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Extension Toxicology Network

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.


Publication Date: 9/93


Common names include metomil and mesomile. Trade names include Lannate, Lanox, Methavin, and Nudrin.


Methomyl is classified as Restricted Use Pesticide (RUP) by the Environmental Protection Agency because of its high acute toxicity to humans (28). Restricted Use Pesticides may be purchased and used only by certified applicators. Reentry periods for farm workers of 1 to 7 days are required, depending on the crop (30). Check the product label for details.


Methomyl was introduced in 1966 (26) as a broad spectrum insecticide. It is also used as an acaricide to control ticks and spiders. It is used for foliar treatment of vegetable, fruit and field crops, cotton, commercial ornamentals, and in and around poultry houses and dairies. It is also used as a fly bait (6). Methomyl is effective in two ways: (a) as a 'contact insecticide,' because it kills target insects upon direct contact, and; (b) as a 'systemic insecticide' because of its capability to cause overall 'systemic' poisoning in target insects, after it is absorbed and transported throughout the pests that feed on treated plants. It is capable of being absorbed by plants without being 'phytotoxic' or harmful, to the plant. It is one of a class of chemicals called 'carbamates' (8, 13, 15, 25). The carbamates work by inhibiting cholinesterase, an essential enzyme for proper functioning of the nervous system.



Methomyl is potentially a highly poisonous material in humans (6). It is highly toxic if it is ingested or absorbed through the eyes, moderately poisonous when inhaled, but of lower toxicity with skin, or 'dermal,' exposure (18, 30). Methomyl is a highly toxic inhibitor of cholinesterase, an essential nervous system enzyme. Symptoms of anti- cholinesterase activity include weakness, blurred vision, headache, nausea, abdominal cramps, chest discomfort, constriction of pupils, sweating, muscle tremors, and decreased pulse. If there is severe poisoning, symptoms of twitching, giddiness, confusion, muscle incoordination, slurred speech, low blood pressure, heart irregularities, and loss of reflexes may also be experienced. Death can result from discontinued breathing, paralysis of muscles of the respiratory system, intense constriction of the openings of the lung, or all three (6, 16). The onset of symptoms may be delayed up to 12 hours (16). The route, duration, and concentration of methomyl exposure will affect the severity of poisoning and the number and types of symptoms that occur. Complete recovery from an acute poisoning by methomyl, with no long term health effects, is possible if exposure ceases and the victim has time to reform their normal level of cholinesterase and to recover from symptoms (7, 26). (For more information on cholinesterase, please refer to the Toxicology Information Brief on Cholinesterase- Inhibition).

Carbamates generally are excreted rapidly and do not accumulate in mammalian tissue. If exposure does not continue, cholinesterase inhibition reverses rapidly. In non-fatal cases, the illness generally lasts less than 24 hours (32).

In addition to cholinesterase-inhibition symptoms which may be observed within 15 minutes to four hours of methomyl ingestion, gastrointestinal disturbances may occur, such as lack of appetite, nausea, vomiting, abdominal cramps and diarrhea (16). Liquid concentrate may be fatal if swallowed (2). Three men died after accidentally eating approximately 12 to 15 mg of methomyl for each kg of body weight when it was mistaken for leavening and baked into their bread (6, 9).

Methomyl is poisonous if inhaled, and may be absorbed through the mucous membranes of the respiratory tract, resulting in systemic intoxication and cholinesterase inhibition. Inhalation of dust or aerosol may cause irritation, lung and eye problems, with symptoms of chest tightness, blurred vision, tearing, wheezing and headaches appearing upon exposure. Other systemic symptoms of cholinesterase inhibition may appear within a few minutes or several hours of exposure (2, 3, 16, 30, 32).

Methomyl is not readily absorbed by the skin and is therefore only slightly toxic via dermal exposure (26, 32). However, if sufficient amounts are absorbed through the skin, symptoms similar to those induced by ingestion or inhalation will develop (32). Within fifteen minutes to four hours of exposure, the immediate area of contact may have localized sweating and uncoordinated muscular contractions. Other symptoms associated with excess dermal exposure may include vomiting, nausea, diarrhea, abdominal cramping, dizziness, and headaches (or any of the other symptoms previously mentioned) (16).

Application of the dry material or a 10% solution caused mild inflammation, but no injury to the cornea in the eyes of rabbits (32). Pain, short-sightedness, blurring of distant vision, tearing, and other eye disturbances, as well as previously mentioned symptoms of cholinesterase-inhibition, may occur within a few minutes of eye contact with methomyl (16, 32). Absorption through the eyes may be fatal.

The amount of methomyl that is deadly to one-half (50%) of experimental animals is called its acute oral lethal dose fifty or LD50. The LD50 for methomyl in rats is 12-48 mg/kg, in mice it is 10 mg/kg, and in guinea pigs it is 15 mg/kg (2, 19, 26). When applied to the skin of rabbits, the dermal LD50 was 5,880 mg/kg (2, 32). The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it for a set time period. The inhalation LC50 for male rats is 0.3 mg/liter (30).


Prolonged or repeated exposure to methomyl may cause symptoms similar to the pesticide's acute effects (32). Repeated exposure to small amounts of methomyl may cause an unsuspected inhibition of cholinesterase, resulting in flu-like symptoms, such as weakness, lack of appetite, and muscle aches. Cholinesterase-inhibition may persist for two to six weeks. This condition is reversible if exposure is discontinued. Since cholinesterase is increasingly inhibited with each exposure, severe cholinesterase-inhibition symptoms may be produced in a person who has had previous methomyl exposure, while a person without previous exposure may not experience any symptoms at all (16).

In a 24 month study with rats fed doses of 0, 2.5, 5 or 20 mg/kg, the NOEL was 20 mg/kg. At 20 mg/kg, red blood cell counts and hemoglobin levels were significantly reduced in female rats (30).

Based on a 5 mg/kg NOEL in a two-year feeding study with dogs, and utilizing a 100 fold safety margin, the EPA has established an ADI (Acceptable Daily Intake) for methomyl of 0.025 mg/kg of body weight/day (27, 28, 30).

EPA has established a lifetime Health Advisory level of 200 ppb for methomyl. Water containing methomyl at or below this level is acceptable for drinking everyday over the course of one's lifetime and does not pose any health risk.

Reproductive Effects

Methomyl fed to rats at dietary doses of 2.5 or 5 mg/kg for three generations caused no adverse effect on reproduction, nor was there any evidence of congenital abnormalities. The NOEL in this study was 5 mg/kg (9, 30).

A two-generation study at 3,780 and 60 mg/kg in the diet showed no adverse effects on the fertility of rats (27, 28).

Teratogenic Effects

No teratogenic effects were found in the fetuses of female rabbits that were fed 50 to 100 parts per million, (ppm) during the 8th to 16th day of gestation (9). In rats, no embryonic or teratogenic effects were observed at the highest dietary dose administered (400 ppm) (27, 28, 30).

Mutagenic Effects

In all of several assays (including Ames test, a reverse mutation assay, a recessive lethal assay, three DNA damage studies, an unscheduled DNA synthesis assay, and in vivo and in vitro cytogenetic assays), methomyl was not mutagenic (9, 27, 28). Methomyl showed no transforming activity in a host mediated hamster cell culture (26). There is no evidence that methomyl is a mutagen (30).

Carcinogenic Effects

There was no evidence of carcinogenicity in either rats or dogs that were involved in two-year feeding studies (11). Methomyl was not carcinogenic in 22 and 24 month studies with rats fed doses of up to 20 mg/kg, nor in a two year study with mice fed dietary doses of up to 93.4 mg/kg of body wgt/day (26).

In a two year feeding study with mice fed 0, 2.5, 3.75 or 10 mg/kg no compound related tumors formed at any level. In another two year feeding study with dogs fed 0, 1.25, 2.5, 10 or 25 mg/kg the NOEL was 2.5 mg/kg based on the occurrence of hemolytic anemia and non-neoplastic changes in the kidney and spleen at higher doses. No tumors were observed at any dose (27, 28). Methomyl does not cause tumors in rats or mice (30).

Acetamide, a suspected oncogen, is a minor metabolite of methomyl. No valid study of the metabolism of methomyl in the human body is available. Tests for acetamide levels are needed and have been called for by the EPA (30).

Organ Toxicity

Lungs, skin, eyes, gastrointestinal tract, kidneys, and spleen have been affected in various experiments, depending on route of entry, duration of exposure, and dosage (16). Chronic feeding studies in rats and dogs showed dose related changes in tissues of the kidney and spleen. The NOEL in both rat and dog was 100 ppm or 2.5 mg/kg/day (30).

The autopsies of methomyl-induced suicide victims revealed congested and fluid-filled tissue in many locations, including the stomach and lungs. This condition apparently results from decreased or inadequate circulation (19).

Fate in Humans and Animals

Carbamates, the class of active ingredients in which methomyl is included, are quickly absorbed from the skin, lungs and gastrointestinal tract and are broken down and transformed in the liver. Although they do not appear to accumulate in any particular body tissue, they do alter many other enzyme systems besides the cholinesterases (1, 7, 9, 11, 19).


Methomyl is toxic to fish, birds and other wildlife (5).

Effects on Birds

Methomyl is highly toxic to birds. The acute oral LD50 for bobwhite quail is 24.2 mg/kg (30). The oral LD50 of methomyl was 28 mg/kg in hens. All deaths occurred within ten minutes of dosing. The clinical signs of toxicity included tearing of the eyes, salivation, occasional convulsions, and respiratory disorders. In Japanese quail, the LD50 was 34 mg/kg (11). The LD50 of a 90% pure formulation was 15.9 mg/kg in eight-month old mallards, and 15.4 mg/kg in three-to-four month old male pheasants (20). The LD50 for starlings was 42 mg/kg and for redwinged blackbirds was 10 mg/kg (29).

Effects on Aquatic Organisms

Methomyl is moderately to highly toxic to fish and highly toxic to aquatic invertebrates (11, 30). The 96-hour LC50 in rainbow trout for a liquid formulation of methomyl is 3.4 milligrams per liter (mg/l); for bluegill sunfish, it is 0.8 mg/l (8). A 28-day fish residue study indicated that methomyl did not accumulate in fish tissue (11). The 48- hour LC50 for Daphnia magna ( a small, freshwater crustacean) is 28.7 ppb (29).

Effects on Other Animals (Nontarget species)

Methomyl is highly toxic to bees both by direct contact and through ingestion (8, 11, 30). Applications should be coordinated with periods of minimum bee activity so that methomyl is never applied while bees are actively visiting treatment areas (5).

The LD50 for a 90% pure formulation of methomyl was 11.0 to 22.0 mg/kg in mule deer (20). Symptoms of acute poisoning in these animals included drowsiness, drooling, diarrhea, and tremors (20).


Breakdown of Chemical in Soil and Groundwater

Because of its high solubility in water (58,000 ug/ml) and its soil half-life (33 days), methomyl may have potential for groundwater contamination (31). It is very mobile in sandy loam and silty clay loam soils, but only slight leaching was observed in a silt loam and in a sandy soil. Adsorption of methomyl to soil particles is weak to moderate (26, 30). In one national survey which did not detect methomyl in groundwater, methomyl was found in drinking water from groundwater sources. It was also found, in a survey of widely used pesticides in Palm Beach County, Florida (15, 23). Methomyl has been detected at very low levels, 9 ppb and 1.2 ppb respectively, in groundwater in New York and New Jersey (30). Lifetime Health Advisory level of 200 ppb has been established for methomyl.

Methomyl is rapidly degraded by soil microbes (14). The dissipation half-life for methomyl in soil is reportedly three to six weeks (23, 24). However, one month after methomyl-treatment, test soil had traces of the insecticide and some of its breakdown byproducts, or 'metabolites' (14). Methomyl residues are not expected to be found in treated soil after the growing season in which it is applied (15).

Under aerobic conditions, methomyl has a soil half-life of 30-45 days and degrades predominately to carbon dioxide. It is relatively stable to hydrolysis under neutral and acidic conditions. Under basic conditions, it degrades with a half-life of 30 days. Under anaerobic conditions, acetonitrile is the major metabolite in the early stages of degradation, but carbon dioxide is the end product, with total conversion within 8 days (30).

Breakdown of Chemical in Water

Methomyl should be kept out of any body of water and should not be applied where runoff is likely to occur (5). Aqueous solutions of methomyl have been reported to decompose more rapidly on aeration, in sunlight or in alkaline media (33). One study indicated a half-life of six days for the insecticide in water (15). Its 'hydrolysis half-life' in soil, or the time that it takes for half of it to be broken down in groundwater, is estimated at over 25 weeks (23). In one experiment the hydrolysis half lives of methomyl in solutions at pHs of 6.0, 7.0 and 8.0 were 54, 38, and 20 weeks respectively. In pure water, the hydrolysis half-life has been estimated to be 262 days. Methomyl is unlikely to bioconcentrate in aquatic systems (33).

Breakdown of Chemical in Vegetation

Following soil treatment, plants take up methomyl through their roots and move it throughout the plant by a process called 'translocation.' When methomyl is applied to plants, its residues are short-lived (13). After it is applied to leaves, it has a three-to- seven day half-life (8, 14). Less than 3% methomyl remained in cabbage plants one week after they were given foliar treatment with the insecticide (19).


Breathing of dust, and skin contact with methomyl dust or solutions, should be avoided and prevented. Appropriate protective clothing, including respirator mask, goggles, and gloves, should be worn to prevent the possibility of skin contact with this toxic material (16). Like most organic powders or crystals, under extremely dusty conditions, methomyl may form explosive mixtures in air (27). A reentry interval of 24 hours may lessen the possibility of poisoning (9). Methomyl users should not contaminate water by cleaning of equipment or disposal of wastes associated with the insecticide (5). Discarded methomyl is considered a hazardous waste product under the Resource Conservation and Recovery Act (RCRA) (2).

Methomyl is a white crystalline solid with a slight sulfurous odor (16). Liquid formulations are flammable and should be kept away from heat, sparks, and open flames (2). When heated to decomposition or combustion, methomyl emits very toxic fumes of nitrogen oxides, sulfur oxides and hydrogen cyanide. Explosion may occur if methomyl confined in containers is heated above 136 degrees C (18, 27, 28). Methomyl will auto ignite at temperatures at or above 290 degrees C (29). Methomyl is stable under normal temperatures and storage conditions (27, 28). It is stable in aqueous neutral suspensions and solutions, but hydrolyses in alkaline media (8). Aqueous methomyl solutions are non corrosive (25). Microcoulometric gas chromatography is recommended for residue detection (1).

Occupational Exposure Limits:

OSHA: 2.5 mg/m3 TWA
ACGIH: 2.5 mg/m3 TWA
NIOSH: 2.5 mg/m3 recommended TWA

Physical Properties:

CAS #: 16752-77-5
H20 solubility: 5,800 ppm; 5.8% at 25 degrees C (16); 5.8 g/100 g (2); 58,000 mg/l (58 g/l) (24)
Solubility in other solvents: soluble in methanol, acetone, ethanol, isopropanol (16); 73 g/100 g acetone, 22 g/100 g isopropanol, 3 g/100 g toluene (8)
Melting point: 172 degrees F (78 degrees C) (16)
Vapor pressure: 5 x 10 to the minus 5 power Torr at 25 degrees C (1)
log Kow: -3.24 (12); = 2.38 (10); = 0.69 (23)
Koc: 160 (23); 27 (calculated) (23); log Koc: 2.63 (10); = 0.38 (12)
Kd: approximately equal to two, assuming that adsorption is described by a linear isotherm, and therefore equal to one (24).
Chemical Class/Use: carbamate insecticide, nematicide, and acaricide.


E.I. DuPont de Nemours and Co., Inc.
Agricultural Products Company
DuPont Building
Wilmington, DE 19898

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: November, 1992


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