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Mevinphos

Publication Date: 9/93

TRADE OR OTHER NAMES

Apavinphos, CMDP, ENT 22374, Fosdrin, Gesfid, Meniphos, Menite, Mevinox, OS-2046, PD5, Mevinphos, Phosfene and Phosdrin.

REGULATORY STATUS

All uses of emulsifiable and liquid concentrates of mevinphos are classified as Restricted Use Pesticides (RUP) by the U.S. Environmental Protection Agency (EPA), due to their acute oral and dermal toxicity and residue effects on mammalian, aquatic and bird species (20). Restricted Use Pesticides may be purchased and used only by certified applicators. Products containing mevinphos must bear the signal words "Danger" and "Poison" (26). Check with specific state regulations for local restrictions which may apply.

INTRODUCTION

Mevinphos is a broad spectrum insecticide, an organophosphate chemical that is used for control of a variety of insects, including aphids, grasshoppers, leafhoppers, cutworms, caterpillars, and many other insects on a broad range of field, forage, vegetable and fruit crops (2). It is also an acaricide that kills or controls mites and ticks. It acts quickly both as a contact insecticide, acting through direct contact with target pests, and as a systemic insecticide which becomes absorbed by plants on which insects feed. It dissipates quickly and has short-term residual activity. It is extremely effective at very low dosage rates (17). It is available in concentrate or liquid formulations (26).

Mevinphos is one of a class of insecticides referred to as organophosphates. These chemicals act by interfering with the activities of cholinesterase, an enzyme that is essential for the proper working of the nervous systems of both humans and insects. Please refer to the Toxicology Information Brief on cholinesterase-inhibition for a more detailed description of this topic.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Mevinphos is highly toxic through all routes of exposure, including ingestion, dermal absorption and inhalation. Poisoning affects the central nervous system, the cardiovascular system, the respiratory system and the eyes (13). The greatest occupational hazard is absorption of mevinphos through the skin, lungs, and mucous membranes (1). Its toxic action is direct and quick, regardless of the route of exposure. In humans, symptoms of poisoning have appeared within as little as 15 minutes or 2 hours after exposure to mevinphos, but onset of symptoms have been delayed for as long as 2 days (25). As with all organophosphates, mevinphos is readily absorbed through the skin. Skin which has come in contact with this material should be washed immediately with soap and water and all contaminated clothing should be removed. The severity of mevinphos poisoning will determine the number and types of symptoms which will result. Poisoning is also influenced by the length and concentration of exposure (13). Persons with respiratory ailments, recent exposure to cholinesterase inhibitors, impaired cholinesterase production, or with liver malfunction may be at increased risk from exposure to mevinphos (28).

An early and important symptom of mevinphos poisoning from dermal exposure is impairment of judgment or the ability to reason (13, 25). Other symptoms of poisoning from exposure to the insecticide include giddiness, tightness in the chest, blurred vision, tearing, hearing irregularities, loss of muscle coordination, slurred speech, mental confusion, breathing difficulty, increased blood pressure, convulsions, coma. Several children were made ill by unknowingly wearing clothing which had been contaminated with mevinphos (6).

The organophosphate insecticides are cholinesterase inhibitors. They are highly toxic by all routes of exposure. When inhaled, the first effects are usually respiratory and may include bloody or runny nose, coughing, chest discomfort, difficulty breathing or shortness of breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact with organophosphates may cause localized sweating and involuntary muscle contractions. Eye contact will cause pain, bleeding, tears, pupil constriction, and blurred vision. Following exposure by any route, other systemic effects may begin within a few minutes or be delayed for up to 12 hours. These may include pallor, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred vision, constriction or dilation of the eye pupils, tears, salivation, sweating, and confusion. Severe poisoning will affect the central nervous system, producing incoordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids, and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beats, unconsciousness, convulsions and coma. Death may be caused by respiratory failure or cardiac arrest (28).

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. The oral LD50 for mevinphos in rats is 3 to 12 mg/kg, and in mice is 4 mg/kg. The dermal LD50 for mevinphos is 4.2 mg/kg in rats, 12 mg/kg in mice, and 4.7 to 33 mg/kg in rabbits (2, 12, 26).

The lethal concentration fifty, or LC50, is the concentration of a material in air or water that causes death in 50% of animals exposed to it for a specified length of time. The 1-hour LC50 for mevinphos in rats is 14.4 parts per million (ppm) (12, 26).

CHRONIC TOXICITY

The TDLo, or Toxic Dose Low, is the lowest dose of a substance introduced over a given time period by any route of exposure, other than inhalation, that has produced toxic effects in humans. The oral TDLo in humans is 690 ug/kg when it was given intermittently over 28 days. During this time, peripheral nervous system effects were observed (12).

Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure. Cholinesterase-inhibition resulting from mevinphos exposure can persist for two to six weeks. Repeated exposure to small amounts of this material may result in an unsuspected inhibition in cholinesterase levels. This can cause symptoms, such as weakness, lack of energy, and lack of appetite, that are similar to other illnesses, such as the flu. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia (28). Severe symptoms of cholinesterase-inhibition may be produced in a previously exposed person, whereas symptoms of cholinesterase-inhibition may not be obvious in a person that has not been previously exposed to the same concentration of mevinphos. The monitoring of cholinesterase levels through regular blood testing is highly recommended for those persons with exposure to this material.

In a 2-year feeding study with rats given dietary doses of 0, 0.5, 1.5, 5 and 15 ppm, the NOEL for cholinesterase inhibition was 0.025 mg/kg/day (0.5 ppm). The same NOEL for cholinesterase inhibition was found in a 2-year feeding study with dogs (29). No effect on general health and no significantly obvious poisoning symptoms were seen in a two-year study with rats fed 4 mg/kg, nor in dogs given dietary doses of 5 mg/kg (24). However, rats were killed when given 20 mg/kg mevinphos in their diets for 13 weeks. Dietary doses of 10 mg/kg for 14 weeks were lethal for dogs (17).

Reproductive Effects

In a 3-generation reproduction study with rats, there were no reproductive effects at 1.2 mg/kg (24 ppm) (29). Once in the bloodstream, mevinphos may cross the placenta (28).

Teratogenic Effects

No teratogenic effects were seen in rabbits given doses of 1.0 mg/kg (29).

Mutagenic Effects

No information found.

Carcinogenic Effects

A 2-year study with rats fed dietary doses of up to 0.75 mg/kg mevinphos produced no evidence of tumor formation (29).

Organ Toxicity

Mevinphos primarily affects the nervous system through cholinesterase inhibition, by which there is a deactivation of cholinesterase, an enzyme required for proper nerve functioning.

Acute pulmonary edema, or the filling up of lungs with fluid, and changes in the structure or function of salivary glands, were seen in rats that were exposed to an air concentration of 14 ppm for one hour (12). Rats given dietary doses of 10 or 20 mg/kg for 13 weeks exhibited degeneration of livers, kidneys and cells lining the salivary, tear and other glands, as well as clinical signs of poisoning (25).

Fate in Humans and Animals

Mevinphos is rapidly degraded by the liver. It is more toxic by peripheral exposure routes, such as dermal or intravenous exposure than by routes that go through, and are detoxified by, the liver such as injection into the abdominal cavity.

Samples taken by autopsy from a man who had died within 45 minutes of drinking mevinphos showed the following bodily concentrations of the compound: 3,400 ppm in the stomach wall, 360 ppm in blood, 240 ppm in the liver, 86 ppm in skeletal muscle, 20 ppm in the kidneys, 8 ppm in urine, and 3 ppm in the brain (6).

In cases of moderate poisoning associated with occupational exposure to mevinphos, the concentration of metabolites of mevinphos in the urine collected during the first 12 hours after onset of symptoms was 0.4 ppm. The concentration declined rapidly until 36 hours after onset, and excretion was nearly complete within 50 hours (25).

When labeled mevinphos was fed to cows, blood levels of mevinphos breakdown products, or 'metabolites,' reached the highest point between 2 and 4 hours after feeding. The blood was essentially free of these metabolites within 24 hours. Within 3 days, 77% of the administered dose was excreted. Half of this was excreted via urine within 12 hours (10). When oral doses of 15 ppm of radio-labeled mevinphos were given to a lactating goat for 6 days, no mevinphos was detected in the milk, meat or meat by-products 22-hours after the final dose (10).

ECOLOGICAL EFFECTS

Effects on Birds

Mevinphos is highly toxic to birds. The acute symptoms of mevinphos poisoning in birds include: lack of muscle coordination, curled toes, salivation, diarrhea, trembling and wing beating. Pheasant deaths all occurred 8 to 18 minutes after treatment; deaths of mallards and grouse occurred 5 to 40 minutes post-treatment (18). The oral LD50 for mevinphos in chickens is 7.52 mg/kg, 3 mg/kg in wild bird species, 4.63 mg/kg in female mallards, 1.37 mg/kg in male pheasants, and 0.75-1.50 mg/kg in male grouse. Its dermal LD50 in ducks is 11 mg/kg (12, 14).

Effects on Aquatic Organisms

Mevinphos is highly toxic to fish. The 96-hour LC50 for technical mevinphos in rainbow trout is 11.9 parts per billion (ppb), and 22.5 ppb in bluegill sunfish (26). The 48-hour LC50 for mevinphos in rainbow trout is 17 ppb (14). The 24-hour LC50 in rainbow trout is 34 ppb, 41 ppb in bluegills, and 800 ppb in mosquito fish (14, 24).

Effects on Other Animals (Nontarget species)

Mevinphos is highly toxic to bees, especially when they are exposed to direct treatment or residues on crops (4, 11). Severe losses may be expected if mevinphos is used when bees are present at treatment time or within a day thereafter. Areas frequented by wildlife, including lakes or ponds inhabited by fish, should not be contaminated by use of this material (16).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Mevinphos does not readily adsorb to soil particles, and that which does become adsorbed comes unbound, or 'desorbed,' easily. It therefore has a high tendency to leach, or move with soil moisture. Mevinphos is very mobile in sandy loam, silt loam, loam, and clay loam soils (26). It is more active in moist soils than in dry soils (23, 3).

Mevinphos disappears from soil in approximately one day (8). A soil half-life of 3 days has been reported (27). No harmful effects to soil microorganisms have been observed from applications of mevinphos formulations (16). One study indicated that this material lost its insecticidal capability in two to four weeks (7).

Breakdown of Chemical in Water

Mevinphos dissolves in water and is readily broken down by water (hydrolyzed), losing its insecticidal activity within 2 to 4 weeks (23). In aqueous solution, mevinphos is hydrolyzed with a half-lives of 1.4 hr at pH 11, 3 days at pH 9, 35 days at pH 7, and 120 days at pH 6 (25).

Breakdown of Chemical in Vegetation

When mevinphos is used as directed, it is not phytotoxic, or poisonous to plants (17). There seem to be at least two ways by which a plant breaks down mevinphos (10). However, some crops may be sensitive to solvents with which the active ingredient is formulated, as well as to excessive dosages (16).

PHYSICAL PROPERTIES AND GUIDELINES

Pure mevinphos is a colorless to yellow liquid that has a very mild odor or is odorless (6). It is compatible with alkaline pesticides and fertilizers (24). Mevinphos is corrosive to cast iron, some stainless steels, and brass. Some forms of plastic, rubber, and coatings may be deteriorated by mevinphos (13, 24). Decomposition by lime sulfur is rapid (25). Mevinphos also hydrolyzes in the presence of water and alkalis (28).

Mevinphos is stable under normal temperatures and pressures, but decomposes vigorously above 300 degrees C (572 degrees F), causing containers to burst (28). The temperature of the product should not exceed 25-30 degrees C. Containers should be kept away from heat sources, free flames, or spark- generating equipment. When heated to decomposition, mevinphos emits toxic fumes of phosphorous oxides and oxides of carbon (15, 28). Contact with oxidizers may cause fire or explosion (28). Storage areas should be located at a suitable distance from inhabited buildings, animal shelters, and food stores. They should also be inaccessible to unauthorized persons, children and domestic animals (2).

Mevinphos must be stored in sealed original containers, in well ventilated, fresh and dry storehouses or in shaded, well aired places.

In aqueous solution, mevinphos is hydrolyzed with a half-life of 1.4 hr at pH 11, 3 days at pH 9, 35 days at pH 7, and 120 days at pH 6 (25).

Persons who work with organophosphate materials for long periods of time should have frequent blood tests of their cholinesterase levels. If the cholinesterase level falls below a critical point, no further exposure should be allowed until it returns to normal (30).

Protective clothing must be worn when handling mevinphos. Before removing gloves, wash them with soap and water. Always wash hands, face and arms with soap and water before smoking, eating or drinking.

After work, remove all work clothes and shoes. Shower with soap and water. Wear only clean clothes when leaving the job. Wash contaminated clothing and equipment with soap and water after each use. Keep contaminated work clothes separate from regular laundry.

Exposure Guidelines:

Air concentration of 40 mg/m3 is immediately dangerous to life or health (28).

OSHA TWA: (skin) 0.1 mg/m3 (28)
OSHA STEL: 0.3 mg/m3 (28)
ACGIH TWA (skin): 0.1 mg/m3 (28)
ACGIH STEL: 0.3 mg/m3 (28)
NIOSH Recommended TWA (skin): 0.1 mg/m3 (28)
NIOSH Recommended STEL: 0.3 mg/m3 (28)
ADI: 0.0025 mg/kg/day, based on a 2-year rat feeding study and a 10-fold safety factor (29).

Physical Properties:

CAS #: 7786-34-7
Specific gravity: 1.25 (25)
H20 solubility: miscible (22)
Solubility in other solvents: Technical mevinphos is miscible in alcohols, ketones, chlorinated hydrocarbons and aromatic hydrocarbons and most organic solvents.
It is slightly soluble in aliphatic hydrocarbons and petroleum ether.
It is highly soluble in acetone and benzene (9, 25, 26).
Melting point: 21 degrees C (cis-isomer); 6.9 degrees C (trans-isomer) (24)
Boiling point: 99 - 103 degrees C at 0.03 mm Hg (26); 617 degrees F (325 degrees C) (28).
Flash point: 30 degrees C (26); 175 degrees F (79 degrees C) (28).
Vapor pressure: 2.2 x 10 to the minus 3 mm Hg at 20 degrees C (9); 0.0029 mm Hg at 70 degrees F (22)
Koc: 1 g/ml (27)
Chemical Class/Use: organophosphate insecticide

BASIC MANUFACTURER

Amvac Chemical Corp.
4100 E. Washington Blvd.
Los Angeles, CA 90023

Review by Basic Manufacturer:

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

REFERENCES

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  2. Berg, G. L., ed. 1986. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing Company.
  3. Doull, J., C. D. Klaassen, and M. O. Amdur. 1980. Casarett and Doull's Toxicology: The basic science of poisons. Second edition. NY: MacMillan Publishing Company.
  4. Gillett, J. W. 1970. The biological impact of pesticides in the environment. Environmental Health Sciences Series No. 1. Corvallis, OR: Oregon State University.
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  7. Kahn, S. U. 1980. Pesticides in the soil environment. Amsterdam: Elsevier.
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  11. Morse, R. A. 1987. Bee poisoning. In 1988 New York State pesticide recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11. Cornell University, Ithaca, NY.
  12. National Institute for Occupational Safety and Health (NIOSH). 1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH: NIOSH.
  13. Occupational Health Services, Inc. 1986. Material safety data sheet on mevinphos. Secaucus, NJ: OHS, Inc.
  14. Pimentel, D. 1971 (June). Ecological effects of pesticides on nontarget species. Executive Office of the President's Office of Science and Technology. Washington, DC: U. S. Government Printing Office.
  15. Sax, N. I. 1979. Dangerous properties of industrial materials. Sixth edition. NY: VanNostrand Reinhold Co.
  16. Shell Chemical Company. 1972. Summary of basic data for mevinphos insecticide. Technical data bulletin. San Ramon, CA: Shell.
  17. TOXNET. 1986. National library of medicine's toxicology data network. Hazardous Substances Databank (HSDB). Public Health Service. National Institute of Health, United States Department of Health and Human Services. Bethesda, MD: NLM.
  18. Tucker, R. and D. G. Crabtree. 1970. Handbook of toxicity of pesticides to wildlife. U.S. Department of Agriculture, Fish and Wildlife Service. Bureau of Sport Fisheries and Wildlife. Washington, DC: U S. Government Printing Office.
  19. U. S. Department of Transportation. 1983. 1984 Emergency response guidebook. Guidebook for hazardous materials incidents. G-31. Washington, DC: D.O.T.
  20. U.S. Environmental Protection Agency. 1987 (Oct. 23). Subject: Active ingredients subject to restricted use classification. Office of Pesticide Programs, Registration Division. Washington, DC.
  21. _____. 1986. Memorandum from Ferial S. Bishop. List of federally restricted products. Registration Support and Emergency Response Branch (TS- 767). Washington, DC.
  22. _____. 1985 (Oct. 31). EPA chemical profile: Mevinphos. Washington, DC.
  23. 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.
  24. Worthing, C. R., ed. 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.
  25. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  26. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  27. 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.
  28. Occupational Health Services, Inc. 1991 (May 2). MSDS for Mevinphos. OHS Inc., Secaucus, NJ.
  29. US Environmental Protection Agency. 1984 (March 28). Methyl 3- [(Dimethoxyphosphinyl)Oxy] Butenoate, alpha and beta isomers; Proposed tolerance. Federal Register 49 (61): 11854.
  30. Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet : Dimethoate. Cheminova, Lemvig, Denmark.
  31. Wu, J., et. al. Metabolic fate of mevinphos in the lactating goat. AMVAC Chemical Corp., City of Commerce, CA.