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DEET

Technical Fact Sheet

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 The old collection of technical fact sheets will remain available in this archive, but they may contain out-of-date material.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 -
DEET

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.

Chemical Class and Type:

Physical / Chemical Properties:

Uses:

Mode of Action:

Target Organisms

Non-target Organisms

Acute Toxicity:

Oral

TOXICITY CLASSIFICATION - DEET
High Toxicity Moderate Toxicity Low Toxicity Very Low Toxicity
Acute Oral LD50 Up to and including 50 mg/kg
(≤ 50 mg/kg)
Greater than 50 through 500 mg/kg
(>50-500 mg/kg)
Greater than 500 through 5000 mg/kg
(>500-5000 mg/kg)
Greater than 5000 mg/kg
(>5000 mg/kg)
Inhalation LC50 Up to and including 0.05 mg/L
(≤0.05 mg/L)
Greater than 0.05 through 0.5 mg/L
(>0.05-0.5 mg/L)
Greater than 0.5 through 2.0 mg/L
(>0.5-2.0 mg/L)
Greater than 2.0 mg/L
(>2.0 mg/L)
Dermal LD50 Up to and including 200 mg/kg
(≤200 mg/kg)
Greater than 200 through 2000 mg/kg
(>200-2000 mg/kg)
Greater than 2000 through 5000 mg/kg
(>2000-5000 mg/kg)
Greater than 5000 mg/kg
(>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 - 21 days 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 erythema)
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. http://www.epa.gov/oppfead1/labeling/lrm/chap-07.pdf

Dermal

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.

Inhalation

Signs of Toxicity - Animals

Signs of Toxicity - Humans

Chronic Toxicity:

Animals

Oral

Dermal

Humans

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.

Endocrine Disruption:

Carcinogenicity:

Animals

Humans

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.

Reproductive or Teratogenic Effects:

Animals

Humans

Fate in the Body:

Absorption

Animals

Humans

Distribution

Animals

Humans

Metabolism

Animals

Humans

Excretion

Animals

Humans

Medical Tests and Monitoring:

Environmental Fate:

Soil

Water

Air

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 toxicological significance.

Indoor

Food Residue

Ecotoxicity Studies:

Birds

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 monitored.

Newman, M.C.; Unger, M.A. Fundamentals of Ecotoxicology; CRC Press, LLC.: Boca Raton, FL, 2003; p 178.

Fish and Aquatic Life

Regulatory Guidelines:

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.

References:

  1. Reregistration Eligibility Decision (RED) DEET; EPA 738-R-98-010; U.S. Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1998; pp 1-34.
  2. Hazardous Substances Data Bank (HSDB), DEET; HSDB Number 1582; U.S. Department of Health and Human Services, National Institutes of Health, National Library of Medicine. http://toxnet.nlm.nih.gov (accessed Jan 2008), updated March 2003.
  3. Technical Guide No. 36: Personal Protective Measures Against Insects and Other Arthropods of Military Significance; Defense Pest Management Information Analysis Center (DPMIAC), Armed Forces Pest Management Board (AFPMB): Washington, DC, 2002; pp 21-25.
  4. Pesticide Products. Pest Bank [CD-ROM] 2007.
  5. Toxicity and Exposure Assessment for Children's Health (TEACH) Summaries: Diethyltoluamide (DEET) Chemical Summary; U.S. Environmental Protection Agency. http://www.epa.gov/teach/chem_summ/DEET_summary.pdf (accessed Aug 2007), updated April 2007.
  6. Davis, E. E.; Sokolove, P. G. Lactic Acid-sensitive Receptors on the Antennae of the Mosquito, Aedes aegypti. J. Comp. Physiol. 1976, 105, 43-54.
  7. McIver, S. B. A model for the mechanism of action of the repellent DEET on the Aedes Aegypti (Diptera: Culicidae). J. Med. Entomol. 1981, 18 (5), 357-361.
  8. Snow, W. F. The effect of a reduction in expired carbon dioxide on the attractiveness of human subjects to mosquitoes. Bull. Ent. Res. 1970, 60, 43-48.
  9. Sudakin, D. L.; Trevathan, W. R. DEET: A review and update of safety and risk in the general population. J. Toxicol. Clin. Toxicol. 2003, 41 (6), 831-839.
  10. Lewis, C. M., Silva, M., Sanborn, J. N,N-Diethyl-Meta-Toluamide (DEET) Risk Characterization Document; California Environmental Protection Agency, Department of Pesticide Regulation: Sacramento, CA, 2000; pp 18-21, 32-33.
  11. Gwaltney-Brant, S. Insecticides and Molluscicides. Clinical Veterinary Toxicology; Plumlee, K. H., Ed.; Mosby, Inc.: St. Louis, 2004; pp 177-192.
  12. Bell, J. W.; Veltri, J. C.; Page, 12. B. C. Human Exposures to N,N-diethyl-m-toluamide Insect Repellents Reported to the American Association of Poison Control Centers 1993-1997. Int. J. Toxicol. 2002, 21 (5), 341-352.
  13. Reigart, J. R.; Roberts, J. R. Other Insecticides, Acaricides, and Repellents. Recognition and Management of Pesticide Poisonings, 5th ed.; U.S. Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1999; pp 80-82.
  14. Schoenig, G. P.; Osimitz, T. G.; Gabriel, K. L.; Hartnagel, R.; Gill, M. W.; Goldenthal, E. I. Evaluation of the Chronic Toxicity and Oncogenicity of N,N-diethyl-m-toluamide (DEET). Toxicol. Sci. 1999, 47 (1), 99-109.
  15. Schoenig, G. P.; Osimitz, T. G. DEET. Handbook of Pesticide Toxicology, 2nd ed.; Krieger, R. I., Ed.; Academic Press, Inc.: San Diego, 2001; Vol. 2, pp 1439-1455.
  16. Knowles, C. O. Miscellaneous Pesticides. Handbook of Pesticide Toxicology; Hayes Jr., W. J., Laws Jr., E.R., Eds.; Academic Press, Inc.: San Diego, 1991; Vol. 3, pp 1500-1505.
  17. Ross, E. A.; Savage, K. A.; Utley, L. J.; Tebbett, I. R. Insect repellent interactions: sunscreens enhance DEET (N,N-diethyl-mtoluamide) absorption. Drug Metab. Dispos. 2004, 32 (8), 783-785.
  18. Kasichayanula, S.; House, J. D.; Wang, T.; Gu, X. Percutaneous characterization of the insect repellent DEET and the sunscreen oxybenzone from topical skin application. Toxicol. Appl. Pharmacol. 2007, 223 (2), 187-194.
  19. Selim, S.; Hartnagel, R. E., Jr.; Osimitz, T. G.; Gabriel, K. L.; Schoenig, G. P. Absorption, Metabolism, and Excretion of N,N,- Dietyl-m-toluamide Following Dermal Application to Human Volunteers. Environ. Appli. Toxicol. 1995, 25, 95-100.
  20. Stinecipher, J.; Shah, J. Percutaneous Permeation of N,N-Diethyl-m-toluamide (DEET) From Commercial Mosquito Repellents and the Effect of Solvent. J. Toxicol. Environ. Health 1997, 52, 119-135.
  21. Brand, R. M.; Jendrzejewski, J. L.; Henery, E. M.; Charron, A. R. A Single Oral Dose of Ethanol Can Alter Transdermal Absorption of Topically Applied Chemicals in Rats. Toxicol. Sci. 2006, 92 (2), 349-355.
  22. Usmani, K. A.; Rose, R. L.; Goldstein, J. A.; Taylor, W. G.; Brimfield, A. A.; Hodgson, E. In Vitro Human Metabolism and Interactions of Repellent N,N-Diethyl-m-toluamide. Drug Metab. Dispos. 2002, 30 (3), 289-294.
  23. Snodgrass, H. L.; Nelson, D. C.; Weeks, M. H. Dermal penetration and potential for placental transfer of the insect repellent, N,N-diethyl-m-toluamide. Am. Ind. Hyg. Assoc. J. 1982, 43 (10), 747-753.
  24. Schoenig, G. P.; Hartnagel, R. E., Jr.; Osimitz, T. G.; Llanso, S. Absorption, distribution, metabolism, and excretion of N,Ndiethyl- M-toluamide in the rat. Drug Metab. Dispos. 1996, 24 (2), 156-163.
  25. CDC. Third National Report on Human Exposure to Environmental Chemicals; U.S. Department of Health and Human Services, Centers for Disease Control and Prevention: Atlanta, 2005.
  26. Rivera-Cancel, G.; Bocioaga, D.; Hay, A. G. Bacterial Degradation of N,N-Diethyl-m-Toluamide (DEET): Cloning and Heterologous Expression of DEET Hydrolase. Appl. Environ. Microbiol. 2007, 73 (9), 3105-3108.
  27. Seo, J.; Lee, Y. G.; Kim, S. D.; Cha, C. J.; Ahn, J. H.; Hur, H. G. Biodegradation of the Insecticide N,N-Diethyl-m-Toluamide by Fungi: Identification and Toxicity of Metabolites. Arch. Environ. Contam. Toxicol. 2005, 48 (3), 323-328.
  28. Sandstrom, M. W.; Kolpin, D. W.; Thurman, E. M.; Zaugg, S. D. Widespread detection of N,N-diethyl-m-toluamide in U.S. streams: comparison with concentrations of pesticides, personal care products, and other organic wastewater compounds. Environ. Toxicol. Chem. 2005, 24 (5), 1029-1034.
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