E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
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University of California at Davis. Major support and funding was provided
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Pesticide
Information
Profile
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Dimethoate
Publication Date: 9/93
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TRADE OR OTHER NAMES
Trade names include Cekuthoate, Chimigor 40, Cygon 400, Daphene,
De-Fend, Demos NF, Devigon, Dimate 267, Dimet, Dimethoat Tech 95%,
Dimethopgen, Ferkethion, Fostion MM, Perfekthion, Rogodan, Rogodial,
Rogor, Roxion, Sevigor, Trimetion.
REGULATORY STATUS
Products containing dimethoate must bear the signal word "Warning"
(3).
INTRODUCTION
Dimethoate is an insecticide used to kill mites and insects
systemically and on contact. It is used against a wide range of
insects, including aphids, thrips, planthoppers and whiteflies on
ornamental plants, alfalfa, apples, corn, cotton, grapefruit, grapes,
lemons, melons, oranges, pears, pecans, safflower, sorghum, soybeans,
tangerines, tobacco, tomatoes, watermelons, wheat and other vegetables.
It is also used as a residual wall spray in farm buildings for house
flies. Dimethoate has been administered to livestock for control of
botflies. Dimethoate is available in aerosol spray, dust, emulsifiable
concentrate, and ULV concentrate formulations (2, 3).
Dimethoate is one of a class of insecticides referred to as
organophosphates. These chemicals act by interfering with the
activities of cholinesterase, an enzyme that is essential for the proper
working of the nervous systems of both humans and insects. Please refer
to the Toxicology Information Brief on cholinesterase-inhibition for a
more detailed description of this topic.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Dimethoate is moderately toxic by ingestion, inhalation and dermal
absorption. As with all organophosphates, dimethoate is readily
absorbed through the skin. Skin which has come in contact with this
material should be washed immediately with soap and water and all
contaminated clothing should be removed. Organophosphates are easily
absorbed through the lungs. Persons with respiratory ailments, recent
exposure to cholinesterase inhibitors, impaired cholinesterase
production, or with liver malfunction may be at increased risk from
exposure to dimethoate. High environmental temperatures or exposure of
dimethoate to visible or UV light may enhance its toxicity (10).
Dimethoate is not irritating to the eyes of lab animals. Severe
eye irritation has occurred in workers manufacturing dimethoate.
Another chemical in the formula is thought to be the cause.
Firefighters exposed to fumes of burning dimethoate have developed eye
irritations (A. Medicina 42 (4):381-384. 1982). Splashing of
dimethoate into the eye may cause very swollen eyelids and damage to the
cornea (the outer surface of the eye). Both of these symptoms should
rapidly clear up (Grant. Tox. of the Eye. 1974).
The organophosphate insecticides are cholinesterase inhibitors.
They are highly toxic by all routes of exposure. When inhaled, the
first effects are usually respiratory and may include bloody or runny
nose, coughing, chest discomfort, difficult or short breath, and
wheezing due to constriction or excess fluid in the bronchial tubes.
Skin contact with organophosphates may cause localized sweating and
involuntary muscle contractions. Eye contact will cause pain, bleeding,
tears, pupil constriction, and blurred vision. Following exposure by
any route, other systemic effects may begin within a few minutes or be
delayed for up to 12 hours. These may include pallor, nausea, vomiting,
diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred
vision, constriction or dilation of the eye pupils, tears, salivation,
sweating, and confusion. Severe poisoning will affect the central
nervous system, producing incoordination, slurred speech, loss of
reflexes, weakness, fatigue, involuntary muscle contractions, twitching,
tremors of the tongue or eyelids, and eventually paralysis of the body
extremities and the respiratory muscles. In severe cases there may also
be involuntary defecation or urination, psychosis, irregular heart
beats, unconsciousness, convulsions and coma. Death may be caused by
respiratory failure or cardiac arrest (10).
Some organophosphates may cause delayed symptoms beginning 1 to 4
weeks after an acute exposure which may or may not have produced
immediate symptoms. In such cases, numbness, tingling, weakness and
cramping may appear in the lower limbs and progress to incoordination
and paralysis. Improvement may occur over months or years, but some
residual impairment will remain (10).
The amount of a chemical that is lethal to one-half (50%) of
experimental animals fed the material is referred to as its acute oral
lethal dose fifty, or LD50. The oral LD50 for technical dimethoate in
rats is 60 to 387 mg/kg, 60 mg/kg in mice, 400 mg/kg in dogs, 200 mg/kg
in hamsters, 300 mg/kg in rabbits, 350 mg/kg in guinea pigs, and 100
mg/kg in cats (3, 10). The dermal LD50 in rabbits is 1,000 mg/kg, and
353 mg/kg in rats (10). A dermal LD50 of greater than 2,000 mg/kg in
rats has also been reported (11).
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 4-hour LC50 for dimethoate in
rats is 1.2 mg/l (11).
CHRONIC TOXICITY
There was no cholinesterase inhibition in an adult human who
ingested 18 mg (about 0.26 mg/kg/day) of dimethoate/day for 21 days. No
toxic effects and no cholinesterase inhibition were observed in
individuals who ingested 2.5 mg/day (about 0.04 mg/kg/day) for 4 weeks.
In another study with humans given oral doses of 5, 15, 30, 45 or 60
mg/day for 57 days, cholinesterase inhibition was observed only in the
30 mg/day or higher dosage groups (2).
Repeated or prolonged exposure to organophosphates may result in
the same effects as acute exposure, including the delayed symptoms.
Other effects reported in workers repeatedly exposed include impaired
memory and concentration, disorientation, severe depressions,
irritability, confusion, headache, speech difficulties, delayed reaction
times, nightmares, sleepwalking and drowsiness or insomnia. An
influenza-like condition with headache, nausea, weakness, loss of
appetite, and malaise has also been reported (10).
Reproductive Effects
When mice were given 60 ppm (9.5 to 10.5 mg/kg/day) dimethoate in
their drinking water, there was decreased reproduction, pup survival,
and growth rates of surviving pups. Adults in this study exhibited
reduced weight gain, but their survival was not affected. In a 3-
generation study with mice, 2.5 mg/kg/day did not decrease reproductive
performance or pup survival (2). Once in the bloodstream, dimethoate
may cross the placenta (10).
Teratogenic Effects
Dimethoate is possibly a human teratogen (14). It was teratogenic
in cats and rats (6). A dosage of 12 mg/kg/day given to pregnant cats
increased the incidence of extra toes on kittens. The same dosage given
to pregnant rats produced birth defects related to bone formation,
runting and defects related to malfunction of the bladder. Dosages of 3
or 6 mg/kg/day were not teratogenic in cats or rats (2). The NOEL for
both cats and rats was 2.8 mg/kg/day (12). There were no teratogenic
effects seen in the offspring of mice given (9.5 - 10.5 mg/kg/day)
dimethoate in their drinking water (2).
Mutagenic Effects
Dimethoate is possibly a mutagen (6, 14, Mutation Res. 88 (3):307-
326. 1981). Mutagenic effects (dominant lethal) were more prominent in
male mice given a single high dose of dimethoate than in male mice given
one-twelfth of the same dose daily for 30 days (2).
Carcinogenic Effects
Dimethoate is possibly carcinogenic (6, 14). An increase in
malignant tumors was reported in rats given oral doses of 5, 15 or 30
mg/kg dimethoate for 511 to 627 days (2).
Organ Toxicity
The testicles of male rats exposed to dimethoate decreased in size.
These rats also developed chronic kidney problems (Environ. Res. 34
(2):193-211. 1984).
Fate in Humans and Animals
Dimethoate is rapidly metabolized by mammals. Rats excreted about
60% of an administered dose in urine and expired air within 24 hours.
In another study, rats given a single oral dose, excreted 50% in the
urine and 25% in the feces within 24 hours. Nine days later, only 0.9
to 1.1% of the dose remained in the rats' tissues . Human volunteers
excreted 76 to 100% of administered dimethoate within 24 hours (2).
The rate of metabolism and elimination varied in several species
tested. Amongst several mammalian species tested, dimethoate appears to
be less toxic to those animals with higher liver-to-body weight ratios
and to those with the highest rate of dimethoate metabolism (2).
Following application of radio-labeled dimethoate to the backs of
cows at the rate of 30 mg/kg, the concentration of dimethoate reached a
maximum level of 0.02 ppm in blood and milk in about 3 hours. The level
then dropped to 0.01 ppm by 9 hours after application (2).
ECOLOGICAL EFFECTS
Effects on Birds
Dimethoate is very toxic to birds. Birds are not able to
metabolize dimethoate quickly like mammals (4, White-Stevens. Pest. in
Environ. Vol. I. 1971). 7 mg/kg of dimethoate will kill one-half of
the wild birds exposed (LC50). The LC50 for birds in general is 22
mg/kg of dimethoate (NIOSH RTECS Online File 84/8310). The oral LD50
for mallard ducks is 41.7 mg/kg (11).
Effects on Aquatic Organisms
Dimethoate is highly toxic to fish and to aquatic invertebrates.
The 96-hour LC50 for dimethoate in rainbow trout is 6.2 ug/l (11). The
LC50 in mosquito fish is 40 to 60 mg/l (3). The 48-hour LC50 in Daphnia
magna, a small freshwater crustacean, is 2.5 ug/l (11).
Effects on Other Animals (Nontarget species)
Dimethoate is highly toxic to honey bees. The 24-hour topical LD50
for dimethoate in bees is 0.12 ug/bee. The 24-hour oral LD50 in bees is
0.15 ug/bee (11).
It is very toxic to livestock (Clarke. Vet. Tox. 1981) and other
wildlife. Oral LD50's range from 30 mg/kg (humans) to 400 mg/kg (dogs)
(NIOSH RTECS Online File 84/8310). Dimethoate is 300 times more toxic
to insects (house flies) than to mice.
ENVIRONMENTAL FATE
Dimethoate is biodegradable. It undergoes rapid degradation in the
environment and in sewage treatment plants (11).
Breakdown of Chemical in Soil and Groundwater
Because dimethoate is highly soluble in water and it adsorbs only
very weakly to soil particles, it may be subject to considerable
leaching (8, 9). It may be subject to degradation by hydrolysis,
especially in alkaline soils, and to evaporation from dry soil surfaces.
Losses due to evaporation of 23 to 40% of applied dimethoate have been
reported. Biodegradation may be significant, with 77% degradation
reported for a non-sterile clay loam soil in 2 weeks reported (9).
Dimethoate does not persist. Soil half-lives of 4 to 16 days, or
as high as 122 days have been reported. Half-lives between 2.5 and 4
days were reported during drought and moderate rainfall conditions (9).
Dimethoate breaks down faster in moist soils. It is rapidly broken down
by most soil microorganisms.
Breakdown of Chemical in Water
In water, dimethoate is not expected to adsorb to sediments or
suspended particles, nor to bioaccumulate in aquatic organisms. It is
subject to significant hydrolysis, especially in alkaline waters.
Hydrolysis half-lives of 3.7 and 118 days at pH 9 and pH 7,
respectively, have been estimated. Photolysis and evaporation from open
waters is not expected to be significant. The half-life for dimethoate
in raw river water was 8 days, with disappearance possibly due to
microbial action or chemical degradation (9).
Breakdown of Chemical in Vegetation
Dimethoate is not toxic to plants (5).
PHYSICAL PROPERTIES AND GUIDELINES
Dimethoate is a colorless crystalline solid with a camphor-like
(mercaptan) odor (5, 10). It will decompose rapidly when heated to
temperatures above 80 degrees C, creating the possibility of explosion.
It should never be heated above 35 degrees C. Thermal decomposition may
release toxic and hazardous fumes of dimethylsulfide, methyl mercaptane,
carbon monoxide, carbon dioxide, phosphorus pentoxide, nitrogenoxides
(3, 10, 11).
Persons who work with organophosphate materials for long periods of
time should have frequent blood tests of their cholinesterase levels.
If the cholinesterase level falls below a critical point, no further
exposure should be allowed until it returns to normal (13).
Protective clothing must be worn when handling dimethoate. Before
removing gloves, wash them with soap and water. Always wash hands, face
and arms with soap and water before smoking, eating or drinking.
After work, remove all work clothes and shoes. Shower with soap
and water. Wear only clean clothes when leaving the job. Wash
contaminated clothing and equipment with soap and water after each use.
Keep contaminated work clothes separate from regular laundry.
Exposure Guidelines:
No occupational exposure limits have been established for
dimethoate by OSHA, NIOSH or ACGIH (10).
Physical Properties:
| CAS#: | 60-51-5 |
| Specific gravity: | 1.28 at 20 degrees C (10) |
| Solubility in water: | 2.5% at 70 degrees F (21 degrees C) (3); 25 mg/ml (8). |
| Solubility: | Soluble in methanol and cyclohexane.
Slightly soluble in aliphatic hydrocarbons, aromatic hydrocarbons, diethyl ether, carbon tetrachloride, hexane and xylene.
Very soluble in chloroform, benzene, toluene, alcohols, esters, ketones, methylene chloride, acetone and ethanol.
Insoluble in petroleum ether (1, 18, Spencer. Guide to Chem. in Crop prot. 1982). |
| Boiling point: | 225 degrees F (107 degrees C) at 0.05 mm Hg (10) |
| Melting point: | 45-48 degrees C (1); 124-126 degrees F (51-52 degrees C) (10, 17) |
| Flash point: | 124 degrees F (16); 107 degrees C for technical dimethoate (3); 266 degrees F (130 degrees C) (10). |
| Vapor pressure: | 8.5 x 10 to the minus 6 power mm Hg at 25 degrees C (5)
1.85 x 10 to the minus 6 power mm Hg at 20 degrees C (11)
2.9 x 10 to the minus 4 power mm Hg at 50 degrees C (11) |
| Oil: | water partition coefficient - 5.959 (J. Envir. Sci. Health B18 (6):667-83.1983). |
| Koc: | 8 g/ml (8) |
BASIC MANUFACTURER
BASF Corp.
Agricultural Products Group
PO Box 13528
2505 Meridian Pkwy.
Research Triangle Park, NC 27709-3528
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received:
REFERENCES
Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby,
OH: Meister Publishing Co.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
Tucker, Richard. 1970. Handbook of toxicity of pesticides to
wildlife. USDI Fish & Wildlife Service.
Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council. Croydon,
England.
Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore,
MD: Williams & Wilkins.
Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides:
chemistry, degradation, and mode of action. 2nd Ed. Vol. 1 & 2. New
York: M. Dekker.
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.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis
Publishers, Chelsea, MI.
Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for
Dimethoate. OHS Inc., Secaucus, NJ.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
US Environmental Protection Agency. 1983 (Nov. 23). Dimethoate:
Proposed tolerance. Federal Register 48 (227): 52951-2.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and
human health. New York: Springer-Verlag.
Gosselin, R.E. 1984. Clinical toxicology of commercial products.
5th Ed. Baltimore, MD: Williams & Wilkins.
National Fire Protection Association (NFPA). 1978. Fire
Protection Guide. Hazardous Materials.
Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of
chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
Sunshine, Irving. 1969. Handbook of analytical toxicology.
Cleveland, OH: Chemical Rubber Co.
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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.
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