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
Publication Date: 9/93
TRADE OR OTHER NAMES
Trade names include Afalon, Afalon Inuron, DuPont 326, Garnitan,
Hoe 002810, Linex, Linorox, Linurex, Lorox, Premalin, Sarclex, and
Sinuron. Linuron is often used in formulations with other herbicides,
insecticides and fungicides.
Linuron is a substituted urea herbicide used to control annual and
perennial broadleaf and grassy weeds on crop and noncrop sites. It is
used as a pre and a postemergent herbicide. It works by inhibiting
photosynthesis in target weed plants. It is labeled for use in soybean,
cotton, potato, corn, bean, pea, winter wheat, asparagus, carrot, and
fruit crops. It is also used on crops stored in warehouses and
Linuron is a Restricted Use Pesticide (RUP). Restricted Use
Pesticides may be purchased and used only by certified applicators.
Linuron is of low toxicity and is labeled with a CAUTION signal
word. The oral LD50 is 1,500 mg/kg for rats (8) and 2,400 mg/kg for
Rabbits' eyes were mildly irritated when exposed to one high dose
of dry linuron powder. The irritation subsided in two days (4).
Linuron is mildly irritating to eyes and skin. Chronic effects
have been noted relating to the production of tumors in the liver and
testes of rats and mice as noted under "Carcinogenicity."
The EPA is requiring additional long term testing to fully assess
the reproductive potential of linuron (11). There is some evidence to
suggest that linuron interferes with the hormone testosterone in horses
at relatively low doses. No effects on reproduction were noted.
Pregnant rabbits fed high doses of linuron during the sensitive
period of pregnancy had normal offspring (7). This suggests that
linuron does not cause birth defects, but further studies are needed to
confirm this conclusion.
Linuron caused mutations in one microbial assay (2). But, in
another study (Ames test) and in several tests using mice, linuron was
not mutagenic. Thus, it appears that linuron is either non-mutagenic or
possibly only slightly mutagenic.
Several tests have shown that linuron has little or no mutagenic
potential. Additional studies are being required before EPA will
determine what the mutagenic risks is to humans.
Linuron is classified by the EPA as a possible human carcinogen.
Several animal studies of mice, rats and dogs have shown that linuron
produces benign liver or testicular tumors, but no malignant (cancerous)
ones. In these two-year studies, rats and mice were fed low doses (2.5
mg/kg/day) of linuron (7).
Rats and dogs fed various doses of linuron for two years had very
small levels of residues from linuron in their blood, fat, liver, kidney
and spleen. However, these did not seem to be associated with adverse
effects (3, 7).
Fate in Humans and Animals
In rats, linuron breaks down completely to several products after
passing through the liver (3, 7). Rats fed a wide range of doses (up to
125 mg/kg) for 2 years had only a minute portion of the amount ingested
in their body tissues at the end of the 2 years. The highest level
observed in tissue was 100 ppm (3).
Linuron is highly toxic to non-target aquatic organisms such as
fish and shellfish. The LC50 for linuron in trout and bluegill is 16
mg/l, and 40 mg/l in crawfish. It is moderately toxic to wild birds.
Its LC50 in mallard ducks is 3,000 mg/kg, 3,500 mg/kg in pheasants, and
5,000 mg/kg in quail (4, 6, 7, 9). Product labeling states that the
compound should not be allowed to enter lakes or streams.
Linuron is non-toxic to bees.
In the environment, linuron is broken down, mainly by microbes,
into a much less active metabolite: 3,4-dichloroaniline (4), and carbon
Linuron is a selective herbicide which is most readily absorbed
through the root system. It accumulates and metabolizes differently in
different plants. Susceptible plants transport linuron through the
foliage, while tolerant plants can metabolize linuron into inactive
products (1). Linuron inhibits photosynthesis in susceptible plants
causing them to lose color, wilt, and die. In crops, linuron has low
residual action and persistence.
Linuron is moderately persistent in soils. In the presence of
oxygen in soil (aerobic conditions in the lab), linuron's half-life was
75 days, while it was 230 days under field conditions (5). This
chemical is bound to soil (especially clay) and organic matter and does
not move freely. The movement of the compound decreases as the organic
content of the soil increases, however its herbicidal activity also
decreases with increasing organic content (10). Accumulation is not
expected in soil or in living organisms. If erosion occurs, linuron
moves with the eroding soil.
Linuron is slightly to moderately soluble in water, and is not
readily broken down in water. Humans have been exposed to linuron
through the runoff of linuron into surface waters after heavy spring
rains in Northwestern Ohio. It has also been found at very low
concentrations in well and groundwater in several states. The
concentrations were around 2 to 3 parts per billion.
PHYSICAL PROPERTIES AND GUIDELINES
Linuron is a substituted phenylurea herbicide. It is an odorless,
white crystalline solid. Its molecular weight is 249.11. The chemical
name for linuron is 3-(3,4-Dichlorophenyl)-1-methoxy -1-methylurea.
|NOEL: ||2.5 mg/kg/day
|RfD: ||0.002 mg/kg/day
|LEL: ||0.625 mg/kg/day
|CAS #: ||330-55-2
|Solubility in water: ||75 mg/l (8) at 25 degrees C (slightly to moderately soluble)
|Solubility in solvents: ||slightly soluble in aliphatic hydrocarbons moderately soluble in ethanol (15 x 104 ppm) (1), soluble in acetone (50 x 104 ppm) (1)
|Melting point: ||93-94 degrees C
|Boiling point: ||180-190 degrees C
|Vapor pressure: ||1.5 x 10 to the minus 5 power torr at 24 degrees C(8)
Drexel Chemical Company
P.O. Box 9306
2487 Pennsylvania St.
Memphis, Tennessee 38109
Du Pont Agricultural Products
P.O. Box 80038
Walker's Mill, Barley Mill Pl.
Wilmington, DE 19880-0038
Review by Basic Manufacturer - Drexel:
Comments solicited: October, 1992
Comments received: November, 1992
Review by Basic Manufacturer - Du Pont:
Comments solicited: October, 1992
Comments received: November, 1992
Ashton, F.M. and Crafts, A.S. 1973. Mode of Action of Herbicides.
pg. 22. New York: John Wiley & Sons Inc.
Epstein, S.S. and Legator, M.S. 1971. The Mutagenicity of
Pesticides. p. 182. The Massachusetts Institute of Technology.
National Library of Medicine. 1992. Hazardous Substances Databank
E.I. duPont de Nemours & Co. Product Information booklet on LOROX.
Rao, P.S.C., and Davidson, J.M. 1980. Estimation of pesticide
retention and transformation parameters required in nonpoint source
pollution models. In Environmental Impact of Nonpoint Source Pollution.
M.R. Overcashand J.M. Davidson, eds. Ann Arbor Science.
U.S. Environmental Protection Agency. Office of Pesticide
Programs. Pesticide Fact Sheet for Linuron. Fact Sheet No. 28. June
Wagner, S.L. Linuron. 1983. Clinical Toxicology of Agricultural
Chemicals. pp. 273-274. Noyes Data Corp.
Windholz, M., et al., eds. 1983. Linuron. pg. 790. The Merck
Index. 10th edition. Merck & Co. Inc.
The Agrochemicals Handbook. 1991. The Royal Society of Chemistry.
Menzer, Robert E. 1991. Water and Soil Pollutants in Casarett
and Doull's Toxicology: The Basic Science of Poisons. Mary O. Amdur,
John Doull, and Curtis D. Klaassen editors. Pergamon Press, NY.
Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet
Database. Lewis Publishers. Chelsea, MI.