PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> 2,4-D to Captan --> Bendiocarb

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 Assessment Program.


Publication Date: 5/94


Ficam, Dycarb, Garvox, Multamat, Multimet, Niomil, Rotate, Seedox, Turcam (24).


Most formulations of bendiocarb are classified as general use pesticides, with the exception of Turcam, Turcam 2.5 G and Turcam Fertilizer GC, which are classified as Restricted Use Pesticides (RUP) (28, 30). Restricted use pesticides may be purchased and used only by certified applicators.


Bendiocarb is a carbamate insecticide. It is effective against a wide range of nuisance and disease vector insects. It is used to control mosquitoes, flies, wasps, ants, fleas, cockroaches, silverfish, ticks and other pests in homes, industrial plants, and food storage sites. In agriculture it is used against a variety of insects, especially those in the soil. Bendiocarb is also used as a seed treatment on sugar beets and maize and against snails and slugs (24, 14, 16, Res. Discl. 158:67, 1977). Pesticides containing bendiocarb are formulated as dusts, granules, ultra- low volume sprays, and as wettable powders (28).



Bendiocarb is highly toxic if it is ingested or if it is absorbed through the skin (27). Absorption through the skin is the most likely route of exposure. Individuals exposed under conditions of high temperature and humidity are at the greatest risk because these conditions promote rapid absorption of bendiocarb across the skin (24). Persons with asthma, diabetes, cardiovascular disease, mechanical obstruction of the gastrointestinal or ureogenital tract, and those in vagotonic states are at special risk from any route of exposure (27).

Irritation and pain, blurred vision, tearing, muscle spasms and unresponsive pupils (to changes in light) may all occur if bendiocarb gets in the eye(s). These effects are due to anti-cholinesterase activity.

In one case of exposure while applying bendiocarb, the victim experienced symptoms of severe headache, vomiting and excessive salivation and his cholinesterase level was depressed by 63%. He recovered from these symptoms in less than three hours with no medical treatment and his cholinesterase level returned to normal within 24 hours. In another case, poisoning occurred when an applicator who was not wearing protective equipment attempted to clean contaminated equipment. The victim experienced nausea, vomiting, incoordination, pain in his arms, hands and legs, muscle spasms, and breathing difficulty. These symptoms abated within two hours after decontamination and treatment with atropine. The victim was fully recovered by the following day (24).

Like other carbamate insecticides, bendiocarb is a reversible inhibitor of cholinesterase, an essential nervous system enzyme. Symptoms of bendiocarb poisoning 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 (16, 26). Carbamates generally do not accumulate in mammalian tissue and the cholinesterase inhibition reverses rapidly once exposure ceases. Complete recovery from an acute poisoning by bendiocarb, with no long term health effects, is possible if exposure ceases and the victim has time to recover their normal level of cholinesterase before succumbing to symptoms. In non-fatal cases, the illness usually lasts less than 24 hours (24, 27). (For more information on cholinesterase, please refer to the Toxicology Information Brief on Cholinesterase-Inhibition).

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 bendiocarb in rats is 34-156 mg/kg, 35-40 mg/kg for rabbits, and 35 mg/kg for guinea pigs. The dermal LD50 for rats is 566 mg/kg (24, 27, NIOSH RTECS Online File # 84/8310).


Chronic exposure to bendiocarb can cause the same symptoms as acute exposure. Long term feeding studies with test animals show depressed levels of cholinesterase activity. A two-year study with dogs fed doses of 12.5 mg/kg showed elevated serum cholesterol and decreased levels of calcium in the bloodstream. A two-year study with rats fed doses of 10 mg/kg/day showed a wide range of changes in organ weights, blood and urinalysis characteristics, as well as an increased incidence of stomach and eye lesions (24).

Reproductive Effects

In a three generation study with rats, fertility and reproduction were not affected by bendiocarb at dietary levels of up to 12.5 mg/kg. Prenatal and postnatal doses of 40 mg/kg were toxic to rat dams and reduced pup weight and survival rates. No effects were seen at 20 mg/kg (24).

Teratogenic Effects

No teratogenic effects were seen in the offspring of rats given 4 mg/kg/day or in rabbits given 5 mg/kg/day of bendiocarb during gestation (24).

Mutagenic Effects

Numerous studies show that bendiocarb is not mutagenic (24).

Carcinogenic Effects

Bendiocarb was not carcinogenic in two-year studies of rats and mice (24).

Organ Toxicity

No changes in organ weight or harmful effects in tissues were observed in a two-year dietary study of dogs fed doses of up to 12.5 mg/kg/day. In a two-year study with rats fed doses of 10 mg/kg/day, changes in organ weight and an increased incidence of stomach and eye lesions were observed (24).

Fate in Humans and Animals

Bendiocarb is absorbed through all the normal routes of exposure, but dermal absorption is especially rapid.

Carbamates generally are excreted rapidly and do not accumulate in mammalian tissue. If exposure does not continue, cholinesterase inhibition and its symptoms reverse rapidly. In non-fatal cases, the illness generally lasts less than 24 hours (26). Within 2 days after feeding doses of up to 10 mg/kg of bendiocarb to rats, 89 to 90 % of the dose was eliminated in the urine, 2 to 6% was exhaled, and another 2 to 6% was eliminated in the feces. This same pattern of elimination was observed in a human subject given an oral dose of bendiocarb (24).


Effects on Birds

Bendiocarb is highly toxic to birds. The LD50 for mallard ducks is 3.1 mg/kg, and for quail is 19 mg/kg.

Effects on Fish

The LC50 for bendiocarb in fish is 0.4-1.8 mg/L (5).

Effects on Other Animals (Nontarget Species)

Earthworm populations under turf were reduced by 99% within one week after a single application of 4.48 kg/hectare of bendiocarb. This rate is twice the highest application rate permitted on labels for products containing bendiocarb (26).


Bendiocarb does not accumulate in soil, water, or plants.

Breakdown of Chemical in Soil and Groundwater

The half-life of bendiocarb varies with soil type from less than one week to up to four weeks (8, 28).

Breakdown of Chemical in Water

Bendiocarb is degraded in solution by hydrolysis. It does not accumulate in water.


Bendiocarb is an odorless, white crystalline solid. It is stable under normal temperatures and pressures, but should not be mixed with alkaline preparations. Thermal decomposition products may include toxic oxides of nitrogen (27).

Occupational Exposure Limits:

No occupational exposure limits have been established for bendiocarb by OSHA, ACGIH, or NIOSH.

Physical Properties:

CAS #: 22781-23-3
Koc: 200 calculated from log P (28)
Density: 1.25 g/ml
H20 solubility: 260 ppm (28)
Solubility in other solvents:
Acetone 2-3 x 10 to the minus 5 ppm
Dichloromethane 3-6 x 10 to the minus 5 ppm
Dimethyl sulfoxide 2-3 x 10 to the minus 5 ppm
Ethanol 3-5 x 10 to the minus 4 ppm
Xylene 1.6 x 10 to the minus 4 ppm (30)
Melting point: 124-129 degrees C (264 degrees F)(27, 30)
Vapor pressure: 3.5 x 10 to the minus 5 mm Hg at 25 degrees C (28).
Water: hexane partition coefficient: 1:9 at 25 degrees C (5)
Chemical Class/Use: Carbamate insecticide


NOR-AM Chemical Company
Little Falls Centre One
2711 Centerville Rd.
Wilmington, DE 19808
Telephone: 302-892-3000

Review by Basic Manufacturer:

Comments solicited: June, 1992
Comments received: January, 1994


  1. Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby, OH: Meister Pub. Co.
  2. WSSA Herbicide Handbook Committee. 1983. Herbicide Handbook of the Weed Science Society of America. 5th Ed. WSSA, Champaign, IL.
  3. Hazardous Materials Advisory Committee. 1974. EPA-SAB-74-001 Herbicide Report Chemical Analysis, Environmental Effects, Agriculture and Other Applied Uses. EPA: May.
  4. Tucker, Richard. 1970. Handbook of toxicity of pesticides to wildlife. USDI Fish & Wildlife Service.
  5. Worthing, C.R. (ed.). 1987. The pesticide manual: A world compendium. 8th Ed. The British Crop Protection Council. Croydon, England.
  6. Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore, MD: Williams & Wilkins.
  7. Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides: chemistry, degradation, and mode of action. 2nd Ed. Vol. 1 & 2. New York: M. Dekker.
  8. Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. Crop Protection Chemicals Reference. 1986. 2nd Ed. New York: Chemical and Pharmaceutical Pub. Corp.
  10. Shepard, T.H. 1973. Catalog of teratogenic agents. Baltimore, MD: John Hopkins University Press.
  11. Schardein, James. 1985. Chemically induced birth defects. New York: Marcel Dekker.
  12. U.S. Department of Health, Education and Welfare. 1976. Suspected Carcinogens. A subfile of the registry of toxic effects of chemical substances. Washington, DC: EPA.
  13. Department of Transportation. 1984. Emergency Response Guidebook: Guidebook for hazardous materials incidents. Washington, DC: U.S. DOT.
  14. Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and human health. New York: Springer-Verlag.
  15. Lef'evre, M.J. 1980. First aid manual for chemical accidents. New York: Van Nostrand Reinhold.
  16. TOXNET. 1985. 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.
  17. Sax, N.I. 1975. Dangerous properties of industrial materials. 4th Ed. New York: Van Nostrand Reinhold Co.
  18. Casarett, L.J. 1980. Casarett & Doull's Toxicology: the basic science of poisons. 2nd Ed. New York: Macmillan.
  19. Gosselin, R.E. 1984. Clinical toxicology of commercial products. 5th Ed. Baltimore, MD: Williams & Wilkins.
  20. National Fire Protection Association (NFPA). 1978. Fire Protection Guide. Hazardous Materials.
  21. Morgan, D.P. 1982. Recognition and management of pesticide poisonings. Iowa Pesticide Hazardous Assessment Project. 1982. Iowa City, IA.
  22. Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
  23. Sunshine, Irving. 1969. Handbook of analytical toxicology. Cleveland, OH: Chemical Rubber Co.
  24. Hayes, W.J. and E.R. Lawes (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., New York.
  25. Meister, R.T. (ed.). 1991. Farm Chemicals Handbook '91. Meister Publishing Company, Willoughby, Ohio.
  26. DuPont. 1991. Technical Bulletin for Lannate Insecticide, DuPont Agricultural Products, Wilmington, DE.
  27. Occupational Health Services. 1991 (Sept. 29). MSDS for bendiocarb. OHS, Inc., Secaucus, NJ.
  28. Nor-Am Chemical Company. 1992 (Aug. 5). Letter from Richard R. Stevens. Discussion of properties of bendiocarb. Nor-Am Chemical Co., Wilmington, DE.
  29. Occupational Health Services. 1991. MSDS for methomyl. OHS, Inc., Secaucus, NJ.
  30. Review by Nor-Am Chemical Co. January 3, 1994.