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.
| |
Pesticide
Information
Profile
|
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
U.S. Environmental Protection Agency (1983-85). Chemical
Information Fact Sheet. Office of Pesticides and Toxic Substances,
Office of Pesticide Programs (TS-766C)
National Library of Medicine (1992). Hazardous Substances
Databank. TOXNET, Medlars Management Section, Bethesda, MD.
U.S. Environmental Protection Agency (1987). Health Advisory,
Office of Drinking Water. August.
Beste, C.E., Chairman (1983). Herbicide Handbook of the Weed
Science Society of America. Weed Science Society of America, Champaign,
IL.
Chemical Information Systems, Inc. (1988). Oil and Hazardous
Materials/Technical Assistance Data System, Baltimore, MD.
Worthing, Charles R., Editor (1983). The Pesticide Manual, A World
Compendium. The British Crop Protection Council, The Ravenham Press
Limited, Ravenham, Suffolk, England.
Food and Drug Administration (1986). The FDA Surveillance Index.
Bureau of Foods, Dept of Commerce, National Technical Information
Service, Springfield, VA.
Howard, Philip H. 1991. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals. Lewis Publishers, Chelsea, MI.
The Agrochemicals Handbook. 1991. The Royal Society of Chemistry.
Cambridge, England.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
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.
To Top
For more information relative to pesticides and their use in New York State, please contact the PMEP staff at:
| |
5123 Comstock Hall
Cornell University
Ithaca, NY 14853-0901
(607) 255-1866
|
PLEASE NOTE: If you are not in New York State, you must contact the appropriate
agency for your area.
|
 |
This site is supported, in part, by funding from the
 |
Questions regarding the development of this web site should be directed to the
PMEP Webmaster