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Diethyltoluamide (DEET) 

From Other Insecticides, Acaricides, and Repellents Recognition and Management of Pesticide Poisonings
5th Edition 1999, Chapter 8, pp.80-82

Brand Names
  • Auton
  • Detamide
  • Metadelphene
  • MGK
  • Muskol
  • Off!
  • Skeeter Beater
  • Skeeter Cheater
  • Skintastic for Kids

This chemical is a widely-used liquid insect repellent, suitable for application to skin or to fabrics. It comes in a wide range of concentrations from 5% (Off!, Skintastic for Kids R ) to 100% (Muskol R ). Compared to the widespread use of the product, there are relatively few cases of toxicity.16 However, if used improperly, ingested, or a very high concentration is used on children, especially repeatedly over large skin surfaces, the potential for severe toxicity exists.17 DEET is formulated with ethyl or isopropyl alcohol.

Toxicology For many years, diethyltoluamide has been effective and generally well tolerated as an insect repellent applied to human skin, although tingling, mild irritation, and sometimes desquamation have followed repeated application. In some cases, DEET has caused contact dermatitis and excerbation of preexisting skin disease.18,19 It is very irritating to the eyes, but not corrosive.

Serious adverse effects have occurred when used under tropical condition, when it was applied to areas of skin that were occluded during sleep (mainly the antecubital and popliteal fossae). Under these conditions, the skin became red and tender, then exhibited blistering and erosion, leaving painful weeping denuded areas that were slow to heal. Severe scarring occasionally resulted from some of these severe reactions.20

DEET is efficiently absorbed across the skin and by the gut. Blood concentrations of about 0.3 mg/dL have been reported several hours after dermal application in the prescribed fashion.17 The amount absorbed increases as the concentration of DEET rises. In addition, many commercial formulations are prepared with ethanol as a solvent, which further increases absorption.21 Toxic encephalopathic reactions have apparently occurred in rare instances following dermal application, mainly in children who were intensively treated.22, 23, 24 The more frequent cause of systemic toxicity has been ingestion: deliberate in adults and accidental in young children.

Manifestations of toxic encephalopathy have been behavioral disorders including headache, restlessness, irritability, ataxia, rapid loss of consciousness, hypotension, and seizures. Some cases have shown flaccid paralysis and areflexia Deaths have occurred following very large doses.16, 17, 22 Blood levels of DEET found in fatal systemic poisonings have ranged from 168 to 240 mg per liter.17 Interpretation of DEET toxicity in some fatal cases has been complicated by effects of simultaneously ingested ethanol, tranquilizers, and other drugs. One well-documented case of anaphylactic reaction to DEET has been reported. One fatal case of encephalopathy in a child heterozygous for ornithine carbamoyl transferase deficiency resembled Reyes syndrome, but the postmortem appearance of the liver was not characteristic of the syndrome.

Discretion should be exercised in recommending DEET for persons who have acne, psoriasis, an atopic predisposition, or other chronic skin condition. It should not be applied to any skin area that is likely to be opposed to another skin surface for a significant period of time (antecubital and popliteal fossae, inguinal areas).22

Great caution should be exercised in using DEET on children. Avoid repeated application day after day. Applications should be limited to exposed areas of skin, using as little repellent as possible and washing off after use. Do not apply to eyes and mouth and, with young children, do not apply to their hands. Low concentrations (10% or below) are effective and may be preferred in most situations. There are formulations labeled for children that have concentrations of 5 to 6.5% DEET.25 If continuous repellent protection is necessary, DEET should be alternated with a repellent having another active ingredient. If headache or any kind of emotional or behavioral change occurs, use of DEET should be discontinued immediately.

Confirmation of Poisoning

Methods exist for measurement of DEET in blood and tissues and of metabolites in urine, but these are not widely available.

Treatment

1. Skin decontamination. Wash skin with soap and water as outlined in Chapter 2. Eye contamination should be removed by prolonged flushing of the eye with copious amounts of clean water or saline. If irritation persists, specialized medical treatment should be obtained. Topical steroids and oral antihistamines have been used for severe skin reactions that occasionally follow application of DEET.21

2. Gastrointestinal decontamination. If a substantial amount of DEET has been ingested within an hour of treatment, gastrointestinal decontamination should be considered as outlined in Chapter 2. Induced emesis is.usually considered contraindicated in these poisonings due to the rapid onset of seizures.

3. Seizures. Treatment is primarily supportive, with control of seizures by anticonvulsants, as outlined in Chapter 2. Persons surviving poisoning by ingestion of DEET have usually recovered within 36 hours or less.16,17

References 

(only references applicable to this section)

  1. Veltri JC, Osimitz TG, Bradford DC, et al. Retrospective analysis of calls to poison control centers resulting from exposure to the insect repellent N, N-diethyltoluamide (DEET) from 1985-1989. Clin Toxicol 1994;32:1.

  2. Tenebein M. Severe toxic reactions and death following ingestion of diethyltoluamide-containing insect repellents. JAMA 1987;258:1509.

  3. Maibach HI and Johnson HL. Contact urticaria syndrome. Arch Dermatol 1975;111:726.

  4. Wantke F, Focke M, Hemmer W, et al. Generalized urticaria induced by a diethyltoluamide-containing insect repellent in a child. Contact Dermatitis 1996;35(3):186.

  5. Reuveni H.and Yagupsky P. Diethyltoluamide-containing insect repellent: Adverse effects in worldwide use. Arch Dermatol 1982;118:582.

  6. Stinecipher J and Shaw 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.

  7. Lipscomb JW, Kramer JE, and Leikin JB. Seizure following brief exposure to the insect repellent N,N-diethyl-m-toluamide. Ann Emerg Med 1992;21(3):315-17. 

  8. Zadikoff CM. Toxic encephalopathy associated with use of insect repellent. J Pediatr 1979;95:140-2. 

  9. Pronczuk de Garbino J and Laborda A. Toxicity of an insect repellent: N,N- diethyltoluamide.Vet Hum Toxicol 1983;25:422-3.

  10. Hebert AA and Carlton S. Getting bugs to bug off: A review of insect repellents. Contemp Pediatr 1998;15:85-95. 


Authors

J. Routt Reigart, M.D.
Professor of Pediatrics, Medical University of South Carolina

James R. Roberts, M.D., M.P.H.
Assistant Professor of Pediatrics, Medical University of South Carolina

Support for this publication was provided by:
Certification and Worker Protection Branch
Field and External Affairs Division
Office of Pesticide Programs
U.S. Environmental Protection Agency
401 M Street SW (7506C)
Washington, DC 20460

For additional copies or more information:
Tel: 703-305-7666
Fax: 703-308-2962

The manual is available in electronic format on the Internet at: http://www.epa.gov/oppfead1/safety/healthcare/handbook/handbook.htm

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