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DIMETHYLFORMAMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dimethylformamide is widely used as an organic solvent in the chemical industry and in laboratories. It is well absorbed via inhalation, dermal or oral exposure. The primary target organ following acute or chronic exposure is the liver in both humans and animals.

Specific Substances

    1) Formic acid dimethylamide
    2) N,N-dimethylformamide
    3) NIOSH/RTECS LQ 2100000
    4) DMF
    5) DMFA
    6) Formyldimethylamine
    7) Dimethylformamide (German)
    8) Dimetiformamide (Italian)
    9) Dwumethyloformamide (Polish)
    10) NCI-c 60913
    11) NSC 5354
    12) CAS 68-12-2
    1.2.1) MOLECULAR FORMULA
    1) C3-H7-N-O

Available Forms Sources

    A) FORMS
    1) Dimethylformamide is a colorless to slightly yellow liquid, with a fishy or amine-like odor (HSDB , 2001).
    2) Dimethylformamide is a colorless, mobile liquid (Lewis, 2000).
    B) SOURCES
    1) Dimethylformamide is formed by the following reactions (Bingham et al, 2001; HSDB , 2001; Lewis, 1996):
    1) Carbon monoxide and dimethylamine
    2) Methyl formate and dimethylamine
    3) Formic acid and dimethylamine
    4) Hydrogen cyanide and methanol
    5) Hydrogen cyanide and dimethylamine
    C) USES
    1) Dimethylformamide, an organic solvent, is used whenever a solvent with a slow evaporation rate is needed. It is referred to as the "universal organic solvent" (Budavari, 2000).
    2) It is a solvent most often used for polar polymers and resins. It also is used in adhesives, cleaners, zinc electroplating, protective coatings, inks, film, paint removers, and in selective gas absorption (ACGIH, 1991; Ashford, 1994).
    3) It is used in orlon and acrylic fiber spinning, synthetic leather, polyurethanes, wire enamels, chemical manufacturing, pharmaceutical production, vinyl, acid gases, polyacrylic fibers, and resins. It is a catalyst in the carboxylation reaction and is used in organic synthesis and as a carrier for gases (Bingham et al, 2001; Budavari, 2000; Clayton & Clayton, 1994; Lewis, 1997).
    4) Dimethylformamide often is utilized to recover or remove acetylene, to extract butadiene from hydrocarbon streams, and to increase the amount of ethylene dichloride from direct chlorination. It is used as a reagent to determine nithiazide in feed (Bingham et al, 2001; HSDB , 2001).
    5) Dimethylformamide has also been shown to be an occasional contaminant in the sodium fluorescein used in fluorescein angiography (Jacob et al, 1982).
    6) Dimethylformamide is a solvent for a veterinary euthanasia drug, T-61(R) (Hantson et al, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Dimethyl formamide (DMF) is mildly irritating to the eyes, skin, and mucous membranes. Signs and symptoms of exposure may include vertigo; sleep disorders; blurred vision; flushing of the face, neck, arms, hands, and chest; nausea, vomiting, and abdominal pain; and hypertension. DMF is a known hepatotoxin. Hepatomegaly, jaundice, and altered liver function tests may be observed. Renal, hematologic, cardiovascular, and dermatologic effects have also been noted.
    B) Alcohol intolerance has been noted. The liver appears to be the main target organ following acute or chronic exposures.
    0.2.4) HEENT
    A) Conjunctivitis has been noted after exposure. Effects have been mild when tested in animals.
    B) Periorbital swelling may occur.
    0.2.5) CARDIOVASCULAR
    A) Hypertension has been noted in animals.
    0.2.6) RESPIRATORY
    A) Bronchoconstriction and wheezing have occurred.
    0.2.7) NEUROLOGIC
    A) Sleep disorders, dizziness, and various functional CNS effects have been noted. Poisoned animals showed agitation and hind leg paralysis.
    0.2.8) GASTROINTESTINAL
    A) Anorexia, vomiting, and abdominal pain have been seen, even after inhalation.
    0.2.9) HEPATIC
    A) DMF is a hepatotoxin in both animals and man.
    B) A single acute ingestion resulted in severe liver injury.
    0.2.10) GENITOURINARY
    A) Kidney damage has been observed in animals.
    0.2.13) HEMATOLOGIC
    A) Anemia, leukopenia, and thrombocytopenia may occur in humans and have been reported in animals.
    0.2.14) DERMATOLOGIC
    A) Contact dermatitis, as well as dermatitis due to skin defatting may occur. Alcohol-induced flushing may occur.
    0.2.15) MUSCULOSKELETAL
    A) Elevated CPK isoenzyme levels have been reported.
    0.2.17) METABOLISM
    A) Hypercholesterolemia may occur with exposure.
    0.2.20) REPRODUCTIVE
    A) Data would indicate an increase rate of abortions and miscarriages rather than teratogenesis.
    0.2.21) CARCINOGENICITY
    A) There is some limited evidence that DMF may promote testicular cancer.

Laboratory Monitoring

    A) Monitor kidney and liver function.
    B) CBC, and coagulation time may be indicated for chronically exposed patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is no antidote for dimethylformamide poisoning. Treatment is symptomatic and supportive.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) HYPERTENSION: Monitor vital signs regularly. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary. Sedation with benzodiazepines may be helpful in agitated patients with hypertension and tachycardia. For severe hypertension sodium nitroprusside is preferred. Labetalol, nitroglycerin, and phentolamine are alternatives. See main treatment section for doses.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    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) 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).
    0.4.6) PARENTERAL EXPOSURE
    A) Acute toxicity has been reported following intentional injections of veterinary drugs containing dimethylformamide as the solvent in human cases. Treatment is symptomatic and supportive.
    B) Monitor for liver toxicity and possible renal toxicity.
    C) HYPERTENSION: Monitor vital signs regularly. For mild/moderate asymptomatic hypertension (no end organ damage), pharmacologic treatment is generally not necessary. Sedation with benzodiazepines may be helpful in agitated patients with hypertension and tachycardia. For severe hypertension sodium nitroprusside is preferred. Labetalol, nitroglycerin, and phentolamine are alternatives. See main treatment section for doses.

Range Of Toxicity

    A) No specific data were available. The estimated human lethal dose is 10 g.
    B) Experimental animal LD50s (oral) are 1 to 3.7 g/kg. The TCLo (human) is estimated at 20 ppm.

Clinical Effects

Summary Of Exposure

    A) Dimethyl formamide (DMF) is mildly irritating to the eyes, skin, and mucous membranes. Signs and symptoms of exposure may include vertigo; sleep disorders; blurred vision; flushing of the face, neck, arms, hands, and chest; nausea, vomiting, and abdominal pain; and hypertension. DMF is a known hepatotoxin. Hepatomegaly, jaundice, and altered liver function tests may be observed. Renal, hematologic, cardiovascular, and dermatologic effects have also been noted.
    B) Alcohol intolerance has been noted. The liver appears to be the main target organ following acute or chronic exposures.

Heent

    3.4.1) SUMMARY
    A) Conjunctivitis has been noted after exposure. Effects have been mild when tested in animals.
    B) Periorbital swelling may occur.
    3.4.2) HEAD
    A) Flushing of the face (especially after alcohol ingestion) may be seen (Sittig, 1985; Cox & Mustchin, 1991).
    3.4.3) EYES
    A) Conjunctivitis may be seen on exposure (ITI, 1985).
    B) Periorbital swelling may be seen in DMF exposures with alcohol-induced flushing (Cox & Mustchin, 1991).
    C) ANIMAL TESTING - A 25% solution drop tested in rabbit eyes had no effect, a 50% solution was a slight irritant, 75% to 100% produced a rare severe reaction (Massmann, 1956).
    D) SPLASH CONTACT - When a drop of 100% DMF was placed in rabbit eyes followed 2 minutes later by brief irrigation with water, edema of the corneal epithelium was seen, which normalized in 2 days (Grant & Schuman, 1993).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypertension has been noted in animals.
    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) Hypertension may occur (Sittig, 1985) and has been seen in some animal experiments (Imbriani et al, 1986).
    B) PALPITATIONS
    1) Palpitations may occur, associated with alcohol intolerance following DMF exposure (NIOSH, 1990).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BRADYCARDIA
    a) Experimental animals developed bradycardia, hypotension, and degenerative changes in the myocardium (Gosselin et al, 1984). These effects have not been reported in exposed humans.

Respiratory

    3.6.1) SUMMARY
    A) Bronchoconstriction and wheezing have occurred.
    3.6.2) CLINICAL EFFECTS
    A) BRONCHOSPASM
    1) Bronchoconstriction may occur with wheezing associated with spontaneous and alcohol-induced flushing after DMF exposures (Cox & Mustchin, 1991).

Neurologic

    3.7.1) SUMMARY
    A) Sleep disorders, dizziness, and various functional CNS effects have been noted. Poisoned animals showed agitation and hind leg paralysis.
    3.7.2) CLINICAL EFFECTS
    A) SLEEP DISORDER
    1) Sleep disorders have been seen after exposure (O'Donoghue, 1985).
    B) DIZZINESS
    1) Vertigo may occur postexposure (O'Donoghue, 1985).
    C) NEUROPATHY
    1) Functional nervous system disorders have been reported (O'Donoghue, 1985).
    D) HEADACHE
    1) Headache as well as weakness may occur (NIOSH, 1990).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) AGITATION
    a) Fatally poisoned mice developed agitation followed by hind leg paralysis (Gosselin et al, 1984).

Gastrointestinal

    3.8.1) SUMMARY
    A) Anorexia, vomiting, and abdominal pain have been seen, even after inhalation.
    3.8.2) CLINICAL EFFECTS
    A) LOSS OF APPETITE
    1) Anorexia and various digestive disturbances, including nausea, epigastric pain, and vomiting, have been reported in exposed workers (Gosselin et al, 1984; ITI, 1985) ACGIH, 1986; (Huang et al, 1998).
    B) ABDOMINAL PAIN
    1) Nausea, vomiting, constipation, diarrhea, and colic may occur after either inhalation or skin contact (Sittig, 1985; Hathaway et al, 1996; Huang et al, 1998). Exposure to 20 ppm and sometimes higher concentrations for 32 weeks produced such symptoms (Procter et al, 1991; NIOSH, 1990). Abdominal pain may be a common effect of occupational dimethylformamide exposure (Yang et al, 1996).
    C) LOSS OF TASTE
    1) DYSGEUSIA - Abnormal taste may develop in DMF exposures with ethanol intolerance (Cox & Mustchin, 1991).

Hepatic

    3.9.1) SUMMARY
    A) DMF is a hepatotoxin in both animals and man.
    B) A single acute ingestion resulted in severe liver injury.
    3.9.2) CLINICAL EFFECTS
    A) LARGE LIVER
    1) Hepatomegaly and other signs of hepatic damage may be seen after exposure via inhalation or skin contact (Sittig, 1985; Redlich et al, 1988; Finkel, 1983; Huang et al, 1998). Following chronic exposures, the most significant liver biopsy finding is steatosis, mainly macrovesicular (Hantson et al, 1996). Toxicity appears to be dose dependent and may be delayed following a higher dose (Van den Bulcke et al, 1994).
    2) After working in an enclosed and poorly-ventilated workplace for one day, an episode of acute hepatitis with jaundice and elevated serum liver enzymes due to dimethylformamide exposure was reported in a previously healthy 42-year-old male. He was admitted to the hospital and discharged 10 days asymptomatic (Huang et al, 1998).
    B) LIVER ENZYMES ABNORMAL
    1) Redlich et al (1988) recently investigated a fabric-coating plant and found workers exposed to DMF (and other solvents) in poorly ventilated areas without appropriate skin protection. Blood tests revealed elevated liver enzymes (suggesting liver injury) in 35 of the 46 production workers tested; this percentage of abnormal tests (76%) was unusually high. The enzyme levels generally returned to normal within 1 to 5 months after removal from this exposure. However, four workers whose tests remained abnormal underwent liver biopsies. Examination of the biopsied tissues revealed damage that could have been caused by a chemical exposure (NIOSH, 1990a).
    2) Nicolas et al (1990) reported the occurrence of elevated serum total and conjugated bilirubin, elevated serum transaminase levels, decreased prothrombin factors, and decreased factor V (50%) 48 hours after self-injection of 0.3 mL/kg intramuscularly of an euthanasia drug (0.18 mL/kg of DMF).
    3) An intracardiac injection of T-61(R), a veterinary euthanasia drug containing dimethylformamide as the solvent, was self-administered in a suicide attempt by a 44-year-old male. Delayed, transient abnormal liver function tests, which peaked on day 14, were reported to be possibly due to the solvent, dimethylformamide or its metabolites (Hantson et al, 1996).
    4) Fiorito et al (1997) performed a cross-sectional study of the prevalence of chronic liver function alterations in 75 workers employed in a synthetic leather factory exposed to DMF air concentrations below TLVs (30 mg/m(3)). The study revealed a high percentage of gastrointestinal symptoms (50%) and liver function abnormalities (22.7%), compared with a demographically similar group of unexposed workers.
    a) Covariance analysis (ANCOVA) revealed that transaminase levels were significantly higher in exposed workers than in controls after data were corrected for age, alcohol consumption, body mass index, and cholesterol levels. DMF induced liver damage even if air TLVs were respected because accidental skin contact with liquid DMF significantly increased DMF uptake.
    C) LIVER DAMAGE
    1) Seven patients exposed occupationally to DMF presented with toxic liver injury. In the 3 exposed less than 3 months, aminotransferase activities were markedly increased. Liver biopsies indicated focal hepatocellular necrosis and microvesicular steatosis with prominence of smooth endoplasmic reticulum (SER), complex lysosomes, and pleomorphic mitochondria having crystalline inclusions. In the 4 exposed during more than a year, liver biopsies revealed macrovesicular steatosis, pleomorphic mitochondria without crystalline inclusions, and prominent SER; no persistent acute injury or fibrosis was evident (Redlich et al, 1990).
    D) HEPATIC FAILURE
    1) Hepatotoxicity ranging from mild hepatitis to fatal fulminant hepatic failure has been reported after ingestion or intravenous injection of veterinary euthanasia drugs containing DMF (Trevisani et al, 1993). Hepatotoxicity and fulminant liver failure have been reported to occur within 3 to 22 days following exposure to this drug (Hantson et al, 1996).
    2) Fulminant hepatic failure developed 48 hours after ingestion of 0.6 mL/kg of DMF. Fulminant hepatitis with onset of jaundice, and flopping tremor developed on the sixth day, coma on the seventh day, and death on the ninth day (Nicolas et al, 1990).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC NECROSIS
    a) Hepatic necrosis has been seen in tested animals along with fatty degeneration (Massmann, 1956; Clayton et al, 1963; Lundberg et al, 1986; Malley et al, 1994).
    b) Van den Bulcke et al (1994) reported on the metabolism and hepatotoxicity of dimethylformamide (DMF) in rats. DMF and 2 of its metabolites were evaluated over a 4 day period. It was observed that DMF toxicity was dose dependent, with delayed toxicity occurring after administration of a high dose (13.7 mmol/kg) in comparison to a lower dose (4.1 mmol/kg). Hepatotoxicity occurred later for DMF than for its metabolites.
    2) HEPATOMEGALY
    a) Liver hypertrophy and necrosis were seen in rats and mice exposed at concentrations up to 400 ppm DMF by inhalation for 6 hours per day, 5 days per week, for 2 years or 18 months, respectively (Malley et al, 1994).

Genitourinary

    3.10.1) SUMMARY
    A) Kidney damage has been observed in animals.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FAILURE
    a) Kidney damage may be seen. It has been reported in animals exposed to 100 to 450 ppm for 4 months (Massmann, 1956; Sittig, 1985).
    2) CARCINOMA
    a) Testicular cancer has been suggested by animal studies (Pham et al, 1971) and a few case reports (Levin et al, 1987; (Ducatman et al, 1986) but has not been demonstrated in other cohort studies (Chen & Kennedy, 1988). More work needs to be done to determine risk.

Hematologic

    3.13.1) SUMMARY
    A) Anemia, leukopenia, and thrombocytopenia may occur in humans and have been reported in animals.
    3.13.2) CLINICAL EFFECTS
    A) THROMBOCYTOPENIC DISORDER
    1) PLATELET ACTIVITY - 15 workers who had been exposed to DMF for about 8 years (no concentrations available) were studied and found to have a decrease in platelets and longer coagulation times than a control group of 28 workers (Imbriani et al, 1986).
    B) LEUKOPENIA
    1) Leukopenia with relative or absolute lymphocytosis has been seen after exposures (Clayton et al, 1963; DiLorenzo & Grazioli, 1972).
    C) PROTHROMBIN TIME LOW
    1) Following hepatotoxicity, a patient was observed to have severely depressed prothrombin activity and increased activated partial thromboplastin time (Trevisani et al, 1993).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANEMIA
    a) Anemia of moderate severity was seen in animal studies after chronic exposure to DMF (Clayton et al, 1963).
    2) POLYCYTHEMIA
    a) Experimental animals developed polycythemia (Gosselin et al, 1984).

Dermatologic

    3.14.1) SUMMARY
    A) Contact dermatitis, as well as dermatitis due to skin defatting may occur. Alcohol-induced flushing may occur.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Dermatitis may be seen after exposure (Sittig, 1985), including itching and desquamation of the skin (ITI, 1985). Contact dermatitis resulting in vesicular and intensely pruriginous eczema has been reported in people working with DMF (Camarasa, 1987).
    B) FLUSHING
    1) Prolonged spontaneous and alcohol-induced flushing has been reported in industrial exposures to DMF (Proctor & Hughes, 1978). In one patient, symptoms persisted for many months following discontinuance of exposure (Cox & Mustchin, 1991).
    C) ERUPTION
    1) Dimethyl formamide exposure can cause nausea and irritation of the eyes, mucous membranes, and skin (CHRIS, 1985; (Finkel, 1983; Sax & Lewis, 1989; ITI, 1985). Dermal absorption readily occurs (Finkel, 1983) ACGIH, 1986).
    2) CASE REPORT - A worker who had direct dermal contact over about 20 percent of the body developed initial skin irritation and hyperemia. Abdominal pain and vomiting developed 62 hours later, and hypertension was noted. All symptoms had cleared by the seventh day after exposure (Proctor & Hughes, 1978).

Musculoskeletal

    3.15.1) SUMMARY
    A) Elevated CPK isoenzyme levels have been reported.
    3.15.2) CLINICAL EFFECTS
    A) ENZYMES/SPECIFIC PROTEIN LEVELS - FINDING
    1) Industrial exposure to DMF have been associated with increased CPK isoenzyme levels but no specific damage to muscles has been reported (Wang & Lai, 1991).

Reproductive

    3.20.1) SUMMARY
    A) Data would indicate an increase rate of abortions and miscarriages rather than teratogenesis.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Dimethylformamide exposure during pregnancy has caused fetotoxicity, reductions in the number of implants, and musculoskeletal and craniofacial abnormalities in the offspring in rats (RTECS , 2000).
    2) The NOAEL for developmental toxicity in rats has been given as 50 mg/kg per day by gavage (Saillenfait et al, 1997). A NOAEL could not be established for mice in a continuous breeding study of DMF in drinking water at concentrations up to 4,000 ppm (Fail et al, 1998).
    3) DMF has also been embryotoxic, fetotoxic, and teratogenic in several species of animals, including rabbits (Merkle & Zeller, 1980; Stula & Krauss, 1977), rats (Stula & Krauss, 1977; Gofmekler, 1974; Gofmekler et al, 1970; Kimmerle & Machemer, 1975; pp 119-123), and mice (Scheufler, 1976; Scheufler & Freye, 1975). Generally it has been active by any route of exposure.
    4) The primary metabolite monomethylformamide was a more potent teratogen in rabbits than the parent compound (Merkle & Zeller, 1980; Von-Kreybid, 1968).
    5) In a mouse limb bud assay, the toxicity of DMF was shown to be related to the magnitude of glutathione binding (Klug et al, 1998).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) ABORTION
    a) DMF has been associated with adverse reproductive effects in humans. Women exposed to 100 mg/m(3) (10X the TLV) had a tenfold increase in miscarriages (pp 119-123). There were 3 cases of intrauterine death in the last trimester among female laboratory workers who were exposed to DMF and other solvents (Farquaharson et al, 1983).
    b) Various studies have been done to evaluate DMF's effects in pregnancy. The results are inconsistent, with the best conclusion being that DMF does not cause malformations of the fetus, but can produce increased embryonal deaths, especially when near the lethal dose for the mother (ACGIH, 1986).
    B) ANIMAL STUDIES
    1) DMF causes abortions in pregnant rats but not mice (CHRIS, 1985). Miscarriages have been noted in workers in synthetic fiber industry (Schardein, 1985) and laboratory workers (Farquaharson et al, 1983).
    2) DMF applied to the skin of pregnant rats resulted in reduced body weight, weight gain, and pregnancy rate. Reduced numbers of live fetuses and fetal weight, and increased postimplantation loss were noted. These effects appeared to be dose related (Hansen & Meyer, 1990).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS68-12-2 (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) IARC Classification
    a) Listed as: Dimethylformamide
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) There is some limited evidence that DMF may promote testicular cancer.
    3.21.3) HUMAN STUDIES
    A) TESTIS NEOPLASM MALIGNANT
    1) Dimethylformamide has been linked with testicular cancer in humans from occupational exposures in two separate studies (Hathaway et al, 1991; (Ducatman et al, 1986; Levine et al, 1987). Excess cases of cancers of the buccal cavity and pharynx, and malignant melanoma, were also seen in another occupational study. Prostate cancers occurred with mixed exposures to acrylonitrile (Chen & Kennedy, 1988).
    a) More research needs to be done to determine whether industries have associated testicular cancer with DMF exposure. It has been suggested that DMF may be a co-carcinogen (Gollins, 1991).
    b) Other case reports from leather tanning and aircraft maintenance industries have associated testicular cancer with DMF exposure. DMF may be a co-carcinogen (Gollins, 1991).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) SUMMARY - Animal studies published to date have failed to establish a link between DMF and cancer. The International Agency for Research on Cancer (IARC) recently classified the evidence associating DMF with cancer in animals as "inadequate." However, on the basis of the published literature reviewed above, IARC found "limited evidence" that DMF causes cancer in humans and classified DMF as "possibly carcinogenic to humans" (IARC Group 2 B) (NIOSH, 1990a).
    2) DMF was not carcinogenic in rats or mice by the inhalation route at concentrations up to 400 ppm (Malley et al, 1994).
    B) TESTIS NEOPLASM MALIGNANT
    1) TESTICULAR CANCER has been suggested by animal studies (Pham et al, 1971) and a few case reports (Levin et al, 1987; (Ducatman et al, 1986; Calvert et al, 1990) but has not been demonstrated in other cohort studies (Chen & Kennedy, 1988).
    C) LACK OF EFFECT
    1) TUMORS - Rats given 75 to 150 mg/kg orally over an extended period of time (total dose of 380 g/kg) showed NO tumors. Similarly, injecting rats subcutaneously with 200 to 400 mg/kg/week (total dose 8 to 10 g) produced NO tumors (ACGIH, 1986).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor kidney and liver function.
    B) CBC, and coagulation time may be indicated for chronically exposed patients.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor for liver toxicity.
    B) HEMATOLOGIC
    1) Monitor CBC.
    C) COAGULATION STUDIES
    1) Monitor coagulation time.
    4.1.3) URINE
    A) OTHER
    1) The presence of monomethylformamide (the metabolite) is used as a biological indicator of exposure (Finkel, 1983). Urinary levels of N-methylformamide may be used as an indicator of exposure, and as a biomarker to assess the body burden of dimethylformamide exposure (Chang et al, 2004).
    2) Biological monitoring should be instituted if skin contact with liquid DMF might occur. Such monitoring may be accomplished by collecting urine at the end of the exposure period and analyzing it for certain metabolites of DMF. Biological monitoring can provide additional information regarding the effectiveness of engineering controls, work practices, and personal protective equipment (NIOSH, 1990a).

Methods

    A) CHROMATOGRAPHY
    1) BLOOD - Both dimethyl and methyl formamide have been identified in blood after extraction into ethanol by nitrogen-selective gas chromatography (Kimmerle & Eben, 1975a).
    2) URINE DETERMINATIONS - Methylformamide levels have been ascertained using flame-ionization gas chromatography (Barnes & Henry, 1974; Lauwerys et al, 1980).
    3) AIR - Gas chromatography has been used to measure air concentrations of DMF (Wang & Lai, 1991).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor kidney and liver function.
    B) CBC, and coagulation time may be indicated for chronically exposed patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive, there is no specific antidote.
    B) MONITORING OF PATIENT
    1) LIVER FUNCTION - This agent is a hepatotoxin, with the liver being the primary target organ of toxic exposures.
    2) KIDNEY FUNCTION - Renal toxicity has been seen in animals.
    3) CBC - Anemia and lymphocytosis have been reported in animals; decreased platelets and increased coagulation time has been seen in humans chronically exposed.
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) FLUID LOSS may occur if vomiting is extensive.
    D) HYPERTENSIVE EPISODE
    1) Monitor vital signs regularly. For mild/moderate hypertension without evidence of end organ damage, pharmacologic intervention is generally not necessary. Sedative agents such as benzodiazepines may be helpful in treating hypertension and tachycardia in agitated patients, especially if a sympathomimetic agent is involved in the poisoning.
    2) For hypertensive emergencies (severe hypertension with evidence of end organ injury (CNS, cardiac, renal), or emergent need to lower mean arterial pressure 20% to 25% within one hour), sodium nitroprusside is preferred. Nitroglycerin and phentolamine are possible alternatives.
    E) MALIGNANT HYPERTENSION
    1) SODIUM NITROPRUSSIDE/INDICATIONS
    a) Useful for emergent treatment of severe hypertension secondary to poisonings. Sodium nitroprusside has a rapid onset of action, a short duration of action and a half-life of about 2 minutes (Prod Info NITROPRESS(R) injection for IV infusion, 2007) that can allow accurate titration of blood pressure, as the hypertensive effects of drug overdoses are often short lived.
    2) SODIUM NITROPRUSSIDE/DOSE
    a) ADULT: Begin intravenous infusion at 0.1 microgram/kilogram/minute and titrate to desired effect; up to 10 micrograms/kilogram/minute may be required (American Heart Association, 2005). Frequent hemodynamic monitoring and administration by an infusion pump that ensures a precise flow rate is mandatory (Prod Info NITROPRESS(R) injection for IV infusion, 2007). PEDIATRIC: Initial: 0.5 to 1 microgram/kilogram/minute; titrate to effect up to 8 micrograms/kilogram/minute (Kleinman et al, 2010).
    3) SODIUM NITROPRUSSIDE/SOLUTION PREPARATION
    a) The reconstituted 50 mg solution must be further diluted in 250 to 1000 mL D5W to desired concentration (recommended 50 to 200 mcg/mL) (Prod Info NITROPRESS(R) injection, 2004). Prepare fresh every 24 hours; wrap in aluminum foil. Discard discolored solution (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    4) SODIUM NITROPRUSSIDE/MAJOR ADVERSE REACTIONS
    a) Severe hypotension; headaches, nausea, vomiting, abdominal cramps; thiocyanate or cyanide toxicity (generally from prolonged, high dose infusion); methemoglobinemia; lactic acidosis; chest pain or dysrhythmias (high doses) (Prod Info NITROPRESS(R) injection for IV infusion, 2007). The addition of 1 gram of sodium thiosulfate to each 100 milligrams of sodium nitroprusside for infusion may help to prevent cyanide toxicity in patients receiving prolonged or high dose infusions (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    5) SODIUM NITROPRUSSIDE/MONITORING PARAMETERS
    a) Monitor blood pressure every 30 to 60 seconds at onset of infusion; once stabilized, monitor every 5 minutes. Continuous blood pressure monitoring with an intra-arterial catheter is advised (Prod Info NITROPRESS(R) injection for IV infusion, 2007).
    6) NITROGLYCERIN/INDICATIONS
    a) May be used to control hypertension, and is particularly useful in patients with acute coronary syndromes or acute pulmonary edema (Rhoney & Peacock, 2009).
    7) NITROGLYCERIN/ADULT DOSE
    a) Begin infusion at 10 to 20 mcg/min and increase by 5 or 10 mcg/min every 5 to 10 minutes until the desired hemodynamic response is achieved (American Heart Association, 2005). Maximum rate 200 mcg/min (Rhoney & Peacock, 2009).
    8) NITROGLYCERIN/PEDIATRIC DOSE
    a) Usual Dose: 29 days or Older: 1 to 5 mcg/kg/min continuous IV infusion. Maximum 60 mcg/kg/min (Laitinen et al, 1997; Nam et al, 1989; Rasch & Lancaster, 1987; Ilbawi et al, 1985; Friedman & George, 1985).

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.

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).

Enhanced Elimination

    A) HEMOFILTRATION
    1) Hantson et al (1996) reported the use of continuous arteriovenous hemofiltration (CAVH) from day 2 to day 15, while intermittent hemodialysis was performed from day 6 to day 21 in an adult following the intracardiac injection of T-61(R), a veterinary euthanasia drug containing dimethylformamide (DMF) as the solvent. The authors reported significant amounts of the metabolite, N-hydroxymethyl-N-methylformamide, were found in the hemodialysis and CAVH fluids.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) DERMAL
    a) ADULT
    1) A worker had DMF liquid splashed on greater than 20% of his body and initially experienced only redness and dermal irritation. 62 hours later abdominal pain occurred which progressed to vomiting. Blood pressure of 190/100 was also noted. The effects gradually subsided to normal over the next 7 days (Potter, 1973).
    2) ORAL
    a) ADULT
    1) A 30 year-old female ingested 50 mL of T61 (0.75 mg/kg) and presented to the hospital with drowsiness, disorientation, muscle hypertonia, and upper limb myoclonus. Severe liver injury developed 2 days after ingestion; treatment included intravenous reduced glutathione therapy. Her liver function tests normalized completely within 2 months (Trevisani et al, 1993).

Range Of Toxicity

Summary

    A) No specific data were available. The estimated human lethal dose is 10 g.
    B) Experimental animal LD50s (oral) are 1 to 3.7 g/kg. The TCLo (human) is estimated at 20 ppm.

Minimum Lethal Exposure

    A) ACUTE
    1) Estimated lethal dose in humans is 10 grams, (ACGIH, 1986), but there are no reports of human deaths.
    B) ANIMAL DATA
    1) Exposure to air saturated with 5000 ppm of dimethylformamide for 6 hours killed rats and caused lung, liver, and kidney injury. Five 6-hour exposures to 2500 ppm of dimethylformamide in air also killed rats (ACGIH, 1991).
    2) Maternal mortality resulted when rats were fed 1510 mg/kg of dimethylformamide from gestational days 6 through 15. The same oral doses also produced reduced fetal weights, increased skeletal variations, and malformations (Bingham et al, 2001).

Maximum Tolerated Exposure

    A) ADULT
    1) Exposure to airborne concentrations of 25 to 60 ppm was associated with elevated alanine aminotransferase (ALT) levels (Wang & Lai, 1991).
    2) Three men whose skin was continually exposed to dye containing dimethylformamide developed testicular tumors and presented with similar histological findings following 8- to 14-year latency periods (Hathaway et al, 1996).
    3) CARCINOGENICITY RATINGS:
    a) IARC Rating - Group 2B, possibly carcinogenic to humans (ACGIH, 1991).
    B) ANIMAL DATA
    1) Rats had liver damage after exposure for 6 months to 5000 ppm of dimethylformamide in the drinking water. Mice, guinea pigs, gerbils, and dogs had liver damage after oral treatment with the compound (Bingham et al, 2001).
    2) Dogs exposed to concentrations greater than 20 ppm had a decreased pulse rate, degenerative changes in the heart muscle, and a decline in systolic pressure (HSDB , 2001).
    3) Cats showed liver damage after repeated exposures to concentrations of dimethyl formamide at 100 ppm (HSDB , 2001).
    4) Chronic exposures caused abortions in pregnant rats. The implication is, it can possibly occur in humans (CHRIS , 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ROUTE OF EXPOSURE
    a) When 21 ppm for 4 hours was inhaled, DMF levels reached 2.8 milligrams/liter and were not detectable at 4 hours. The metabolite, methylformamide, averaged 1 to 2 milligrams/liter and was found for 4 hours postexposure (Baselt, 1982).
    b) When 87 ppm were used for 4 hours, the peak level of DMF was 14 milligrams/liter and the peak methylformamide level was 8 milligrams/liter (Kimmerle & Eben, 1975).
    c) Workers in 2 plants, both with airborne concentrations of N,N-dimethylformamide (DMF) of 4 ppm, were monitored. In one plant, workers' hands were also exposed to liquid DMF at an average daily concentration of 7.62 mcg/cm(2). A significant pattern of linear accumulation across a 5-day work week was found in workers with dermal exposure, but not in those exposed only to airborne DMF (Chang et al, 2005).

Workplace Standards

    A) ACGIH TLV Values for CAS68-12-2 (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) Dimethylformamide
    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
    d) Molecular Weight: 73.09
    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) Dimethylformamide
    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 CAS68-12-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Dimethylformamide
    2) REL:
    a) TWA: 10 ppm (30 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: 500 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS68-12-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Dimethylformamide
    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: Dimethylformamide
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: N,N-Dimethylformamide
    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): 3 ; Listed as: Dimethylformamide
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Dimethylformamide
    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 CAS68-12-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Dimethylformamide
    2) Table Z-1 for Dimethylformamide:
    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: 30
    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) References: ACGIH, 1991 Bingham et al, 2001 Budavari, 2000 CHRIS, 2001 HSDB, 2001 ITI, 1995 Lewis, 2000 RTECS, 2001
    1) LD50- (INHALATION)MOUSE:
    a) 3000 mg/kg for 2H (Bingham et al, 2001)
    2) LD50- (INTRAMUSCULAR)MOUSE:
    a) 3800 mg/kg (Lewis, 2000)
    b) 3900 mg/kg
    3) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1120 mg/kg (HSDB, 2001)
    b) 650 mg/kg
    c) 6.2 mL/kg (Budavari, 2000)
    d) 1100-6200 mg/kg (Bingham et al, 2001)
    4) LD50- (ORAL)MOUSE:
    a) 6.8 mL/kg (Budavari, 2000)
    b) 2900 mg/kg
    c) 3750 mg/kg (Lewis, 2000)
    d) 3800-6800 mg/kg (Bingham et al, 2001)
    5) LD50- (SUBCUTANEOUS)MOUSE:
    a) 4500 mg/kg
    b) 3500-5100 mg/kg (Bingham et al, 2001)
    6) LD50- (INHALATION)RAT:
    a) >2500 mg/kg for 4-and 6H (Bingham et al, 2001)
    b) 3000 mg/kg (Bingham et al, 2001)
    7) LD50- (INTRAPERITONEAL)RAT:
    a) 1400 mg/kg
    b) 1400-4800 mg/kg (Bingham et al, 2001)
    c) 4.7 mL/kg (Budavari, 2000)
    8) LD50- (ORAL)RAT:
    a) 7.6 mL/kg (Budavari, 2000)
    b) 1500 mg/kg (ITI, 1995)
    c) 2800 mg/kg
    d) 2000-2200 mg/kg (Bingham et al, 2001)
    e) 3500 mg/kg (ACGIH, 1991)
    f) 5-15 g/kg (Grade 1) (CHRIS, 2001)
    9) LD50- (SKIN)RAT:
    a) 1700-4000 mg/kg (Bingham et al, 2001)
    10) LD50- (SUBCUTANEOUS)RAT:
    a) 3800 mg/kg
    b) 3000-3500 mg/kg (Bingham et al, 2001)
    11) TCLo- (INHALATION)HUMAN:
    a) 20 ppm (ITI, 1995)
    12) TCLo- (INHALATION)MOUSE:
    a) Female, 200 ppm for 6H at 13W prior to mating -- maternal effects and effects on menstrual cycle
    b) 800 ppm for 6H/13W - intermittent -- liver, bladder, and weight loss or decreased weight gain
    13) TCLo- (INHALATION)RAT:
    a) 4 mg/m(3) for 4H at 1-19D pregnancy -- pre-implantation mortality, fetotoxicity (except death), fetal death
    b) Female, 300 ppm for 6H at 6-15D of pregnancy -- fetotoxicity (except death)
    c) Female, 287 ppm for 6H at 0-19D of pregnancy -- post-implantation mortality, fetotoxicity (except death), extra-embryonic structures
    d) Male, 50 ppm for 6H at 13W prior to mating -- spermatogenesis
    e) Female, 800 ppm for 6H at 13W prior to mating -- maternal and endocrine effects
    f) Female, 600 mg/m(3) for 24H at 1-19D of pregnancy -- behavioral effects on newborn
    g) 2523 ppm for 6H/5D - intermittent -- death
    h) 300 mg/m(3) for 4H/26W - intermittent -- CNS effects, altered sleep time
    i) 500 mcg/m(3) for 24H/60D - continuous -- urine and biochemical changes
    j) 400 ppm for 6H/13W - intermittent -- liver, blood, and biochemical changes

Pharmacology Toxicology

Toxicologic Mechanism

    A) No exact mechanism of toxicity has been determined, but Whitby et al (1984) found that N-methylformamide (not dimethylformamide, N-hydroxymethylformamide or formamide) to dose dependently decrease the ability of the liver mitochondria to sequester calcium ions. They propose that the metabolite affecting the mitochondria calcium pump may be at least part of the toxic mechanism.
    B) The toxic profiles show that toxicity of DMF and its metabolites is N-methylformamide greater than N-hydroxymethyl-N-methylformamide greater than dimethylformamide (Scailteur & Lauwerys, 1984).
    C) Depression of cytosylic alcohol dehydrogenase, leading to elevated acetaldehyde levels following ethanol ingestion is the probable toxic mechanism of DMF-induced alcohol intolerance. Alcohol delays excretion of DMF (Cox & Mustchin, 1991).

Physicochemical

Physical Characteristics

    A) Dimethylformamide is a colorless to slightly yellow liquid (Budavari, 2000). It also is described as a water-white colored liquid (Lewis, 1997).
    B) It has a faint amine or "fishy" odor (AAR, 1994; (Budavari, 2000).

Ph

    A) 6.7 (for a 0.5 M aqueous solution) (Budavari, 2000)

Molecular Weight

    A) 73.38

References

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