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
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,
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
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
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.
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.
A variety of microbial mutagenicity assays with various strains and
with numerous concentration were all negative.
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.
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
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).
|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
|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
800 N Lindbergh Blvd
St Louis, MO 63167
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received: November, 1992
The Agrochemicals Handbook. (1991) The Royal Society of Chemistry,
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.
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.
National Library of Medicine (1992). Hazardous Substances
Databank. TOXNET, Medlars Management Section, Bethesda, MD.
U. S. Environmental Protection Agency (1987). Health Advisory,
Office of Drinking Water.
Beste, C.E., Chairman (1983). Herbicide Handbook of the Weed
Science Society of America. Weed Science Society of America, Champaign,
Food and Drug Administration (1986). The FDA Surveillance Index.
Bureau of Foods, Dept of Commerce, National Technical Information
Service, Springfield, VA.
National Research Council (1987). Regulating Pesticides in Food,
The Delaney Paradox, National Academy Press, Washington, D.C.
Occupational Health Services, Inc. (1988). Hazardline, New York,
Walker, Mary M. and Lawrence H. Keith. (1992). EPA's Pesticide
Fact Sheet Database. Lewis Publishers. Chelsea, MI.
Alachlor Technical (94%) Material Safety Data Sheet. (1991).
Monsanto Company, St Louis, MO.
Farm Chemicals Handbook. (1992). Meister Publishing.
Holden, Larry, and Jeffery A. Graham. (1992). Results of the
National Alachlor Well Water Survey. Environmental Science and
Technology 26: 935-943.