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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.


Publication Date: 9/93


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 storerooms.

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 mice (3).

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."

Reproductive Effects

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.

Teratogenic Effects

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.

Mutagenic Effects

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.

Carcinogenic Effects

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).

Organ Toxicity

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 dioxide.

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.


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.

Exposure Guidelines:

NOEL: 2.5 mg/kg/day
RfD: 0.002 mg/kg/day
LEL: 0.625 mg/kg/day

Physical Properties:

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)
Koc: 860
Kd: nonionic


Drexel Chemical Company
P.O. Box 9306
2487 Pennsylvania St.
Memphis, Tennessee 38109
Telephone 901-774-4370

Du Pont Agricultural Products
P.O. Box 80038
Walker's Mill, Barley Mill Pl.
Wilmington, DE 19880-0038
Telephone: 800-441-7515

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


  1. Ashton, F.M. and Crafts, A.S. 1973. Mode of Action of Herbicides. pg. 22. New York: John Wiley & Sons Inc.
  2. Epstein, S.S. and Legator, M.S. 1971. The Mutagenicity of Pesticides. p. 182. The Massachusetts Institute of Technology.
  3. National Library of Medicine. 1992. Hazardous Substances Databank Linuron.
  4. E.I. duPont de Nemours & Co. Product Information booklet on LOROX.
  5. 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.
  6. U.S. Environmental Protection Agency. Office of Pesticide Programs. Pesticide Fact Sheet for Linuron. Fact Sheet No. 28. June 30, 1984.
  7. Wagner, S.L. Linuron. 1983. Clinical Toxicology of Agricultural Chemicals. pp. 273-274. Noyes Data Corp.
  8. Windholz, M., et al., eds. 1983. Linuron. pg. 790. The Merck Index. 10th edition. Merck & Co. Inc.
  9. The Agrochemicals Handbook. 1991. The Royal Society of Chemistry. Cambridge, England.
  10. 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.
  11. Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet Database. Lewis Publishers. Chelsea, MI.