E X T O X N E T
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
Publication Date: 9/93
TRADE OR OTHER NAMES
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
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-
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
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.
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).
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).
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).
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).
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
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
PHYSICAL PROPERTIES AND GUIDELINES
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
Occupational Exposure Limits:
|OSHA: ||2.5 mg/m3 TWA
|ACGIH: ||2.5 mg/m3 TWA
|NIOSH: ||2.5 mg/m3 recommended TWA
|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
Wilmington, DE 19898
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received: November, 1992
American Conference of Governmental Industrial Hygienists, Inc.
1986. Documentation of the threshold limit values and biological
exposure indices. Fifth edition. Cincinnati, OH: Publications
Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Chemical & Pharmaceutical Press. 1987. Crop protection chemicals
reference. Third edition. NY: John Wiley & Sons.
Cornell University. 1987. 1988 New York State pesticide
recommendations. Forty-ninth annual pest control conference. Nov. 9,
10, 11. Ithaca, NY.
DuPont de Nemours and Company. 1983. Technical data sheet for
methomyl. Agricultural Chemicals Department. Wilmington, DE: DuPont.
Gosselin, R. E., et al. 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides
and human health. NY: Springer-Verlag.
Hartley, D. and H. Kidd, eds. 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD:
Williams and Wilkins.
Hunter, R. L., et al. 1984. User's manual for QSAR System.
Center for Data Systems and Analysis, Montana State University.
Kaplan, M. A. and H. Sherman. 1977. Toxicity studies with methyl
N-[[Methylamino) carbonyl]oxy]-ethanimidothioate. Toxicology and
Applied Pharmacology 40:1-17. Great Britain: Academic Press, Inc.
Li, F. 1982. Technical data submitted in support of the San Luis
drain report of waste discharge. File Report, Branch of Scientific
Resources, US Department of Interior, (Contract #2-0-20-X0221).
McEwen, F. L. and G. R. Stephenson. 1979. The use and
significance of pesticides in the environment. NY: John Wiley and
Menzie, C. M. 1980. Metabolism of pesticides. Update III. U.S.
Dept. of the Interior. Fish and Wildlife Service. Special Scientific
Report. Wildlife no. 232. Washington, DC: U. S. Government Printing
National Research Council, Safe Drinking Water Committee. 1977.
Drinking water and health. Washington, DC: National Academy of
Occupational Health Services, Inc. 1986. Material safety data
sheet. Secaucus, NJ: OHS, Inc.
Rom, W. N., ed. 1983. Environmental and Occupational Medicine.
Boston: Little, Brown, and Company.
Sax, N. I. 1984. Dangerous properties of industrial materials.
Sixth NY: VanNostrand Reinhold Company.
TOXNET. 1975-1986. National library of medicine's toxicology
data network. Hazardous Substances Databank. Public Health Service.
National Institute of Health, U. S. Department of Health and Human
Services. Bethesda, MD: NLM.
Tucker, R. and D. G. Crabtree. 1970. Handbook of toxicity of
pesticides to wildlife. U.S. Department of Agriculture, Fish and
Wildlife Service. Bureau of Sport Fisheries and Wildlife.
U. S. Environmental Protection Agency. 1987 (Oct. 23). Subject:
Active ingredients subject to restricted use classification. Office of
Pesticide Programs, Registration Division. Washington, DC.
_____. 1986. List of federally restricted products.
Registration Support and Emergency Response Branch (TS-767).
_____. 1984. Memorandum from Stuart Z. Cohen. List of potential
groundwater contaminants. Office of Pesticides and Toxic Substances.
Washington, DC. Photocopy.
Wagenet, L. P. et al. 1985. A review of physical-chemical
parameters related to the soil and groundwater fate of selected
pesticides in New York state. Cornell University Agricultural
Experiment Station, New York State College of Agriculture and Life
Sciences. Ithaca, NY. Number 30. ISSN 0362-2754.
Worthing, C. R., ed. 1983. The pesticide manual: A world
compendium. Croydon, England: The British Crop Protection Council.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
DuPont Agricultural Products. 1991 (Aug.). MSDS for methomyl
technical. DuPont, Wilmington, DE.
DuPont Agricultural Products. 1991 (June). MSDS for Lannate
Insecticide. DuPont, Wilmington, DE.
DuPont Agricultural Products. 1989 (Nov.). Technical Data Sheet
for Methomyl. DuPont, Wilmington, DE.
US EPA. 1989 (April). Registration standard for pesticide
products containing methomyl as the active ingredient. EPA, Office of
Pesticide Programs, Washington, DC.
U. S. Department of Agriculture, Soil Conservation Service. 1990
(Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0
(Summary). USDA - Soil Conservation Service, Syracuse, NY.
Occupational Health Services, Inc. 1991. MSDS for Methomyl. OHS
Inc., Secaucus, NJ.
Howard, Philip H. 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III, Pesticides. Lewis
Publishers: Chelsea, MI.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
Questions regarding the development of this web site should be directed to the
For more information relative to pesticides and their use in New York State, please contact the PMEP staff at:
5123 Comstock Hall
Ithaca, NY 14853-0901
This site is supported, in part, by funding from the