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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 for products containing metolachlor include Bicep, CGA-24705, Dual, Pennant, and Pimagram. The compound may be used in formulations with other pesticides (often herbicides that control broad leaved weeds) including atrazine, cyanazine, and fluometuron.


Metolachlor is usually applied to crops before plants emerge from the soil. It is used to control certain broadleaf and annual grassy weeds in field corn, soybeans, peanuts, grain sorghum, potatoes, pod crops, cotton, safflower, stone fruits, nut trees, highway right-of-ways and woody ornamentals.

Metolachlor acts by inhibiting protein synthesis. High-protein crops can be adversely affected by metolachlor applications (13). Certain additives included in product formulations to help protect sensitive crops like sorghum from injury.

Metolachlor is a general use pesticide.



Metolachlor is a slightly toxic chemical with a CAUTION signal word on its product labels. Metolachlor is not very acutely toxic to humans. Human exposure most commonly occurs through skin or eye contact. It is more dangerous when inhaled than when ingested. Signs of human intoxication from metolachlor include abdominal cramps, anemia, shortness of breath, dark urine, convulsions, diarrhea, jaundice, weakness, nausea, sweating, and dizziness (12).

The acute oral LD50 in rats for technical grade metolachlor is from 1,200 mg/kg (7) to 2,780 mg/kg (11). The oral LD50 of Dual 8E, a product containing metolachlor, is 2534 mg/kg in rats (5, 10). The 4-hour exposure inhalation LC50 of technical metolachlor for rats is greater than 1.7 ppm (11). The inhalation LC50 of Dual 8E in rats is greater than 6.0 ppm for 4 hours (5). The dermal LD50 in rabbits is greater than 10,000 mg/kg for technical-grade metolachlor, and is greater than 5,009 mg/kg for the product Dual 8E (5, 11). Moderate exposure to metolachlor can cause slight skin irritation. While these results indicate that metolachlor has a low dermal toxicity to humans, this chemical could cause skin sensitivity.


While metolachlor is not readily absorbed by the skin, repeated dermal exposures may create skin sensitization, especially among those who work with metolachlor. Except for skin sensitization studies, not enough information is available to accurately determine the chronic effects of metolachlor in humans.

In rats fed metolachlor for ninety days, the level at which no adverse compound related effects were noted was about 90 mg/kg/day (15). This indicates that the compound is capable of causing chronic toxic effects at exposure levels substantially below levels that cause acute toxicity.

Reproductive Effects

Overall the evidence suggests that metolachlor has little or no effect on reproduction at commonly encountered levels. In two long-term rat reproduction studies, mating, gestation, lactation, and fertility were not affected at the low doses administered (50 mg/kg) (12). However, pup weights and parental food consumption decreased at this low dose. Another two-year test caused the wasting of testicles at moderate doses (150 mg/kg) (12).

Teratogenic Effects

Studies to date indicate that metolachlor does not cause birth defects, even at doses which cause toxic effects in the mother. In one rat study, pregnant rats fed high doses of metolachlor during the sensitive period of pregnancy had normal offspring. No toxic effects in the fetuses were seen. At the highest dose, a decrease in food consumption was observed in the mother (4, 11). In another study, pregnant rabbits were fed high doses during the sensitive period. While the mothers showed toxicity to the chemical, none of the 319 offspring showed any birth defects (12).

Mutagenic Effects

Metolachlor is clearly non-mutagenic. Metolachlor tested negative in two bacterial assays. In studies on mice, no effects were noted on fertility, zygote or embryo survival rates after very high single oral doses. No malformations of embryos were reported (4). Also, no mutagenicity effects were noted in a standard mouse test (11). From this evidence it is unlikely that the compound would pose a major mutagenic threat to humans.

Carcinogenic Effects

Metolachlor shows limited carcino-genicity in animals. Male and female mice exposed to high doses for 18 to 20 months did not develop cancer (12). But, female rats given high doses for two years showed a significant increase in new growths, nodules, and lesions in livers (11, 12). Because of the limited, evidence of carcinogenicity and lack of human data, metolachlor is classified as a possible human carcinogen (9, 12).

Organ Toxicity

Exposure to metolachlor can damage the liver and irritate the skin, eyes, and mucous membranes. It has also caused skin sensitization in guinea pigs (11, 12).

In a two-year study of rats fed moderate doses (150 mg/kg), no negative effects on mortality or organ weights were observed. However, females fed metolachlor did not gain as much weight as the female controls, and both sexes showed microscopic changes in their livers (12).

Fate in Humans and Animals

Metabolism studies show that orally administered metolachlor is quickly broken down into metabolites and is almost totally eliminated in the urine and feces of goats, rats, and poultry. Metolachlor itself was not detected in the urine, feces, or body tissues (4). Rats, given a single oral dose of metolachlor, excreted 70 to 90 percent of the metolachlor as metabolites within 48 hours (12).

In animals, trace amounts of metolachlor metabolites were found in kidneys, liver, blood, and milk. But, no residues were found in eggs, meat, or fat samples of laying chickens. It is unlikely the compound would concentrate in organisms through the food chain.


Metolachlor is moderately toxic to both cold and warm water fish, including rainbow trout, carp, and bluegill sunfish. The 96 hr LC50 values for this compound in rainbow trout, carp and bluegill sunfish are 2.0, 4.9 and 15.0 mg/kg respectively.

Studies on algae and fish exposed to metolachlor in water indicate that very little is accumulated and that any accumulated material is excreted rapidly when the organisms are placed in clean water (4). Residues in fish were quite low and do not pose a threat to human health.

Wildfowl can tolerate metolachlor exposure. Both the mallard and the bobwhite quail can survive five day exposures of greater than 10,000 mg/kg, an indication that metolachlor is practically nontoxic to upland game birds and waterfowl (4). However, although mallard ducks showed no impairment of reproductive capabilities at high level long-term exposures, bobwhite quail fed a diet containing high levels of metolachlor for 17 weeks during mating, egg laying, and egg hatching produced fewer chicks.


Metolachlor, applied before plants emerge, is absorbed through shoots just above the seed, and may be absorbed from the soil into and through the roots. This chemical acts by inhibiting the production of essential plant components like chlorophyll and protein. Thus, metolachlor is a growth inhibitor affecting root and shoot growth after seeds have germinated.

The breakdown of metolachlor in corn, soybean, peanuts, and sorghum is similar. Metabolites are found in varying levels throughout the plant. For example, the roots, grain, and oil contain little, if any, residues of metolachlor or its metabolites. However the plants retain their metolachlor metabolites. Animals which eat these plants are able to rapidly break down and eliminate the chemical. Livestock should not be fed foliage from crops such as cotton because the leaves can hold metolachlor residues at much higher levels than the seeds.

Metolachlor is mobile in the soil, is easily leached, and resists breakdown for long periods of time. The breakdown of the compound is affected by temperature, moisture, microbe activity, amount of leaching, soil type, nitrification, oxygen concentrations and sunlight. Soil metabolism primarily occurs by both aerobic and anaerobic microorganisms. Some of these microorganisms can rapidly break down the chemical if the organisms are provided with enough energy. In one study using an aerobic bacterium, complete breakdown occurred in 16 days (8). Anaerobic degradation rates are even slower (4).

Any temperature and moisture changes which affect microbial activity will also affect the breakdown of this herbicide. As temperature increases, the degradation rate also increases. Also, the deeper the chemical is in the soil, the less organic matter and fewer soil microbes are present, so the herbicide takes longer to degrade. Most of acetanilide herbicides, of which metolachlor is a member, are lost through microbial decomposition (17).

Breakdown by sunlight is another important degradation pathway. About fifty percent of applied metolachlor was found to have degraded on sunlit soil over a period of eight days. But, if this chemical was incorporated into the top two inches of soil, then degradation by photolysis was minimal (6% over one month) (4).

Metolachlor degradation also depends on binding to the soil. Breakdown rates decrease, and binding increases, with increased soil organic matter and clay content. Half-lives of 30 to 50 days in northern areas, and 15 to 25 days in southern areas have been observed (17). However, clay loams have significant soil water content and this contributes to more rapid breakdown. Half-lives found in the field were 17 days in clay loams at an average temperature of 20 degrees C, and 23 days in sandy loams at an average temperature of 23 degrees C (17).

Metolachlor is moderately persistent in silt loams, taking 10.1 weeks to halve the initial herbicide concentration from a depth of 10 to 20 cm at 23 degrees C (1). Extensive leaching occurs, especially in soils with low organic content (4). Very little metolachlor volatilizes from the soil.

Metolachlor is stable to breakdown in water over a wide water acidity. Its half-life at 20 degrees C is more than 200 days in highly acid waters and, in highly basic waters, the half-life is 97 days (4). Metolachlor is also relatively stable in water under natural sunlight. About 6.6 percent was degraded by sunlight in 30 days, a slow and minimal rate (4).

Because of the slow microbial and anaerobic degradation rates of this chemical and its ability to leach through soil, metolachlor has the potential to contaminate groundwater. Leaching is greatest if the soils are coarse and the ground water is near the surface. Metolachlor was one of four pesticides that were extensively studied throughout the nation in the National Alachlor Well Water Survey. This several year project analyzed the contents of over six million private and domestic well. Metolachlor was detected in about one percent of the wells (about 60,000 wells) at concentrations ranging from 0.1 to 1.0 ppb (11, 12, 18).

Metolachlor has been found in 1,644 of 1,997 surface water samples from 312 locations in 14 states, at the maximum concentration of 138 ppb (12). These levels may result from runoff during spring and summer applications in crop fields (11).


Pure metolachlor is an odorless, off-white to colorless liquid at room temperature. In formulations, its color ranges from opaque white to tan. It is a member of the chloracetanilide chemical family, with a molecular weight of 283.46. The chemical name for metolachlor is 2-chloro-N-(2-ethyl-6- methylphenyl)-N-(2-methoxy-1-methylethyl) acetamide.

Technical metolachlor is stable for at least one year at room temperature (4). The shelf storage life of Dual 8E is 3-5 years when in a dry place (5).

Exposure Guidelines:

NOEL: 1.5 mg/kg/day (dog); 2.5 mg/kg/day (rat)
ADI: 0.092 mg/kg/day (11)
MPI: 0.075 mg/day (4)
Drinking water
health advisory:
Drinking water equivalent level: 0.525 mg/L

Physical Properties:

CAS #: 51218-45-2
Solubility in water: 530 ppm (at 20 degrees C) (15)
Solubility in solvents: very soluble in benzene, dichloromethane, hexane, methanol, and octan-1-ol;
miscible with xylene toluene, dimethyl formamide, methyl cellusolve, butyl cellusolve, ethylene dichloride, and cyclohexanone.
Insoluble in ethylene glycol and propylene glycol.
Boiling point: 100 degrees C (at 0.001 mm Hg) (15)
Vapor pressure: 1.3 X 10 to the minus 5 mm Hg at 20 degrees C (14)
Koc: 1.48 at a soil depth of 10-20 cm; 0.92 at 40-50 cm (1)
Kd: 2.73 (3)


Ciba-Geigy Agricultural Division
P.O. Box 18300
Greensboro, NC 27419-8300
Telephone 919-632-6000
Fax 919-299-8318

Review by Basic Manufacturer:

Comments solicited: January, 1992
Comments received: April, 1992


  1. Bouchard, D.C, T.L Lavy and D.B. Marx. 1982. Fate of metribuzin, metolachlor, and fluometuron in soil. Weed Sci. 30: 629-632.
  2. Braverman, M.P.; T.L. Lavy, and C.J. Barnes. 1986. The degradation and bioactivity of metolachlor in the soil. Weed Sci. 34: 479-484.
  3. Burkhard, N. and J.A. Guth. 1981. Rate of volatilisation of pesticides from soil surfaces. Pestic. Sci. 12: 37-44.
  4. U.S. Environmental Protection Agency. Pesticide Regulation Standard for Metolachlor. September 1980.
  5. Meister, R.T., ed. dir. 1992. Farm Chemical Handbook. Meister Pub. Co.
  6. Fuerst, E.P. and J.W. Gronwald. 1986. Induction of rapid metabolism of metolachlor in sorghum shoots by CGA-92194 and other antidotes. Weed Sci. 34: 354-361.
  7. Gosselin, R.E., R.P. Smith, H.C. Hodge and J.E. Braddock. 1984. Clinical Toxicology of Commercial Products. 5th edition. Williams & Wilkins.
  8. Krause, A. et al. 1985. Microbial transformation of the herbicide metolachlor by a soil actinomycete. J. Agric. Food Chem. 33: 545-589.
  9. "Review board urges Agriculture Canada to reinstate alachlor." Pesticide and Toxic Chemical News. pg. 15. 25 November 1987.
  10. RTECS Quarterly Microfiche. April 1987. "Metolachlor." AN3430000.
  11. U.S. Environmental Protection Agency. Office of Pesticide Programs. "Metolachlor." Chemical Fact Sheet No. 106. January 1987.
  12. U.S. Environmental Protection Agency. Office of Drinking Water. Metolachlor Health Advisory. Draft Report. August 1987.
  13. Wilkinson, R.E. 1981. Metolachlor influence on growth and terpenoid synthesis. Pest. Biochem. and Physiol. 16:63-71.
  14. Windholz, M., et al., eds. 1983. Metolachlor. pg. 880. The Merck Index. 10th ed. Merck & Co., Inc.
  15. Worthing, C.R., ed. 1983. "Metolachlor." pg 377. The Pesticide Manual. 7th edition. British Crop Protection Council.
  16. Zama, P. and K.K. Hatzios. 1987. Interactions between the bioicide metolachlor and the safener CGA-92194 in sorghum leaf protoplasts. Pesticide Biochem. and Physiology. 27: 86-96.
  17. Zimdahl, R.L. and S.K. Clark. 1982. Degradation of three acetanilide herbicides in soil. Weed Sci. 30: 545-548.
  18. Holden, Larry R. and Jeffery A. Grahm. 1992. Results of the National Alachlor Well Water Surver. Environmental Science and Technology. 26: 935-943.