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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.

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Carbofuran

Publication Date: 9/93

TRADE OR OTHER NAMES

Furadan, Bay 70143, Curaterr, D 1221, ENT 27164, Yaltox, Furacarb (25).

REGULATORY STATUS

Following a Special Review which began in 1985, the EPA initiated a ban on all granular formulations of carbofuran, with five minor-use exceptions, to become effective on September 1, 1994. Phase-out began on September 1, 1991 with a ban on the use of granular carbofuran in certain ecologically sensitive areas. Before 1991, 80 percent of the total usage of carbofuran was in granular formulations. The ban has been established to protect birds and is not related to human health concerns. Bird kills have occurred when birds ingested carbofuran granules, which resemble grain seeds in size and shape, or when predatory or scavenging birds have ingested small birds or mammals which had eaten carbofuran pellets. There is no ban on liquid formulations of carbofuran (27, 28).

Liquid formulations of carbofuran are classified as Restricted Use Pesticides (RUP) because of their acute oral and inhalation toxicity to humans. Granular formulations are also classified as RUP's, but for a different reason, their toxicity to birds. Liquid formulations bear the signal word "Danger." Granular formulations bear the signal word "Caution" (25).

INTRODUCTION

Carbofuran is a broad spectrum carbamate pesticide that kills insects, mites and nematodes on contact or after ingestion. It is used against soil and foliar pests of field, fruit, vegetable and forest crops. Carbofuran is available in liquid and granular formulations (5, 25, 27, 28).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Carbofuran is highly toxic by inhalation and ingestion and moderately toxic by dermal absorption (6, 30). Risks from exposure to carbofuran are especially high for persons with asthma, diabetes, cardiovascular disease, mechanical obstruction of the gastrointestinal or urogenital tracts, or those in vagotonic states (30).

Carbofuran may cause contact burns to the skin or eyes (13). Eye protection should be worn when handling carbofuran. A respirator should be worn by applicators of carbofuran (1). Fires, and the run off from fire control, may produce irritating or poisonous gases (13). Closed spaces (storage, etc.) should be aired before entering (13).

As with other carbamate compounds, carbofuran's cholinesterase- inhibiting effect is short-term and reversible (7). Symptoms of carbofuran poisoning include: nausea, vomiting, abdominal cramps, sweating, diarrhea, excessive salivation, weakness, imbalance, blurring of vision, breathing difficulty, increased blood pressure or 'hypertension,' and lack of control of urine or feces release, referred to as 'incontinence.' Death may result from respiratory system failure associated with carbofuran exposure (4). Complete recovery from an acute poisoning by carbofuran, 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, 24). (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 (30).

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 rats is 5 mg/kg, for mice is 2 mg/kg, and for dogs is 19 mg/kg. The dermal LD50 for rabbits is 885 mg/kg (30).

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 inhalation of carbofuran in guinea pigs is 43 mg/m3. The LC50 for rats is 85 mg/L and 52 mg/L for dogs (30).

CHRONIC TOXICITY

Prolonged or repeated exposure to carbofuran may cause the same symptoms as an acute exposure (30). The EPA has established a Lifetime Health Advisory (LHA) level of 40 ppb of carbofuran in drinking water. This means that a person may drink water containing carbofuran at or below this level daily over the course of their lifetime with no health effects. Consuming carbofuran at high levels well above the LHA level over a long period of time has caused damage to the testes and uterus of test animals. It has also caused cholinesterase inhibition in both humans and test animals (29).

Reproductive Effects

Daily feeding of 100 ppm of carbofuran to pregnant rats greatly reduced the ability of the pups to survive. Non-fatal liver changes occurred in mice pups (6).

Teratogenic Effects

The lowest amount of carbofuran that proved teratogenic to mice in the mother's diet (TDlo) was 210 ug/kg (fed throughout pregnancy) (NIOSH RTECS Online File 304/8311).

Mutagenic Effects

No mutagenic effects have been reported in animals or bacteria (using the Ames Assay: J. Toxicol. Environ. Health 7(3-4):519- 531.1981). Genetic changes have been shown in algae (Microbios. Lett. 12(46):79.1979).

Carcinogenic Effects

Sufficient data are available from animal studies to indicate that carbofuran does not pose a risk of cancer to humans (29). However, N- nitrosocarbamates are potent mutagens and carcinogens. They can be made under the acidic conditions of the stomach of some animals. Humans are possible candidates (J. Toxicol. Environ. Health 14(2-3):279- 290.1984).

Fate in Humans and Animals

Carbofuran is poorly absorbed through the skin (19). It is metabolized (broken-down) in the liver and eventually excreted in the urine. The half-life is from 6-12 hours. About 3% of the mother's intake will be excreted in the milk (Menzie. Metab. Pesticides. 1974).

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 (30).

ECOLOGICAL EFFECTS

Effects on Birds

Carbofuran is highly toxic to birds. One granule is sufficient to kill a small bird. Bird kills have occurred when birds ingested carbofuran granules, which resemble grain seeds in size and shape, or when predatory or scavenging birds have ingested small birds or mammals which had eaten carbofuran pellets (28).

Carbofuran is very toxic to pheasants, chickens, fulvous tree ducks and Japanese quail (4). Red shouldered hawks have been poisoned after eating prey from carbofuran treated fields (J. Wildlife Manage. 47(4):1129. 1983). Levels of carbofuran occurring in Kansas fields have been high enough to cause a reduction in the weight, food intake and ability to move of adult male bobwhites (Arch. Environ. Contam. Toxicol. 11(5):611-615.1982).

Effects on Fish

Carbofuran may be teratogenic to frogs (Toxicol. Lett. 22(1):7- 13.1984). It is very toxic to trout, Coho salmon, perch (Hdbk. Acut. Tox. Chem. Fish & Aqua. Invert. 1980), bluegills (8), and catfish (Toxicology 23(4):337-345.1982). The 96-hour LD50 for fish is 150 ug/L.

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Carbofuran is soluble in water and has a moderately lengthy soil half-life (3-60 days). It is therefore expected to have a high potential for groundwater contamination (31, Curr. Sci. 53(17):925.1984.). Carbofuran was mobile to very mobile in sandy , silt loam, silty clay and silty clay loam soils; moderately mobile in silty clay and silty clay loam soils; and only slightly mobile in muck soils. Carbofuran has been detected at very low (1 to 5 ppb) in water table aquifers beneath sandy soils in New York and Wisconsin (29).

In soil, carbofuran is degraded by chemical hydrolysis and microbial processes. Hydrolysis occurs more rapidly in alkaline soils (29). Soil microorganisms are better at breaking down large amounts of carbofuran if the soil is pretreated with a small amount of carbofuran (J. Environ. Sci. Health Part B, B-19 (1):111.1984). Carbofuran breaks down in sunlight (Menzie. Metab. Pesticides. 1969.).

Breakdown of Chemical in Water

In water, carbofuran is subject to degradation by chemical hydrolysis under alkaline conditions. Photodegradation and aquatic microbes may also contribute to degradation. The hydrolysis half-lives of carbofuran in water at 25 degree C are 690, 8.2, and 1.0 weeks at pH's of 6.0., 7.0, and 8.0 respectively. Carbofuran does not volatilize from water nor does it adsorb to sediment or suspended particles. It does not bioaccumulate in aquatic systems (29).

Fire control run-off or dilution water may cause pollution of lakes and/or streams (13).

Breakdown of Chemical in Vegetation

The half-life of carbofuran on crops, when applied to the roots, is about 4 days and longer than 4 days if applied to the leaves (Menzie. Metab. Pesticides. 1974).

PHYSICAL PROPERTIES AND GUIDELINES

Carbofuran is an odorless, white crystalline solid. Thermal decomposition may include toxic oxides of nitrogen (28, 30).

Applicators and handlers of carbofuran should wear protective/impervious clothing and equipment to prevent skin contact (30).

Occupational Exposure Limits:

OSHA: 2.5 mm/m3 TWA
ACGIH: 2.5 mm/m3 TWA
NIOSH: 2.5 mm/m3 TWA

Physical Properties:

CAS #: 1563-66-2
Melting point: 150-153 degrees C (22, 30)
Vapor pressure: 2 x 10 to the minus 5 mm Hg at 33 degrees C (1, 30)
Specific gravity: 1.180 at 20 degrees C (1)
Solubility:
SolventSolubility
Water 25,700 ppm
Acetone 150 g/kg
Acetonitrile 140 g/kg
Benzene 40 g/kg
Cyclohexone 90 g/kg
Dimethylformade 270 g/kg
Dimethyl sulfoxide 250 g/kg (6)
Chemical class: carbamate insecticide

BASIC MANUFACTURER:

FMC Corporation
Agricultural Chemicals Group
2000 Market Street
Philadelphia. PA 19103

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received:

REFERENCES

  1. Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing 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 Healtyh. 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. Gosselin, R.E. 1984. Clinical toxicology of commercial products. 5th Ed. Baltimore, MD: Williams & Wilkins.
  19. National Fire Protection Association (NFPA). 1978. Fire Protection Guide. Hazardous Materials.
  20. Morgan, D.P. 1982. Recognition and management of pesticide poisonings. Iowa Pesticide Hazardous Assessment Project. 1982. Iowa City, IA.
  21. Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
  22. Sunshine, Irving. 1969. Handbook of analytical toxicology. Cleveland, OH: Chemical Rubber Co.
  23. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., New York.
  24. Meister, R.T. (ed.). 1991. Farm Chemicals Handbook '91. Meister Publishing Company, Willoughby, Ohio.
  25. U.S. Environmental Protection Agency. 1990 (Oct. 18). Carbofuran: Requests to amend registrations to delete certain uses and final determination with respect to those uses. Federal Register 55 (202): 42266-8.
  26. U.S. Environmental Protection Agency. 1991 (May 14). Pesticide carbofuran phased out under settlement agreement. Environmental News, R-84. Al Heir, Communications and Public Affairs, US EPA, Washington, DC.
  27. U.S. Environmental Protection Agency. 1991(?). Environmental Fact Sheet for Carbofuran. Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  28. U.S. Environmental Protection Agency. 1989 (Jan.). Health Advisory Summary for Carbofuran. US EPA, Washington, DC.
  29. Occupational Health Services, Inc. 1991 (Oct. 29). MSDS for carbofuran. OHS Inc., Secaucus, NJ.
  30. 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.
  31. Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers, Chelsea, MI.