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Oxamyl

Publication Date: 9/93

TRADE OR OTHER NAMES

Some trade names include Vydate, DPX 1410, Oxamimidic Acid, Thioxamyl and Oxamyl.

REGULATORY STATUS

The U.S. Environmental Protection Agency (EPA) has classified most products containing oxamyl as Restricted Use Pesticides (RUP) due to oxamyl's acute toxicity to humans and its toxicity to birds and mammals (21). Restricted Use Pesticides may be purchased and used only by certified applicators. Granular formulations of oxamyl are banned in the United States, where this pesticide is available only in liquid formulations (22). Containers of oxamyl and/or its formulated products should bear labels with the signal words "DANGER-POISON" (1).

INTRODUCTION

Oxamyl is used as an insecticide to kill and control a broad spectrum of insects, as an acaricide to control mites and ticks, and as a nematicide against roundworms. Its action is both systemic and contact. Oxamyl is used on field crops, vegetables, fruits, and ornamental plants (20). Oxamyl may be applied directly on plants or on the soil surface (15).

Oxamyl belongs to a family of pesticides called carbamates (7). These insecticides work by blocking the normal functioning of cholinesterase, an essential nervous system enzyme. Please refer to the Toxicology Information Brief on cholinesterase-inhibition for more information.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Oxamyl has been rated as extremely poisonous to humans. Oxamyl can enter the body by three routes of exposure: inhalation, ingestion, or skin absorption (4, 7, 10). Acute oral exposure to oxamyl has caused human deaths (7). Oral, skin ('dermal'), and eye ('ocular') exposure may cause poisoning, although absorption through the skin is slow (4). Exposure of rabbit's eyes to technical oxamyl caused decreased pupil size and congestion of the iris, the colored portion of the eye; the cornea was not damaged (3).

As with other carbamate compounds, oxamyl's cholinesterase-inhibiting effect is short-term and reversible (7). Symptoms of oxamyl poisoning include nausea, vomiting, abdominal cramps, sweating, diarrhea, excessive salivation, weakness, imbalance, blurring of vision, breathing difficulty, increased blood pressure or 'hypertension,' and lack of control of urine or feces release. Death may result from respiratory system failure associated with oxamyl exposure (4). Complete recovery from an acute poisoning by oxamyl, with no long term health effects, is possible if exposure ceases and the victim has time to reform their normal level of cholinesterase and to recover from symptoms (7, 19).

Carbamates generally are excreted rapidly and do not accumulate in mammalian tissue. If exposure does not continue, cholinesterase inhibition reverses rapidly. In non-fatal cases, the illness generally lasts less than 24 hours (26).

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. In rats the oral LD50 of technical oxamyl is 5.4 mg/kg. A 24% liquid formulation of this insecticide has an acute oral LD50 of 37 mg/kg in rats. The dermal LD50 for technical oxamyl is 2,960 mg/kg in rabbits (1, 20).

CHRONIC TOXICITY

Prolonged or repeated exposure to oxamyl may cause symptoms similar to the pesticide's acute effects.

In a two-year rat feeding study, the no-observable effect level (NOEL) was 2.5 mg/kg. At 5 and 7.5 mg/kg, the average body weights of the animals were decreased. In a two-year mouse feeding study, the NOEL was 1.25 mg/kg. At 2.5 and 3.75 mg/kg there was decreased body weight and changed nutritional performance (3). No cumulative toxicity was seen when rats were given twice the LD50 in divided doses over a two-week period (4).

The EPA's Lifetime Health Advisory (LHA) level for oxamyl is 200 micrograms/liter. Water containing oxamyl at or below this level is acceptable for drinking every day over the course of one's life with no health concerns (25).

Reproductive Effects

Litter size, viability, lactation and body weights of offspring were decreased in a three-generation, six litter reproduction study in rats fed 100 and 150 ppm of technical oxamyl. (There were two litters per generation). The body weights of rats fed 5 or 7.5 mg/kg/day were also lowered (23).

Teratogenic Effects

When pregnant rats were fed oxamyl, there was a dose related decrease in the maternal body weight and in food consumption rates in rats fed doses of 5, 7.5 or 15 mg/kg/day on days 6 through 15 of pregnancy, but not in rats fed doses of 0 and 2.5 mg/kg/day. No effects were observed on the number of implantation sites, resorptions and live fetuses. The NOEL was calculated at 2.5 mg/kg/day (23).

No teratogenic effects were observed in the offspring of rabbits fed 2 and 4 mg/kg during days 6 through 19 of gestation (23).

Oxamyl was not teratogenic or embryotoxic in the offspring of pregnant rats fed up to 15 mg/kg/day of the insecticide (3, 23). However, embryotoxic effects were produced in rabbits at 4 mg/kg/day. No teratogenic effects were observed in rabbits given oxamyl levels approximately equal to 130 ppm in the diet (3).

Mutagenic Effects

Oxamyl was not reported to be mutagenic after several tests (3, 23).

Carcinogenic Effects

Sufficient data is available from animal studies to indicate that oxamyl does not increase the risk of cancer in humans (25). No evidence of carcinogenic potential has been seen following long-term dietary exposure in rats and mice (23).

Organ Toxicity

Liver impairment was suggested by a slight biochemical change seen in dogs that were fed 3.75 mg/kg/day as a part of a two-year feeding study (3).

In a two-year study, male rats fed 7.5 mg/kg/day oxamyl for two years had decreased organ weight of the heart, testes and adrenals. In females, there was an increase in the relative weights of the brain, heart, lungs and adrenals (23).

Fate in Humans and Animals

When oxamyl was administered to rats, most of the dose was rapidly eliminated in the urine and feces as breakdown byproducts, or metabolites (4). Carbamates generally are excreted rapidly and do not accumulate in mammalian tissue (26).

ECOLOGICAL EFFECTS

Oxamyl is toxic to fish, birds, and other wildlife (3). It does not bioaccumulate to any great extent (23).

Effects on Birds

Oxamyl is extremely toxic to birds (3). The acute oral LD50 for oxamyl in quail is 4.18 mg/kg (6). Hens given single oral doses of oxamyl at 20 to 40 mg/kg of body weight followed by intramuscular injections of 0.5 mg of atropine, an antidote, exhibited early symptoms of cholinesterase inhibition with full recovery after 12 hours. No signs of delayed neurotoxicity were observed in these same hens (23). The oral LD50 for oxamyl is 3.83 mg/kg in male mallard ducks and 2.61 mg/kg in female mallard ducks (3). Egg production was decreased in mallard ducks to which oxamyl was fed at 50 ppm dietary levels over a 28-week period (3).

Effects on Aquatic Organisms

Oxamyl is moderately toxic to fish (3). The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it for a set time period. The 96-hour LC50, for oxamyl in bluegill sunfish is 5.6 mg/l, 27.5 mg/l in goldfish, and 42 mg/l in rainbow trout (6).

Effects on Other Animals (Nontarget species)

Oxamyl is highly toxic to bees (22).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Oxamyl does not readily bind, or 'adsorb,' to soil or sediments and has been shown to leach in soil (23). No single soil property appears to influence the tendency of this insecticide to adsorb. Its adsorption is strongest in soils of high organic matter. Its adsorption on sandy loam is fairly weak. An increase in temperature causes a decrease in adsorption. The effectiveness of this material is affected by how deeply it is incorporated in treated soil (17).

Oxamyl is a nonpersistent pesticide which rapidly degrades in the soil (20, 23). Loss is due to decomposition by aerobic and anaerobic bacteria (17, 23). Its soil/field dissipation half-life is one to eight weeks (16). Its soil half-life is one to five weeks, with residual levels found for up to six to 12 months later (23). Oxamyl is hydrolyzed rapidly in neutral and alkaline soils and more slowly in acid soils (23).

Rain readily leaches oxamyl from soil (17). Oxamyl is highly soluble in water (280 g/liter at 25 degrees C). Generally, high solubility promotes groundwater contamination. However, oxamyl is rapidly broken down by plants after application and by both aerobic and anaerobic bacteria in the soil. Oxamyl is therefore considered to be a non-persistent pesticide with a low potential for groundwater contamination under most soil-water conditions. Wherever conditions favor very rapid movement of leachate, oxamyl dissolved in the soil-water may reach the groundwater. Sites where the water table is very close to the surface, where large volumes of water are applied to the site (as irrigation or precipitation), or where there are sandy soils low in organic matter, are sites where oxamyl contamination of the groundwater may occur (23, 24).

Oxamyl is rapidly hydrolyzed, or broken down by groundwater in neutral and alkaline soil. This occurs more slowly in acid soil. Since oxamyl degrades relatively quickly in the presence of bacteria, it is more likely to be found in groundwater than in surface water. It has been found in parts per billion (ppb) levels in the states of New York (1-60 ppb) and Rhode Island (1 ppb) (2, 8, 23).

Breakdown of Chemical in Water

In a river water study, oxamyl had a half-life of one to two days (23). Another study indicates that its hydrolysis half-life is from less than one week to a few weeks (16). This insecticide should not be applied directly to water, nor where runoff is likely to occur. Cleaning of equipment or disposal of wastes can also contaminate water, so precautions should be taken to avoid such contamination (3).

Breakdown of Chemical in Vegetation

Oxamyl has a residual period in plants of approximately one to two weeks. It is considered non-toxic to plants (5). Plants take oxamyl up through both leaves and roots; it is transported downward to the roots in treated plants (6). Oxamyl is metabolized rapidly by plants (23).

PHYSICAL PROPERTIES AND GUIDELINES

Oxamyl is an off-white crystalline powder (23) or a white crystalline solid with a slight sulfurous odor (1, 7, 19). As a carbamate, it tends to have poor stability (18). While oxamyl is stable in solid form and in most solutions, it decomposes to innocuous materials in natural waters and in soils. Aeration, sunlight, alkalinity, and higher temperatures increase its rate of decomposition (7). Toxic fumes of nitrogen oxides and sulfur oxides are emitted if oxamyl is heated to decomposition (10). It is noncorrosive (6). Oxamyl is available in a variety of formulations, such as a 24% water- soluble liquid and 10% granules (7).

Protective clothing and respirators should be worn by applicators so that skin, eye and clothing contact can be carefully avoided. Oxamyl should be kept away from children, unauthorized persons, domestic and other animals, food, and feedstuffs (6).

Occupational Exposure Limits:

No occupational exposure limits have been established for oxamyl by OSHA, ACGIH or NIOSH.

Physical Properties:

CAS #: 23135-22-0
H20 solubility: 280 g/l at 25 degrees C (15); 280,000 ppm (16)
Solubility in other solvents: (per 100 g. solvent at 25 degrees C): 67 g in acetone, 33 g in ethanol, 11 g in 2-propanol, 144 g in methanol, 1 g in toluene (7)
Melting Point: 100 - 102 degrees C (15); at this point it changes to a different crystalline form with a melting point of 108 degrees C to 10 degrees C (7, 19, 20)
Vapor pressure: 2.3 x 104 mm Hg at 25 degrees C (19)
Partitioning Model: PCMC1 (mole fraction): 0.023
PCMC2 (mg/l): 2.8 x 10 to the minus 5
PCMC3 (ug/l): 1,280,000 (16)
Kow: 0.3 (14)
Koc: 0.2 - 8.6; 4.4 (calc) (16)
Kd: 0.02-0.3 (16)
pH: 2.37 x 10 to the minus 7 atm x m/3 mole, suggesting that aeration is not likely to be a suitable water treatment technique for oxamyl removal (15).
Chemical Class/Use: Carbamate insecticide, nematicide, acaricide.
ADI: a temporary ADI of 0.01 mg/kg/day was calculated by WHO using a two-year dog feeding study (15).

BASIC MANUFACTURER

Du Pont Agricultural Products
Walker's Mill, Barley Mill Plaza
PO Box 80038
Wilmington, DE 19880-0038

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: November, 1992

REFERENCES

  1. Berg, G. L., ed. 1986. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing Company.
  2. Cohen, S. Z., et al. 1986. Monitoring groundwater for pesticides. Office of Pesticide Programs (TS-769C), U.S. Environmental Protection Agency. Published by the American Chemicals Society. Washington, DC.
  3. DuPont de Nemours and Company. 1984 (Mar.). Technical data sheet for oxamyl. Agricultural Chemicals Department. Wilmington, DE: DuPont.
  4. Gosselin, R. E., et al. 1984. Clinical toxicology of commercial products. Fifth edition. Baltimore: Williams and Wilkins.
  5. Harding, W.C. 1979. Pesticide profiles. Part one: Insecticides and miticides. Bulletin 267. Cooperative Extension Service. University of Maryland.
  6. Hartley, D. and H. Kidd, eds. 1983. The Agrochemicals Handbook. Nottingham, England: Royal Society of Chemistry.
  7. Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD: Williams and Wilkins.
  8. Holden, P. W. 1986. Pesticides and groundwater quality issues and problems in four states. Washington, DC: National Academy Press.
  9. Morse, R. A. 1987. Bee poisoning. 1988. New York state pesticide recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11. Cornell University. Ithaca, NY.
  10. Sax, N. I. 1984. Dangerous properties of industrial materials. Sixth edition. NY: VanNostrand-Reinhold Co.
  11. Thomson, W.T. 1976. Insecticides, acaricides and ovicides. Agricultural Chemicals, Book I. Indianapolis, IN: Thomson Publications.
  12. USEPA. 1987 (Oct. 23). Subject: Active ingredients subject to restricted use classification. Office of Pesticide Programs, Registration Division. Washington, DC.
  13. _____. 1987 (Feb. 4). Environmental News. Office of Public Affairs (A-107). Washington, DC.
  14. _____. 1986. (Jan.). Estimating pesticide sorption coefficients for soils and sediments. Richard E. Green and Samuel W. Karickhoff. Environmental Research Laboratory. Office of Research and Development. Athens, GA.
  15. _____. 1985 (Sept. 30). Draft health advisory: Oxamyl. Office of Drinking Water. Washington, DC.
  16. _____. 1984 (Dec.). User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  17. Wagenet, L. P., et al. 1985. A review of physical-chemical parameters related to the soil and groundwater fate of selected pesticides in New York State. Cornell University Agricultural Experiment Station, New York State College of Agriculture and Life Sciences. Ithaca, NY. Number 30. ISSN 0362-2754.
  18. Witt, J. M., ed. 1985. Chemistry, biochemistry, and toxicology of pesticides. Proceedings of an Extension Service Short Course at Oregon State University. Pest control education program. Eugene, OR.
  19. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  20. Meister, R.T. (ed.). 1991. Farm Chemicals Handbook '91. Meister Publishing Company, Willoughby, OH.
  21. DuPont Agricultural Products. 1990 (Aug.). Material Safety Data Sheet for "Vydate L" Insecticide/Nematicide. DuPont, Wilmington, DE.
  22. DuPont Agricultural Products. 1989 (Sept.). Technical Bulletin for Vydate, Insecticide/Nematicide. DuPont, Wilmington, DE.
  23. US Environmental Protection Agency. 1987 (March 31). Health Advisory: Oxamyl. Office of Drinking Water, US EPA, Washington, DC.
  24. U. S. Department of Agriculture, Soil Conservation Service. 1990 (Nov). SCS/ARS/CES Pesticide Properties Database: Version 2.0 (Summary). USDA - Soil Conservation Service, Syracuse, NY.
  25. US Environmental Protection Agency. 1989 (Jan.). Health Advisory Summary: Oxamyl. US EPA, Washington, DC.
  26. Occupational Health Services, Inc. 1991. MSDS for Methomyl. OHS Inc., Secaucus, NJ.