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3D model (JSmol)
ECHA InfoCard 100.004.682
Molar mass 191.27 g/mol
Density 0.998 g/mL
Melting point −45 °C (−49 °F; 228 K)
Boiling point 288-292 °C
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R-phrases (outdated) R23 R24 R25
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N,N-Diethyl-meta-toluamide, abbreviated DEET, is a slightly yellow oil. It is the most common active ingredient in insect repellents. It is intended to be applied to the skin or to clothing, and provides protection against tick bites, mosquito bites, chiggers, and other insects that can transmit disease.


DEET was developed by the United States Army, following its experience of jungle warfare during World War II. It was originally tested as a pesticide on farm fields, and entered military use in 1946 and civilian use in 1957. It was used in Vietnam and Southeast Asia.[1]


A slightly yellow liquid at room temperature, it can be prepared by converting m-toluic acid (3-methylbenzoic acid) to the corresponding acyl chloride, and allowing it to react with diethylamine:[2][3]

Preparation of DEET.png

Mechanism of action

DEET was historically believed to work by blocking insect olfactory receptors for 1-octen-3-ol, a volatile substance that is contained in human sweat and breath. The prevailing theory was that DEET effectively "blinds" the insect's senses so that the biting/feeding instinct is not triggered by humans or other animals which produce these chemicals. DEET does not appear to affect the insect's ability to smell carbon dioxide, as had been suspected earlier.[4][5]

However, more recent evidence shows that DEET serves as a true repellent in that mosquitoes intensely dislike the smell of the chemical repellent.[6] A type of olfactory receptor neuron in special antennal sensilla of mosquitoes that is activated by DEET as well as other known insect repellents such as eucalyptol, linalool, and thujone has been identified. Moreover, in a behavioral test DEET had a strong repellent activity in the absence of body odor attractants such as 1-octen-3-ol, lactic acid, or carbon dioxide. Female and male mosquitoes showed the same response.[7][8]

A recent structural study has revealed that DEET binds to Anopheles gambiae Odorant binding protein 1 (AgamOBP1) with high shape complementarity, suggesting that AgamOBP1 is a molecular target of DEET and perhaps other repellents.[9]


DEET is often sold and used in spray or lotion in concentrations up to 100%.[10] Consumer Reports found a direct correlation between DEET concentration and hours of protection against insect bites. 100% DEET was found to offer up to 12 hours of protection while several lower concentration DEET formulations (20%-34%) offered 3–6 hours of protection.[11] Other research has corroborated the effectiveness of DEET.[12] The Center for Disease Control recommends 30-50% DEET to prevent the spread of pathogens carried by insects.[13]

Effects on health

As a precaution, manufacturers advise that DEET products should not be used under clothing or on damaged skin, and that preparations be washed off after they are no longer needed or between applications.[14] DEET can act as an irritant;[4] in rare cases, it may cause severe epidermal reactions.[14]

In the DEET Reregistration Eligibility Decision (RED), the United States Environmental Protection Agency (EPA) reported 14 to 46 cases of potential DEET-associated seizures, including 4 deaths. The EPA states: "... it does appear that some cases are likely related to DEET toxicity," but observed that with 30% of the US population using DEET, the likely seizure rate is only about one per 100 million users.[15]

The Pesticide Information Project of Cooperative Extension Offices of Cornell University states that "Everglades National Park employees having extensive DEET exposure were more likely to have insomnia, mood disturbances and impaired cognitive function than were lesser exposed co-workers".[16]

When used as directed, products containing between 10% to 30% DEET have been found by The American Academy of Pediatrics to be safe to use on children as well as adults but recommends that DEET not be used on infants less than two months old.[14]

Citing human health reasons, Health Canada barred the sale of insect repellents for human use that contained more than 30% DEET in a 2002 re-evaluation. The agency recommended that DEET-based products be used on children between the ages of 2 and 12 only if the concentration of DEET is 10% or less and that repellents be applied no more than 3 times a day, children under 2 should not receive more than 1 application of repellent in a day and DEET-based products of any concentration not be used on infants under 6 months.[17][18]

DEET has been found to inhibit the activity of a central nervous system enzyme, acetylcholinesterase, in both insects and mammals.[19] This enzyme is involved in the hydrolysis of the neurotransmitter acetylcholine, thus playing a role in the function of the neurons which control muscles. Because of this property, many insecticides are used to block acetylcholinesterase, which leads to an excessive accumulation of acetylcholine at the synaptic cleft, causing neuromuscular paralysis and death by asphyxiation.[20] DEET is commonly used in combination with insecticides and has the capacity to strengthen the toxicity of carbamates,[21] a class of insecticides known to block acetylcholinesterase. These findings bring evidence that, besides having known toxic effects on the olfactory system, DEET also acts on the brain of insects, and that its toxicity is strengthened in combination with other insecticides.

In 2012 media reported that two Canadian sisters had died after ingesting the chemical while in Thailand.[22] (It is reportedly used as a cocktail ingredient there in a drink called "4x100".)[22]

Effects on materials

DEET is an effective solvent,[4] and may dissolve some plastics, rayon, spandex, other synthetic fabrics, and painted or varnished surfaces including nail polish.

Effects on the environment

Though DEET is not expected to bioaccumulate, it has been found to have a slight toxicity for coldwater fish such as the rainbow trout[23] and the tilapia,[24] and it has also been shown to be toxic for some species of freshwater zooplankton.[25] DEET has been detected at low concentrations in waterbodies as a result of production and use, such as in the Mississippi River and its tributaries, where a 1991 study detected levels varying from 5 to 201 ng/L.[26]

See also


  1. ^ Committee on Gulf War and Health: Literature Review of Pesticides and Solvents (2003). Gulf War and Health: Volume 2. Insecticides and Solvents (available online). Washington, D.C.: National Academies Press. ISBN 978-0-309-11389-2.
  2. ^ Wang, Benjamin J-S. (1974). "An interesting and successful organic experiment (CEC)". J. Chem. Ed. 51 (10): 631. doi:10.1021/ed051p631.2.
  3. ^ Donald L. Pavia (2004). Introduction to organic laboratory techniques (Google Books excerpt). Cengage Learning. pp. 370–376. ISBN 978-0-534-40833-6.
  4. ^ a b c Anna Petherick (2008-03-13). "How DEET jams insects' smell sensors". Nature News. Retrieved 2008-03-16.
  5. ^ Mathias Ditzen, Maurizio Pellegrino, Leslie B. Vosshall (2008). "Insect Odorant Receptors Are Molecular Targets of the Insect Repellent DEET". Sciencexpress. 319 (5871): 1838–42. doi:10.1126/science.1153121. PMID 18339904.CS1 maint: multiple names: authors list (link)
  6. ^ Mosquitoes smell and avoid the insect repellent DEET, Proceedings of the National Academy of Sciences of the United States of America, June 12, 2008.
  7. ^ Fox, Maggie; David Wiessler (Aug 18, 2008). "For mosquitoes, DEET just plain stinks". Washington. Reuters. Archived from the original on August 11, 2011. Retrieved August 11, 2011. Cite uses deprecated parameter |deadurl= (help)
  8. ^ Syed, Z.; Leal, WS (2008). "Mosquitoes smell and avoid the insect repellent DEET". Proc. Natl. Acad. Sci. USA. 105 (36): 13598–603. doi:10.1073/pnas.0805312105. PMC 2518096. PMID 18711137.
  9. ^ Tsitsanou, K.E.; et al. (2011). "Anopheles gambiae odorant binding protein crystal complex with the synthetic repellent DEET: implications for structure-based design of novel mosquito repellents". Cell Mol Life Sci. 69 (2): 283–97. doi:10.1007/s00018-011-0745-z. PMID 21671117.
  10. ^ Record in the Household Products Database of NLM
  11. ^ Matsuda, Brent M.; Surgeoner, Gordon A.; Heal, James D.; Tucker, Arthur O.; Maciarello, Michael J. (1996). "Essential oil analysis and field evaluation of the citrosa plant "Pelargonium citrosum" as a repellent against populations of Aedes mosquitoes". Journal of the American Mosquito Control Association. 12 (1): 69–74. PMID 8723261.CS1 maint: multiple names: authors list (link)
  12. ^ David Williamson (3 July 2002). "Independent study: DEET products superior for fending off mosquito bites" (Press release). University of North Carolina.
  13. ^ "Protection against Mosquitoes, Ticks, Fleas and Other Insects and Arthropods". Travelers' Health - Yellow Book. Centers for Disease Control and Prevention. 2009-02-05.
  14. ^ a b c "Insect Repellent Use and Safety". West Nile Virus. Centers for Disease Control and Prevention. 2007-01-12.
  15. ^ "Reregistration Eligibility Decision: DEET" (PDF). U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances. pp. pp39–40. Retrieved 2012-09-08.CS1 maint: extra text (link)
  16. ^ "DEET". Pesticide Information Profile. EXTOXNET. October 1997. Retrieved 2007-09-26.
  17. ^ "Insect Repellents". Healthy Living. Health Canada. August 2009. Retrieved 2010-07-09.
  18. ^ "Re-evaluation Decision Document: Personal insect repellents containing DEET (N,N-diethyl-m-toluamide and related compounds)". Consumer Product Safety. Health Canada. 2002-04-15. Retrieved 2010-07-09.
  19. ^ Corbel; et al. (2009). "Evidence for inhibition of cholinesterases in insect and mammalian nervous systems by the insect repellent deet". BMC Biology. 7: 47. doi:10.1186/1741-7007-7-47. PMC 2739159. PMID 19656357.
  20. ^ Purves, Dale, George J. Augustine, David Fitzpatrick, William C. Hall, Anthony-Samuel LaMantia, James O. McNamara, and Leonard E. White (2008). Neuroscience. 4th ed. Sinauer Associates. pp. 121–2. ISBN 978-0-87893-697-7.CS1 maint: multiple names: authors list (link)
  21. ^ Moss (1996). "Synergism of Toxicity of N,N-Diethyl-m-toluamide to German Cockroaches (Othoptera: Blattellidae) by Hydrolytic Enzyme Inhibitors". J. Econ. Entomol. 89 (5): 1151–1155. PMID 17450648.
  22. ^ a b "DEET in drinks killed sisters". Retrieved 2012-09-08.
  23. ^ U.S. Environmental Protection Agency. 1980. Office of Pesticides and Toxic Substances. N,N-diethyl-m-toluamide (Deet) Pesticide Registration Standard. December, 1980. 83 pp.
  24. ^ Mathai, AT; Pillai, KS; Deshmukh, PB (1989). "Acute toxicity of deet to a freshwater fish, Tilapia mossambica : Effect on tissue glutathione levels". Journal of Environmental Biology. 10 (2): 87–91.CS1 maint: multiple names: authors list (link)
  25. ^ J. Seo, Y. G. Lee, S. D. Kim, C. J. Cha, J. H. Ahn and H. G. Hur (2005). "Biodegradation of the Insecticide N,N-Diethyl-m-Toluamide by Fungi: Identification and Toxicity of Metabolites". Archives of Environmental Contamination and Toxicology. 48 (3): 323–328. doi:10.1007/s00244-004-0029-9. PMID 15750774.CS1 maint: multiple names: authors list (link)
  26. ^ "Errol Zeiger, Raymond Tice, Brigette Brevard, (1999) N,N-Diethyl-m-toluamide (DEET) [134-62-3] - Review of Toxicological Literature" (PDF). Retrieved July 20. Check date values in: |accessdate= (help)

Further reading

External links