N,N-DIETHYL-meta-TOLUAMIDE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
N,N-DIETHYL-meta-TOLUAMIDE m-TOLUAMIDE, N,N-DIETHYL- AI 3-22542 AUTAN BAKER'S ANTIFOL BENZAMIDE, N,N-DIETHYL-3-METHYL- CHEMFORM DEET DELPHENE m-DELPHENE DET DETA m-DETA DETA-20 DETAMIDE DIELTAMID N,N-DIETHYL-3-METHYLBENZAMIDE DIETHYLTOLUAMIDE DIETHYL-m-TOLUAMIDE N,N-DIETHYL-m-TOLUAMIDE M-DET FLYPEL METADELPHENE 3-METHYL-N,N-DIETHYLBENZAMIDE MGK DIETHYLTOLUAMIDE NAUGATUCK DET OFF REPEL REPPER-DET REPUDIN-SPECIAL m-TOLUIC ACID DIETHYLAMIDE
IDENTIFIERS
USES/FORMS/SOURCES
DEET is one of the most widely used insect repellents, estimated to be used by 30 percent of Americans every year (Veltri et al, 1994). It is particularly effective against mosquitoes. Typically, commercial formulations use DEET dissolved in ALCOHOL (HSDB). It is the active ingredient in OFF!(R).
N,N-DIETHYL-meta-TOLUAMIDE (DEET(TM)) is a nearly odorless liquid which is soluble in alcohol, benzene, and ether, and is practically insoluble in water (Budavari, 1996). It is miscible with ethanol, isopropanol, propylene glycol, and cottonseed oil (Hayes & Laws, 1991). The commercial grade is 85 percent meta- isomer, with the remainder being the ortho- and para- isomers (HSDB).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- Editor's Note: An ERG guide with information appropriate to this material does not exist.
ACUTE CLINICAL EFFECTS
- Acute and chronic exposure can produce hypotension, bradycardia, erythematous bullous skin eruptions, urticaria, confusion, slurred speech, muscle cramps, insomnia, tremor, clonic jerking, psychosis, seizures, coma, or anaphylactic reaction (Budavari, 1996).
- In acute exposures, DEET is not very toxic to experimental animals with oral and dermal LD50's in the range of 2 to 5 g/kg and inhalation LC50's typically being approximately 5,000 mg/m(3) (Hayes & Laws, 1991). DEET was a primary irritant when applied to the skin or eyes of rabbits, and has produced desquamation when repeatedly applied to human skin (HSDB). Rats exposed to airborne concentrations of 2,300 to 4,000 mg/m(3) for 4 hours had behavioral effects (Sherman, 1979).
- Contact urticaria has been described after topical application of DEET (Maibach & Johnson, 1975; Von Mayenburg & Rakoski, 1983). A bullous eruption in the antecubital and popliteal fossae that may progress to painful skin necrosis and permanent scarring has been described after topical use of 50 to 75 percent DEET preparations (Lamberg & Mulrennan, 1969; Reuveni & Yagupsky, 1982). Anaphylaxis has been reported after topical DEET application (Miller, 1982).
- Inhalation and ocular exposure routes are most likely to result in signs or symptoms; death may occur following suicidal ingestion (Veltri et al, 1994).
- Hypotension has been reported after ingestion of large amounts (Tenenbein, 1987). Bradycardia is rare but has been reported after dermal exposure to DEET (Clem et al, 1993).
- Toxic encephalopathy has been reported after ingestion or excessive dermal application of DEET. Signs and symptoms include restlessness, drowsiness, irritability, weakness, ataxia, tremors, confusion, agitation, slurred speech, headaches, athetosis and, in severe cases, coma (Zadikoff, 1979; (Edwards & Johnson, 1987; Heick et al, 1980; Roland et al, 1985; Tenenbein, 1987). Neurologic symptoms may develop within 30 minutes of ingestion (Tenenbein, 1987).
- Generalized tonic-clonic seizures may develop within 30 minutes after excessive dermal use or ingestion of DEET (Zadikoff, 1979; (Tenenbein, 1987; Roland et al, 1985; CDC, 1989) Lipscomb et at, 1992). Most case reports have described a prodrome of ataxia, irritability, confusion, and/or disorientation prior to the onset of seizures; rarely seizures have occurred without warning (Lipscomb et al, 1992). Tremors, ataxia, opisthotonos, athetosis and myoclonic jerking may develop with DEET-induced encephalopathy (Zadikoff, 1979; (Tenenbein, 1987; Edwards & Johnson, 1987). Cerebral edema has been found at autopsy in fatal cases of DEET exposure (Zadikoff, 1979; Heick et al, 1987).
- (14-C)-DEET was well absorbed by the oral route in rats, with 85 to 91 percent of the administered dose appearing in the urine, and 3 to 5 percent in the feces. A total of 74 to 78 percent of the dose was in the urinary fraction, and 4 to 7 percent in the feces after a single dermal application of 100 mg/kg, but the rate of absorption and excretion were much slower from the dermal route than orally (Schoenig et al, 1996).
- It is rapidly absorbed after dermal application in experimental animals (Hayes & Laws, 1991). Metabolism and elimination are also rapid, with the major urinary metabolites in rats and rabbits being m-toluric, hippuric, and benzoic acids (Hayes & Laws, 1991). Known human urinary metabolites are m-carboxyl-N,N-diethylbenzoylamide and N-hydroxyethyl-N-ethyl-m-toluamide glucuronide (Hayes & Laws, 1991).
- Nausea and vomiting may develop after ingestion or dermal exposure to DEET (Heick et al, 1980; Pronczuk de Garbino & Laborde, 1983; Roland et al, 1985). Abdominal pain developed in a 6-year-old girl with suspected ornithine carbamoyl transferase deficiency after copious use of a DEET containing insect repellent (Heick et al, 1980). Toxic hepatitis has been reported in patients developing severe neurologic toxicity after topical exposure or ingestion of DEET (Konovalov & Romanov, 1980; Heick et al, 1980).
- Acute manic psychosis with paranoid and grandiose delusions, pressured speech, and flight of ideas developed in a 30-year-old man after two weeks of daily application of a 70 percent DEET preparation to treat a skin rash (Snyder et al, 1986). The patient would apply the DEET to half of his body followed by 60 to 90 minutes in a sauna, and then repeat the exposure to the other side of his body. Symptoms resolved after five days of treatment with haloperidol and cessation of exposure.
- Acute oral lethality of DEET co-administered with pyridostigmine bromide and permethrin was increased in a greater than additive fashion in rats. The combination of DEET and pyridostigmine also had greater than additive acute lethality (McCain et al, 1997).
CHRONIC CLINICAL EFFECTS
- Several fatal cases of DEET overexposure have occurred in children, and exposures greater than 4 grams per week may produce neurotoxic effects (Robbins & Cherniack, 1986). Behavioral effects were seen in a child who had been heavily treated with DEET over a period of 2 weeks. These effects included disorientation, loss of coordination, slurred speech, and sudden movements (Gryboski, 1961).
- Chronic DEET usage can produce very high exposures. In a study of employees at Everglades National Park, NIOSH found that field personnel may use a cumulative dose of 100 g per week (McConnel et al, 1985).
- When used regularly, the estimated human exposure is 442 grams (nearly a pound) over 6 months (Robbins & Cherniack, 1986). DEET has been extensively studied by the US Army, where it was used in field trials. Significant depot storage occurs in the skin with chronic dermal application (Robbins & Cherniack, 1986).
- DEET was not a sensitizer when applied to the skin of guinea pigs (Ambrose, 1959). Behavioral effects were noted in rats and dogs exposed to 250 to 1,500 mg/m(3) for 13 weeks, and SPERM HEAD ABNORMALITIES were seen in both species in the same study (Macko & Bergman, 1979).
- Serious bullous skin eruptions with blisters and necrosis have occurred in soldiers using DEET, and several cases of allergic dermatitis have been seen (Hayes & Laws, 1991).
- DEET, given at a dose of 500 mg/kg/day subcutaneously, had minimal neurotoxicity in the standard hen assay, but the neurotoxicity was enhanced by co-administration of pyridostigmine bromide, an anti-nerve gas agent, and/or permethrin, an insecticide. These agents may compete for the same detoxifying esterases, such that their presence may lead to higher levels of unmetabolized compounds (Abou-Donia et al, 1996).
- Severe neurologic deficit and neuropathological changes were induced in hens co-exposed for 2 months to 500 mg/day of DEET subcutaneously and other agents used by soldiers in the Gulf War: 5 mg/day of pyridostigmine bromide (3-dimethylaminocarbonyloxy-N-methylpyridinium bromide) or 10 mg/kg/day of chlorpyrifos. Binary exposures produced greater neurotoxicity than exposure to single agents, and exposure to all three produced even greater effects. Brain neurotoxicity target esterase (NTE) was inhibited by the combination of DEET and chlorpyrifos, and by the triple combination (Abou-Donia et al, 1996).
-RANGE OF TOXICITY
MAXIMUM TOLERATED EXPOSURE
- Carcinogenicity Ratings for CAS134-62-3 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): Not Listed 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 NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS134-62-3 (U.S. Environmental Protection Agency, 2011):
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS134-62-3 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS134-62-3 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS134-62-3 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS134-62-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS134-62-3 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS134-62-3 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS134-62-3 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS134-62-3 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS134-62-3 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS134-62-3 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS134-62-3 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS134-62-3 (EPA, 2005):
LABELS
- NFPA Hazard Ratings for CAS134-62-3 (NFPA, 2002):
-PERSONAL PROTECTION
SUMMARY
- Editor's Note: An ERG guide with information appropriate to this material does not exist.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 134-62-3.
-PHYSICAL HAZARDS
FIRE HAZARD
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS134-62-3 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- Editor's Note: An ERG guide with information appropriate to this material does not exist.
- NFPA Extinguishing Methods for CAS134-62-3 (NFPA, 2002):
EVACUATION PROCEDURES
- Editor's Note: An ERG guide with information appropriate to this material does not exist.
- AIHA ERPG Values for CAS134-62-3 (AIHA, 2006):
- DOE TEEL Values for CAS134-62-3 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS134-62-3 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 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62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS134-62-3 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
-PHYSICAL/CHEMICAL PROPERTIES
-REFERENCES
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