N,N-Diethyl-meta-toluamide, also called diethyltoluamide or DEET (/diːt/, from DET, the initials of di- + ethyl + toluamide),[1][2] is the oldest, most effective and most common active ingredient in commercial insect repellents. It is a slightly yellow oil intended to be applied to the skin or to clothing and provides protection against mosquitoes, flies, ticks, fleas, chiggers, leeches, and many other biting insects.
Unlike Icaridin, DEET emits an odor that many find unpleasant, leaves skin greasy, dissolves plastics and synthetic fabrics[3] and interacts negatively with sunscreen.[4][5]
Effectiveness
DEET and icaridin are the most effective insect repellents available.[6] DEET is effective against a variety of invertebrates, including ticks, flies, mosquitos, and some parasitic worms.[6]
A 2018 systematic review found no consistent performance difference between DEET and icaridin in field studies and concluded that they are equally preferred mosquito repellents, noting that 50% DEET offers longer protection but is not available in some countries.[7]
Concentrations
The concentration of DEET in products may range from less than 10% to nearly 100%, but concentrations greater than 50% do not increase the duration of protection.[8] Higher concentrations can be safely applied to clothing, although it may damage some types of synthetic fibers. In the United Kingdom, the publicly-funded healthcare system, the National Health Service (NHS), recommends that UK citizens should use a concentration of 50% when visiting areas of the world with malaria.[9] A lower concentration of 10% is recommended for infants and children.[10][11]Health Canada decided to limit DEET concentration to 30% in the country since 2002 due to an increased long-term risk observed with repeated applications.[12]
DEET is often sold and used in spray or lotion in concentrations up to 100%.[13]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.[citation needed] Other research has corroborated the effectiveness of DEET.[14] The Centers for Disease Control and Prevention recommends 30–50% DEET to prevent the spread of pathogens carried by insects.[15]
A 2008 study found that higher concentrations of DEET have an improved ability to repel insects through fabric.[16]
Contraindications
DEET should not be used on children younger than 2 months of age.[17]
Adverse effects
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.[17]
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.[17] DEET can irritate the eyes and, unlike icaridin, it can cause breathing difficulty, headaches,[18] or, in rare cases, it may cause severe epidermal reactions.[17]
... this repellent has been subjected to more scientific and toxicologic scrutiny than any other repellent substance. ... DEET has a remarkable safety profile after 40 years of use and nearly 8 billion human applications. Fewer than 50 cases of serious toxic effects have been documented in ... medical literature since 1960 ... Many of these cases of toxic effects involved long-term, heavy, frequent, or whole-body application of DEET. No correlation has been found between the concentration of DEET used and the risk of toxic effects. ... When applied with common sense, DEET-based repellents can be expected to provide a safe as well as a long-lasting repellent effect ... under circumstances in which it is crucial to be protected against arthropod bites that might transmit disease.
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.[20]
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".[21]
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.[22][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 inflammation, immune, liver, and kidney functions, and found no "evidence that DEET exposure has any impact on the biomarkers identified."[24]
Detection in body fluids
DEET may be measured 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]
Overdose
Applying DEET to the skin is safe if done as directed. Adverse reactions are very rare, about 1 in 100 million people. However, repeated use of DEET in very high concentrations can lead to toxic encephalopathy with severe neurological symptoms including seizures, tremors and slurred speech. The risk is higher for children since they have a greater surface area to body weight ratio.[27][28]
Interactions
Limited data indicates that combining insect repellents with DEET and sunscreen decreases the sun protection factor of the sunscreen by about a third.[4] Unlike icaridin, the combination also increases the absorption of both significantly.[5] When the two need to be used together, the repellent should be applied after the sunscreen has been absorbed, about 30 or more minutes later.[29]
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.[30]
Damage to materials
Unlike icaridin, DEET is an effective solvent[31] and may dissolve some watch crystals,[32] 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.[33]
Environmental impact
Though DEET is not expected to bioaccumulate, it has been found to have a slight toxicity for fresh-water fish such as rainbow trout[34] and tilapia,[35] and it also has been shown to be toxic for some species of freshwater zooplankton.[36] 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.[37]
A 1975 study analyzed the effects of DEET on communities of freshwater organisms native to Chinese waterways and found that DEET was moderately toxic to aquatic organisms compared to other commercial insect repellants. 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.[38]
DEET is biodegraded by fungi into products less toxic to zooplankton.[36] It degrades well under aerobic conditions, but poorly and slowly under anaerobic conditions.[39]
Mechanism of action
DEET is thought to provide protection from mosquitos via two pathways, both by negatively impacting mosquito odorant receptors at a distance, and by negatively impacting mosquito chemoreceptors upon contact.[6] 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 "bewilderment hypothesis" (that smelling DEET confuses insects).[6]
In its original form, known as "bug juice", the application solution was composed of 75% DEET and 25% ethanol.[32] Later, a new version of the repellent was developed by the U.S. Army and the USDA. This formulation consisted of DEET and a mixture of polymers that extended its release and reduced its evaporation rate.[45] This extended-release application was registered by the Environmental Protection Agency in 1991.[32]
^"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.
^"DEET". Pesticide Information Profile. EXTOXNET. October 1997. Archived from the original on 2020-11-19. Retrieved 2007-09-26.
^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. PMID3625951.
^Baselt RC (2014). Disposition of toxic drugs and chemicals in man, 10th edition. Seal Beach, Ca.: Biomedical Publications. p. 650. ISBN978-0-9626523-9-4.
^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. PMID17450648.
^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.
^ abSeo 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. PMID15750774. S2CID31723995.
^Weeks JA, Guiney PD, Nikiforov AI (January 2012). "Assessment of the environmental fate and ecotoxicity of N,N-diethyl-m-toluamide (DEET)". Integrated Environmental Assessment and Management. 8 (1): 120–34. doi:10.1002/ieam.1246. PMID22006575. S2CID5370204.
