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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


The compound is found in a variety of commercial herbicides including Lasso, Lariat, and Crop Star. It also mixes well with other herbicides such as Bullet, Freedom, and Rasta and in mixed formulations with atrazine, glyphosate, trifluralin and imazaquin (1,12).

Alachlor is a Restricted Use Pesticide (RUP). Restricted Use Pesticides may be purchased and used only by certified applicators.


Alachlor is an aniline herbicide used to control annual grasses and certain broadleaf weeds in field corn, soybeans and peanuts. It is a selective systemic herbicide, absorbed by germinating shoots and by roots. The compound works by interfering with a plants ability to produce (synthesize) protein and by interfering with root elongation (4, 10).



Alachlor carries the signal word DANGER on the label not because of its acute oral toxicity, which is fairly low, but rather due to its potential to cause cancer in laboratory animals (see subsection on carcinogenicity).

The rat oral LD50 is between 930 mg/kg and 1,350 mg/kg. The LD50 of alachlor is between 1,910 and 2,310 mg/kg in the mouse (5). The dermal LD50 in rabbits is 13,300 mg/kg, but some of the formulated materials can be more toxic, with dermal LD50 values ranging from 7,800 to 16,000 mg/kg (6). Skin irritation is slight to moderate. The inhalation LD50 in rats is greater than 5.1 g/m3 for four hours of exposure(5) and greater than 23.4 g/m3 for six hours of exposure (1).


An early study on rats and dogs given diets containing low to moderate amounts of alachlor (1 to 100 mg/kg/day) showed no adverse effects over the 90 day study (6). However, a six-month dog study showed related liver toxicity at all doses above 5 mg/kg/day and a one- year study established a No Observable Effect Level (NOEL) of 1 mg/kg based on effects in the liver, spleen and kidney. In two-year rat studies the NOEL was placed at 2.5 mg/kg based on irreversible degeneration of the iris and related structures of the eye (5). While the record may be a bit confusing it is clear that there are distinct chronic effects to rats and dogs at relatively low doses over a period of time.

Reproductive Effects

Rats fed small amounts of alachlor (3, 10 and 30 mg/kg) over three generations produced renal toxicity in second generation males and in third generation males and females (7). In another rat study, high oral doses (400 mg/kg) fed during the sensitive period of gestation resulted in maternal and fetal toxicity (5). There was no indication in the report that reproduction was affected.

Teratogenic Effects

In a rabbit study moderate oral doses of 50 to 450 mg/kg resulted in only maternal and fetal toxicity (no birth defects appeared in the offspring) at the 150 mg/kg dose (11). There is little or no teratogenic potential of the compound (5) and it poses little risk of birth defects among humans.

Mutagenic Effects

A variety of microbial mutagenicity assays with various strains and with numerous concentration were all negative.

Carcinogenic Effects

Two rat studies at high doses have clearly demonstrated the development of stomach, thyroid, and nasal turbinate tumors (5).

A mouse study of 18 months with levels from 26 to 260 mg/kg/day showed an (equivocal) increase of lung tumors at the highest dose for females but not males (5). These findings however are not widely accepted. There is still some debate about the oncogenic potential of alachlor in mice.

Alachlor is classified by the United States Environmental Protection Agency as a (Group B2) probable human carcinogen. While the information is adequate for animal studies it is incomplete for human risks of cancer. Despite the incomplete record of human carcinogenicity due to alachlor, the EPA has required the Danger signal word on product labels based on alachlor's potential to cause tumors in rats.

Organ Toxicity

Other than cancer, liver toxicity and eye lesions are the principal chronic toxic effects to organs seen in various studies (5).

Fate in Humans and Animals

Rats given a single low dose of alachlor (14 mg/kg) eliminated nearly all of the compound in 10 days, most within the first 48 hours (5). About a third to a half of the alachlor and its breakdown products were excreted in urine and nearly a half in feces. Rats absorbed close to three quarters of a single low dose (14 mg/kg) while only 8-10 percent was absorbed through the skin in monkeys (5). In animals, alachlor is rapidly broken down to mercapturic acid, glucuronic acid, and sulfate which pose little toxic threat to the organism.

Cattle and poultry fed very small amounts of alachlor for 30 days had no residues in the milk, eggs or tissue. There were very low levels of alachlor found in the muscle of swine (7). A two-year rodent study showed the amount of alachlor in tissue was related to the amount of blood in an organ (5). There is no evidence that the compound accumulates in animal tissue.


Alachlor is only moderately toxic to aquatic invertebrates and to fish. The 96-hour LC50 for alachlor is 2.4 mg/l in rainbow trout and 4.3 mg/l bluegill sunfish (2). Other 96-hour LC50 values for the pesticide are: 6.5 mg/l (catfish), 4.6 mg/l (carp), and 19.5 mg/l (crayfish) (4).

The compound is slightly toxic to practically non-toxic to wildfowl. Alachlor has a five-day LC50 of greater than 5,000 ppm in young mallards and bobwhite quail (6). The LD50 of alachlor in other mallards was greater than 2,000 mg/kg (3). Pheasants have an LC50 of greater than 10,000 ppm (4).

Alachlor should not pose a problem for bees when used as directed. The product is practically non-toxic to earthworms (11).


Alachlor persists in soil from two weeks to a month, depending on soil type and climate (1). About half of the compound remains in soil after eight days (7). The main means of degradation is by soil microbes (6). It has moderate mobility in sandy and silty soils and thus can migrate to groundwater (5). The single largest groundwater testing program (National Alachlor Well Water Survey) for a pesticide was conducted for alachlor throughout the last half of the 1980s. Over six million private and domestic wells were tested for the presence of the compound (13). Less than one percent of all of the wells had detectable levels of alachlor. Detection of the chemical in well water was more common where the herbicide was used more intensively (13). Concentrations of the pesticide in the one percent of the wells where the compound was detected ranged from 0.1 ppb to 1.0 ppb. The majority of these wells had concentrations around 0.2 ppb (13).

No parent compound was found after three weeks when alachlor was applied to plants. It rapidly metabolized to water-soluble products with the acid product accumulating in the plant (7). Absorption is primarily by germinating shoots (2) and it is readily translocated throughout the plant. Higher concentrations appear in the vegetative parts than in the reproductive parts of the plant. In plants alachlor is almost completely metabolized within ten days (4).

Physical Properties:

Common Name: alachlor
CAS #: 2-chloro-N-(2,6-diethylphenyl)-N-(methoxymethyl) acetamide
Chemical class/use: aniline/herbicide
Solubility in water: 240 mg/l at 25 degrees C
Solubility in other solvents: soluble in most organic solvents
Melting Point: 39.5-41.5 degrees C
Vapor Pressure: 1.4 x 10 to the minus 5 power mm Hg
Partition Coefficient: 434

Exposure Guidelines:

NOEL (dog): 1 mg/kg/day, based on an increase in iron stores
ADI: 0.0025 mg/kg (EPA, disputed study)
DWEL: 0.4 mg/l at 10 to the minus 4 power
Q*: 6.0 x 10 to the minus 2 power
TLV-TWA: 5 mg/m3 total dust
LEL (dog): 3 mg/kg/day
RfD: 0.01 mg/kg/day
MCL: 0.002 mg/l


Monsanto Company
800 N Lindbergh Blvd
St Louis, MO 63167
Telephone: 314/694-1000
Emergency: 314/694-4000

Review by Basic Manufacturer:

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


  1. The Agrochemicals Handbook. (1991) The Royal Society of Chemistry, Cambridge, England.
  2. Johnson, W.W. and M.T. Finley (1980). Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. U. S. Dept of the Interior, Fish and Wildlife Service, Resource Publication 137.
  3. Hudson, R.H., R.K. Tucker, and M.A. Haegele (1984). Handbook of Toxicity of Pesticides to Wildlife. U. S. Dept of the Interior, Fish and Wildlife Service, Resource Publication 153.
  4. National Library of Medicine (1992). Hazardous Substances Databank. TOXNET, Medlars Management Section, Bethesda, MD.
  5. U. S. Environmental Protection Agency (1987). Health Advisory, Office of Drinking Water.
  6. Beste, C.E., Chairman (1983). Herbicide Handbook of the Weed Science Society of America. Weed Science Society of America, Champaign, IL.
  7. Food and Drug Administration (1986). The FDA Surveillance Index. Bureau of Foods, Dept of Commerce, National Technical Information Service, Springfield, VA.
  8. National Research Council (1987). Regulating Pesticides in Food, The Delaney Paradox, National Academy Press, Washington, D.C.
  9. Occupational Health Services, Inc. (1988). Hazardline, New York, NY.
  10. Walker, Mary M. and Lawrence H. Keith. (1992). EPA's Pesticide Fact Sheet Database. Lewis Publishers. Chelsea, MI.
  11. Alachlor Technical (94%) Material Safety Data Sheet. (1991). Monsanto Company, St Louis, MO.
  12. Farm Chemicals Handbook. (1992). Meister Publishing. Willoughby, OH.
  13. Holden, Larry, and Jeffery A. Graham. (1992). Results of the National Alachlor Well Water Survey. Environmental Science and Technology 26: 935-943.