As of 2011, NPIC stopped creating technical pesticide fact sheets. The old collection of technical fact sheets will remain available in this archive, but they may contain out-of-date material. NPIC no longer has the capacity to consistently update them. To visit our general fact sheets, click here. For up-to-date technical fact sheets, please visit the Environmental Protection Agency’s webpage.
Molecular Structure -
Laboratory Testing: Before pesticides are registered by
the U.S. EPA, they must undergo laboratory testing for
short-term (acute) and long-term (chronic) health effects.
Laboratory animals are purposely given high enough doses
to cause toxic effects. These tests help scientists judge how
these chemicals might affect humans, domestic animals,
and wildlife in cases of overexposure.
- DEET is an insect and acarid repellent. The International Union of Pure and Applied Chemistry (IUPAC) name for DEET is
N,N-diethyl-m-toluamide and other isomers, and it is a member of the N,N-dialkylamide family of chemicals. The Chemical
Abstracts Service (CAS) registry number for DEET is 134-62-3.1
- DEET was developed by the U.S. Army in 1946 for protection of military
personnel in insect-infested areas. DEET was registered in the
United States for use by the general public in 1957, and has been
commercially marketed as a personal insect repellent since 1965.
A Registration Standard was established for DEET by the United
States Environmental Protection Agency (U.S. EPA) in 1980. DEET
was reregistered in 1998 following a review of the Registration
Standard and additional animal and avian toxicity data from a Data
Call-In (DCI) in 1988.1 See the text box on Laboratory Testing.
- DEET is a liquid with a distinct, faint odor and is almost colorless.1
- Vapor pressure2: 5.6 x 10-3 mmHg at 20 °C
- Octanol-Water Partition Coefficient (log Kow)2: 2.02
- Henry's constant2: 2.1 x 10-8 atm·m3/mol
- Molecular weight2: 191.3 g/mol
- Solubility (water)1: >1.0 g/L (>1000 mg/L) at 25 °C
- Soil Sorption Coefficient (Koc)2: 3.00 x 102
- DEET is a plasticizer and can damage certain rubber, plastic, vinyl, or elastic
materials such as contact lenses, eyeglass frames and lenses, watch crystals,
combs, painted and varnished surfaces, and certain synthetic or treated fabrics.
DEET does not damage natural fibers including cotton and wool.3
- DEET is used to repel biting and flying insects such as biting flies and midges, black flies, chiggers, no-see-ums, fleas, mosquitoes,
and ticks. Repellents containing DEET are used on a variety of sites, including the human body, clothing, headgear,
and horses. Formulations of the repellent include liquids, pressurized liquids, lotions, sticks, foams, and impregnated materials
such as towelettes.1,4 Uses for individual products containing DEET vary widely. Always read and follow the label when
applying pesticide products.
- It has been previously estimated that approximately 30% of the U.S. population uses DEET annually as a personal insect
- Signal words for products containing DEET may range from Caution to Danger. The signal word reflects the combined
toxicity of the active ingredient and other ingredients in the product. See the pesticide label on the product and refer to
the NPIC fact sheets on Signal Words and Inert or "Other" Ingredients.
- To find a list of products containing DEET which are registered in your state, visit the website
http://npic.orst.edu/reg/state_agencies.html select your state then click on the link for "State Products."
- Sunscreen: The U.S. EPA is reviewing additional information regarding the use of DEET in combination with sunscreen.
Instructions to apply sunscreen "generously and frequently" are in contrast to the U.S. EPA's recommendation to use DEET
- Scientists have not definitively determined the exact mode of action of DEET in target organisms. Research indicates that
DEET interferes with receptors in mosquito (and other biting insects) antennae that detect L-lactic acid and carbon dioxide,
the primary attractants emitted by humans and other animals. Insects exposed to DEET are thereby unable to effectively
locate a host.6,7,8
- Scientists have not determined the exact mechanism by which DEET may affect the nervous system in humans.9
- DEET is low in toxicity to rats when ingested. The acute oral LD50 in rats is 2170 to 3664 mg/kg.1 See the text boxes on Toxicity
Classification and LD50/LC50.
|TOXICITY CLASSIFICATION - DEET
||Very Low Toxicity
|Acute Oral LD50
||Up to and including 50 mg/kg
(≤ 50 mg/kg)
|Greater than 50 through 500 mg/kg
|Greater than 500 through 5000 mg/kg
|Greater than 5000 mg/kg
||Up to and including 0.05 mg/L
|Greater than 0.05 through 0.5 mg/L
|Greater than 0.5 through 2.0 mg/L
|Greater than 2.0 mg/L
||Up to and including 200 mg/kg
|Greater than 200 through 2000 mg/kg
|Greater than 2000 through 5000 mg/kg
|Greater than 5000 mg/kg
|Primary Eye Irritation
||Corrosive (irreversible destruction of
ocular tissue) or corneal involvement or
irritation persisting for more than 21 days
||Corneal involvement or other
eye irritation clearing in 8 -
||Corneal involvement or other
eye irritation clearing in 7
days or less
||Minimal effects clearing in less than 24 hours
|Primary Skin Irritation
||Corrosive (tissue destruction into the
dermis and/or scarring)
||Severe irritation at 72 hours
(severe erythema or edema)
||Moderate irritation at 72
hours (moderate erythema)
||Mild or slight irritation at
72 hours (no irritation or
|The highlighted boxes reflect the values in the "Acute Toxicity" section of this fact sheet. Modeled after the U.S. Environmental Protection Agency, Office of Pesticide Programs, Label Review Manual, Chapter 7: Precautionary Labeling. https://www.epa.gov/sites/default/files/2018-04/documents/chap-07-mar-2018.pdf
- DEET is low in toxicity to rabbits when applied to the skin. The acute dermal LD50 in rabbits is 4280 mg/kg.1
- Researchers observed slight to moderate dermal irritation and slight edema in studies exposing rabbits to technical grade
DEET. Dermal irritation resolved within seven days.10
- Investigators did not observe skin sensitization in guinea pigs or humans treated with technical grade or formulated
- Researchers observed slight to moderate corneal opacity, slight iritis, and moderate to severe conjunctivitis following 24-
hour ocular exposure studies in rabbits with technical grade DEET. Symptoms generally cleared within five to seven days.
Conjunctivitis persisted beyond seven days in some studies.10
LD50/LC50: A common measure of acute toxicity is the lethal
dose (LD50) or lethal concentration (LC50) that causes death
(resulting from a single or limited exposure) in 50 percent
of the treated animals. LD50 is generally expressed as the
dose in milligrams (mg) of chemical per kilogram (kg) of
body weight. LC50 is often expressed as mg of chemical
per volume (e.g., liter (L)) of medium (i.e., air or water) the
organism is exposed to. Chemicals are considered highly
toxic when the LD50/LC50 is small and practically non-toxic
when the value is large. However, the LD50/LC50 does not
reflect any effects from long-term exposure (i.e., cancer,
birth defects or reproductive toxicity) that may occur at
levels below those that cause death.
- DEET is very low in toxicity to rats when inhaled. The acute inhalation
LC50 in rats is 5.95 mg/L.1
Signs of Toxicity - Animals
- Reports of DEET toxicosis in animals are rare. Clinical signs in
dogs and cats may include vomiting, tremors, excitation, ataxia,
Signs of Toxicity - Humans
- Poison control center data from 1993-1997 revealed that symptoms
were dependent on the pathway of exposure. Reported
symptoms were most frequently associated with ocular exposure,
with effects including eye irritation or pain, and excess tearing.12
- Dermal symptoms were reported in 5% of reports to poison control centers following DEET exposure. Symptoms included
irritation, redness, rash, and swelling.12
- Gastrointestinal symptoms reported to poison control centers following exposure to DEET primarily occurred following
ingestion. Gastrointestinal symptoms included oral irritation, nausea, and vomiting.12
- Neurological reactions from DEET exposure are rare. The incidence of seizure following DEET exposure is estimated to be 1
per 100 million users between 1961 and 1998. Reports of neurological reactions are predominately the result of accidental
or deliberate ingestion, or dermal applications not consistent with label directions. Reported neurological signs of toxicity
include encephalopathy, seizure, tremor, slurred speech, coma, and death.1,5,13
- The U.S. EPA and FIFRA Scientific Advisory Panel concluded that the reported incidences of seizures among children that
were potentially related to DEET use are "inconclusive" and do not support a causal link between DEET and seizures in
- Always follow label instructions and take steps to minimize exposure. If any exposure occurs, be sure to follow the First Aid
instructions on the product label carefully. For additional treatment advice, contact the Poison Control Center at 1-800-
222-1222. If you wish to discuss an incident with the National Pesticide Information Center, please call 1-800-858-7378.
- Researchers administered DEET in the diet of male and female rats at doses
of 10, 30, or 100 mg/kg/day for males, and 30, 100 or 400 mg/kg/day for
females for 2 years. Researchers observed no toxicity among males at any
dose level, and observed decreased body weight, decreased food consumption,
and increased cholesterol levels among females at the highest
dose tested. The NOELs for oral toxicity are 100 and 400 mg/kg/day for
male and female rats, respectively.1 See the text box on NOAEL, NOEL,
LOAEL, and LOEL.
NOAEL: No Observable Adverse Effect Level
NOEL: No Observed Effect Level
LOAEL: Lowest Observable Adverse Effect Level
LOEL: Lowest Observed Effect Level
- Researchers administered DEET in the form of gel capsules to dogs at doses of 0, 30, 100, and 400 mg/kg/day for one year.
At the highest dose tested, investigators noted decreased body weight, and increased incidence of drooling/salivation, and
decreased cholesterol levels.1
- Investigators applied DEET to the shaved backs of male and female rats at doses of 0, 100, 300, or 1000 mg/kg/day for 90
days. Researchers observed no effect on general behavior among any treatment group. Dermal irritation presented as red
and scabbed areas of the skin for all treatment groups. Researchers also observed decreased body weights of male rats at
the highest dose tested. The systemic NOEL determined from this study was 300 mg/kg/day for decreased body weights,
and 100 mg/kg/day for local effects based on dermal irritation.10
- Researchers applied DEET to the skin of micropigs® at doses of 0, 100, 300, or 1000 mg/kg/day, five days per week for 13
weeks. Investigators observed skin effects, including dryness and desquamation at the site of application for all doses. Severity
of skin effects increased with increased dose level. Investigators did not observe systemic effects at any dose tested.
The LOEL for skin irritation was 100 mg/kg, and the NOEL for systemic toxicity was determined to be equal to or greater
than 1000 mg/kg/day.1,10
- No data were found on chronic health effects from DEET exposure in humans. See the text box on Exposure.
Exposure: Effects of DEET on human health and the environment depend on how much
DEET is present and the length and frequency of exposure. Effects also depend on the health
of a person and/or certain environmental factors.
- No data were found on endocrine effects from DEET exposure.
- Researchers fed DEET to male and female rats in the diet for two years at doses of 10, 30, or 100 mg/kg/day, and 30, 100, or
400 mg/kg/day, respectively. Researchers fed mice 250, 500, or 1,000 mg/kg/day for 18 months, and dogs 30, 100, or 400
mg/kg/day. No specific target organ toxicity or oncogenicity was observed in any of the animals.14
- Researchers often use studies designed to test for mutagenicity to screen chemicals for carcinogenicity. Sufficient evidence
indicates that DEET does not have significant potential for mutagenicity.15
- The U.S. EPA classified DEET as "Group D - not classifiable as to human carcinogenicity" based on inadequate evidence of
carcinogenicity, or lack of data in laboratory animals and humans.1 See the text box on Cancer.
Cancer: Government agencies in the United States and abroad have developed programs to evaluate the
potential for a chemical to cause cancer. Testing guidelines and classification systems vary. To learn more
about the meaning of various cancer classification descriptors listed in this fact sheet, please visit the
appropriate reference, or call NPIC.
- In a two-generation study, researchers fed rats 0, 25, 100, or 250 mg/kg/day of DEET in the diet. There were no adverse reproductive
effects on fertility, gestation, or viability. At the highest dose tested, male pups exhibited reduced body weight
at day 7 of lactation. Female pups experienced a significant reduction in body weight at 100 mg/kg/day at day 14 of lactation.
The NOEL for reproductive toxicity was 250 mg/kg/day.1
- Researchers applied DEET at 1000 mg/kg/day to the skin of rats throughout pregnancy. Prenatal mortality increased relative
to the control (34.1% vs. 20.9%). Mortality between birth and weaning increased relative to the control (44.0% vs.
- Researchers administered DEET to pregnant female rabbits (route of exposure not specified) at doses of 0, 30, 100 or 325
mg/kg/day from days 6 through 18 of gestation. Scientists did not observe any compound-related maternal toxicity or
developmental toxicity. The NOEL for maternal and development toxicity was 325 mg/kg/day.1
- In a double-blind, randomized trial of the safety of DEET to prevent malaria during pregnancy, females in the second and
third trimester of pregnancy applied 20% DEET in carrier solution, or carrier solution alone to exposed areas of the arms
and legs daily until delivery. DEET crossed the placental barrier and was detected in 8% of cord blood samples. No significant
adverse effects were detected in either the mother or the fetus during pregnancy, and infants showed no differences
in development or survival at birth or at age one.14
- Researchers fed DEET to rats and found peak blood concentrations occurring at 0.5 hours following exposure for males
and at 2.0 hours following exposure for females. Male and female rats absorbed 53.3% and 65.3% of the administered dose,
- Researchers dermally applied DEET to rats and found that blood levels reached a plateau 1.5 hours after application, and
remained at that level for 24 hours (until termination of study), indicating that a small amount of DEET is continuously
absorbed from the site of application. Following dermal application, male and female rats absorbed 17.0% and 5.3% of the
applied dose, respectively.1
- Investigators analyzed absorption rates of a commercial sunscreen products containing 9.5% DEET compared to a 20.0%
DEET solution applied to mouse skin. The sunscreen product was initially absorbed faster, and at a rate 3.4 times higher,
than the 20.0% DEET solution.17 Scientists treated pigs with 10% DEET alone and in combination with 5% oxybenzone
sunscreen in a skin penetration study. Compared to DEET alone, the combination of DEET and sunscreen significantly increased
the absorption of DEET into the skin of laboratory animals.18 See sunscreen information under Uses.
- Investigators applied DEET to the skin of rats following oral administration of ethanol at doses of 1.5, 3.0, 4.3, 6.0, or 10.0 g/
kg to observe the effect of ethanol ingestion on DEET dermal penetration. At two hours post-treatment, ingested ethanol
caused a statistically significant dose-dependent increase in DEET absorption through the skin at 4.3, 6.0, and 10.0 g/kg
ethanol. At 24 hours following treatment, researchers observed enhanced absorption of DEET at doses of 6.0 g/kg and 10.0
g/kg ethanol. Doses of ethanol that caused increased absorption are relevant to human levels of alcohol consumption.21
- Researchers applied technical grade DEET, and DEET formulated in a 15% ethanol solution, to the forearm skin of male
human volunteers for an 8-hour exposure period. DEET was absorbed within two hours after application and absorption
continued at a constant rate over the 8-hour exposure period. Researchers determined that a total of 5.6% of the dose of
technical grade DEET, compared to 8.4% of the dose of DEET in ethanol solution, was absorbed through the skin.19
- In a study to determine the effect of ethanol on the skin permeation of DEET, investigators found that 10% DEET formulated
with 30-45% ethanol demonstrated higher skin permeation than a solution containing only DEET.20
- Researchers detected very small concentrations of radio-labeled DEET primarily in the liver, kidney, lung, spleen, whole
blood, and carcass of experimental animals. Total radioactivity found in all tissues accounted for between 0.15% and 0.67%
of the administered dose.1
- Researchers applied DEET to the forearm skin of male human volunteers for an 8-hour exposure period and found quantifiable
levels in plasma for 12 hours following the initial application. DEET did not accumulate in superficial layers of human
- In rats, DEET is primarily metabolized via oxidation of the methyl group on the aromatic ring, which represents 50% of an
administered oral dose. The other metabolic pathway of DEET (18% of the administered oral dose) is via ring methyl oxidation
in combination with N-dealkylation of an ethyl substituent on the amide moiety.1,9
- Researchers applied DEET to the forearm skin of male human volunteers for an 8-hour exposure period and found that the
entire absorbed dose (5.6% and 8.3% of the applied dose, depending on formulation) was metabolized prior to excretion.
Researchers found six metabolites, with the two major metabolites (up to 68% of total) resulting from metabolic processes
similar to those observed in rat studies.1,19
- An in vitro study with human liver microsomes determined that ring methyl hydroxylation is the major metabolic pathway
for DEET in humans. This pathway is dependent on specific CYP450 isoforms, whose levels vary considerably among individuals.9,22
- DEET is excreted primarily in the urine in laboratory animals.1
- Researchers compared the absorption and elimination of DEET in three species of animals following a single topical application.
In each species, at least 75% of the absorbed dose was detected in the urine within the first day, with elimination
essentially complete within 3-4 days for all animals.23
- A pharmacokinetic study in rats exposed to radio-labeled DEET monitored excretion of the compound in the urine after
single and multiple oral doses, as well as a single dermal dose. Recovery rates at seven days post-exposure for the singleand
multiple-oral doses were between 85-91% from the urine and 3-5% from the feces. From the dermal dose, 74.0-78.0%
was recovered from the urine, 4.0-7.0% from the feces and 6.5% from the application site at seven days post-exposure.24
- Researchers applied DEET to the forearm skin of male human volunteers for an 8-hour exposure period and found that
most of the absorbed dose was eliminated within 12 hours following application, and nearly all of the absorbed dose was
eliminated within 24 hours following application. Essentially all of the absorbed dose (less than 10% of the applied dose)
was excreted in the urine.19
- Methods exist for testing DEET in blood and tissue, and DEET metabolites in urine. However, these methods are not widely
- Researchers analyzed urine samples from a random, representative sub-sample of 2535 participants from the 2001-2002
National Health and Nutrition Environmental Analyses Survey (NHANES) for metabolites of DEET. Ninety-five percent (95%)
of the urine samples tested for DEET were below the limit of detection (0.17 μg/L).25
- DEET is moderately mobile in soil.2
- DEET is stable to hydrolysis at soil pH levels typically found in the environment.1
- Investigators observed microbial degradation of DEET by the soil bacterium P. putida, under conditions where DEET was
the sole carbon source. The resulting metabolic products are 3-methyl benzoate and diethylamine. The metabolic pathway
used by P. putida is different compared to observed pathways used by other eukaryotes.26
- Researchers observed metabolism of DEET in cultures of soil fungi. C. elegans and M. ramannianus effectively metabolized
DEET yielding several metabolites by proposed mechanisms of N-oxidation and N-deethylation. Metabolic products of the
fungi breakdown demonstrated lower toxicity to Daphnia magna compared to the parent compound.27
- DEET is practically insoluble in water.15
- DEET has been found in water where wastewater is thought to
contribute to stream-flow. The median level found was 0.05 μg/L,
with the highest levels (1.10 μg/L) found in streams with urban
- DEET will exist as a vapor in ambient air and degrade via hydroxyl-
radicals with an estimated half-life of 15 hours.2 See the text
box on Half-life.
The "half-life" is the time required for half of the
compound to break down in the environment.
1 half-life = 50% remaining
2 half-lives = 25% remaining
3 half-lives = 12% remaining
4 half-lives = 6% remaining
5 half-lives = 3% remaining
Half-lives can vary widely based on environmental
factors. The amount of chemical remaining after a
half-life will always depend on the amount of the
chemical originally applied. It should be noted that
some chemicals may degrade into compounds of
- No indoor fate data were found for DEET.
- No food tolerances have been established for DEET.
- DEET is slightly toxic to birds (oral LD50 = 1375 mg/kg).1
EC50: The median effective concentration (EC50) may be
reported for sublethal or ambiguously lethal effects. This
measure is used in tests involving species such as aquatic
invertebrates where death may be difficult to determine.
This term is also used if sublethal events are being
Newman, M.C.; Unger, M.A. Fundamentals of Ecotoxicology; CRC Press, LLC.:
Boca Raton, FL, 2003; p 178.
Fish and Aquatic Life
- DEET is slightly toxic to freshwater fish (LC50 = 75 mg/L).1
- DEET is slightly toxic to aquatic invertebrates (EC50 = 75 ppm).1 See the text box on EC50.
- The U.S. EPA has classified DEET as "Group D - not classifiable as to human carcinogenicity" based on inadequate evidence
of carcinogenicity, or lack of data in laboratory animals and humans.1 See the text box on Cancer.
- The Centers for Disease Control and Prevention (CDC), National Institute for Occupational Safety and Health (NIOSH) and
the Occupational Safety and Health Administration (OSHA) have not established recommended or regulatory occupational
exposure limits for DEET.
Date Reviewed: July 2008
Please cite as: Jackson, D.; Luukinen, B.; Buhl, K.; Stone, D. 2008. DEET Technical Fact Sheet; National Pesticide Information
Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/archive/DEETtech.html.