N,N-Diethyl-meta-toluamide, also called diethyltoluamide or DEET (/diːt/, from DET, the initials of di- + ethyl + toluamide),[1][2] is the oldest, one of the most effective, and most common active ingredients 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.

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.

[7][8] 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.

[14] 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 irritate the eyes and, unlike icaridin, it can cause breathing difficulty, headaches,[15] or, in rare cases, it may cause severe epidermal reactions.

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.

"[21] 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.

However, repeated use of DEET in very high concentrations can lead to toxic encephalopathy with severe neurological symptoms including seizures, tremors and slurred speech.

[29] Unlike icaridin, DEET is an effective solvent[30] and may dissolve some watch crystals,[31] plastics, rayon, spandex, other synthetic fabrics, and painted or varnished surfaces including nail polish.

[39] 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:[40][41] DEET was developed in 1944[42] by Samuel Gertler[42] of the United States Department of Agriculture for use by the United States Army,[43] following its experience of jungle warfare during World War II.