DEET

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DEET
DEET.svg
DEET Ball and Stick.png
Names
Preferred IUPAC name
N,N-Diethyl-3-methylbenzamide
Other names
N,N-Diethyl-m-toluamide
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.004.682 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C12H17NO/c1-4-13(5-2)12(14)11-8-6-7-10(3)9-11/h6-9H,4-5H2,1-3H3 checkY
    Key: MMOXZBCLCQITDF-UHFFFAOYSA-N checkY
  • InChI=1S/C12H17NO/c1-4-13(5-2)12(14)11-8-6-7-10(3)9-11/h6-9H,4-5H2,1-3H3
    Key: MMOXZBCLCQITDF-UHFFFAOYAE
  • O=C(c1cc(ccc1)C)N(CC)CC
Properties
C12H17NO
Molar mass 191.27 g/mol
Density 0.998 g/mL
Melting point −33 °C (−27 °F; 240 K)
Boiling point 288 to 292 °C (550 to 558 °F; 561 to 565 K)
Pharmacology
P03BX02 (WHO) QP53GX01 (WHO)
Hazards
GHS labelling:
GHS07: Exclamation mark
Danger
H302, H315, H319, H402
NFPA 704 (fire diamond)
2
1
0
Safety data sheet (SDS) External MSDS
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

N,N-Diethyl-meta-toluamide, also called DEET (/dt/) or diethyltoluamide, is the most common active ingredient in insect repellents. It is a slightly yellow oil intended to be applied to the skin or to clothing and provides protection against mosquitoes, ticks, fleas, chiggers, leeches and many biting insects.

History[edit]

DEET was developed in 1944[1] by Samuel Gertler[1] of the United States Department of Agriculture for use by the United States Army,[2] 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.[3]

In its original form, known as "bug juice", the application solution was composed of 75% DEET and 25% ethanol.[4] Later, a new version of the repellent was developed by the U.S. Army and the USDA. This incarnation consisted of DEET and a mixture of polymers that extended its release and reduced its evaporation rate.[4] This extended-release application was registered by the Environmental Protection Agency in 1991.[4]

Preparation[edit]

A slightly yellow liquid at room temperature, it can be prepared by converting m-toluic acid (3-methylbenzoic acid) to the corresponding acyl chloride using thionyl chloride (SOCl2), and then allowing that product to react with diethylamine:[5][6]

Preparation of DEET.png

Mechanism and effectiveness[edit]

DEET is an extremely effective insect repellant, the most effective available.[7] It is effective against a variety of invertebrates, including ticks, flies, mosquitos, and some parasitic worms.[7] DEET is suspected to affect two pathways in mosquitos: it affects odorant receptors at a distance, and it affects chemoreceptors upon contact.[7] The exact mechanisms are still being researched, but the two most likely hypotheses are the "smell and avoid hypothesis" (that DEET has an unpleasant odor to insects), and the "confusant hypothesis" (that smelling DEET confuses insects).[7]

Concentrations[edit]

The concentration of DEET in products may range from less than 10 percent to nearly 100 percent. Concentrations of 10 to 30 percent are recommended for infants and children. DEET should not be used on children under 2 months of age.[8]

DEET is often sold and used in spray or lotion in concentrations up to 100%.[9] 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.[10] Other research has corroborated the effectiveness of DEET.[11] The Centers for Disease Control and Prevention recommends 30–50% DEET to prevent the spread of pathogens carried by insects.[12]

A 2008 study found that higher concentrations of DEET have an improved ability to repel insects through fabric.[13]

Effects on health[edit]

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;[15] in rare cases, it may cause severe epidermal reactions.[14] Other symptoms that can occur are breathing difficulty, burning eyes, or headaches.[16]

The authors of a 2002 study published in The New England Journal of Medicine wrote, "Despite the substantial attention paid by the lay press every year to the safety of DEET, this repellent has been subjected to more scientific and toxicological scrutiny than any other repellent substance," continuing, "DEET has a remarkable safety profile after 40 years of use and nearly 8 billion human applications," concluding, "When applied with common sense, DEET-based repellents can be expected to provide a safe as well as long-lasting repellent effect."[17]

When DEET is used in combination with insecticides for cockroaches it can strengthen the toxicity of carbamate, an acetylcholinesterase inhibitor. These 1996 findings indicate that DEET has neurological effects on insects in addition to known olfactory effects, and that its toxicity is strengthened in combination with other insecticides.[18]

In the DEET Reregistration Eligibility Decision (RED) in 1998, the United States Environmental Protection Agency (EPA) reported 14 to 46 cases of potential DEET-associated seizures, including four deaths. The EPA states: "... it does appear that some cases are likely related to DEET toxicity," which may underreport the risk as physicians may fail to check for history of DEET use or fail to report cases of seizure subsequent to DEET use.[19]

In 1997, the Pesticide Information Project of Cooperative Extension Offices of Cornell University stated that "Everglades National Park employees having extensive DEET exposure were more likely to have insomnia, mood disturbances and impaired cognitive function than lesser exposed co-workers".[20]

When used as directed, products containing between 10% and 30% DEET have been found by the American Academy of Pediatrics to be safe to use on children, as well as adults, but the Academy 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 "based on a human health risk assessment that considered daily application of DEET over a prolonged period of time". 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 should not be used on infants under 6 months.[21][22] Some experts recommend against applying DEET and sunscreen simultaneously since that would increase DEET penetration; Xiaochen Gu, a professor at the University of Manitoba’s faculty of Pharmacy who led a study about mosquitos, advises that DEET should be applied 30 or more minutes later.[23]

A 2020 study performed by students within the University of Florida's College of Public Health and Health Professions analyzed data from the National Health and Nutrition Examination Survey and identified 1,205 participants who had "DEET metabolic levels recorded at or above detection limits". They analyzed biomarkers related to systemic inflation, immune, liver, and kidney functions, and found no "evidence that DEET exposure has any impact on the biomarkers identified."[24]

Detection in body fluids[edit]

DEET may be quantitated in blood, plasma, or urine by gas or liquid chromatography-mass spectrometry to confirm a diagnosis of poisoning in hospitalized patients or to provide evidence in a medicolegal death investigation. Blood or plasma DEET concentrations are expected to be in a range of 0.3–3.0 mg/L during the first 8 hours after dermal application in persons using the chemical appropriately, >6 mg/L in intoxicated patients and >100 mg/L in victims of acute intentional oral overdose.[25][26]

Effects on materials[edit]

DEET is an effective solvent,[15] and may dissolve some watch crystals,[4] plastics, rayon, spandex, other synthetic fabrics, and painted or varnished surfaces including nail polish. It also may act as a plasticizer by remaining inside some formerly hard plastics, leaving them softened and more flexible. DEET is incompatible with rayon, acetate, or dynel clothing.

Effects on the environment[edit]

Though DEET is not expected to bioaccumulate, it has been found to have a slight toxicity for fresh-water fish such as rainbow trout[27] and tilapia,[28] and it also has been shown to be toxic for some species of freshwater zooplankton.[29] DEET has been detected at low concentrations in water bodies 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.[30]

A 1975 study analyzed the effects of DEET on communities of freshwater organisms native to Chinese waterways and found that compared to other commercial insect repellants, DEET was moderately toxic to aquatic organisms. The most-at-risk organisms were algae colonies which often experienced "significant biomass decline and community composition shift[s]" when exposed to DEET at 500 ng/L.[31]

See also[edit]

References[edit]

  1. ^ a b US 2408389, Gertler S, "N,N-diethylbenzamide as an insect repellent", published 1946-10-01 
  2. ^ Katz TM, Miller JH, Hebert AA (May 2008). "Insect repellents: historical perspectives and new developments". Journal of the American Academy of Dermatology. 58 (5): 865–71. doi:10.1016/j.jaad.2007.10.005. PMID 18272250. Retrieved 2015-08-16.
  3. ^ Committee on Gulf War and Health: Literature Review of Pesticides and Solvents (2003). Gulf War and Health: Volume 2. Insecticides and Solvents. Washington, D.C.: National Academies Press. doi:10.17226/10628. ISBN 978-0-309-11389-2.
  4. ^ a b c d Kitchen LW, Lawrence KL, Coleman RE (June 2009). "The role of the United States military in the development of vector control products, including insect repellents, insecticides, and bed nets". Journal of Vector Ecology. 34 (1): 50–61. doi:10.1111/j.1948-7134.2009.00007.x. PMID 20836805.[permanent dead link]
  5. ^ Wang BJ (1974). "An interesting and successful organic experiment (CEC)". J. Chem. Educ. 51 (10): 631. doi:10.1021/ed051p631.2.
  6. ^ Pavia DL (2004). Introduction to organic laboratory techniques (Google Books excerpt). Cengage Learning. pp. 370–376. ISBN 978-0-534-40833-6.
  7. ^ a b c d DeGennaro, Matthew (2015). "The mysterious multi-modal repellency of DEET". Fly. 9 (1): 45–51. doi:10.1080/19336934.2015.1079360. ISSN 1933-6942. PMC 4594586. PMID 26252744.
  8. ^ American Academy of Pediatrics, “Summer Safety Tips,” Dec 2, 2017 https://www.healthychildren.org/English/safety-prevention/at-play/Pages/Summer-Safety-Tips-Staying-Safe-Outdoors.aspx
  9. ^ Record in the Household Products Database of NLM
  10. ^ Matsuda BM, Surgeoner GA, Heal JD, Tucker AO, Maciarello MJ (March 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.
  11. ^ Williamson D (3 July 2002). "Independent study: DEET products superior for fending off mosquito bites" (Press release). University of North Carolina.
  12. ^ "Protection against Mosquitoes, Ticks, Fleas and Other Insects and Arthropods". Travelers' Health – Yellow Book. Centers for Disease Control and Prevention. 2009-02-05.
  13. ^ Ditzen M, Pellegrino M, Vosshall LB (2008). "Insect odorant receptors are molecular targets of the insect repellent DEET". Science. 319 (5871): 1838–42. Bibcode:2008Sci...319.1838D. doi:10.1126/science.1153121. PMID 18339904. S2CID 18499590.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ a b c "Insect Repellent Use and Safety". West Nile Virus. Centers for Disease Control and Prevention. 2007-01-12.
  15. ^ a b Petherick A (2008-03-13). "How DEET jams insects' smell sensors". Nature News. doi:10.1038/news.2008.672. Retrieved 2008-03-16.
  16. ^ "Bug spray poisoning". U.S. National Library of Medicine. October 2015. Retrieved 2016-06-25.
  17. ^ Fradin MS, Day JF (July 2002). "Comparative efficacy of insect repellents against mosquito bites". The New England Journal of Medicine. 347 (1): 13–8. doi:10.1056/NEJMoa011699. PMID 12097535.
  18. ^ Moss JI (October 1996). "Synergism of toxicity of N,N-diethyl-m-toluamide to German cockroaches (Orthoptera: Blattellidae) by hydrolytic enzyme inhibitors". Journal of Economic Entomology. 89 (5): 1151–5. doi:10.1093/jee/89.5.1151. PMID 17450648.
  19. ^ "Reregistration Eligibility Decision: DEET" (PDF). U.S. Environmental Protection Agency, Office of Prevention, Pesticides, and Toxic Substances. September 1998. pp. 39–40. Archived from the original (PDF) on October 21, 2012. Retrieved 2012-09-08.
  20. ^ "DEET". Pesticide Information Profile. EXTOXNET. October 1997. Retrieved 2007-09-26.
  21. ^ "Insect Repellents". Healthy Living. Health Canada. August 2009. Archived from the original on 2010-04-11. Retrieved 2010-07-09.
  22. ^ "Re-evaluation Decision Document: Personal insect repellents containing DEET (N,N-diethyl-m-toluamide and related compounds)" (PDF). Consumer Product Safety. Health Canada. 2002-04-15. Retrieved 2010-07-09.
  23. ^ "How to choose the best bug repellent". Best Health. Reader's Digest Association, Inc. January 2000. Retrieved June 14, 2016. ‘Anything intended for topical use only shouldn’t be going into the body,’ says Xiaochen Gu, a professor at the University of Manitoba’s faculty of pharmacy, who led the study.
  24. ^ Haleem ZM, Yadav S, Cushion ML, Tanner RJ, Carek PJ, Mainous AG (2020). "Exposure to N,N-Diethyl-Meta-Toluamide Insect Repellent and Human Health Markers: Population Based Estimates from the National Health and Nutrition Examination Survey". Am J Trop Med Hyg. 103 (2): 812–814. doi:10.4269/ajtmh.20-0226. PMC 7410448. PMID 32458781.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Tenenbein M (September 1987). "Severe toxic reactions and death following the ingestion of diethyltoluamide-containing insect repellents". JAMA. 258 (11): 1509–11. doi:10.1001/jama.258.11.1509. PMID 3625951.
  26. ^ Baselt RC (2014). Disposition of toxic drugs and chemicals in man, 10th edition. Seal Beach, Ca.: Biomedical Publications. p. 650. ISBN 978-0-9626523-9-4.
  27. ^ 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.
  28. ^ 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. Archived from the original on 2007-11-07.
  29. ^ Seo J, Lee YG, Kim SD, Cha CJ, Ahn JH, Hur HG (April 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): 323–8. doi:10.1007/s00244-004-0029-9. PMID 15750774. S2CID 31723995.
  30. ^ Zeiger E, Tice R, Brevard B (1999). "N,N-Diethyl-m-toluamide (DEET) [134-62-3] – Review of Toxicological Literature" (PDF). Archived from the original (PDF) on October 9, 2012.
  31. ^ Schmoldt A; Benthe HF; Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. doi:10.1016/0006-2952(75)90094-5. PMID 10.

Further reading[edit]

External links[edit]