---

The information in this profile may be out-of-date. It was last revised in 1996. EXTOXNET no longer updates this information, but it may be useful as a reference or resource.

Please visit the National Pesticide Information Center (NPIC) to find updated pesticide fact sheets. If you don't find a fact sheet related to your question, feel free to call 1-800-858-7378. NPIC is open five days a week from 8:00am to 12:00pm Pacific Time.

---

E X T O X N E T

Extension Toxicology Network

Pesticide Information Profiles

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

EXTOXNET primary files maintained and archived at Oregon State University

Revised June 1996

Dimethoate

Trade and Other Names: Trade names include Cekuthoate, Chimigor 40, Cygon 400, Daphene, De-Fend, Demos NF, Devigon, Dicap, Dimate 267, Dimet, Dimethoat Tech 95%, Dimethopgen, Ferkethion, Fostion MM, Perfekthion, Rogodan, Rogodial, Rogor, Roxion, Sevigor, Trimetion.

Regulatory Status: Dimethoate is moderately toxic compound in EPA toxicity class II. Labels for products containing dimethoate must bear the Signal Word WARNING. Dimethoate is a General Use Pesticide (GUP).

Chemical Class: organophosphate

Introduction: Dimethoate is an organophosphate 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. Unless otherwise specified, the data summarized in this profile refer to the technical product.

Formulation: Dimethoate is available in aerosol spray, dust, emulsifiable concentrate, and ULV concentrate formulations.

Toxicological Effects:

• Acute toxicity: Dimethoate is moderately toxic by ingestion, inhalation, and dermal absorption. The reported acute oral LD50 values for the technical product range from 180 to 330 mg/kg in the rat; although an oral LD50 of as low as 28 to 30 mg/kg has been reported, it is regarded by some as less reflective of the toxicity of current products [2,13]. Reported oral LD50 values in other species are 160 mg/kg in mice and 400 to 500 mg/kg in rabbits [2,13]. In guinea pigs, the oral toxicity is reported as 550 to 600 mg/kg for the pure and laboratory grade of the compound, but for the technical grade is only 350 to 400 mg/kg [2]. It is not clear whether the increased toxicity results from impurities present initially in the technical product or whether these may be formed from degradation over time [2]. Reported dermal LD50 values for dimethoate are 100 to 600 mg/kg in rats, again with a much lower value for an earlier product [2,13]. Dimethoate is reportedly not irritating to the skin and eyes of lab animals [8,13]. Severe eye irritation has occurred in workers manufacturing dimethoate, although this may be due to impurities [2]. Via the inhalation route, the reported 4-hour LC50 is greater than 2.0 mg/L, indicating slight toxicity [13]. Effects of acute exposure are those typical of organophosphates. 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. Persons with respiratory ailments, recent exposure to cholinesterase inhibitors, impaired cholinesterase production, or 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 [2].
• 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 and 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 depression, 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 [2].
• Reproductive effects: When mice were given 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 three-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 [2]. Impaired reproductive function in humans is not likely under normal conditions.
• Teratogenic effects: Dimethoate is teratogenic in cats and rats [8,2]. A dosage of 12 mg/kg/day given to pregnant cats increased the incidence of extra toes on kittens [2,8]. The same dosage given to pregnant rats produced birth defects related to bone formation, runting and malfunction of the bladder. Dosages of 3 or 6 mg/kg/day were not teratogenic in cats or rats [2]. No effects were observed in cats and rats at doses of 2.8 mg/kg/day. There were no teratogenic effects seen in the offspring of mice given 9.5 to 10.5 mg/kg/day dimethoate in their drinking water [2]. It is not likely that teratogenic effects will be seen in humans under normal circumstances.
• Mutagenic effects: Mutagenic effects due to dimethoate exposure were seen in mice. They 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]. Mutagenic effects are unlikely in humans under normal circumstances.
• Carcinogenic effects: An increase in malignant tumors was reported in rats given oral doses of 5, 15 or 30 mg/kg/day dimethoate for over a year. The increases were not, however, dose dependent [2]. That is, higher doses did not necessarily result in higher tumor rates. Thus the evidence of carcinogenicity, even with high-dose, long-term exposure, is inconclusive. This suggests carcinogenic effects in humans are unlikely.
• Organ toxicity: Target organs as determined through animal tests include the testicles, kidneys, liver, and spleen [2].

• Fate in humans and animals: Dimethoate is rapidly metabolized by mammals. Rats excreted about 50 to 60% of administered doses in urine, expired air and feces within 24 hours [2]. 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 dimethoate to the backs of cows at 30 mg/kg, the concentration of dimethoate reached a maximum level of 0.02 ppm in blood and milk in about 3 hours, and decreased to 0.01 ppm within 9 hours [2].

Ecological Effects:

• Effects on birds: Dimethoate is moderately to very highly toxic to birds. In Japanese quail, a 5-day dietary LC50 of 341 ppm is reported [14]. It may be very highly toxic to other birds; reported acute oral LD50 values are 41.7 to 63.5 mg/kg in mallards and 20.0 mg/kg in pheasants [6]. Birds are not able to metabolize dimethoate as rapidly as mammals do, which may account for its relatively higher toxicity in these species [26].
• Effects on aquatic organisms: Dimethoate is moderately toxic to fish, with reported LC50 values of 6.2 mg/L in rainbow trout, and 6.0 mg/L in bluegill sunfish [16]. It is more toxic to aquatic invertebrate species such as stoneflies and scuds [16].
• Effects on other organisms: Dimethoate is highly toxic to honeybees. The 24-hour topical LD50 for dimethoate in bees is 0.12 ug per bee [13].

Environmental Fate:

• Breakdown in soil and groundwater: Dimethoate is of low persistence in the soil environment. Soil half-lives of 4 to 16 days, or as high as 122 days have been reported, but a representative value may be on the order of 20 days [12,19]. Because it is rapidly broken down by soil microorganisms, it will be broken down faster in moist soils. Dimethoate is highly soluble in water, and it adsorbs only very weakly to soil particles so it may be subject to considerable leaching [12,19]. However, it is degraded by hydrolysis, especially in alkaline soils, and evaporates from dry soil surfaces. Losses due to evaporation of 23 to 40% of applied dimethoate have been reported [12]. Biodegradation may be significant, with a 77% loss reported in a nonsterile clay loam soil after 2 weeks [12].
• Breakdown in water: In water, dimethoate is not expected to adsorb to sediments or suspended particles, nor to bioaccumulate in aquatic organisms [12]. It is subject to significant hydrolysis, especially in alkaline waters. The half-life for dimethoate in raw river water was 8 days, with disappearance possibly due to microbial action or chemical degradation [12]. Photolysis and evaporation from open waters are not expected to be significant [12].
• Breakdown in vegetation: Dimethoate is not toxic to plants [13].

Physical Properties:

• Appearance: Dimethoate is a grey-white crystalline solid at room temperature [13].
• Chemical Name: O,O-dimethyl S-methylcarbamoylmethyl phosphorodithioate [13]
• CAS Number: 60-51-5
• Molecular Weight: 229.28
• Water Solubility: 25 g/L @ 21 C [13]
• Solubility in Other Solvents: s. in methanol and cyclohexane; s.s in aliphatic hydrocarbons, aromatic hydrocarbons, diethyl ether, carbon tetrachloride, hexane, and xylene; v.s. in chloroform, benzene
• Melting Point: 43-45 C (technical) [13]
• Vapor Pressure: 1.1 mPa @ 25 C [13]
• Partition Coefficient: 0.6990 [13]
• Adsorption Coefficient: 20 [19]

Exposure Guidelines:

• ADI: 0.01 mg/kg/day [38]
• MCL: Not Available
• RfD: 0.0002 mg/kg/day [53]
• PEL: Not Available
• HA: Not Available
• TLV: Not Available

Basic Manufacturer:

BASF Corporation
Agricultural Products Group
P.O. Box 13528
Research Triangle Park, NC 27709-3528

• Phone: 800-669-2273
• Emergency: 800-832-4357
  

References:

References for the information in this PIP can be found in Reference List Number 5

DISCLAIMER: The information in this profile does not in any way replace or supersede the information on the pesticide product labeling or other regulatory requirements. Please refer to the pesticide product labeling.