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
Trade names for some of the products containing MCPA are Agritox,
Agroxone, Chiptox, Rhonox, and Weed-Rhap. This herbicide may be used in
formulations with many other types of pesticides including 2,4-D,
dicamba, MCPB, bromoxynil, mecoprop and bentazone.
MCPA is a systemic phenoxy herbicide used to control annual and
perennial weeds (including thistle and dock) in cereals, grasslands,
trees and turf. As with some of the other phenoxy herbicides, MCPA is
an acid, but it is often formulated as a salt such as diethanolamine
salt. Unless otherwise indicated, this document will refer to the acid
form. The herbicide works by concentrating in the actively growing
regions of a plant (meristematic tissue) where it interferes with
protein synthesis, cell division and ultimately the growth of the plant.
This compound is a Restricted Use Pesticide (RUP). Restricted Use
Pesticides may be purchased and used only by certified applicators.
MCPA carries a DANGER signal word on the label even though the
acute toxicity of the product indicates that it is only slightly toxic.
This is due to its potential to cause severe eye irritation. Symptoms
in humans from acute toxic exposure include slurred speech, twitching,
jerking and spasms, drooling, low blood pressure, and unconsciousness.
The LD50 for MCPA in rats ranges from 700 mg/kg to 1,330 mg/kg and
the LD50 of MCPA in the mouse ranges from 550 to 800 mg/kg. The dermal
LD50 is 4,800 mg/kg in male rabbits and 3,400 mg/kg in female rabbits.
The estimated human lethal oral dose is from 250 to 450 mg/kg (6).
Three ninety day studies of rats revealed chronic toxic effects at
doses around 20 to 25 mg/kg/day. Growth retardation and increased
kidney weight were the effects noted in all three studies. Another
study of this type indicated that the lowest dose that caused chronic
toxic effects in the rat was about 5 mg/kg/day. These levels are
substantially below the LD50 values for the organism indicating that
chronic toxicity can occur at low exposure levels.
A two-generation rat study at doses of up to 15 mg/kg affected
reproductive function. Even smaller amounts of the compound were toxic
to the fetuses. Dogs receiving relatively small amounts of MCPA (8 and
16 mg/kg) for 13 weeks had various adverse sperm and testes changes (8).
Pregnant rats fed low to moderate doses of MCPA (20 to 125 mg/kg)
on days 6 to 15 of gestation, had no birth defects in their offspring.
However, when the ethyl ester form of MCPA was fed to pregnant rats at
low to moderate levels (2 to 100 mg/kg) on days 8 to 15 of gestation,
cleft palate, heart defect, and kidney anomalies were observed in the
offspring (7). Mice fed 5 to 100 mg/kg of MCPA on days 6 to 15 showed
significantly reduced fetal weight and delayed bone development at the
The EPA, however, has stated that these studies are unacceptable
under current guidelines and are requiring additional testing of the
compound with regard to its potential to cause birth defects in two
animal species. No conclusions can be drawn about human birth defect
risk from the currently available information.
MCPA was only weakly mutagenic to bone marrow and ovarian cells of
hamsters and negative results were reported for all other mutagenic
tests (10). While another test has been requested by the EPA (a gene
mutation study) it appears that the compound poses little mutagenic risk
All of the available cancer evidence on MCPA indicates that the
compound does not cause cancer (10).
Farm worker exposure has resulted in reversible anemia, muscular
weakness, stomach problems, and slight liver damage (6).
Fate in Humans and Animals
Rats eliminated nearly all of a single oral dose within 24 hours,
mostly in their urine. In another rat study, three quarters of the dose
was eliminated within two days. All was gone by the eighth day. Humans
excreted about half of a 5 mg dose in the urine within a few days. No
residues were found after day five. Rats given intravenous MCPA had
residues in tissues within 1.5 hours.
Cattle and sheep fed MCPA in low to moderate doses in the diet for
two weeks had no residues from levels less than about 18 mg/kg. At
moderate continuous ingestion there was greater than 0.05 ppm in whole-
milk or cream. This level declined to non-detectable levels one or
three days after the removal of MCPA from the diet.
The major metabolite of MCPA is 2-methyl-4-chlorophenol in the free
and conjugated form which is formed in the liver (2).
MCPA is moderately toxic to wildfowl and has an LC50 for
bobwhites, pheasants, and mallard. For example the acute avian LD50 of
MCPA in bobwhite quail is 377 mg/kg. MCPA is only slightly toxic to
freshwater fish with LC50 values around 90 mg/l for rainbow trout and
for bluegill. MCPA is practically non-toxic to freshwater
invertebrates, and estuarine and marine organisms. It is non-toxic to
bees (9, 10).
The organic content of soil determines in large part the
persistence of MCPA. With less than 10% organic matter in soil, the
compound is degraded in one day and, with greater than 10% levels in
soil, it takes three to nine days to degrade. No MCPA was detected in
forest soils at a depth of 3 to 15 cm 40 days after application. The
half-life is five to six days in slightly acidic to slightly alkaline
MCPA leaches in most soils, but its mobility increases as organic
matter decreases (2). The compound has been found in well water in
Missouri and is of concern to the EPA as a potential groundwater
In sterilized water, it takes about three weeks for half of the
compound to degrade due to the action of sunlight. In rice paddy water
however, MCPA is almost totally degraded by aquatic microorganisms in
under two weeks (2). MCPA is absorbed, translocated, and actively
broken down by vegetation. Forest litter had 32 ppm 10 months after
application. Levels in moss declined to 7% of the initial level within
40 days. The metabolite found in plants is 2-methyl-4-chlorophenol.
|NOEL (dog): ||0.15 mg/kg/day, based on kidney effects, 1 year
|DWEL: ||0.05 mg/l
|HA: ||0.01 mg/l (lifetime)
|RfD: ||0.0005 mg/kg/day (EPA); 0.0015 mg/kg/day (WHO)
|LEL: ||0.75 mg/kg/day
|CAS #: ||94-74-6
|Chemical name: ||(4-chloro-2-methylphenoxy) acetic acid
|Chemical class/use: ||phenoxy herbicide
|Solubility in water: ||for the amine salt, 866,000 mg/l; for the ester, 5 mg/l (estimate)
|Solubility in other solvents: ||ether 77 g/100 g; ethanol 153 g/100 g; toluene 6.2 g/100 g
|Melting Point: ||118-119 degrees C
|Vapor Pressure: ||1.5 x 10 to the minus 6 power mm Hg
|Partition Coefficient: ||2.07 calculated (octanol/water)
5501 Murray Road
Memphis, TN 38119-3703
Review by Basic Manufacturer:
Comments solicited: October, 1992
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,
Chemical Information Systems, Inc. (1988). Oil and Hazardous
Materials/Technical Assistance Data System, Baltimore, MD.
Worthing, Charles R., Editor (1983). The Pesticide Manual, A World
Compendium. The British Crop Protection Council, The Ravenham Press
Limited, Ravenham, Suffolk, England.
Stevens, James T. and Darrell D. Sumner. 1991. Herbicides in
Handbook of Pesticide Toxicology, Volume 3, Classes of Pesticides.
Wayland J. Hayes and Edward R. Laws editors. Academic Press, NY.
National Research Council Canada (1978). Phenoxy Herbicides -
Their Effects on Environmental Quality with Accompanying Scientific
Criteria for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD). Subcommittee
on Pesticides and Related Compounds, NRC Associate Committee on
Scientific Criteria for Environmental Quality, Ottawa, Canada.
Food and Drug Administration (1986). The FDA Surveillance Index.
Bureau of Foods, Dept of Commerce, National Technical Information
Service, Springfield, VA.
The Agrochemicals Handbook. 1991. The Royal Society of Chemistry,
Walker, Mary M. and Lawrence H. Keith. 1992. EPA's Pesticide
Fact Sheet Database. Lewis Publishers. Chelsea, MI.
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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