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 methoxychlor include Marlate, Chemform and Methoxy-DDT.
Methoxychlor is a contact and stomach insecticide effective against a
wide range of pests encountered in agriculture, households, and ornamental
plantings. It is registered for use on fruits, vegetables, forage crops and
on shade trees. Methoxychlor is also registered for veterinary use as a
poison to kill parasites on dairy and beef cattle.
Methoxychlor is one of a few organochlorine pesticides that have seen an
increase in use since the ban on DDT in 1972. This is due to its relatively
low toxicity and relatively short persistence in biological systems (9).
Methoxychlor is a general use pesticide.
Methoxychlor is classified as slightly toxic and carries the signal word
CAUTION. It has a very low toxicity (9). The oral LD50 for rats is 5,000 to
6,000 mg/kg and 2,000 mg/kg for mice. A 50% mortality was not achieved for
monkeys at 2,500 mg/kg or for hamsters at 2000 mg/kg. The lowest oral dose
that can cause lethal effects for humans is estimated to be 6,400 mg/kg and
the lowest dose through the skin that produces toxic effects in humans is
2,400 mg/kg based on behavioral symptoms (3). Rabbit skin dosed at 2,800
mg/kg produced no symptoms. Symptoms close to the lethal dose include Central
Nervous System depression, progressive weakness and diarrhea. Extremely high
doses can cause death within 36 to 48 hours.
Rats fed from very low to high doses of methoxychlor (10 to 2,000 mg/kg)
for two years had growth retardation above 200 ppm but no tissue damage from
the methoxychlor. Human volunteers taking oral doses of 0.5 to 2.0 mg/kg/day
for six weeks had no adverse effects measured by routine enzyme (biochemical)
or (blood) hematologic parameters. Loss of body weight and growth retardation
were the most frequent effects in lab animal studies. These effects were
attributed to food refusal rather than to methoxychlor toxicity (4).
Rats fed low doses (about 50 mg/kg/day) in their diet had normal
reproduction but slightly higher doses (150 mg/kg/day) fewer animals mated and
many did not produce litters. At about 250 mg/kg/day none of the rats had
litters or embryo implantation. In another study male rats given 100 to 200
mg/kg/day suffered arrested sperm production after 70 consecutive days and
females rats produced ovarian effects. Chronic exposure to this pesticide may
present a reproductive risk to humans.
When a methoxychlor formulation containing 50% active ingredient and 50%
unknown compounds was administered to pregnant female rats, adverse effects in
the fetus occured only at doses large enough to be toxic to the dams. These
effects were thought to be due to the disruption of the maturation process
rather than due to the direct toxic effects of methoxychlor (12). At 400
mg/kg, the pesticide killed rat embryos and at 200 mg/kg there was increased
incidence of resorption, small litter size, and low fetal weights. This
suggests that there may be a potential risk to human development following
Most mutation assays have proven to be negative. There is no convincing
evidence that methoxychlor is toxic to genetic material.
Two strains of mice were fed diets containing low levels (40 mg/kg)
methoxychlor for two years. There was no significant incidence of liver
tumors but one strain did have increased testicular tumors (1). After
evaluating the data, National Cancer Institute and the International Agency
for Research on Cancer both conclude that methoxychlor is not an animal
carcinogen. The U.S. EPA has not made an official determination on the
carcinogenic status of the compound (10).
Chronic effects include liver cell degeneration and kidney damage. Death
is usually due to respiratory failure from paralysis in the brain. Central
nervous depression is more prominent than excitation.
Methoxychlor does not accumulate to any significant degree in fat or
other tissues of mammals (9). At high dietary doses, low levels of
methoxychlor were detected in the fat of rats though it cleared the body
readily after dietary intake stopped (two weeks). Mice excreted 98.3% of a 50
mg/kg dose in the urine and feces within 24 hours. When rats were injected
with 3 mg/kg, 50% was excreted in the feces and 5 to 10% in the urine in four
days. The major metabolites in mouse feces and urine were the monophenol and
bisphenol. Other metabolites were present also but methoxychlor itself does
not appear to undergo dehydrochlorination.
Lactating cows treated twice in 14 days with sprays of 0.25 to 0.5% (2
quarts per animal) had residues of 2 to 3 ppm in milk. After 14 days, levels
were at the limit of detection (0.005 ppm).
Methoxychlor shows low toxicity to mallards, Japanese quail, pheasants
and bobwhite quail. No mortality occurred in these species after being exposed
at 250 mg/kg in their diets for five days. Most fish, however, are sensitive
to the pesticide. The 96-hour LC50 for fish ranges from 1.7 ppb for Atlantic
salmon to 5,200 ppm for channel catfish. The bioconcentration factors for
fish ranges from 138 in sheepshead minnows to 8,300 in the fathead minnow.
Bioconcentration factors were the highest in the mussel (12,000) and in the
snail (8,570). This indicates that methoxychlor would accumulate in aquatic
organisms that do not rapidly metabolize the compound. Fish do metabolize
methoxychlor fairly rapidly and thus tend not to accumulate it appreciably
Methoxychlor is very persistent in soil and its half-life is greater than
six months. However, rates may be as fast as one week in some instances. The
chemical is tightly bound to soil and is insoluble in water, so it leaches
slowly, if at all. Methoxychlor degrades much more rapidly in soil that has a
supply of oxygen (aerobic) than in soil without oxygen (anaerobic). Any
movement of the pesticide is expected to take place while attached to
suspended soil particles in runoff. In the EPA pilot groundwater survey,
methoxychlor was found in a number of wells in New Jersey (not quantified) and
at extremely low concentrations (from 0.1 to 1.0 ppt) in water from the
Niagara River, the James river, and a Lake Michigan tributary. Many other
rivers tested throughout the United States did not contain methoxychlor.
In water the major products of breakdown in a neutral solution are
anisoin, anisil, and DMDE. The half-life in distilled water is 37 days but in
some river waters the half-life is as rapid as two to five hours (3).
Methoxychlor evaporates very slowly, but the evaporation may contribute to the
cycling of the product in the environment (11).
On mature soybean foliage, the washoff rate was 8% per cm of rainfall
with a total of 33.5% washoff for a season. Dislodgeable residues account for
less than 1% of the amount applied.
|NOEL (rabbit): ||5.01 mg/kg/day
|MCL: ||0.1 mg/l/day (ppm)
|DWEL: ||0.2 mg/l
|HA: ||0.04 mg/l (lifetime)
|TLV-TWA: ||10.0 mg/m3
|ADI: ||0.1 mg/kg/day (WHO)
|RfD: ||0.05 mg/kg/day
|LEL: ||35.5 mg/kg/day (rabbit)
|CAS #: ||72-43-5
|Chemical name: ||1,1'-(2,2,2-trichloro-ethylidene)bis[4-methoxybenzene]
|Chemical class/use: ||diphenyl alkane insecticide
|Solubility in water: ||0.1 mg/l
|Solubility in other solvents: ||chloroform 44 g/100 g; methanol 5 g/100 g
|Melting Point: ||86-88 degrees C
|Vapor Pressure: ||very low
|Partition Coefficient: ||3.05 to 4.30 (octanol/water)
Drexel Chemical Co.
PO Box 9366
2487 Pennsylvania St.
Memphis, Tennessee 38109
Review by Basic Manufacturer:
Comments solicited: October, 1991
National Research Council (1977). Drinking Water and Health, Advisory
Center on Toxicology, Assembly of Life Sciences. Safe Drinking Water
Committee, National Academy of Sciences, Washington, DC.
Trabalka, J.R. and C.T. Garten, Jr. (No date). Development of
Predictive Models for Xenobiotic Bioaccumulation in Terrestrial Ecosystems.
Environmental Sciences Div Publication No. 2037, Oak Ridge National
Laboratory, Oak Ridge, TN.
National Library of Medicine (1992). Hazardous Subtances Databank.
TOXNET, Medlars Management Section, Bethesda, MD.
U. S. Environmental Protection Agency (1987). Health Advisory, Office
of Drinking Water.
Menzie, Calvin M. (1980). Metabolism of Pesticides, Update III. U.
S. Dept of the Interior, Fish and Wildlife Service, Special Scientific Report,
Wildlife No. 232.
Worthing, Charles R., Editor (1983). The Pesticide Manual, A World
Compendium. The British Crop Protection Council, The Ravenham Press Limited,
Ravenham, Suffolk, England.
National Institute for Occupational Safety and Health (1985-86)
Registry of Toxic Effects of Chemical Substances, U. S. Department of Health
and Human Services, Centers for Disease Control.
Khera, K. S., C. Whalen, and G. Trivett (1978). Teratogenicity
Studies on Linuron, Malathion, and Methoxychlor in Rats, Toxic and Applied
Smith, Andrew G. (1991). Chlorinated Hydrocarbon Insecticides. in
Handbook of Pesticide Toxicology, Volume 3, Classes of Pesticides. Wayland J.
Hayes Jr. and Edward R. Laws, Jr. editors. Academic Press, Inc., NY.
U.S. EPA Health Advisory Summaries. (1989). Methoxychlor. Office of
Howard, Philip H. (1991). Handbook of Environmental Fate and
Exposure Data for Organic Chemicals. Volune III, Pesticides. Lewis
Publishers, Chelsea, MI.
U.S. EPA Health Advisories for 16 Pesticides. Office of Drinking
Water. March 31.