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Fluometuron. 1994 Pesticide Information Profile. EXTOXNET.

http://pmep.cce.cornell.edu/profiles/extoxnet/dienochlor-glyphosate/fluometuron-ext.html

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.

  Pesticide
Information
Profile 		Fluometuron

Publication Date: 3/94

TRADE OR OTHER NAMES

Trade names include C-2059, Cotoran, Cotorex, Cottonex, Ciba-2059, Higalcoton, Lanex, Pakhtaran.

REGULATORY STATUS

Fluometuron is registered by the U.S. Environmental Protection Agency (EPA) for use on cotton and sugarcane (2). It may only be manufactured into formulations intended for herbicide use on these crops (13). Container labels of fluometuron products must bear the signal word "WARNING" (1). Check with specific state regulations for local restrictions that may apply.

INTRODUCTION

Fluometuron is a selective herbicide used to control weeds in cotton (16). It acts on susceptible plants by inhibiting photosynthesis. It can be applied preemergence, for weed control before planting, or postemergence, after target crops and weeds come up (15). It has prolonged residual action of two to five months (6). Fluometuron is available as liquid, dry flowable, and wettable powder formulations (16).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Fluometuron is moderately toxic to humans by ingestion and slightly toxic by dermal absorption (18). The major routes of exposure to this herbicide are from inhalation and absorption through the skin (13). It may be fatal if inhaled, swallowed, or absorbed through skin, as it is irritating to the mucous membrane lining the skin, gastrointestinal tract, and respiratory system (2). While there have been no reports of cases of fluometuron poisoning in humans, this herbicide is considered a mild inhibitor of cholinesterase. Cholinesterase is an essential enzyme of the nervous system. Cholinesterase inhibition was observed in guinea pigs exposed by inhalation to 588 mg/m3 for 2 hours (18). (For more information, refer to the Toxicology Information Brief on Cholinesterase-Inhibition). Fluometuron caused an increased white blood cell count in agricultural workers (3).

Symptoms of fluometuron poisoning in rats include muscular weakness, tearing or watery eyes, extreme exhaustion and collapse (15).

Fluometuron is a mild skin and eye irritant. It has caused skin sensitization in guinea pigs and in humans (18). It affects the cornea of the eye in such a way that light cannot pass through it. This condition is referred to as corneal opacity (1, 13, 15). Skin or eye contact with it may cause burning (11).

The amount of a chemical that is deadly when given by mouth to one- half (50%) of test animals, is referred to as its acute oral lethal dose fifty, or LD50. The acute oral LD50 for fluometuron in rats is 1,515 to 8,900 mg/kg, and in rabbits is 2,500 mg/kg. In mice and guinea pigs, it has an LD50 of about 800 to 900 mg/kg of body weight. In rabbits, its dermal LD50 is approximately 3,000 - 10,000 mg/kg (3, 15, 16, 18).

CHRONIC TOXICITY

Rats were fed 7.5, 75, or 750 mg/kg/day for 90 days. At the 750 mg/kg dose, decreased body weight and congestion in the spleen, adrenals, liver, and kidneys were evident. The NOAEL for this study was 7.5 mg/kg/day (100 ppm). When doses of 1.5, 15 or 150 mg/kg/day were fed to puppies for 90 days, congestion of the liver, kidneys and spleen occurred at the 150 mg/kg dose. No effects were seen at 15 mg/kg/day (400 ppm) (20).

Prolonged or repeated exposure to fluometuron may cause conjunctivitis (18).

The EPA has established a Lifetime Health Advisory (LHA) level of 90 micrograms per liter (ug/l) for fluometuron in drinking water. This means that EPA believes that water containing fluometuron at or below this level is acceptable for drinking every day over the course of one's lifetime, and does not pose any health concerns. However, consumption of fluometuron at high levels well above the LHA level over a long period of time has been shown to cause damage to the liver, kidneys and spleen in animals studies (19).

Reproductive Effects

There is a data gap in the information on the reproductive effects of fluometuron (13).

Teratogenic Effects

Pregnant rabbits were given doses of 50, 500 or 1,000 mg/kg/day by gavage during days 6 through 19 of gestation. An increase in the number of resorbed fetuses was found at all treatment doses. Reduction in maternal body weight and food consumption occurred at doses of 500 and 1,000 mg/kg/day (20).

Mutagenic Effects

In two separate assays, one on yeast and the other on bacterial cell cultures, fluometuron failed to cause mutations. Fluometuron interfered with DNA synthesis in the testes of mice given a single oral dose of 2,000 mg/kg (20).

Carcinogenic Effects

EPA has determined that there is not enough evidence that fluometuron causes cancer in animals to justify its classification as a carcinogen. Fluometuron is not classified as a carcinogen by the EPA (20). An increased incidence of liver-cell tumors in male mice was noted in a study of rats and mice. In the same study, no carcinogenic effects were observed in female mice or in rats of either sex (18). Mice that were given oral doses of 87 mg/kg for two years had evidence of liver tumors and leukemia, a condition characterized by uncontrolled growth in the number of white blood cells in the blood stream (7).

Organ Toxicity

Toxic injury to the liver, kidneys, gut and brain is induced when lethal doses of fluometuron are administered experimentally (10). An increase in spleen weight and in the incidence of abnormalities in red-blood cells, and decreased weight gain in females were observed in a 90-day study of rats (18).

Fate in Humans and Animals

Fluometuron is absorbed only slowly into the body from the gastrointestinal tract. 72 hours after rats were given oral doses of 50 mg/kg radio-labeled fluometuron, 15% of the dose was excreted in the urine and 49% in the feces. At the same time, radioactivity was detected in the rats' livers, kidneys, adrenal glands, pituitary glands, red blood cells, blood plasma and spleens, with the highest concentration found in red blood cells (20).

Excretion in the feces indicates that the compound remained in the gastrointestinal tract and was not absorbed into the bloodstream. Since fluometuron is stored only briefly in body tissues, a substantial amount of the herbicide is excreted intact (10).

ECOLOGICAL EFFECTS

Effects on Birds

The EPA characterizes fluometuron as ranging from being slightly toxic to practically nontoxic to birds (13). Eighty percent wettable powder fluometuron had an oral LD50 of more than 2,000 mg/kg in three- to four-month old female mallards. Signs of herbicide poisoning in these ducks included imbalance, falling, fluffed feathers, and hyperexcitability. These signs showed up in the ducks within 15 minutes of treatment and persisted for up to a week (5).

The lethal concentration fifty, or LC50, is concentration of a chemical in water or air which causes death in 50% of an experimental animal population after exposure for a specified length of time. The 8- day dietary LC50 in ppm for technical fluometuron is 4,620 for Japanese quail, 4,500 for mallard ducks, and 3,150 for ring-neck pheasants (15).

Effects on Aquatic Organisms

Fluometuron is slightly toxic to fish. The 96-hour LC50 of technical fluometuron is 47 ppm in rainbow trout, 96 ppm in bluegill sunfish, and 55 ppm in catfish (15).

Effects on Other Animals (Nontarget species)

Fluometuron is relatively nontoxic to wildlife and bees (15).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

The capacity for fluometuron to move through the ground varies with the soil type to which it is applied. It was very mobile in both sandy and silt loam soils (20). Its mobility and herbicidal activity both decrease as the organic matter content of the soil increases (10). Fluometuron is readily soluble in water (110 ug/ml) (17). While the relatively easy movement of this herbicide through the soil improves its capacity to control weeds that germinate deep in soil, such mobility, or leaching, increases its potential to contaminate groundwater (15). Fluometuron has been placed on the EPA list of possible groundwater contaminants (13). Although it was not found in groundwater during a national survey, the EPA considers fluometuron to be one of the pesticide compounds with the greatest potential for leaching into groundwater (14).

Degradation of fluometuron by soil microbes may be very rapid. Some field and lab soil dissipation studies show a half-life of approximately 30 days, while others indicate that this period is less than 24 weeks (14). Residues of fluometuron have dissipated to levels that were not detectable (less than 0.10 ppm) within four months of the last application at normal usage rates (15). A European study indicated that in sandy clay loams, fluometuron dissipates with a half-life of less than 340 days (13). A soil half-life as short as 11 days has been reported (17). Field studies show that runoff from soil into surface waters is insignificant, with an average loss of less than 1% of the total fluometuron applied (15).

Photodecomposition is not expected to occur in the field because of application methods. Volatilization is not a significant route of dissipation of fluometuron in the field (15).

Breakdown of Chemical in Water

Fluometuron products should not be applied to water or wetlands, and cleaning of equipment or disposal of waste related to this herbicide can contaminate water (13). The half-life of fluometuron in water (hydrolysis half-life) is 110 to 144 weeks (14). At 20 degrees C, half- life values of fluometuron aqueous solutions with pH 5 to 9, are between 730 and 1,010 days. It is stable at pH values ranging from one to 13, at this temperature (15). Exposure of 10 ppm aqueous solutions of fluometuron to natural sunlight resulted in 88% decomposition in 3 days, with a half-life of 1.2 days.

Breakdown of Chemical in Vegetation

Fluometuron is more readily absorbed by roots from soil application, than by leaves from foliar application. The addition of a surfactant or nonphytotoxic oil to spray solutions improves the absorption of fluometuron by leaves. Fluometuron has been shown to undergo a 3-step degradation process in plants. The rate at which it is absorbed, translocated, and subsequently broken down, or metabolized, differs with various plant species. An understanding of these differences is important in determining the tolerance or susceptibility of plants and weeds to this chemical (15). Cotton exhibits a remarkable ability to breakdown fluometuron (10). All fluometuron product labels warn against the crop injury which may result if any crops other than sugarcane or cotton are planted within a one-year period after the last application of this material (13). The following crop plants may have special sensitivities to fluometuron: sugarbeets, red beets, cole crops, cucurbits, and eggplant (15).

PHYSICAL PROPERTIES AND GUIDELINES

Fluometuron is a white to tan powder or crystalline material with an amine-like odor. It is nonflammable and noncorrosive (15, 18). It is compatible with other herbicides (10). While it is stable at room temperature, fluometuron is broken down (hydrolyzed) by acids or bases at elevated temperatures (13, 18). It poses a fire and explosion hazard in the presence of strong oxidizers. Fluometuron is stable under normal temperatures and pressures, but it may pose a slight fire hazard if exposed to heat or flame and containers may explode in the heat of a fire. Thermal decomposition may release highly toxic fumes of fluorides and oxides of nitrogen and carbon (18). Runoff from fire control water may also give off poisonous gases and cause pollution (11).

Fluometuron should be kept out of the reach of children and domestic animals. It may be harmful if swallowed. Breathing of, and eye contact with, fluometuron dust should be avoided. Dust may be irritating to the lungs and eyes (15). Mixers, loaders and applicators must wear protective clothing when handling this product. Protective clothing includes coveralls, long-sleeved shirt, shoes, impermeable gloves, and eye protection (13).

Formulations of fluometuron intended for cotton use should not be applied within six days of cotton harvest. Foliage from fluometuron- treated cotton plants must not be fed to livestock. Sugarcane formulations should not be applied within 180 days of harvest, and livestock must not be grazed in treated fields (13).

Occupational Exposure Limits:

No occupational exposure limits have been established for fluometuron by OSHA, NIOSH, or ACGIH (18).

Physical Properties:

CAS #: 2164-17-2
Specific gravity: 1.39 (18)
H20 solubility: 90 ppm (14) 0.0105 % at 20 degrees C (18)
Solubility in other solvents: at 20 degrees C, acetone, 15%; chloroform, 2%; methanol, 14%; hexane <4%(13). Fluometuron is readily soluble in organic solvents (16). Slightly soluble in hexane (18).
Melting Point: 163-164 degrees C (325-329 degrees C) (15)
Vapor pressure: 5 x 10 to the minus 7 power mm Hg at 20 degrees C (15)
Kow: log Kow: 1.34 (9)
Koc: 175; 370 (calc) (14)
Kd: Class 3, Intermediate (14); (PC - partition coefficient): 174 (8)
Chemical Class/Use: Substituted urea herbicide
NOEL: 7.5 mg/kg for rats; 400 ppm for dogs (13)

BASIC MANUFACTURER

Ciba-Geigy Corporation
Agricultural Division
PO Box 18300
Greensboro, NC 27419

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received: April, 1992

REFERENCES

  1. Berg, G. L., ed. 1988. Farm chemicals handbook. Willoughby, OH: Meister Publishing Company.
  2. Dreisbach, R. H. 1983. Handbook of poisoning: prevention, diagnosis and treatment. Eleventh edition. Los Altos, CA: Lange Medical Publications.
  3. Gosselin, R. E., et al. 1984. Clinical toxicology of commercial products. Fifth edition. Baltimore, MD: Williams and Wilkins.
  4. Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and human health. NY: Springer-Verlag.
  5. Hudson, R. H., et al. 1984. Handbook of toxicity of pesticides to wildlife. Second edition. U. S. Department of the Interior. Fish and Wildlife Service. Resource Publication 153. Washington, DC: US Government Printing Office.
  6. Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer- Verlag, Inc.
  7. National Institute for Occupational Safety and Health (NIOSH). 1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH: NIOSH.
  8. Rao, P. S. C., et al. 1983 (Sept.). Pesticides and their behavior in soil and water. Florida Cooperative Extension Service. Institute of Food and Agricultural Sciences, University of Florida. Soil Science fact sheet adapted from: Herbicide injury, symptoms and diagnosis, Skroch and Sheet, eds. 1981 (Dec.). North Carolina Agricultural Extension Service. AG-85.
  9. Smith, C. N. 1981. Partition coefficients (Log Kow) for selected chemicals. In US EPA, 1984. User's Manual for the Pesticide Root Zone Model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  10. TOXNET. 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.
  11. U. S. Department of Transportation. 1983. 1984 Emergency response guidebook. Guidebook for hazardous material incidents. G-31. Washington, DC.
  12. U. S. Environmental Protection Agency. 1987 (Feb.). Environmental News. Office of Public Affairs (A-107). Washington, DC.
  13. _____. 1985 (Dec). Chemical fact sheet for fluometuron. Fact sheet no. 88.
  14. _____. 1984. Memorandum from Stuart Z. Cohen. List of potential groundwater contaminants. Office of Pesticides and Toxic Substances. Washington, DC. Photocopy.
  15. WSSA Herbicide Handbook Committee. 1989. Herbicide Handbook of the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL.
  16. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  17. 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.
  18. Occupational Health Services, Inc. 1991 (Feb. 21). MSDS for Fluometuron. OHS Inc., Secaucus, NJ.
  19. U. S. Environmental Protection Agency. 1989 (Jan.). Health Advisory Summary: Fluometuron. US EPA, Washington, DC.
  20. _____. 1988 (Aug.). Fluometuron: Health Advisory. Office of Drinking Water, US EPA, Washington, DC.