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Metabolism of N,N-diethyl-m-toluamide (DEET) by liver microsomes from male and female rats. Simultaneous quantitation of DEET and its metabolites by high performance liquid chromatography.

A simple and sensitive HPLC procedure was developed to separate and quantitate N,N-diethyl-m-toluamide (DEET) and its in vitro metabolites using a gradient elution, a reversed phase C18 column, and an internal standard. This procedure was applied to examine the metabolism of this insect repellent in liver microsomes from normal (untreated) male and female Wistar rats. At a pH of 8.6 and at a substrate concentration of 200 microM, the microsomal preparations from males degraded DEET faster than did those from females. The half-life of DEET was 10 min and 15 min, respectively. The benzylic methyl hydroxylated metabolite and the N-deethylated metabolite were determined over 2 hr in fortified microsomal suspensions. Rate constants for appearance of the metabolites showed significantly higher values for males than for females. These observations suggests that a sex difference may be present in the metabolism of DEET.

Animals↗
PubMed1997

Percutaneous permeation of N,N-diethyl-m-toluamide (DEET) from commercial mosquito repellents and the effect of solvent.

N,N-Diethyl-m-toluamide (DEET), the active ingredient in many commercial mosquito repellents, is thought to be responsible for a wide range of local and systemic adverse reactions following its use. Many investigators have studied the dermal absorption of pure DEET; however, there is only one report in the literature on the absorption of DEET from commercial mosquito repellents and the effect of concentration of DEET on its absorption through skin. The first objective of the present study was to evaluate the permeation characteristics of DEET from four commercial products, Everglades (95%), Repel Deerhunters (52.25%), Off Skintastic (6.65%), and Skedaddle (6.2%), as compared to pure DEET (approximately 100%). The second objective was to study the effects of ethanol, the solvent for DEET, on the permeation of DEET and investigate its potential for enhancing the dermal absorption of DEET. Permeation studies of DEET from commercial mosquito repellents and from solutions containing various percentages of ethanol were conducted across human skin using an infinite dose technique with a Franz diffusion cell. Permeation parameters such as steady-state flux (Jss), lag time (tL), diffusion coefficient (D), permeability (P), and skin/ vehicle partition coefficient (K) were obtained from the permeation profiles in each case. The cumulative amount of DEET permeated can be ranked according to the following order: neat DEET (100%) = Everglades (95%) > Repel (52.25%) > Skedaddle (6.2%) = Off Skintastic (6.65%). Pure DEET exhibited the highest flux value of 63.20 +/- 24.52 micrograms/cm2-h, while Off Skintastic had the lowest value of 21.12 +/- 14.75 micrograms/cm2-h. The tL and D values for each of the products were similar to that of pure DEET. The total amount of DEET permeated from 30-45% ethanolic solutions at the end of 36 h was significantly higher than that from pure DEET and from the 60-90% ethanolic solutions. The Jss, P, and K values of DEET from the 30-45% ethanolic solutions were significantly higher than those from the 75-90% ethanolic solutions, while the tL and D values were similar for each solution. Therefore, there is potential for significant absorption of DEET after the dermal application of commercial mosquito repellents, and ethanol, used as a solvent, may enhance the permeation of DEET.

Analysis of Variance↗
PubMed1997

The influence of diethyl-m-toluamide (DEET) on the percutaneous absorption of permethrin and carbaryl.

Simultaneous exposure to DEET and permethrin was recently proposed to be associated with the "Gulf War Syndrome." However, no studies have reported the percutaneous absorption of DEET and permethrin when applied simultaneously to the skin as a mixture, the relevant route of exposure in the Persian Gulf. The present study quantitates percutaneous absorption of DEET and permethrin after coadministration to rodent and pig skin in vitro. Dosing solutions were also prepared with either acetone, dimethyl sulfoxide (DMSO), or ethanol to compare vehicle effects on percutaneous absorption of permethrin and DEET. The influence of DEET on carbaryl absorption and dermal disposition was also assessed in pig studies to statistically demonstrate DEET effects in acetone or DMSO and different solvent concentrations. Topical application of permethrin + DEET resulted in absorption of DEET (1-20% dose), but no permethrin. Permethrin (1.2-1.7% dose) was detected only when mouse skin was dosed solely with permethrin, a finding suggesting that DEET decreased permethrin absorption. DEET also inhibited carbaryl absorption in acetone mixtures, but had no effect on DMSO mixtures. Irrespective of solvent, DEET did not enhance carbaryl penetration into skin. For DEET, absorption was greater in mouse skin (10.7-20.6% dose) than in rat skin (1.1-5.2% dose) and pig skin (2.8% dose). The extent of DEET absorption was greater with DMSO and acetone than with ethanol in rat and mouse skin. These studies support DEET, but not permethrin or carbaryl, as having sufficient systemic exposure to potentially cause signs of toxicity when simultaneously applied with pesticides. Furthermore, these studies demonstrated that DEET does not necessarily enhance dermal absorption of all toxicants as was originally hypothesized.

Administration, Cutaneous↗
PubMed1999

Anticonvulsant-resistant seizures following pyridostigmine bromide (PB) and N,N-diethyl-m-toluamide (DEET).

An acute toxic interaction has been described, in which sublethal doses of pyridostigmine bromide (PB) and the insect repellent N,N-diethyl-m-toluamide (DEET), when administered concomitantly, resulted in seizures and lethality. To investigate the possible relationships between seizures and lethality and the role of the cholinergic system in this interaction, PB (5 mg/kg), DEET (200 mg/kg) or PB (3 mg/kg) + DEET (200 mg/kg) were administered i.p. to male ICR mice, alone or following i.p. pretreatment, with one of several anticonvulsant agents: diazepam, 10 mg/kg; fosphenytoin, 40 mg/kg; phenobarbital, 45 mg/kg; or dextrophan, 25 mg/kg), or the anticholinergic agents, atropine (5 mg/kg), atropine methyl nitrate (2.7 mg/kg), or mecamylamine (2.5 mg/kg). The anticonvulsants selected for this study act through different mechanisms to reduce seizures. None of the anticonvulsants was able to reduce the incidence of seizures following treatment with PB, DEET or PB + DEET. Only diazepam delayed the onset of seizures. Fosphenytoin or diazepam significantly prolonged the time to lethality following PB, but only fosphenytoin reduced the incidence of PB-induced lethality. Diazepam or phenobarbital significantly prolonged the time to lethality following PB + DEET. Both atropine and atropine methyl nitrate protected against PB and PB + DEET-induced lethality and PB-induced seizures. Neither agent blocked seizures resulting from DEET or PB + DEET. Mecamylamine reduced seizures and lethality in PB-treated mice, but not in mice treated with DEET or PB + DEET. The results indicate that seizure activity is not a causative factor in the toxic interaction between PB and DEET. Furthermore, PB, DEET and PB + DEET induce seizures that are resistant to standard anticonvulsants, and each appears to operate through different mechanisms to produce seizures. Peripheral muscarinic receptors may play a specific role in lethality caused by PB + DEET.

Animals↗
PubMed2001

Toxic encephalopathy associated with use of DEET insect repellents: a case analysis of its toxicity in children.

(1) Respiratory distress and seizures developed in an 18-month-old boy following brief exposure to low-strength (17.6%) N,N-diethyl-m-toluamide (DEET). A review of the literature revealed 17 reports of DEET-induced encephalopathy in children. The objective of this study was to test the hypothesis that the potential toxicity of DEET is high and that available repellents containing DEET, irrespective of their strength, are not safe when applied to children's skin. (2) Although this is a case report, we used the features of published reports of DEET-induced encephalopathy in children to support the diagnosis, since the evidence that the child's illness was caused by DEET was circumstantial. In the following case analysis, clinical reports of children < 16 years old have been reviewed and analyzed in an effort to relate direct DEET toxicity to various clinical, demographic, and toxic compound exposure factors (Fisher's exacttest and logistic regression analysis). (3) DEET-induced encephalopathy in children (56% girls) followed not only ingestion or repeated and extensive application of repellents, but also a brief exposure to DEET (45%). Of those who reported a dermal exposure, 33% reported an exposure to a product containing DEET < 20%. Seizures, the most prominent symptom (72%), were significantly more frequent when DEET solutions were applied to the skin (P<0.01). Mortality (16.6%) did not correlate significantly with the concentration of the DEET liquid used, duration of skin exposure, pattern of use, age, or sex. (4) Data of this case analysis suggest that repellents containing DEET are not safe when applied to children's skin and should be avoided in children. Additionally, since the potential toxicity of DEET is high, less toxic preparations should be probably substituted for DEET-containing repellents, whenever possible.

Administration, Topical↗
PubMed2004

Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity.

Military personnel deployed in the Persian Gulf War (PGW) were exposed to a combination of chemicals, including pyridostigmine bromide (PB), DEET, and permethrin. We investigated the dose-response effects of these chemicals, alone or in combination, on the sensorimotor performance and cholinergic system of male Sprague-Dawley rats. Animals were treated with a daily dermal dose of DEET and/or permethrin for 60 days and/or PB (gavage) during the last 15 days. Neurobehavioral performance was assessed on day 60 following the beginning of the treatment with DEET and permethrin. The rats were sacrificed 24 h after the last treatment for biochemical evaluations. PB alone, or in combination with DEET, or DEET and permethrin resulted in deficits in beam-walk score and longer beam-walk times compared to controls. PB alone, or in combination with DEET, permethrin, or DEET and permethrin caused impairment in incline plane performance and forepaw grip strength. PB alone at all doses slightly inhibited plasma butyrylcholinesterase activity, whereas combination of PB with DEET or permethrin increased its activity. Brainstem acetylcholinesterase (AChE) activity significantly increased following treatment with combinations of either DEET or permethrin at all doses, whereas the cerebellum showed a significant increase in AChE activity following treatment with a combination of PB/DEET/permethrin. Co-exposure to PB, DEET, and permethrin resulted in significant inhibition in AChE in midbrain. PB alone or in combination with DEET and permethrin at all doses increased ligand binding for m2 muscarinic acetylcholine receptor in the cortex. In addition, PB and DEET together or a combination of PB, DEET, and permethrin significantly increased ligand binding for nicotinic acetylcholine receptor. These results suggest that exposure to various doses of PB, alone and in combination with DEET and permethrin, leads to sensorimotor deficits and differential alterations of the cholinergic system in the CNS.

Acetylcholinesterase↗
PubMed2001

Locomotor and sensorimotor performance deficit in rats following exposure to pyridostigmine bromide, DEET, and permethrin, alone and in combination.

Since their return from Persian Gulf War (PGW), many veterans have complained of symptoms including muscle and joint pain, ataxia, chronic fatigue, headache, and difficulty with concentration. The causes of the symptoms remain unknown. Because these veterans were exposed to a combination of chemicals including pyridostigmine bromide (PB), DEET, and permethrin, we investigated the effects of these agents, alone and in combination, on the sensorimotor behavior and central cholinergic system of rats. Male Sprague-Dawley rats (200-250 gm) were treated with DEET (40 mg/kg, dermal) or permethrin (0.13 mg/kg, dermal), alone and in combination with PB (1.3 mg/kg, oral, last 15 days only), for 45 days. Sensorimotor ability was assessed by a battery of behavioral tests that included beam-walk score, beam-walk time, incline plane performance, and forepaw grip on days 30 and 45 following the treatment. On day 45 the animals were sacrificed, and plasma and CNS cholinesterase, and brain choline acetyl transferase, muscarinic and nicotinic acetylcholine receptors were evaluated. Animals treated with PB, alone or in combination with DEET and permethrin, showed a significant deficit in beam-walk score as well as beam-walk time as compared with controls. Treatment with either DEET or permethrin, alone or in combination with each other, did not have a significant effect on beam-walk score. All chemicals, alone or in combination, resulted in a significant impairment in incline plane testing on days 30 and 45 following treatment. Treatment with PB, DEET, or permethrin alone did not have any inhibitory effect on plasma or brain cholinesterase activities, except that PB alone caused moderate inhibition in midbrain acetylcholinesterase (AChE) activity. Treatment with permethrin alone caused significant increase in cortical and cerebellar AChE activity. A combination of DEET and permethrin or PB and DEET led to significant decrease in AChE activity in brainstem and midbrain and brainstem, respectively. A significant decrease in brainstem AChE activity was observed following combined exposure to PB and permethrin. Coexposure with PB, DEET, and permethrin resulted in significant inhibition in AChE in brainstem and midbrain. No effect was observed on choline acetyl transferase activity in brainstem or cortex, except combined exposure to PB, DEET, and permethrin caused a slight but significant increase in cortical choline acetyltransferase activity. Treatment with PB, DEET, and permethrin alone caused a significant increase in ligand binding for m2 muscarinic acetylcholine receptor (mAChR) in the cortex. Coexposure to PB, DEET, and permethrin did not have any effect over that of PB-induced increase in ligand binding. There was no significant change in ligand binding for nicotinic acetylcholine receptor (nAChR) associated with treatment with the chemical alone; a combination of PB and DEET or coexposure with PB, DEET, and permethrin caused a significant increase in nAChR ligand binding in the cortex. Thus, these results suggest that exposure to physiologically relevant doses of PB, DEET, and permethrin, alone or in combination, leads to neurobehavioral deficits and region-specific alterations in AChE and acetylcholine receptors.

Acetylcholinesterase↗
PubMed2002

Topical formulation studies with DEET (N,N-diethyl-3-methylbenzamide) and cyclodextrins.

The purpose of this study was to investigate the utility of cyclodextrins as a safer alternative to the commonly used cosolvent ethanol in topical N,N-diethyl-3-methylbenzamide (DEET) formulations. Ethanol is a known penetration enhancer and would ideally not be used in a formulation containing DEET, a compound known for its potential toxicity. DEET formulations were prepared containing up to 20% w/w gamma-cyclodextrin (GCD) or 30% w/w hydroxypropyl-beta-cyclodextrin (HPBCD). These formulations were evaluated by determining the release rate of DEET from its vehicle through a synthetic membrane into a receiver medium with a high affinity for DEET using a fully automated Franz-diffusion cell system. DEET release was measured by ultraviolet spectrophotometry at 260 nm. Both the traditional Higuchi release model and an alternate repeated measures analysis of variance with nested factors were used to analyze the data. The influence of the cyclodextrins on the volatility of DEET was determined by solid-phase microextraction. Morphological characterization of the formulations was performed by light microscopy. Physical stability of the formulations was evaluated by rheology in an accelerated study performed at 50 degrees C for 28 days. The cyclodextrins caused a decrease in the release of DEET from its vehicle compared with an ethanol-containing formulation. This effect became more pronounced as the amount of cyclodextrin in the formulation was increased. The addition of the cyclodextrins resulted in a cream-like product compared with the ethanol formulation, which was a lotion. The DEET formulations had the following rank order of volatility: ethanol < DEET = GCD < HPBCD. Examination of the formulations by light microscopy indicated that the CD-based formulations produced a smaller and more homogeneous droplet size distribution than the ethanol-based formulations. The accelerated physical stability study indicated that cyclodextrin-based formulations are both technically and commercially feasible. Cyclodextrins are a promising alternative to ethanol in DEET-containing formulations. The reduced release rate of DEET from these formulations suggests that the toxic potential of DEET may be decreased in these products, while its repellency and stability are maintained.

Administration, Topical↗
PubMed2000

Reduction in skin permeation of N,N-diethyl-m-toluamide (DEET) by altering the skin/vehicle partition coefficient.

Reported adverse side effects after using N,N-diethyl-m-toluamide (DEET)-containing mosquito repellent products appear to be the result of significant absorption of DEET through human skin. The overall objective was to develop formulations of DEET with significantly reduced permeation using the basic principles and model of skin permeation based on Fick's laws of diffusion at steady state. Ternary phase diagrams of DEET with water and semipolar solvents, ethanol, PG and PEG 400, showed an increase in the aqueous solubility of DEET. This resulted in a linear decline in octanol/water PC with an increase in the concentration of the solvent. Permeation of DEET across human skin was studied from vehicles containing various amounts of PG and PEG 400 using an infinite dose technique and Franz diffusion cell. DEET's flux reduced with increasing PG concentration and the flux from 90% PG was 9.9+/-2.1 microg/cm(2) h, 6-fold lower than flux of pure DEET control, 63.2+/-24.5 microg/cm(2) h. Flux was reduced 6-fold from 60% PEG 400 solution, and permeation of DEET was totally prevented from 90% PEG 400 which was very viscous. However, a combination of 60% PEG 400 with 30% PG not only reduced permeation 9-fold but was suitable as a vehicle for formulation. The decrease in flux and permeability of DEET with increasing concentration of solvent appeared to be a direct result of decrease in skin/vehicle PC and octanol/water PC. This study clearly demonstrates that alternative formulations can be developed for DEET aimed at reduced permeation and toxicity unlike the current formulations some of which contain ethanol which has been shown to enhance permeation of DEET. A similar approach can be used for developing formulations of other industrial and occupational agents to prevent their skin permeation when a user may be exposed to them.

Algorithms↗
PubMed1999

The potential use of N,N-diethyl-m-toluamide (DEET) as a prophylactic agent in the control of schistosomiasis.

DEET (N, N-diethyl-m-toluamide) is one of the reliable and most widely used insect repellents. This work was planned to study the effect of DEET on Schistosoma mansoni cercariae viability (in vitro) and skin penetration and migration (in vivo). DEET concentrations of 30%, 15% and 7.5% were highly efficient in killing all cercariae in vitro within 30, 60 and 240 minutes respectively. Two concentrations of DEET (15%) and (7.5%) were tested separately for their antipenetrant and protective effects in mice by immersing their tails in the drug and then exposed to cercariae, 30 minutes later. DEET antischistosomal activity was assessed by the number of non penetrating cercariae, worm burden, egg count/gram liver and number of liver granulomata. The maximum prophylactic effect was recorded using DEET (15%) where the percentage of resistance reached 100% compared to 92% using DEET (7.5%). DEET was highly effective in preventing penetration of cercariae as well as its further migration to liver which is proved histopathologically in the liver. The persistence of the antipenetrant and protective effects of DEET over several days post application and following different water wash durations was examined. Treatment of mice tails with DEET (15%) and (7.5%), three days prior to infection, showed significant levels of resistance of 94.8% and 82.7% respectively. DEET (15%) provided 100% and 97.9% resistance even when treated tails were washed for 1 and 2 hours respectively.

Administration, Topical↗
PubMed2001

Subchronic dermal application of N,N-diethyl m-toluamide (DEET) and permethrin to adult rats, alone or in combination, causes diffuse neuronal cell death and cytoskeletal abnormalities in the cerebral cortex and the hippocampus, and Purkinje neuron loss in the cerebellum.

N,N-Diethyl m-toluamide (DEET) and permethrin have been implicated as potential neurotoxic agents that may have played an important role in the development of illnesses in some veterans of the Persian Gulf War. To determine the effect of subchronic dermal application of these chemicals on the adult brain, we evaluated histopathological alterations in the brain of adult male rats following a daily dermal dose of DEET (40 mg/kg in 70% ethanol) or permethrin (0.13 mg/kg in 70% ethanol) or a combination of the two for 60 days. Control rats received a daily dermal dose of 70% ethanol for 60 days. Animals were perfused and brains were processed for morphological and histopathological analyses following the above regimen. Quantification of the density of healthy (or surviving) neurons in the motor cerebral cortex, the dentate gyrus, the CA1 and CA3 subfields of the hippocampus, and the cerebellum revealed significant reductions in all three treated groups compared with the control group. Further, animals receiving either DEET or permethrin exhibited a significant number of degenerating (eosinophilic) neurons in the above brain regions. However, degenerating neurons were infrequent in animals receiving both DEET and permethrin, suggesting that neuronal cell death occurs earlier in animals receiving combined DEET and permethrin than in animals receiving either DEET or permethrin alone. The extent of neuron loss in different brain regions was similar among the three treatment groups except the dentate gyrus, where neurodegeneration was significantly greater with exposure to DEET alone. The neuron loss in the motor cerebral cortex and the CA1 subfield of all treated groups was also corroborated by a significant decrease in microtubule associated protein 2-immunoreactive elements (15-52% reduction), with maximal reductions occurring in rats receiving DEET alone; further, the surviving neurons in animals receiving both DEET and permethrin exhibited wavy and beaded dendrites. Analysis of glial fibrillary acidic protein immunoreactivity revealed significant hypertrophy of astrocytes in the hippocampus and the cerebellum of all treated groups (24-106% increase). Thus, subchronic dermal application of DEET and permethrin to adult rats, alone or in combination, leads to a diffuse neuronal cell death in the cerebral cortex, the hippocampal formation, and the cerebellum. Collectively, the above alterations can lead to many physiological, pharmacological, and behavioral abnormalities, particularly motor deficits and learning and memory dysfunction.

Administration, Cutaneous↗
PubMed2004

Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats.

Malathion (O,O-dimethyl-S-[1,2-carbethoxyethyl]phosphorodithionate), DEET (N,N-diethyl-m-toluamide), and permethrin [(+/-)-cis/trans-3-(2,2-dichloroethenyl)-2,2-dimethylcyclopropane carboxylic acid (3-phenoxyphenyl) methyl ester] are commonly used pesticides. To determine the effects of the dermal application of these chemicals, alone or in combination, the sensorimotor behavior, central cholinergic system, and histopathological alterations were studied in adult male Sprague-Dawley rats following a daily dermal dose of 44.4 mg/kg malathion, 40 mg/kg DEET, and 0.13 mg/kg permethrin, alone and in combination for 30 d. Neurobehavioral evaluations of sensorimotor functions included beam-walking score, beam walk time, inclined plane, and grip response assessments. Twenty-four hours after the last treatment with each chemical alone or in combination all behavioral measures were impaired. The combination of DEET and permethrin, malathion and permethrin, or the three chemicals together resulted in greater impairments in inclined performance than permethrin alone. Only animals treated with a combination of DEET and malathion or with DEET and permethrin exhibited significant increases in plasma butyrlcholinesterase (BChE) activity. Treatment with DEET or permethrin alone, malathion and permethrin, or DEET and permethrin produced significant increases in cortical acetylcholinesterase (AChE) activity. Combinations of malathion and permethrin or of DEET and permethrin produced significant decreases in midbrain AChE activity. Animals treated with DEET alone exhibited a significant increase in cortical m2 muscarinic ACh receptor binding. Quantification of neuron density in the dentate gyrus, CA1 and CA3 subfields of the hippocampus, midbrain, brainstem, and cerebellum revealed significant reductions in the density of surviving neurons with various treatments. These results suggest that exposure to real-life doses of malathion, DEET, and permethrin, alone or in combination, produce no overt signs of neurotoxicity but induce significant neurobehavioral deficits and neuronal degeneration in brain.

Acetylcholinesterase↗
PubMed1999

Microsomal metabolism of N,N-diethyl-m-toluamide (DEET, DET): the extended network of metabolites.

1. The aim was to set out to establish the complete network of metabolites arising from the phenobarbital-treated rat liver microsomal oxidation of N,N-diethyl-m-toluamide (DEET). The products formed from DEET and all its subsequent metabolites were identified by HPLC retention times, UV spectroscopy, mass spectrometry and by comparison with authentic standards. 2. DEET (1a) produces three major metabolites, N-ethyl-m-toluamide (1b), N,N-diethyl-m-(hydroxymethyl)benzamide (2a) and N-ethyl-m-(hydroxymethyl)benzamide (2b), and, at low substrate concentrations or extended reaction times, two minor metabolites, toluamide (1c) and N,N-diethyl-m-formylbenzamide (3a). 1b and 2a are primary metabolites and their formation follows Michaelis-Menten-type kinetics. At low DEET concentrations, ring methyl group oxidation is favoured; at saturation concentrations, methyl group oxidation and N-deethylation proceed at similar rates. The rate of formation of 2b decreases with increasing DEET concentration; 2b is therefore a secondary metabolite of DEET and DEET acts as a competitive inhibitor of the metabolism of 1b and 2a. 3. Except for the primary amides, where N-dealkylation is impossible, metabolism of all subsequent compounds, 1b,c, 2a-c, 3a-c and 4a,b, involves an N-deethylation (NEt2 --> NHEt or NHEt --> NH2) competitive with a ring substituent oxidation (CH3 --> CH2OH, CH2OH --> CHO or CHO --> CO2H). Surprisingly, the aldehydes 3a-c are also reduced to the corresponding alcohols 2a-c (CHO --> CH2OH); CO inhibits the oxidative metabolism of 3a-c, but reduction to 2a-c continues uninhibited. 4. The outcomes of this work are that (1) previously unreported aldehydes 3b and 3c form part of the DEET network of metabolites, (2) the reduction of the aldehydes 3a-c has the potential to inhibit the formation of the more highly oxidized DEET metabolites, (3) amide hydrolysis was not observed for any substrate and (4) no evidence was obtained for N-(1-hydroxyethyl)amide intermediates.

Animals↗
PubMed2001

Soldier acceptability of a camouflage face paint combined with DEET insect repellent.

Under operational conditions, current doctrine requires separate application of the standard military insect repellent and camouflage face paint. Working with an industrial partner, Amon Re, Inc., we developed a combined camouflage face paint and insect repellent that offers excellent protection from arthropod disease vectors. We undertook a study to determine whether the new product was acceptable to soldiers under field conditions. A new formulation of camouflage face paint containing the insect repellent N,N-diethyl-3-methyl-benzamide (DEET) was tested for user acceptability during a joint-service, multinational, military field training exercise (Operation Cobra Gold 1999) in Thailand. Soldiers testing the camouflage face paint were members of one of three companies (A, B, and C) of 1st Battalion, 21st Infantry Regiment, 25th Infantry Division. Soldiers in A company (N = 98) received standard military camouflage face paint and the U.S. military's Extended Duration Topical Insect and Arthropod Repellent containing 33% DEET, soldiers in B company (N = 75) received a new formulation of camouflage face paint without DEET, and soldiers in C company (N = 88) received the new formulation of camouflage face paint containing 30% DEET. Every soldier who volunteered to participate completed the study and submitted responses to the questionnaire. The different treatments were evaluated while soldiers spent 4 days conducting simulated combat exercises in a hot, tropical environment in central Thailand. Soldiers were provided the test materials, given a briefing on the study, and completed an initial questionnaire on May 19, 1999. Soldiers completed a final questionnaire after they returned from the training exercise on May 24, 1999. Results of the study indicated that soldiers found the new formulation of 30% DEET camouflage face paint easier to apply (88% of respondents) and remove (77%) than the current standard issue camouflage face paint. Soldiers liked the new 30% DEET camouflage face paint formulation better (61%) and were more likely to recommend it (67%) than the old camouflage face paint formulation. Although the addition of DEET to the camouflage face paint occasionally caused minor irritation after application for a short period (less than 15 minutes), the new camouflage face paint formulation with 30% DEET was evaluated most often (72%) as either good or excellent. The new 30% DEET camouflage face paint formulation offers significant operational advantages: protection from disease-transmitting arthropods, elimination of the need to carry separate insect repellent and camouflage face paint, and reduction in the time required to apply repellent and camouflage face paint separately.

Adolescent↗
PubMed1995

The present safety assessment of deet.

Deet is considered to be the best "all around" insect repellent ever developed and is the most widely used insect repellent in the world. Since its first use in a consumer product in 1956, billions of applications have been made to human skin. Information about the safety of deet comes from the human clinical literature, animal toxicology studies, and poison control centers' experiences with deet. The clinical literature reports the association of deet with neurotoxicity in 14 individuals. Three of the cases resulted in death, whereas all of the other patients completely recovered. The exact role of deet in the toxicity reported is difficult to determine from the reports. Recently reported animal safety studies have examined potential neurotoxicity following multigenerational dosing. Effects on the nervous system were only seen when generalized toxicity was also observed. Thus deet is not a selective neurotoxin. Important information about deet also comes from an investigation into the reports of adverse affects reported to 71 poison control centers in the USA. An important conclusion from this study is that there is no evidence that increasing deet concentration has any effect on the severity of the symptoms reported. The vast majority of reported cases had either no symptoms or ones that resolved rapidly. In conclusion, a thorough examination of all information available indicates that the risk of serious adverse effects following the use of deet is extremely low.

Animals↗
PubMed1995

Insect repellent formulations of N,N-diethyl-m-toluamide (deet) in a liposphere system: efficacy and skin uptake.

Novel formulations for a deet in liposphere microdispersion in the form of lotion were prepared from natural solid triglycerides and phospholipids dispersed in buffer solution. The formulations containing 6.5, 10, and 20% deet were effective as a repellent against the common aggressive biting mosquitoes, Aedes aegypti and Anopheles stephensi, for up to 6 h. The acute dermal absorption of the 10% loaded formulation was conducted in rabbits using 14C-labeled deet. 14C-labeled deet, 10% in alcohol solution or in liposphere microdispersion was applied to the intact rabbit skin under a porous nonirritating cover for 7 days. Plasma levels of radioactivity were determined for 24 h, and daily for a total of 7 days. The 14C-deet blood levels following intravenous bolus administration were also measured. The bioavailability of deet from 10% ethanol solution was 45%, whereas the bioavailability of deet from lipospheres was 16%, a 3-fold reduction in the amount of deet absorbed. Examination of the rabbits during the experiment and after necropsy showed no evidence of toxicity or irritation. The 10% deet-liposphere formulation was stable at room temperature for at least 1 year.

Aedes↗