VA Class:AP300
ATC Class:P03AX03
Malathion, an organophosphate anticholinesterase insecticide, is used as a pediculicide.1
Malathion is used for the topical treatment of pediculosis capitis (head lice infestation).1, 3, 4, 6, 35, 53, 55, 61, 62, 76, 77, 79 The drug also has been used for the topical treatment of pediculosis pubis† (pubic lice infestation),51, 55, 64, 69, 78 pediculosis corporis† (body lice infestation),89 and scabies† (mite infestation).25, 30, 51
Malathion 0.5% lotion is used for the topical treatment of pediculosis capitis (head lice infestation) in patients infested with Pediculus humanus var. capitis and their ova1, 3, 4, 6, 35, 53, 55, 61, 62, 76, 77, 79 and may be especially useful when lice resistant to permethrin and pyrethrins may be involved.76, 77, 79, 84, 85 The drug has been effective in the treatment of pediculosis capitis in geographic areas where resistance to other pediculicides (e.g., lindane, permethrin, pyrethrins) has been reported.16, 26, 27 In addition, there is in vitro evidence that malathion has more rapid pediculicidal and ovicidal activity than other currently available topical drugs used in the treatment of pediculosis capitis.3, 4, 5, 21, 76, 75, 84, 85
When selecting a pediculicide for the treatment of pediculosis capitis, clinicians should consider efficacy (including both pediculicidal and ovicidal activity), safety, cost, availability, ease of application, age of the patient, presence of other scalp infections, patient preference, severity of the infestation, potential for transmission, number of recurrences, and the pattern of resistance in the geographic region.76, 88 Although no pediculicide possesses true ovicidal activity, drugs with residual activity may kill emerging nymphs.61 The American Academy of Pediatrics (AAP) and others currently recommend use of topical permethrin 1%, topical malathion 0.5%, topical pyrethrins with piperonyl butoxide, topical crotamiton 10%, or oral ivermectin for the treatment of head lice infestations in the US.4, 53, 56, 61, 65, 76, 79 Permethrin 1% generally is considered the treatment of choice and malathion 0.5% is recommended when permethrin resistance is suspected.3, 75, 76, 77, 79, 88, 90 Permethrin 1% has the advantages of a low potential for toxicity and good ovicidal activity; however, widespread resistance to permethrin has been reported in other countries and the prevalence of resistance to the drug in the US is unclear.3, 61, 77 Malathion 0.5% has the advantages of fast pediculicidal and ovicidal activity, a residual effect, and possible efficacy in lice infestations resistant to other pediculicides; however, safety and efficacy of the drug have not been established in children younger than 6 years of age, the topical preparation commercially available in the US has an alcoholic vehicle that is flammable and may be irritating, and the preparation has a characteristic odor that may affect patient preference. (See Cautions: Pediatric Precautions.)1, 3, 61, 76, 77 Some clinicians consider topical pyrethrins with piperonyl butoxide an alternative rather than a preferred treatment for pediculosis capitis3, 53, 65 since the drug has low ovicidal activity without residual activity (a second treatment 7-10 days after the first treatment usually is necessary to kill newly hatched lice)3, 53, 61, 65, 75, 76, 79 and treatment failures have been reported even when dosage and administration recommendations were followed.3, 76 In the past, lindane was widely recommended for the treatment of pediculosis capitis;3, 4, 6, 60, 65, 76 however, the drug is no longer recommended for initial therapy because of reports of resistance and neurotoxicity (e.g., seizures)3, 60, 61, 65, 76 and is now considered a second-line agent that should be used for the treatment of pediculosis only in patients who have not responded to or cannot tolerate other recommended therapies.61, 65, 80 (See Uses: Pediculosis in Lindane 84:04.12.)
In several clinical studies in adults and children, a single application of malathion 0.5% lotion was more effective for the treatment of pediculosis capitis than the isopropyl alcohol vehicle alone.1, 14, 18 The malathion lotion or vehicle control was allowed to air dry and patients shampooed their hair 8-12 hours after application.1, 14, 16, 18 Immediately after shampooing, all patients in both the malathion and vehicle group were free of lice.1 However, 24 hours and 7 days after shampooing, substantially more patients who used malathion 0.5% lotion were free of live lice on their scalps than those who applied the vehicle.1, 14, 18 Although both the malathion lotion and the isopropyl alcohol vehicle demonstrated initial pediculicidal and ovicidal effects, such effects were substantially greater with the malathion lotion.14, 18
In several comparative studies in adults and children, a single application of malathion 0.5% lotion was as effective or more effective than topical application of lindane,16, 26, 28, 52 pyrethrins with piperonyl butoxide,21 or phenothrin lotion (not commercially available in the US).57, 63 However, comparative efficacy of pediculicides is difficult to evaluate because of factors related to the study populations and concerns that adherence to treatment regimens and reinfestation may affect clinical outcome.76, 77 Most comparative clinical studies published to date have involved patients in other countries where resistance to other pediculicides may be widespread or in developing countries among patients with no previous exposure to pediculicides.76, 77 It is unclear whether results of these studies are applicable to the US population and additional study is needed to determine whether malathion actually is a more effective pediculicide in the US than other available drugs.76, 77, 87
Malathion 0.5% has been recommended for the topical treatment of pediculosis pubis† (pubic lice infestation).55, 64, 69, 78
The US Centers for Disease Control and Prevention (CDC) recommends topical permethrin 1% or topical pyrethrins with piperonyl butoxide as the pediculicides of choice for the treatment of pediculosis pubis and topical malathion 0.5% or oral ivermectin as alternatives.69 Other clinicians recommend topical permethrin 1% or oral ivermectin for the treatment of pediculosis pubis.53 The CDC states that malathion 0.5% may be used for the treatment of pediculosis pubis resistant to other pediculicides.69 However, the manufacturer of the malathion 0.5% lotion commercially available in the US and some clinicians state that the drug should not be used in the treatment of pediculosis pubis since the preparation is in an isopropyl alcohol vehicle that may cause burning and irritation of excoriated skin and genitalia.87, 88 In addition, the commercially available preparation has a characteristic odor that may affect patient preference and the longer duration of application may make it a less attractive alternative.1, 3, 61, 69
For further information on the management of pediculosis pubis, see Pediculosis Pubis under Uses: Pediculosis, in Permethrin 84:04.12.
Malathion has been used for the topical treatment of pediculosis corporis† (body lice infestation).90 In some cases, body louse infestations may be treated by improved hygiene and by decontaminating clothes and bedding by washing at temperatures that kill lice.61, 90 If the infestation is severe, a pediculicide also should be used (e.g., topical permethrin, topical pyrethrins with piperonyl butoxide, topical malathion, oral ivermectin).89, 90
Malathion has been used for the treatment of scabies† (usually as an aqueous lotion);25, 30, 51 however, safety and efficacy for the treatment of scabies have not been established.87, 88 The manufacturer of the malathion 0.5% lotion commercially available in the US and some clinicians state that the drug should not be used in the treatment of scabies since the preparation is in an isopropyl alcohol vehicle that may cause burning and irritation of excoriated skin and genitalia.87, 88
For further information on the management of scabies, see Uses: Scabies, in Permethrin 84:04.12.
Malathion 0.5% lotion is applied topically to scalp hair.1
Malathion 0.5% lotion is for external use only.1 The drug should not be administered topically to the skin, eyes, or pubic area and should not be administered orally.1
Contact with the eyes should be avoided.1 The eyes should be closed tightly and covered with a soft towel or washcloth while the lotion is applied to scalp hair or washed off.1 If contact with the eyes occurs, the eyes should immediately be flushed with water.1 If eye irritation persists or if visual changes occur, a clinician should be consulted.1
Malathion 0.5% lotion should be applied to dry hair; after application, the hair should be left uncovered and allowed to dry naturally.1 Malathion 0.5% lotion is flammable .1 Therefore, the lotion or hair wet with the lotion must not be exposed to any open flame, lighted cigarettes, or electric heat sources (e.g., hair dryer, electric curlers).1 Individuals applying the lotion or patients whose hair is wet with the lotion should refrain from smoking.1 (See Cautions: Precautions and Contraindications.)
Individuals applying malathion 0.5% lotion should wash their hands thoroughly after application is completed.1
Measures to Avoid Reinfestation and Transmission
To avoid reinfestation or transmission of lice, most experts recommend that clothing and bed linen that may have been contaminated by the infested individual during the 2 days prior to treatment should be decontaminated (machine-washed in hot water and dried in a hot dryer or dry-cleaned) or removed from body contact for at least 72 hours.69, 66, 79, 81 Items that cannot be laundered or dry-cleaned can be removed from contact and sealed in a plastic bag for 10-14 days.56, 61, 66, 79, 81 Combs and brushes used by the infected patient can be disinfected by soaking in hot water (temperature exceeding 54°C for 5-10 minutes);4, 56, 61, 66, 81 alternatively, they can be soaked in alcohol or a pediculicide for 1 hour.4, 6, 21, 81 It also is recommended that furniture and floors of rooms inhabited by patients infested with lice should be thoroughly vacuumed.56, 61, 65, 66, 79, 81 Fumigation of living areas is not necessary and is not recommended.69, 77, 79, 81
Other family members and close contacts of the individual with pediculosis capitis should be evaluated by a clinician and treated if lice infestation is present.1, 77, 79, 81 Some clinicians suggest that it is prudent to treat family members who share a bed with the infested individual, even if no live lice are found on this family member.61, 79
In the treatment of pediculosis capitis, a fine-toothed comb often is recommended to remove any remaining nits (eggs) or nit shells.1, 4, 6, 21, 56, 66, 70, 79, 81 Some clinicians do not consider nit removal necessary since only live lice can be transmitted, but recommend it for aesthetic reasons and to decrease diagnostic confusion and unnecessary retreatment.54, 61, 79 Other clinicians strongly recommend removal of nits (especially those within 1 cm of the scalp) since no pediculicide is 100% ovicidal and potentially viable nits may remain on the hair after pediculicide treatment.33, 70, 72, 79 Nits are attached to hair shafts by a cylindrical sheath that apparently is composed principally of amino acid derivatives and fatty acids, with an overall composition similar to hair;33, 72 combing is necessary to slide the nit attachment structure off the hair.70 Many solutions (e.g., vinegar mixtures, formic acid solutions) traditionally have been recommended to aid in nit removal,4, 55, 61, 65, 70, 76, 77, 79 but no clinical benefit has been demonstrated65, 77, 79 and an in vitro study showed that none of these commonly used solutions was more than mildly useful in detaching the nits from hair shafts.70, 72 In addition, since the sheath composition is similar to that of hair, any solution that would effectively facilitate nit removal would likely damage the hair.33 Some clinicians suggest that use of a detangler and conditioners applied to and left on the hair while combing may facilitate nit removal and help prevent pulling and breaking of the hair.88 Although many schools will not allow children with nits to attend, the American Academy of Pediatrics (AAP) and other experts consider these no-nit policies excessive.61, 77, 79
For the topical treatment of pediculosis capitis (head lice infestation), malathion 0.5% lotion is applied to dry scalp hair in an amount just sufficient to thoroughly wet the hair and scalp (including the areas on the back of the head and nape of the neck).1 After 8-12 hours, the hair (including areas on the back of the head and neck) should be washed with shampoo, rinsed, and combed with a fine-tooth (nit) comb to remove dead lice and nits.1
Although one treatment with malathion usually is successful,70 treatment may be repeated after 7-10 days if live lice still are present.1 Additional treatments generally are unnecessary.1
Because of in vitro evidence that malathion has rapid pediculicidal and ovicidal activity, it has been suggested that a shorter treatment period (e.g., 20 minutes to 2 hours) may be sufficient for the treatment of pediculosis capitis;62, 75, 76, 88 however, the clinical efficacy of malathion treatment regimens shorter than 8-12 hours has not been fully evaluated in controlled clinical studies.87
Topically applied malathion 0.5% lotion appears to have a low order of toxicity when dosage and administration recommendations are followed.14, 18, 57, 61, 62, 63 (See Dosage and Administration.) The risks associated with the locally irritating (see the opening paragraph under Uses and see Cautions: Pediatric Precautions) and flammable (See Dosage and Administration: Administration) isopropyl alcohol 78% vehicle should be considered.51, 87, 88
Dermatologic and Sensitivity Reactions
Slight stinging or burning has been reported following application of malathion 0.5% lotion,1, 14, 62, 63, 88 which may be due to the effects of the isopropyl alcohol vehicle.14, 62, 63 Adverse local effects may include irritation of the skin and scalp,1 dryness of the hair,16 and a transient increase in dandruff.24
The manufacturer states that it is not known whether malathion 0.5% lotion has the potential to cause allergic contact sensitization.1 However, dermatitis of the scalp has been reported in at least one individual following topical application of malathion 5% lotion (10 times the usually recommended dosage)16 and contact dermatitis has been reported in individuals exposed to agricultural formulations of malathion.1, 73
Accidental contact with the eyes may result in mild conjunctivitis.1 (See Dosage and Administration: Administration.)
The risk of systemic toxicity secondary to transdermal absorption of malathion from the commercially available pediculicidal lotion is not known.1 (See Cautions: Precautions and Contraindications.)
Precautions and Contraindications
Malathion 0.5% lotion is contraindicated in patients with a history of hypersensitivity to the drug or any ingredient in the formulation.1 The lotion also is contraindicated in neonates and infants.1 Some clinicians suggest that the malathion preparation commercially available in the US be avoided in patients with asthma and in small children to prevent exposure to fumes from the isopropyl alcohol vehicle.35, 51 (See Cautions: Pediatric Precautions.)
Malathion lotion is flammable ; therefore, the lotion or hair wet with the lotion must not be exposed to any open flame, lighted cigarettes, or electric heat sources (e.g., hair dryers, electric curlers).1 Individuals applying the lotion or patients whose hair is wet with the lotion should refrain from smoking.1 (See Dosage and Administration: Administration.) After application of malathion lotion, the hair should be left uncovered and allowed to dry naturally.1 Malathion 0.5% lotion should be applied only to the scalp hair.1
Patients using malathion 0.5% lotion for the treatment of pediculosis capitis should be advised that slight stinging sensations may occur after application of the lotion.1 If skin irritation occurs, the scalp and hair should be washed immediately.1 If the irritation clears, the malathion 0.5% lotion may be reapplied, and the patient should be advised to contact a clinician if the irritation recurs.1
Contact of the lotion with the eyes should be avoided since the drug may cause mild conjunctivitis; the eyes should be closed tightly and covered with a soft towel or washcloth while the lotion is applied to scalp hair or washed off.1, 88 If contact with the eye(s) occurs, the affected eye(s) should be rinsed thoroughly with water;1 patients should be advised to consult a clinician if ocular irritation persists or visual changes occur.1
Because the potential for transdermal absorption of malathion from the commercially available pediculicidal lotion is unknown, strict adherence to the recommendations for dosage and administration (e.g., method of application, duration of exposure before the drug is removed, frequency of application) is necessary, especially in children.1 (See Dosage and Administration.) Inadvertent transdermal absorption of malathion has occurred from agricultural formulations, resulting in acute toxicity manifested by excessive cholinergic activity (e.g., increased sweating, salivary and gastric secretion, GI and uterine motility, bradycardia).1 Patients should be advised to seek immediate medical attention if malathion 0.5% lotion is accidentally ingested.1 (See Acute Toxicity.)
Safety and efficacy of malathion 0.5% lotion in children younger than 6 years of age have not been established.1 The topical lotion is contraindicated in infants and neonates because their scalps are more permeable and increased absorption of malathion may occur.1 Some clinicians recommend that the malathion preparation commercially available in the US not be used on small children or in children with asthma35, 51 to prevent exposure to fumes from the isopropyl alcohol vehicle.35, 51
Malathion 0.5% lotion should be used on children only under the direct supervision of an adult and should be kept out of reach of children.1 The malathion lotion commercially available in the US is flammable, and children should be warned to stay away from lighted cigarettes, open flames, and electric heat sources while their hair is wet with the lotion.1
Mutagenicity and Carcinogenicity
The mutagenic and carcinogenic potential of the commercially available malathion 0.5% lotion (0.5% pharmaceutical grade malathion) have not been studied to date.1
The carcinogenic potential of technical grade malathion (95% pure) has been evaluated in long-term studies in rodents.1 There was an increased incidence of hepatocellular neoplastic lesions in mice and rats receiving technical grade malathion via dietary supplementation for 18 and 24 months, respectively.1 These tumors occurred only in association with severe hepatic toxicity and chronic suppression of acetylcholinesterase activity or at doses causing excessive mortality.1 Based on body surface area, carcinogenic effects were observed in rodents following life-time exposures to malathion that were approximately 14-26 times greater than the maximum dose anticipated in a 10-kg child following a single application of topical malathion 0.5% lotion assuming 100% bioavailability (actual systemic exposure in humans is expected to be less than 10% of the dose).1
Conflicting results have been reported in studies evaluating the mutagenic potential of malathion.1 It has been suggested that some of the genetic activity reported may be caused by impurities in the malathion formulations used in the studies.1 Technical grade malathion (95% pure) was not mutagenic in Salmonella typhimurium , but was mutagenic in the mouse lymphoma cell assay and in in vitro chromosomal aberration and sister chromatid exchange assays.1 Although 15 separate in vitro gene mutation studies using malathion of unknown purity were negative, positive results occurred in 3 studies using bacterial cells.1 Both technical grade (94-96.5%) and purified (98-99%) malathion have been reported to cause chromosomal aberrations and sister chromatid exchanges in vitro in human and hamster cell lines.1 In vivo chromosomal aberration and micronucleus studies of technical grade malathion have been positive, whereas an in vivo chromosomal aberration study of more than 99% pure malathion was reported to be negative.1 There was no evidence of chromosome damage in bone marrow cells, spermatogonia, or primary spermatocytes in mice exposed to malathion in their drinking water for 7 weeks.1
Pregnancy, Fertility, and Lactation
There are no adequate and controlled studies to date using topical malathion in pregnant women, and the drug should be used during pregnancy (or handled by a pregnant woman) only when clearly needed.1
Reproduction studies in rats and rabbits using malathion dosages up to 900 and 100 mg/kg daily, respectively, did not reveal evidence of teratogenicity.1, 29, 31 No gross fetal abnormalities attributable to malathion were detected in 3 generations of rats fed the drug in dosages up to approximately 200 mg/kg daily (approximately 40-180 times higher than the anticipated dosage in a 60-kg adult based on body surface area and assuming 100% bioavailability).1 Although a causal relationship to the drug was not established, a condition resembling amyoplasia congenita has been reported in an infant following repeated maternal use of 0.5% malathion lotion for treatment of pediculosis capitis during weeks 11-12 of gestation.32 Little or no fetal activity was noted throughout the second and third trimesters, and the infant died of respiratory insufficiency shortly after birth.32
Reproduction studies in rats using malathion dosages at least 180 times greater than those anticipated in a 60-kg adult (based on body surface area and assuming 100% bioavailability) have not revealed evidence of impaired fertility.1
It is not known whether malathion is distributed into human milk.1 Because many drugs are distributed into milk, caution should be exercised if malathion 0.5% lotion is administered to or handled by a nursing woman.1 Malathion was not detected in milk samples (minimum limits of detection less than 5 mcg/L) from nursing women who resided in geographic areas that received extensive aerial spraying with an agricultural formulation of malathion for insect control.48
Like other organophosphate insecticides, malathion combines with and inactivates acetylcholinesterase, causing accumulation of acetylcholine at the synapses.20, 22, 23, 68, 71 The estimated lethal dose of malathion in mammals is about 1 g/kg.20 However, humans appear to be more susceptible to toxic effects of the drug, and the mean lethal oral dose in humans may be as low as 250 mg/kg if no treatment is given.7
One adult reportedly survived an estimated ingestion of 60 g (about 1 g/kg) of an agricultural formulation of malathion used as an insecticide.39 The patient was treated with atropine and pralidoxime iodide and required a tracheostomy and respiratory support.39 Poisoning also has occurred following topical exposure7, 38, 40 or inhalation.7, 40 Several children developed severe malathion poisoning, including symptoms of hyperglycemia, glycosuria, and hyperinsulinemia, and one died following topical application of malathion 50% in a xylene vehicle formulated for pediculicidal use (not commercially available in the US).38
Malathion formulations for agricultural use may contain malaoxon,7 isomalathion,8, 9, 10, 11 or other organophosphates8, 10, 11, 12, 13 as impurities. These compounds inactivate carboxylesterases, thus increasing malathion toxicity,7, 8, 9, 10, 11, 12, 13 and may be responsible for greater malathion toxicity than would be expected following poisoning with agricultural formulations based on in vitro experiments using highly purified malathion.12
Accidental or deliberate ingestion of an entire bottle (59 mL) of commercially available malathion 0.5% topical lotion would result in a 300-mg dose of malathion, which is considerably less than exposures reported with agricultural formulations of the drug.87
Like other organophosphate anticholinesterase insecticides, accidental ingestion of malathion produces manifestations of cholinergic intoxication that result from inhibition of acetylcholinesterase.1, 5 Compared with some other organophosphate insecticides (e.g., parathion), malathion is a relatively weak cholinesterase inhibitor;1, 5, 7, 24 however, the full range of signs and symptoms of acute intoxication associated with more potent organophosphate anticholinesterase insecticides may occur following accidental ingestion of malathion.1, 5
Manifestations of acute intoxication may include a mix of muscarinic, nicotinic, and CNS effects.22, 41, 42, 43, 68, 71 Symptoms of systemic organophosphate toxicity may appear within minutes or hours depending on the route of exposure.22, 68, 71 Following ingestion of malathion, symptoms may appear rapidly39, 42, 43, 59, 68 or may be delayed up to 12 hours.5 Initial signs and symptoms of malathion poisoning may be largely due to excessive muscarinic effects, which may predominate in milder cases; such effects may include nausea,38, 42, 43 vomiting,40, 42, 43 abdominal cramps,5, 42 diarrhea,5, 39, 43 urinary and/or fecal incontinence,41, 43, 44 hyperhidrosis,5, 38, 42, 43 sialorrhea,38, 39, 40, 42, 43 miosis (pinpoint pupils),5, 38, 39, 40, 42, 43, 44 bradycardia,43, 71 lacrimation,5, 38, 43 and increased nasal,38 pharyngeal,38, 43 and bronchial secretions.39, 41, 43 Anoxia, resulting from retained secretions and pulmonary edema, 42 may result in cyanosis.39, 41, 42, 43, 44, 59 Nicotinic effects, including muscle fasciculation,5, 38, 40, 42, 43, 44 muscle weakness,42, 43, 68 tachycardia,42, 43, 71 weakness or paralysis of respiratory muscles,42 and hypotonia,38, 42 may occur in moderate and severe intoxications.42 CNS effects may include anxiety,5, 42 restlessness,42 and headache.38, 42 In more severe cases, tremors,42 confusion,5, 42 dizziness,5 drowsiness,5 a reduction or loss of deep tendon reflexes,38, 40, 41, 42, 43 seizures,5, 39, 40 bradycardia,5, 39 and coma38, 39, 40, 41, 42 also have been reported; death may occur.7, 38, 45, 46
Hyperglycemia and glycosuria also have been reported following exposure to malathion and other organophosphate insecticides.38, 68, 71 Severe respiratory distress is the major and most serious symptom of organophosphate toxicity1, 5, 22, 41, 42, 44, 68, 71 and has been reported frequently following malathion poisoning.38, 39, 41, 42, 43, 44 Respiratory failure may result from a combination of muscarinic (e.g., increased bronchial secretion, bronchoconstriction, pulmonary edema), nicotinic (e.g., weakness or paralysis of respiratory muscles), and CNS (depression of respiratory centers) effects.22, 41, 42, 43, 44, 71
In children, the signs and symptoms of organophosphate poisoning may be predominantly related to the CNS (e.g., seizures, alterations in mental status including lethargy and coma).22, 38, 40, 42, 59, 67 Hypotonia,38, 40, 67 muscle weakness,22, 42, 67 miosis,22, 38, 40, 42, 67 and excessive salivation also have occurred in children,22, 38, 40, 42, 59, 67 while some of the typical cholinergic effects (e.g., bradycardia, muscular fasciculation, excessive lacrimation, sweating, bronchial secretion) may be observed less frequently than in adults.22, 67 Hyperglycemia, glycosuria, and hyperinsulinemia also have been observed in several children following topical application of malathion in a xylene vehicle formulated for pediculicidal use (not commercially available in the US).38
Manifestations of isopropyl alcohol toxicity also would be expected following ingestion of the pediculicidal lotion commercially available in the US (Ovide®), since the vehicle contains isopropyl alcohol 78%.1
Inadvertent transdermal absorption of malathion has occurred from agricultural formulations, resulting in acute toxicity manifested by excessive cholinergic activity (e.g., increased sweating, salivary and gastric secretion, GI and uterine motility, bradycardia).1 The potential for transdermal absorption of malathion from the commercially available pediculicidal lotion currently is unknown. (See Pharmacokinetics: Absorption.)1
Since severe respiratory distress is the major and most serious manifestation of organophosphate toxicity,1, 5, 22, 41, 42, 44 management of respiratory distress should be initiated in the event of acute toxicity related to malathion by establishing and maintaining an adequate airway, suctioning bronchial secretions, and assisting respiration through artificial or mechanical means as needed.1, 5, 20, 22, 68, 71 Oxygen may be administered.20, 22 Following ingestion of malathion, the stomach should be emptied immediately by inducing emesis or by lavage using a 5% sodium bicarbonate solution.1, 5 If malathion exposure occurred via contamination of skin, clothing, and/or hair, the exposed areas should be thoroughly cleansed with soap and water.22 Care should be taken to prevent absorption of malathion by all personnel involved in the treatment of the patient,22, 71 and rubber gloves should be worn since vinyl gloves do not adequately prevent absorption of organophosphates.22
Supportive and symptomatic treatment aimed at reversing effects of acetylcholine inactivation should be initiated.20, 22 An anticonvulsant (e.g., diazepam, a short-acting barbiturate) may be given to control seizures.5, 20, 22 Atropine may be required to counteract the manifestations of cholinesterase depletion.1, 5, 24, 71 Atropine is used to antagonize the muscarinic effects of acetylcholine, but it has no effect on the nicotinic manifestations (e.g., muscle weakness and fasciculation, respiratory depression) of malathion toxicity.22 Glycopyrrolate has been used as an alternative to atropine.22, 71 A cholinesterase reactivator (e.g., pralidoxime chloride) also may be used to reverse muscle paralysis.5, 20, 22, 24, 71 In acute malathion toxicity, treatment with a cholinesterase reactivator must be initiated early if it is to be effective .5, 7, 22, 71 For additional information on the use and dosages of atropine and pralidoxime in the treatment of acute toxicity caused by organophosphate insecticides such as malathion, see Atropine 12:08.08 and see Pralidoxime Chloride 92:12.
In addition to treatment of cholinergic manifestations of organophosphate toxicity following ingestion of the commercially available malathion lotion, the treatment regimen should include measures directed toward possible adverse effects of isopropyl alcohol, which is present in high concentrations in the vehicle.1, 5
In the management of possible acute toxicity related to malathion, repeated determinations of plasma pseudocholinesterase and erythrocyte acetylcholinesterase (true cholinesterase) concentrations should be performed if possible to assist in establishing the diagnosis and formulating a long-range prognosis.1, 5, 20, 22, 88 Some clinicians suggest that erythrocyte acetylcholinesterase activity may better reflect tissue levels of the enzyme and correlate better with clinical recovery.68, 71 While pseudocholinesterase concentrations do not correlate with severity of manifestations, 22, 39, 71 measurement of plasma pseudocholinesterase concentrations is a useful diagnostic indicator since concentrations are invariably decreased following organophosphate poisoning, and measurement of pseudocholinesterase may be simpler than erythrocyte acetylcholinesterase.68, 71 However, serum pseudocholinesterase concentration alone is insufficient to identify serious organophosphate poisoning since 20% of patients with only mild to moderate initial decreases in pseudocholinesterase developed respiratory failure, 28% experienced sudden cardiovascular collapse, and 18% died in one study.71
Malathion is an organophosphate anticholinesterase insecticide that has pediculicidal and ovicidal activity.1, 4, 5, 16, 19, 57, 62 The drug is an irreversible cholinesterase inhibitor.3, 4, 20, 62
Organophosphates inactivate acetylcholinesterase by phosphorylating the enzyme, which results in inhibition of acetylcholine hydrolysis and an increased concentration of acetylcholine at cholinergic synapses.20, 22, 23 In susceptible insects, malathion is metabolized principally to malaoxon (a more potent anticholinesterase agent) (see Pharmacokinetics: Elimination), which contributes to the insecticidal effects of the drug.24, 25, 37 Following absorption of an acute lethal dose of the drug by Pediculus humanus var. capitis (the head louse), nervous system stimulation develops, resulting in rapid and massive paralysis of locomotory muscles and death.26 The ovicidal action of malathion against nits (eggs) apparently results from nervous system effects that prevent final hatching of the nymph from the nit rather than prevention of embryonic development.26 The high alcohol content of the commercially available malathion lotion also results in rapid dehydration of nits.88
Malathion may be the most rapidly pediculicidal and ovicidal drug commercially available for the topical treatment of lice infestations.3, 4, 5, 21, 76, 75, 84, 85 In one in vitro study using live lice and viable nits obtained from healthy lice-infested children in Panama, exposure to malathion 0.5% lotion killed 90% of the lice within 5 minutes and 100% within 10 minutes; 100% of the nits were killed within 10 minutes.75 In the same study, permethrin 1% killed 30% of the lice within 5 minutes and 100% within 1 hour and killed 89% of the nits within 10 minutes; lindane 1% killed 7% of the lice within 5 minutes and 61% within 3 hours and killed only 24% of the nits within 10 minutes.75
Following topical application of malathion 0.5% lotion to hair, the drug bonds to the hair shaft5, 16, 24, 62 and therefore can exert a residual pediculicidal effect5, 18, 24, 26, 28, 62 that may persist for up to several weeks.5, 16, 17 About 6 hours of exposure to topical malathion results in residual protection5 and 12 hours results in a maximal effect; 5, 24, 26 this effect gradually decreases following repeated washing.28 Although a residual effect has been considered to be beneficial, the importance of this effect in relation to malathion efficacy is unclear84, 87, 88 and it has been suggested that a residual effect may promote resistance.84, 88
Malathion is active in vitro and in vivo against Pediculus humanus var. capitis (the head louse) and its nits (eggs)1, 3, 5, 21, 24, 26, 57, 62 and Phthirus pubis (the pubic or crab louse).24 Malathion also is active against Sarcoptes scabiei , the causative agent of scabies.25, 30
Therapeutic failure and resistance to malathion has been reported in Pediculus humanus var. capitis 34, 35, 62, 75, 83 and some strains of P. humanus var. corporis (body louse) in some areas of the world (e.g., United Kingdom, France, Israel).26, 36, 62, 84, 87 However, the clinical importance of these reports as it relates to treatment of lice infections in the US is unclear since the prevalence of malathion resistance in the US has not been determined.77, 87 Drug resistance assays for P. humanus have not been standardized and are difficult to interpret.3, 83 In addition, some treatment failures or resistance reported with pediculicides may be the result of reinfestation or failure to correctly apply pediculicides, rather than the result of resistance in the lice.4, 35, 82, 83 There is in vitro evidence that malathion is active against some P. capitis resistant to permethrin85 and malathion has been effective for the treatment of some lice infestations resistant to permethrin and pyrethrins.76, 85
It has been suggested that, when malathion resistance occurs, it is the result of acetylcholinesterase modification at the level of nerve synapses in the organism.76
The pharmacokinetics of malathion following topical application of the commercially available 0.5% lotion have not been determined.1, 5 Available information on the pharmacokinetics of the drug is derived principally from reports of topical or systemic exposure to technical grade formulations of malathion (e.g., agricultural), which may contain impurities that contribute to malathion toxicity.7, 8, 9, 10, 11, 12, 13 (See Pharmacokinetics: Elimination.)
Malathion is absorbed systemically following ingestion,7, 20, 38, 39, 40, 41, 42, 43, 44, 45, 46 topical application to skin and mucous membranes,1, 5, 7, 15, 20, 40, 42, 47, 86 or inhalation of dusts or aerosols.7, 20, 42
The potential for transdermal absorption of malathion from the 0.5% pediculicidal lotion commercially available in the US has not been specifically studied to date.1, 87 Results of a study in healthy adults using several different aqueous- and alcohol-based formulations of topical malathion 0.5% (not the preparation commercially available in the US) indicate that small amounts of the drug are absorbed following application to the scalp; the extent of absorption was similar between the aqueous and alcoholic formulations.86
Following topical application to the skin of malathion in an acetone vehicle (not commercially available in the US), approximately 8% of the dose was absorbed.1 In another study, approximately 4.5% of a single dose of malathion was absorbed following topical application to forearm skin (5 mg/cm2); there was no increase in transdermal absorption when the topical dose was repeated once daily for 8 days.47 Inadvertent transdermal absorption of malathion has occurred from agricultural formulations, resulting in acute toxicity.1 (See Acute Toxicity.)
Information on distribution of malathion into human body tissues and fluids following topical application is not available. Following ingestion of agricultural insecticidal formulations, malathion is widely distributed into body tissues and fluids44, 45, 46 including kidneys,45, 46 blood,45, 46 liver,46 bile,45 spleen,45, 46 heart,46 adipose tissue,45 brain,45, 46 lungs,46 and muscles.46
It is not known if malathion crosses the placenta or is distributed into milk following topical application to the skin.1 Malathion was not detected in milk samples from nursing women who resided in geographic areas that received extensive aerial spraying with an agricultural formulation of malathion for insect control.48
Malathion is rapidly metabolized in vivo principally by hydrolysis of the carboxyl ester linkage to inactive metabolites by carboxylesterases.7, 11, 15, 20, 23, 37, 44, 49, 62 Because this detoxification reaction occurs much more rapidly in mammals than in susceptible insects,12, 15, 20, 23, 49 malathion exhibits a relative degree of selective toxicity in insects.5, 12, 14, 15, 20, 23, 49
Malathion also is oxidized by the hepatic microsomal monooxygenase system to malaoxon, an active, toxic metabolite.7, 11, 23, 37, 45, 49 Metabolism of malaoxon typically occurs at a faster rate than its formation from malathion, and little accumulation of this highly toxic metabolite occurs in mammals.37
Technical grade malathion may contain malaoxon,7 isomalathion,8, 9, 10, 11 or other organophosphates9, 10, 11, 12, 13 as impurities. These compounds inactivate carboxylesterases, thus increasing malathion toxicity by decreasing the hydrolysis of the drug7, 8, 9, 10, 11, 12, 13 and increasing the amount of the drug that is oxidized to malaoxon.9
In a patient who injected about 1.8 g of malathion as a 50% solution IV, the apparent half-life was 2.9 hours.50 Patients with impaired hepatic function may be more susceptible to malathion toxicity because of diminished capacity to detoxify the drug.8
Malathion and its metabolites are excreted in urine;42, 45, 46, 86 the monocarboxylic and dicarboxylic acid metabolites of malathion also are excreted in bile.45 In one study following topical application to the scalp of aqueous- or alcohol-based preparations of malathion (not the preparation commercially available in the US), approximately 0.2-3.2% of the applied malathion dose was eliminated in the urine as metabolites within 96 hours.86
Malathion, an organophosphate anticholinesterase insecticide, is used as a pediculicide.1, 3, 4, 6 Malathion occurs as a deep brown to yellow liquid with a characteristic odor.2 Malathion is slightly soluble in water and miscible with many organic solvents (e.g., alcohols, esters, ethers, ketones, aromatic and alkylated hydrocarbons, and vegetable oils).2 The drug has limited solubility in some paraffin hydrocarbons.2
For the topical treatment of pediculosis capitis (head lice infestation), malathion is commercially available as a 0.5% lotion containing isopropyl alcohol 78% with terpineol, dipentene, and pine needle oil.1 Each mL of commercially available malathion 0.5% lotion contains 5 mg of the drug.1
Formulations of malathion intended for use as agricultural insecticides often are less pure than the preparations designed for topical use in humans and these agricultural formulations may contain malaoxon,7 isomalathion,8, 9, 10, 11 or other organophosphates9, 10, 11, 12, 13 as impurities.
Malathion 0.5% lotion should be stored at controlled room temperature between 20-25°C.1
The commercially available malathion 0.5% lotion is flammable and should not be exposed to an open flame (e.g., a lighted cigarette) or heat sources (e.g., hair dryer, electric curlers).1
Malathion is stable in aqueous solutions buffered to pH 5.26; the drug is hydrolyzed at pH less than 5 or exceeding 7.2
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Topical | Lotion | 0.5% | Ovide® | Taro |
Only references cited for selected revisions after 1984 are available electronically.
1. Taro Pharmaceuticals. Ovide® (malathion) lotion 0.5% prescribing information. Hawthorne, NY; 2005 Jul.
2. Budavari S, O'Neil MJ, Smith A et al, eds. The Merck index. 12th ed. Whitehouse Station, NJ: Merck & Co., Inc; 1996:5740.
3. Anon. Drugs for head lice. Med Lett Drugs Ther . 1997; 39:6-7. [PubMed 9008683]
4. Eichenfield LF, Colon-Fontanez F. Treatment of head lice. Pediatr Infect Dis J . 1998; 17:419-20. [PubMed 9613657]
5. GenDerm Corporation. Ovide® lotion (0.5% malathion) monograph. Lincolnshire, IL; 1993.
6. Hogan DJ, Schachner L, Tanglertsampan C. Diagnosis and treatment of childhood scabies and pediculosis. Pediatr Clin North Am . 1991; 38:941-57. [PubMed 1870912]
7. Gosselin RE, Smith RP, Hodge HC et al. Clinical toxicology of commercial products: malathion. 5th ed. Baltimore: Williams & Wilkins Co.; 1984:II-298.K
8. Talcott RE, Denk H, Mallipudi NM. Malathion carboxylesterase activity in human liver and its inactivation by isomalathion. Toxicol Appl Pharmacol . 1979; 49:373-6. [PubMed 494286]
9. Talcott RE, Mallipudi NM, Umetsu N et al. Inactivation of esterases by impurities isolated from technical malathion. Toxicol Appl Pharmacol . 1979; 49:107-12. [PubMed 473195]
10. Mallipudi NM, Talcott RE, Ketterman A et al. Properties and inhibition of rat malathion carboxylesterases. J Toxicol Environ Health . 1980; 6:585-96. [PubMed 7420466]
11. Aldridge WN, Miles JW, Mount DL et al. The toxicological properties of impurities in malathion. Arch Toxicol . 1979; 42:95-106. [PubMed 755464]
12. Talcott RE, Mallipudi NM, Fukuto TR. Malathion carboxylesterase titer and its relationship to malathion toxicity. Toxicol Appl Pharmacol . 1977; 50:501-4.
13. Umetsu N, Mallipudi NM, Toia RF et al. Toxicological properties of phosphorothioate and related esters present as impurities in technical organophosphorus insecticides. J Toxicol Environ Health . 1981; 7:481-97. [PubMed 7288900]
14. Taplin D, Castillero PM, Spiegel J et al. Malathion for treatment of Pediculus humanus var capitis infestation. JAMA . 1982; 247:3103-5. [PubMed 7043013]
15. Walter Z, Czajkowska A, Lipecka K. Effect of malathion on the genetic material of human lymphocytes stimulated by phytohemagglutinin (PHA). Hum Genet . 1980; 53:375-81. [PubMed 6154640]
16. Purdue Frederick Company. The comparative safety and efficacy of Prioderm® lotion (0.5% malathion) in the treatment of head louse infestation: a comprehensive review (product promotion). Norwalk, CT; 1983.
17. Ares Mazas ME, Fandino Salorio ML, Silva Villar MJ et al. Efficacy of a malathion lotion for the treatment of pediculosis capitis. Int J Dermatol . 1988; 27:267-8. [PubMed 3391722]
18. Urcuyo FG, Zaias N. Malathion lotion as an insecticide and ovicide in head louse infestation. Int J Dermatol . 1986; 25:60-2. [PubMed 3512461]
19. Klaassen CD. Nonmetallic environmental toxicants: air pollutants, solvents and vapors and pesticides. In: Hardman JG, Limbird LE, Molinoff PB et al, eds. Goodman and Gilman's the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill; 1995:1687-8.
20. Taylor P. Anticholinesterase agents. In: Hardman JG, Limbird LE, Molinoff PB et al, eds. Goodman and Gilman's the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill; 1995:161-76.
21. Meinking TL, Taplin D, Kalter DC et al. Comparative efficacy of treatments for pediculosis capitis infestations. Arch Dermatol . 1986; 122:267-71. [PubMed 2420284]
22. Organophosphate insecticides. In: Reigart JR, Roberts JR, eds. Recognition and management of pesticide poisonings. 5th ed. Washington, DC: US Environmental Protection Agency; 1999:34-47.
23. Quraishi MS. Organophosphorous compounds. In: Biochemical insect control: its impact on economy, environment, and natural selection. New York: John Wiley & Sons; 1977:27-65.
24. Anon. Malathion. (Dutch; translation supplied by Purdue Frederick.) Pharm Weekbl . 1978; 113:328-30.
25. Ailakis JG. Use of a malathion application for the treatment of scabies in an infant. Aust J Hosp Pharm . 1993; 23:30-3.
26. Maunder JW. Use of malathion in the treatment of lousy children. Community Med . 1971; 126:145-7.
27. Coates KG. Control of head infestation in schoolchildren. Community Med . 1971; 126:148-9.
28. Blommers L, van Lennep M. Miscellaneous notes on the toxicity of some insecticides for the head louse, Pediculus capitis de geer (anoplura). Acta Leiden . 1978; 46:9-15. [PubMed 264208]
29. Kimbrough RD, Gaines TB. Effect of organic phosphorus compounds and alkylating agents on the rat fetus. Arch Environ Health . 1968; 16:805-8. [PubMed 5654550]
30. Burgess I, Robinson RJ, Robinson J et al. Aqueous malathion 0.5% as a scabicide: clinical trial. BMJ . 1986; 292:1172. [PubMedCentral][PubMed 3085770]
31. Machin MGA, McBride WG. Teratological study of malathion in the rabbit. J Toxicol Environ Health . 1989; 26:249-53. [PubMed 2926827]
32. Lindhout D, Hageman G. Amyoplasia congenita-like condition and maternal malathion exposure. Teratology . 1987; 36:7-9. [PubMed 3672379]
33. Reviewers' comments (personal observations) on Permethrin 84:04:12.
34. Silverton N. Malathion-resistant pediculosis capitis. Br Med J . 1972; 3:646-7. [PubMedCentral][PubMed 5071715]
35. Anon. Treating head louse infections. Drug Ther Bull . 1998; 36:45-6. [PubMed 9684423]
36. Cole MM, Clark PH, Washington F et al. Resistance to malathion in a strain of body lice from Burundi. J Econ Entomol . 1973; 66:118-9. [PubMed 4690250]
37. Malathion. From: HSDB. Hazardous Substances Data Bank (database). Bethesda, MD: National Library of Medicine, 1999; HSDB No. 0665. From Toxnet website. [Web]
38. Ramu A, Slonim AE, London M et al. Hyperglycemia in acute malathion poisoning. Isr J Med Sci . 1973; 9:631-4. [PubMed 4717946]
39. Goldin AR, Rubenstein AH, Bradlow BA et al. Malathion poisoning with special reference to the effect of cholinesterase inhibition on erythrocyte survival. N Engl J Med . 1964; 271:1289-93. [PubMed 14214635]
40. Wenzl JE, Burke EC. Poisoning from a malathion-aerosol mixture: a case report. JAMA . 1962; 182:495-7. [PubMed 13999973]
41. Richards AG. Malathion poisoning successfully treated with large doses of atropine. Can Med Assoc J . 1964; 91:82-3. [PubMedCentral][PubMed 14154301]
42. Amos WC, Hall A. Malathion poisoning treated with Protopam. Ann Intern Med . 1965; 62:1013-6. [PubMed 14283379]
43. Crowley WJ, Johns TR. Accidental malathion poisoning. Arch Neurol . 1966; 14:611-6. [PubMed 5935955]
44. Burgess ED, Audette RJ. Case reports: limited effectiveness of charcoal hemoperfusion in malathion poisoning. Pharmacotherapy . 1990; 10:410-2. [PubMed 2287563]
45. Morgade C, Barquet A. Body distribution of malathion and its metabolites in a fatal poisoning by ingestion. J Toxicol Environ Health . 1982; 10:321-5. [PubMed 7143485]
46. Jadhav RK, Sharma VK, Rao GJ et al. Distribution of malathion in body tissues and fluids. Forensic Sci Int . 1992; 52:223-9. [PubMed 1601353]
47. Wester RC, Maibach HI, Bucks DAW et al. Malathion percutaneous absorption after repeated administration to man. Toxicol Appl Pharmacol . 1983; 68:116-9. [PubMed 6845371]
48. Lonnerdal B, Asquith MT. Malathion not detected in breast milk of women living in aerial spraying areas. N Engl J Med . 1982; 307:439. [PubMed 7088119]
49. Murphy SD. Malathion inhibition of esterases as a determinant of malathion toxicity. J Pharmacol Exp Ther . 1967; 156:352-65. [PubMed 6026264]
50. Lyon J, Taylor H, Ackerman B. A case report of intravenous malathion injection with determination of serum half-life. J Toxicol Clin Toxicol . 1987; 25:243-9. [PubMed 3612901]
51. Parfitt K, ed. Martindale: the complete drug reference. 32nd ed. London: The Pharmaceutical Press; 1999:1407-8.
52. Mathias RG, Huggins DR, Leroux SJ et al. Comparative trial of treatment with Prioderm lotion and Kwellada shampoo in children with head lice. Can Med Assoc J . 1984; 130:407-9. [PubMedCentral][PubMed 6198057]
53. Anon. Drugs for parasitic infections. Med Lett Drugs Ther . Aug 2004. From the Medical Letter web site. [Web]
54. Wilson DC, Leyva WH, King LE. Arthropod bites and stings. In: Fitzpatrick TB, Eisen AZ, Wolff K et al, eds. Dermatology in general medicine. Vol II. 4th ed. New York: McGraw-Hill, Inc.; 1993:2810-26.
55. Mathieu ME, Wilson BB. Lice (pediculosis). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's principles and practices of infectious diseases. 5th ed. New York: Churchill Livingstone; 2000:2972-3.
56. Vander Stichele RH, Dezeure EM, Bogaert MG. Systematic review of clinical efficacy of topical treatments for head lice. BMJ . 1995; 311:604-8. [PubMedCentral][PubMed 7545045]
57. Chosidow O, Chastang C, Brue C et al. Controlled study of malathion and d -phenothrin lotions for Pediculus humanus var capitis -infested schoolchildren. Lancet . 1994; 344:1724-7. [PubMed 7997000]
59. Tuthill JWG. Toxic hazards: malathion poisoning. N Engl J Med . 1958; 258:1018-9. [PubMed 13541706]
60. Brown S, Becher J, Brady W. Treatment of ectoparasitic infections: review of the English-language literature, 1982-1992. Clin Infect Dis . 1995; 20(Suppl 1):S104-9. [PubMed 7540875]
61. American Academy of Pediatrics. 2006 Red Book: Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2006.
62. Anon. Malathion for treatment of head lice. Med Lett Drugs Ther . 1999; 41:73-4. [PubMed 10603987]
63. Doss S, Powell CA, Miller AJ. Phenothrin lotion, the latest recruit in the battle against headlice: the results of two controlled comparative studies. J R Soc Health . 1991; 111:47-50. [PubMed 1903813]
64. Rundle PA, Hughes DS. Phthirus pubis infestation of the eyelids. Br J Ophthalmol . 1993; 77:815-6. [PubMedCentral][PubMed 8110680]
65. Burkhart CG, Burkhart CN, Burkhart KM. An assessment of topical and oral prescription and over-the-counter treatments for head lice. J Am Acad Dermatol . 1998; 38:979-82. [PubMed 9632008]
66. Food and Drug Administration. Pediculicide drug products for over-the-counter human use: establishment of a monograph. 21 CFR Part 358. Proposed rule. [Docket No. 81N-0201] Fed Regist . 1982; 47:28312-21. (IDIS 152095)
67. Lifshitz M, Shahak E, Sofer S. Carbamate and organophosphate poisoning in young children. Pediatr Emerg Care . 1999; 15:102-3. [PubMed 10220078]
68. Namba T, Nolte CT, Jackrel J et al. Poisoning due to organophosphate insecticides: acute and chronic manifestations. Am J Med . 1971; 50:475-92. [PubMed 4324629]
69. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines 2006. MMWR Recomm Rep . 2006; 55(RR-11):1-94. [Fulltext MMWR]
70. Burkhart CN, Burkhart CG, Pchalek I et al. The adherent cylindrical nit structure and its chemical denaturation in vitro: an assessment with therapeutic implications for head lice. Arch Pediatr Adolesc Med . 1998; 152:711-2. [PubMed 9667548]
71. Bardin PG, van Eeden SF, Moolman JA et al. Organophosphate and carbamate poisoning. Arch Intern Med . 1994; 154:1433-41. [PubMed 8017998]
72. Burkhart CN, Stankiewicz BA, Pchalek I et al. Molecular composition of the louse sheath. J Parasitol . 1999; 85:559-61. [PubMed 10386454]
73. Milby TH, Epstein WL. Allergic contact sensitivity to malathion. Arch Environ Health . 1964; 9:434-7. [PubMed 14185548]
74. Balaji M, Sasikala K. Cytogenetic effect of malathion in in vitro culture of human peripheral blood. Mutat Res . 1993; 301:13-7. [PubMed 7677938]
75. Meinking TL, Entzel P, Villar ME et al. Comparative efficacy of treatments for pediculosis capitis infections. Arch Dermatol . 2001; 137:287-92. [PubMed 11255326]
76. Jones KN, English JC. Review of common therapeutic options in the United States for the treatment of pediculosis capitis. Clin Infect Dis . 2003; 36:1355-61. [PubMed 12766828]
77. Roberts RJ. Head lice. N Engl J Med . 2002; 346:1645-50. [PubMed 12023998]
78. Wendel K, Rompalo A. Scabies and Pediculosis pubis: an update of treatment regimens and general review. Clin Infect Dis . 2002; 35(Suppl 2):S146-51. [PubMedCentral]
79. American Academy of Pediatrics. Head lice. Pediatrics . 2002; 110:638-43. [PubMed 12205271]
80. Lindane Shampoo, USP, 1% prescribing information. From the FDA web site. Accessed 2003 Apr 4. [Web]
81. Centers for Disease Control and Prevention. Treating head lice. From the CDC website. Accessed 2003 Aug 5. [Web]
82. Dawes M. Evidence for double resistance to permethrin and malathion in head lice. Br J Dermatol . 1999; 142:1047-70.
83. Downs AMR, Stafford KA, Harvey I et al. Evidence for double resistance to permethrin and malathion in head lice. Br J Dermatol . 1999; 141:508-11. [PubMed 10583056]
84. Meinking TL, Serrano L, Hard B et al. Comparative in vitro pediculicidal efficacy of treatments in a resistant head lice population in the United States. Arch Dermatol . 2002; 138:220-224. [PubMed 11843643]
85. Yoon KS, Gao JR, Lee SH et al. Permethrin-resistant human head lice, Pediculus capitis , and their treatment. Arch Dermatol . 2003; 139:994-1000. [PubMed 12925385]
86. Dennis GA, Lee PN. A phase I volunteer study to establish the degree of absorption and effect on cholinesterase activity of four head lice preparations containing malathion. Clin Drug Invest . 1999; 18:106-15.
87. Taro Pharmaceuticals, Hawthorne, NY: Personnel communication.
88. Reviewer comments (personal observations).
89. Centers for Disease Control and Prevention. Body lice infestation. From the CDC website. Accessed 2007 Jun 14. [Web]
90. Flinders DC, De Schweinitz P. Pediculosis and scabies. Am Fam Physician . 2004; 69:341-50. [PubMed 14765774]