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.
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Pesticide
Information
Profile
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Metolachlor
Publication Date: 9/93
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TRADE OR OTHER NAMES
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.
INTRODUCTION
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.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
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.
CHRONIC TOXICITY
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.
ECOLOGICAL EFFECTS
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.
ENVIRONMENTAL FATE
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).
PHYSICAL PROPERTIES AND GUIDELINES
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) |
BASIC MANUFACTURER
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
REFERENCES
Bouchard, D.C, T.L Lavy and D.B. Marx. 1982. Fate of metribuzin,
metolachlor, and fluometuron in soil. Weed Sci. 30: 629-632.
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.
Burkhard, N. and J.A. Guth. 1981. Rate of volatilisation of
pesticides from soil surfaces. Pestic. Sci. 12: 37-44.
U.S. Environmental Protection Agency. Pesticide Regulation Standard
for Metolachlor. September 1980.
Meister, R.T., ed. dir. 1992. Farm Chemical Handbook. Meister Pub. Co.
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.
Gosselin, R.E., R.P. Smith, H.C. Hodge and J.E. Braddock. 1984.
Clinical Toxicology of Commercial Products. 5th edition. Williams & Wilkins.
Krause, A. et al. 1985. Microbial transformation of the herbicide
metolachlor by a soil actinomycete. J. Agric. Food Chem. 33: 545-589.
"Review board urges Agriculture Canada to reinstate alachlor."
Pesticide and Toxic Chemical News. pg. 15. 25 November 1987.
RTECS Quarterly Microfiche. April 1987. "Metolachlor." AN3430000.
U.S. Environmental Protection Agency. Office of Pesticide Programs.
"Metolachlor." Chemical Fact Sheet No. 106. January 1987.
U.S. Environmental Protection Agency. Office of Drinking Water.
Metolachlor Health Advisory. Draft Report. August 1987.
Wilkinson, R.E. 1981. Metolachlor influence on growth and terpenoid
synthesis. Pest. Biochem. and Physiol. 16:63-71.
Windholz, M., et al., eds. 1983. Metolachlor. pg. 880. The Merck
Index. 10th ed. Merck & Co., Inc.
Worthing, C.R., ed. 1983. "Metolachlor." pg 377. The Pesticide
Manual. 7th edition. British Crop Protection Council.
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.
Zimdahl, R.L. and S.K. Clark. 1982. Degradation of three acetanilide
herbicides in soil. Weed Sci. 30: 545-548.
Holden, Larry R. and Jeffery A. Grahm. 1992. Results of the National
Alachlor Well Water Surver. Environmental Science and Technology. 26: 935-943.
Disclaimer: Please read
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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.
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