Toxicology

Diethyltoluamide (DEET)

General overview

Diethyltoluamide, commonly known as DEET, is a widely used insect-repellent ingredient. Products intended for application to the skin are available without prescription and may contain concentrations ranging from approximately 5% to 100%.

Available preparations

DEET is present in many commercial insect repellents and may be supplied as aerosols, pump sprays, lotions, liquids, creams, sticks, or treated wipes. The concentration varies considerably between products, with some preparations containing only a small percentage of DEET and others approaching 100%.

Main use

The primary purpose of DEET is to repel mosquitoes, ticks, and other biting insects when applied to exposed skin or used according to the manufacturer’s instructions.

Toxic dose

Serious toxicity may occur after ingestion of approximately 25–50 mL of a highly concentrated preparation. Repeated excessive application to the skin can also result in significant poisoning.

Normal skin exposure

When DEET is used on the skin at recommended doses, adverse effects are uncommon. Toxicity becomes more likely when large amounts are repeatedly applied over several days.

Mechanism of toxicity

The precise mechanism responsible for DEET poisoning has not been fully established. Its major toxic effects primarily involve the central nervous system.

Absorption through the skin

A substantial proportion of DEET applied to the skin can enter the body. Approximately half of a topical dose may be absorbed within about 6 hours, with peak blood concentrations occurring around 1 hour after application.

Tissue accumulation

DEET and its metabolic products may remain in the skin and fatty tissues for prolonged periods. Persistence for several weeks after application suggests that repeated exposure may allow accumulation within the body.

Frequency of serious poisoning

Although DEET is one of the most commonly used insect repellents, severe poisoning is uncommon when products are used correctly.

Circumstances of severe toxicity

Serious illness and death have been reported mainly after intentional or accidental ingestion of concentrated preparations or repeated application of excessive quantities to the skin.

Common causes of exposure

Most cases of toxicity result from inappropriate or excessive product use rather than normal application.

Exposure in young children

Repeated application of large amounts of DEET-containing repellent to young children has historically been an important cause of significant toxicity because children can absorb proportionally larger amounts through the skin.

Intentional exposure

In very young infants, inappropriate exposure may raise concern for neglect or improper administration. In older children and adolescents, deliberate ingestion or self-harm should be considered when supported by the circumstances.

Damaged skin

Broken, irritated, or unusually permeable skin may increase absorption of DEET and therefore increase the risk of systemic toxicity.

Increased absorption in children

Young children have relatively permeable skin and may absorb clinically important amounts of DEET following frequent or excessive application.

Seizure-related interactions

Medications or substances that reduce the seizure threshold may increase the likelihood of convulsions in a patient experiencing significant DEET toxicity.

Drug metabolism interactions

DEET may influence hepatic cytochrome P450 enzyme activity. This could potentially alter the effects of medications metabolized through these pathways, including some anticonvulsants and other drugs.

Pregnancy considerations

Animal studies have suggested that DEET can be absorbed through the skin during pregnancy. Historical experimental findings raised concern regarding possible fetal effects at sufficient exposure levels.

Exposure reduction during pregnancy

When appropriate, physical methods of insect protection such as mosquito nets, protective clothing, and environmental controls can reduce the amount of repellent required on the skin.

Diagnosis

Differential diagnosis

A number of toxic and medical conditions may produce seizures resembling those associated with severe DEET poisoning.

Toxic causes of seizures

Possible toxicologic causes include central nervous system stimulants, certain antiarrhythmic drugs, isoniazid, tricyclic antidepressants, monoamine oxidase inhibitors, antipsychotic medications, antihistamines, and numerous other substances.

Non-toxic causes of seizures

Medical explanations such as low blood glucose, abnormal sodium concentration, oxygen deprivation, hypothermia, hypothyroidism, intracranial bleeding, central nervous system infection, or an underlying seizure disorder should also be considered.

Main clinical pattern

The characteristic acute pattern of serious DEET poisoning involves central nervous system depression followed by seizures. Convulsions may occur repeatedly in severe cases.

Vital sign abnormalities

Marked overdose may produce a rapid heart rate, low blood pressure, and suppression of normal respiratory activity.

Eye exposure

Direct contact between DEET and the eyes can irritate the cornea and surrounding mucous membranes.

Skin effects

Superficial dermatitis is among the most frequently reported adverse reactions following topical DEET use.

Cardiovascular effects

Sinus tachycardia may occur during significant poisoning. Severe hypotension and cardiovascular collapse have also been reported, although these complications are uncommon.

Respiratory effects

Profound central nervous system depression can interfere with normal breathing and may eventually cause respiratory failure.

Gastrointestinal effects

Nausea and vomiting may follow ingestion of DEET or substantial absorption after heavy skin exposure.

Liver effects

Severe poisoning may occasionally produce acute chemical hepatitis.

Liver injury after repeated use

Rare cases of idiosyncratic toxic hepatitis have also been reported following repeated exposure.

Early neurologic effects

Initial neurologic findings may include poor coordination, irritability, confusion, and disorientation.

Progressive neurologic depression

As toxicity becomes more severe, patients may become increasingly drowsy and less responsive as central nervous system activity is suppressed.

Severe neurologic toxicity

Major poisoning may progress to unresponsiveness, coma, flaccid paralysis, loss of corneal reflexes, reduced deep-tendon reflexes, and recurrent seizures.

Life-threatening complications

Death in severe poisoning may result from respiratory failure associated with profound central nervous system depression.

Investigations

Testing in asymptomatic patients

Patients who remain completely asymptomatic may not require routine laboratory investigations.

Basic metabolic testing

Serum electrolytes, blood urea nitrogen, creatinine, and glucose may be measured in symptomatic patients to identify metabolic abnormalities contributing to central nervous system manifestations.

Oxygenation assessment

Pulse oximetry should be used to assess oxygenation in symptomatic patients. Arterial blood gas analysis may be considered when significant respiratory compromise is present.

Liver assessment

Serum liver enzyme measurements may be useful when chemical hepatitis is suspected.

Screening in overdose

An electrocardiogram and serum acetaminophen and salicylate concentrations may be considered in overdose cases to identify possible hidden coingestants.

Evaluation of altered mental status

When the diagnosis remains uncertain, additional investigations such as brain imaging, lumbar puncture, bacterial cultures, or other appropriate studies may be required to exclude neurologic or infectious causes.

DEET concentration testing

Blood DEET concentrations can be measured by some specialized laboratories, but the clinical value of these levels for guiding treatment is uncertain.

Treatment

Initial management

Early treatment should focus on removing further exposure, protecting the airway, maintaining adequate breathing and circulation, and rapidly controlling seizures when present.

Exposure history

The amount of DEET involved, concentration of the product, route of exposure, and time since exposure should be established whenever possible. Any additional substances involved should also be identified.

Poison control consultation

Specialist poison-control or toxicology advice should be considered when the clinical presentation does not fit typical DEET toxicity or when coingestion, drug interactions, or underlying illness complicate the case.

Referral for medical assessment

Evaluation in a health-care facility is appropriate when intentional poisoning is suspected, the patient or caregiver cannot provide reliable observation, signs of toxicity develop, or another exposure or illness increases risk.

Admission considerations

Hospital admission is generally appropriate for patients who develop altered mental status, respiratory depression, coma, or seizures.

Out-of-hospital gastrointestinal management

The historical source advises against inducing vomiting because seizures can begin suddenly after significant DEET ingestion and may create an aspiration risk.

Skin decontamination

Following substantial dermal exposure, contaminated skin should be thoroughly washed with soap and water to remove remaining product and limit further absorption.

Hospital skin decontamination

Patients presenting to hospital after significant skin exposure should also have affected areas cleaned thoroughly with soap and water.

Gastric aspiration

The historical source describes nasogastric aspiration as a possible consideration in selected patients who present within approximately 1 hour of a major ingestion or who already show serious toxicity.

Activated charcoal

A single dose of activated charcoal was historically recommended after a substantial recent ingestion when clinically appropriate and when the patient’s airway could be safely protected.

Specific antidote

There is no specific antidote capable of directly reversing DEET poisoning.

Seizure management

Patients who develop seizures require immediate attention to airway protection and oxygenation.

Initial anticonvulsant therapy

A benzodiazepine is generally used as first-line medication for acute seizure control.

Persistent seizures

If convulsions continue or recur despite initial treatment, additional anticonvulsant therapy such as phenobarbital may be considered according to clinical circumstances.

Follow-up

Cardiac monitoring

Symptomatic patients should have their heart rate, rhythm, and cardiovascular status monitored because significant poisoning can produce tachycardia, hypotension, or circulatory instability.

Respiratory monitoring

Continuous observation of respiratory function is important in symptomatic patients because central nervous system depression may progress to respiratory failure.

Expected recovery

Most cases of DEET toxicity improve within approximately 24 hours once exposure has stopped and appropriate supportive treatment has been provided.

Severe poisoning

Patients with major neurologic or respiratory toxicity may require hospitalization beyond 24 hours, depending on the persistence of symptoms and complications.

Neurologic complications

Long-term consequences from repeated seizures or oxygen deprivation are uncommon but may occur following particularly severe poisoning.

Persistent neuropsychiatric effects

Some severely affected individuals may experience subtle cognitive, behavioral, or neuropsychiatric abnormalities lasting for several weeks or months after the acute episode.

Emergency department discharge

Patients may be considered for discharge after appropriate decontamination and an observation period of approximately 4–6 hours when they remain asymptomatic and no additional medical concerns are present.

Hospital discharge

Patients admitted to hospital may be discharged when toxic manifestations have resolved or become clinically stable and further inpatient treatment is no longer required.

Psychiatric assessment

A mental health evaluation should be considered when exposure was deliberate or when attempted self-harm is suspected.

Patient education

Use in young children

Highly concentrated DEET preparations should be used cautiously in small children. Products should be selected and applied according to current manufacturer and public-health recommendations.

Avoiding excessive application

Repeated application more frequently than recommended should be avoided because unnecessary accumulation on the skin can increase systemic absorption.

Following product instructions

Parents and caregivers should follow the application frequency, age restrictions, concentration guidance, and other safety instructions supplied with the specific insect-repellent product.

Washing after exposure

When continued protection is no longer required, treated skin can be washed with soap and water to remove residual repellent, particularly in children.

Clinical pitfalls

Alternative diagnoses

Altered mental status, seizures, or coma should not automatically be attributed to DEET exposure. Other toxicologic, neurologic, infectious, and metabolic causes should remain under consideration.

Failure to decontaminate

Clinicians should not overlook skin decontamination after significant dermal exposure because residual DEET on the skin may continue to be absorbed.

Classification

ICD-9-CM 989.4 refers to toxic effects from certain nonmedicinal substances, including pesticides not otherwise classified.