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.
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Pesticide
Information
Profile
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Fluometuron
Publication Date: 3/94
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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
Berg, G. L., ed. 1988. Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Dreisbach, R. H. 1983. Handbook of poisoning: prevention,
diagnosis and treatment. Eleventh edition. Los Altos, CA: Lange
Medical Publications.
Gosselin, R. E., et al. 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides
and human health. NY: Springer-Verlag.
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.
Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer-
Verlag, Inc.
National Institute for Occupational Safety and Health (NIOSH).
1986. Registry of toxic effects of chemical substances (RTECS).
Cincinnati, OH: NIOSH.
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.
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.
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.
U. S. Department of Transportation. 1983. 1984 Emergency
response guidebook. Guidebook for hazardous material incidents. G-31.
Washington, DC.
U. S. Environmental Protection Agency. 1987 (Feb.).
Environmental News. Office of Public Affairs (A-107). Washington, DC.
_____. 1985 (Dec). Chemical fact sheet for fluometuron. Fact
sheet no. 88.
_____. 1984. Memorandum from Stuart Z. Cohen. List of potential
groundwater contaminants. Office of Pesticides and Toxic Substances.
Washington, DC. Photocopy.
WSSA Herbicide Handbook Committee. 1989. Herbicide Handbook of
the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
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.
Occupational Health Services, Inc. 1991 (Feb. 21). MSDS for
Fluometuron. OHS Inc., Secaucus, NJ.
U. S. Environmental Protection Agency. 1989 (Jan.). Health
Advisory Summary: Fluometuron. US EPA, Washington, DC.
_____. 1988 (Aug.). Fluometuron: Health Advisory. Office of
Drinking Water, US EPA, Washington, DC.
Disclaimer: Please read
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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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