Acute toxicity: Malathion is slightly toxic via the oral route, with reported oral LD50 values of 1000 mg/kg to greater than 10,000 mg/kg in the rat, and 400 mg/kg to greater than 4000 mg/kg in the mouse [2,13]. It is also slightly toxic via the dermal route, with reported dermal LD50 values of greater than 4000 mg/kg in rats [2,13]. Effects of malathion are similar to those observed with other organophosphates, except that larger doses are required to produce them [2,8]. It has been reported that single doses of malathion may affect immune system response [2]. Symptoms of acute exposure to organophosphate or cholinesterase-inhibiting compounds may include the following: numbness, tingling sensations, incoordination, headache, dizziness, tremor, nausea, abdominal cramps, sweating, blurred vision, difficulty breathing or respiratory depression, and slow heartbeat. Very high doses may result in unconsciousness, incontinence, and convulsions or fatality. The acute effects of malathion depend on product purity and the route of exposure [33]. Other factors which may influence the observed toxicity of malathion include the amount of protein in the diet and gender. As protein intake decreased, malathion was increasingly toxic to the rats [78]. Malathion has been shown to have different toxicities in male and female rats and humans due to metabolism, storage, and excretion differences between the sexes, with females being much more susceptible than males [79]. Numerous malathion poisoning incidents have occurred among pesticide workers and small children through accidental exposure. In one reported case of malathion poisoning, an infant exhibited severe signs of cholinesterase inhibition after exposure to an aerosol bomb containing 0.5% malathion [44].Chronic toxicity: Human volunteers fed very low doses of malathion for 1 1/2 months showed no significant effects on blood cholinesterase activity. Rats fed dietary doses of 5 mg/kg/day to 25 mg/kg/day over 2 years showed no symptoms apart from depressed cholinesterase activity. When small amounts of the compound were administered for 8 weeks, rats showed no adverse effects on whole-blood cholinesterase activity [2]. Weanling male rats were twice as susceptible to malathion as adults.Reproductive effects: Several studies have documented developmental and reproductive effects due to high doses of malathion in test animals [2]. Rats fed high doses of 240 mg/kg/day during pregnancy showed an increased rate of newborn mortality. However, malathion fed to rats at low dosages caused no reproductive effects [8]. It is not likely that malathion will cause reproductive effects in humans under normal circumstances.Teratogenic effects: Rats fed high doses (240 mg/kg/day) showed no teratogenic effects. Malathion and its metabolites can cross the placenta of the goat and depress cholinesterase activity of the fetus [8]. Chickens fed diets at low doses for 2 years showed no adverse effects on egg hatching [8]. Current evidence indicates that malathion is not teratogenic.Mutagenic effects: Malathion produced detectable mutations in three different types of cultured human cells, including white blood cells and lymph cells [2,8]. It is not clear what the implications of these results are for humans.Carcinogenic effects: Female rats on dietary doses of approximately 500 mg/kg/day of malathion for 2 years did not develop tumors [2]. Adrenal tumors developed in the males at low doses, but not at the high doses [80], suggesting that malathion was not the cause. Three of five studies that have investigated the carcinogenicity of malathion have found that the compound does not produce tumors in the test animals. The two other studies have been determined to be unacceptible studies and the results discounted [2,8,80]. Available evidence suggests that malathion is not carcinogenic but the data are not conclusive.
Organ toxicity: The pesticide has been shown in animal testing and from use experience to affect the central nervous system, immune system, adrenal glands, liver, and blood.
Fate in humans and animals: Malathion is rapidly and effectively absorbed by practically all routes including the gastrointestinal tract, skin, mucous membranes, and lungs. Malathion undergoes similar detoxification mechanisms to other organophosphates, but it can also be rendered nontoxic via another simple mechanism, splitting of either of the carboxy ester linkages. Animal studies indicate it is very rapidly eliminated though urine, feces and expired air with a reported half-life of approximately 8 hours in rats and approximately 2 days in cows [2]. Autopsy samples from one individual who had ingested large amounts of malathion showed a substantial portion in the stomach and intestines, a small amount in fat tissue, and no detectable levels in the liver. Malathion requires conversion to malaoxon to become an active anticholinesterase agent. Most of the occupational evidence indicates a low chronic toxicity for malathion. One important exception to this was traced to impurities in the formulation of the pesticide [2].
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