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Diuron

Publication Date: 9/93

TRADE OR OTHER NAMES

Trade names for products containing diuron include Di-on, Crisuron, Diater, Karmex, and Unidron. It is often used in combination with other pesticides such as bromacil and hexazinone.

INTRODUCTION

Diuron is a substituted urea herbicide used to control a wide variety of annual and perennial broadleaf and grassy weeds. It is used to control weeds and mosses on non-crop areas and among many agricultural crops such as fruit, cotton, sugar cane and legumes. Diuron works by inhibiting photosynthesis.

Diuron is a general use pesticide.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Diuron has a low acute toxicity to mammals even though it carries the signal word WARNING on the label. The signal word is applied because the compound can cause eye and throat irritation. It is much less of an irritant to intact skin. The rat oral LD50 ranges from 1017 mg/kg to 3750 mg/kg. Some signs of central nervous system depression have been noted at high levels of diuron exposure. For humans, the only reported case of acute, oral exposure to the herbicide produced no significant symptoms or toxicity.

CHRONIC TOXICITY

Male rats given extremely high doses of diuron over a two-week period showed changes in their spleen and bone marrow. Other chronic effects attributed to moderate to high doses of the pesticide over time included changes in blood chemistry, increased mortality, growth retardation, abnormal blood pigment, and anemia. When fed small amounts of diuron in food for two years, animal species showed no adverse effects.

Reproductive Effects

Daily low doses of diuron fed to female rats through three successive generations (pregnancies) caused no effects except on body weight of offspring which significantly decreased in the second and third litters. The fertility rate remained unaffected.

Teratogenic Effects

Diuron, administered to pregnant rats on days 6 through 15 of gestation, produced no birth defects in the offspring at doses of up to 125 mg/kg. Moderate doses of 250 mg/kg caused wavy ribs, extra ribs and delayed bone formation. There were also weight decreases in offspring at 500 mg/kg. There was no increase in the severity of the rib deformation at this higher dose.

Pregnant mice given very high doses of diuron (nearly 2,000 mg/kg) exhibited reproductive and embryotoxic effects. Developmental effects were found in their offspring.

Mutagenic Effects

The majority of tests have shown that diuron does not produce mutations in animal cells or in bacterial cells. It is likely that, at levels of exposure normally encountered in the environment, diuron would not pose a mutagenic threat to humans.

Carcinogenic Effects

Limited evidence indicates that diuron, at low exposure levels, does not cause cancer in rats. There is no evidence to suggest it causes cancer in humans.

Organ Toxicity

Low doses of diuron over extended periods of time can cause enlargement to the liver and the spleen. The compound does not cause significant irritation to intact skin, and in test animals does not cause skin sensitization.

Fate in Humans and Animals

Excretion is in feces and urine in test animals. The predominant metabolite in dogs was 3,4-dichlorophenyl urea. Breakdown of the compound is similar in animals, plants and soil. First the methyl groups (CH3) are removed, and then the structure is broken apart.

Cows fed very low doses of diuron in their diets had small amounts of residues in whole milk. Cattle fed small amounts accumulated low levels of diuron in fat and muscle, liver, kidney. Little tissue storage under field conditions is anticipated.

ECOLOGICAL EFFECTS

LC50 values for diuron in several bird species have been established. For bobwhite quail, the oral LC50 is 1730 ppm. For Japanese quail and ring-necked pheasant it is greater than 5000 ppm. Mallard ducks have an LC50 of approximately 5,000 ppm (9). These values indicate that the compound is only slightly toxic to birds.

The 48-hour LC50 values for diuron range from 4.3 ppm to 42 ppm in fish and range from 1 ppm to 2.5 ppm for invertebrates. Thus diuron is moderately toxic to fish and highly toxic to aquatic invertebrates. The compound is non-toxic to bees.

ENVIRONMENTAL FATE

Diuron residues in soil are toxic to plants. Residue levels are lower in soils with low organic content. Residue half-lives are from one month to one year for the parent, five months for the methylurea derivative (DCPMU), and one month for the urea derivative (DCPU). Some pineapple fields contained residues three years after the last application.

Mobility in the soil is related to organic matter and to the type of the residue. The metabolites are less mobile than the parent.

Diuron levels in irrigation water were highest after the initial flush but declined rapidly as a result of dilution. It is relatively stable in neutral water. In California, diuron has been found in groundwater in the 2 to 3 ppb range. It has also been found in Ontario and has been linked with land applications (8). Microbes are the primary factor in the degradation of diuron in aquatic environments. Diuron is not expected to concentrate in aquatic organisms.

Diuron is readily absorbed through the root system of plants and less readily through the leaves and stems. In cotton leaves, DCPU was the main metabolite and in soybean leaves DCPMU was dominant.

Exposure Guidelines:

NOEL (dog): 0.625 mg/kg/day
DWEL: 0.07 mg/l
HA: 0.01 mg/kg/day (lifetime)
TLV-TWA: 10 mg/m3
RfD: 0.0002 mg/kg/day (EPA)
LEL: 3.1 mg/kg/day (dog)

Physical Properties:

CAS #: 330-54-1
Chemical name: N-(3,4-dichlophenyl)-N,N-dimethyl urea
Chemical class/use: substituted urea herbicide
Solubility in water: 42 ppm at 25 degrees C
Solubility in other solvents: acetone 5.3 g/100 g; benzene 0.12 g/100 g; butyl stearate 0.14 g/100 g
Melting Point: 158-159 degrees C
Vapor Pressure: 3.1 x 10 to the minus 6 power mm Hg
Partition Coefficient: 2.77 (octanol/water; log transformed)

BASIC MANUFACTURER

E. I. du Pont
Agric Products Dept
Walker's Mill, Barley Mill Plaza
Wilmington, DE 19880-038
Emergency: 800/441-3637
Toll free: 800/441-7515

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: November, 1992

REFERENCES

  1. U.S. Environmental Protection Agency (1983-85). Chemical Information Fact Sheet. Office of Pesticides and Toxic Substances, Office of Pesticide Programs (TS-766C)
  2. National Library of Medicine (1992). Hazardous Substances Databank. TOXNET, Medlars Management Section, Bethesda, MD.
  3. U.S. Environmental Protection Agency (1987). Health Advisory, Office of Drinking Water. August.
  4. Beste, C.E., Chairman (1983). Herbicide Handbook of the Weed Science Society of America. Weed Science Society of America, Champaign, IL.
  5. Chemical Information Systems, Inc. (1988). Oil and Hazardous Materials/Technical Assistance Data System, Baltimore, MD.
  6. Worthing, Charles R., Editor (1983). The Pesticide Manual, A World Compendium. The British Crop Protection Council, The Ravenham Press Limited, Ravenham, Suffolk, England.
  7. Food and Drug Administration (1986). The FDA Surveillance Index. Bureau of Foods, Dept of Commerce, National Technical Information Service, Springfield, VA.
  8. Howard, Philip H. 1991. Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Lewis Publishers, Chelsea, MI.
  9. The Agrochemicals Handbook. 1991. The Royal Society of Chemistry. Cambridge, England.