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Methoxychlor

Publication Date: 9/93

TRADE OR OTHER NAMES

Trade names for methoxychlor include Marlate, Chemform and Methoxy-DDT.

INTRODUCTION

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.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

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.

CHRONIC TOXICITY

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).

Reproductive Effects

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.

Teratogenic Effects

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 chronic exposure.

Mutagenic Effects

Most mutation assays have proven to be negative. There is no convincing evidence that methoxychlor is toxic to genetic material.

Carcinogenic Effects

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).

Organ Toxicity

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).

ECOLOGICAL EFFECTS

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 (11).

ENVIRONMENTAL FATE

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.

Exposure Guidelines:

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)

Physical Properties:

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)

BASIC MANUFACTURER

Drexel Chemical Co.
PO Box 9366
2487 Pennsylvania St.
Memphis, Tennessee 38109
Telephone 901-774-4370

Review by Basic Manufacturer:

Comments solicited: October, 1991
Comments received:

REFERENCES

  1. 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.
  2. 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.
  3. National Library of Medicine (1992). Hazardous Subtances Databank. TOXNET, Medlars Management Section, Bethesda, MD.
  4. U. S. Environmental Protection Agency (1987). Health Advisory, Office of Drinking Water.
  5. 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.
  6. Worthing, Charles R., Editor (1983). The Pesticide Manual, A World Compendium. The British Crop Protection Council, The Ravenham Press Limited, Ravenham, Suffolk, England.
  7. 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.
  8. Khera, K. S., C. Whalen, and G. Trivett (1978). Teratogenicity Studies on Linuron, Malathion, and Methoxychlor in Rats, Toxic and Applied Pharmacology 45:435-444.
  9. 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.
  10. U.S. EPA Health Advisory Summaries. (1989). Methoxychlor. Office of Water. January.
  11. Howard, Philip H. (1991). Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Volune III, Pesticides. Lewis Publishers, Chelsea, MI.
  12. U.S. EPA Health Advisories for 16 Pesticides. Office of Drinking Water. March 31.