, 1994).
    2) Workers exposed to dimethylacetamide for 2 to 10 years showed abnormal liver function; exposure concentrations were not reported in the study (ACGIH, 1991).
    3) Dimethylacetamide concentrations in a polymer manufacturing operation between 0 and 2 ppm, with occasional excursions between 11 and 34 ppm, caused dizziness, lethargy, and weakness (ACGIH, 1991).
    a) Concentrations between 0 and 3 ppm in metal finishing operations caused the same symptoms (ACGIH, 1991).
    C) ANIMAL DATA
    1) Repeated dermal applications to dogs of dimethylacetamide at 4 mg/kg body weight for 6 weeks produced extensive fatty infiltration of liver tissue (ACGIH, 1991).
    2) Rats exposed 6 hours/day for 2 weeks at 288 ppm dimethylacetamide had nasal irritation and liver hypertrophy (ACGIH, 1991; Hathaway et al, 1991), as well as a transient increase in blood cholesterol (Hathaway et al, 1991). Testicular atrophy was evident 2 weeks post-exposure (Hathaway et al, 1991).
    3) Daily exposure of rats at 195 ppm dimethylacetamide for 6 months produced focal necrosis of the liver (ACGIH, 1991).
    4) Exposures at 40 ppm dimethylacetamide 6 hours/day, 5 days/week for 6 months resulted in no liver damage to dogs and rats (ACGIH, 1991).
    5) Undiluted dimethylacetamide applied to the rabbit eye caused a small area of corneal necrosis (ACGIH, 1991).

Workplace Standards

    A) ACGIH TLV Values for CAS127-19-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) N,N-Dimethylacetamide
    a) TLV:
    1) TLV-TWA: 10 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    c) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): Liver dam; embryo/fetal dam
    d) Molecular Weight: 87.12
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Under Study
    1) N,N-Dimethyl acetamide
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS127-19-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Dimethyl acetamide
    2) REL:
    a) TWA: 10 ppm (35 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 300 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS127-19-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: N,N-Dimethylacetamide
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: N,N-Dimethyl acetamide
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Dimethyl acetamide
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS127-19-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Dimethyl acetamide
    2) Table Z-1 for Dimethyl acetamide:
    a) 8-hour TWA:
    1) ppm: 10
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 35
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (ORAL)MOUSE:
    a) 4620 mg/kg (RTECS, 2000)
    2) LD50- (SKIN)MOUSE:
    a) 9600 mg/kg (RTECS, 2000)
    3) LD50- (ORAL)RAT:
    a) 4300 mg/kg (RTECS, 2000)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) ANTINEOPLASTIC EFFECTS - Mouse studies have shown antineoplastic chemotherapeutic effects of dimethylacetamide by inducing differentiation of PCC4 azal embryonal carcinoma tumors grown in mice by subcutaneous transplantation. This differentiation was associated with a decrease in tumor growth rate, a decreased mitotic index, a decrease in extent of necrosis, and an increase in survival time of the mice (Kim, 1988).
    1) While dimethylacetamide has been shown to have moderate-to-high degree of antitumor effects against mouse tumors, it has also been shown to be cytotoxic to human lymphocytes cultures.
    B) MACROMOLECULAR SYNTHESIS - Dimethylacetamide appears to affect cell membrane and macromolecular synthesis through interaction with cell membranes, changing the entry of nucleotides into the cell and decreasing the synthesis of phospholipids (Kim, 1988).
    C) MYOCARDIAL CONTRACTILITY - In-vitro studies using guinea pig and rat hearts have shown that dimethylacetamide produces a dose-dependent marked positive inotropic response in electrically driven guinea pig left atrial preparations. At concentrations above those causing maximum contractility, dimethylacetamide caused a precipitous decline in tension; irreversible damage to the tissue resulted (Kim, 1988).

Physicochemical

Physical Characteristics

    A) Dimethylacetamide is a clear, colorless to pale yellow, oily liquid with a faint odor of ammonia. It is a high-boiling, polar solvent that readily dissolves gases and numerous organic and inorganic substances. It is miscible with water and all common organic solvents (Anon, 2000; Budavari, 1996; HSDB , 2001). It is a combustible liquid and vapor.
    B) It is a stable compound but is mildly hygroscopic (Kim, 1988). Dimethylacetamide has a boiling point of about 165 degrees (JEF Reynolds , 2000).

Ph

    A) pH 4 at 100 g/L, 20 degrees C (Anon, 2000a)

Molecular Weight

    A) 87.12

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, Vol 1, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991, pp 477-478.
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