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
Assessment Program.
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Pesticide
Information
Profile
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Mevinphos
Publication Date: 9/93
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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
American Conference of Governmental Industrial Hygienists, Inc. 1986.
Documentation of the threshold limit values and biological exposure indices.
Fifth edition. Cincinnati, OH: Publications Office, ACGIH.
Berg, G. L., ed. 1986. Farm Chemicals Handbook. Willoughby, OH:
Meister Publishing Company.
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.
Gillett, J. W. 1970. The biological impact of pesticides in the
environment. Environmental Health Sciences Series No. 1. Corvallis, OR:
Oregon State University.
Gosselin, R. E., et al. 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD:
Williams and Wilkins.
Kahn, S. U. 1980. Pesticides in the soil environment. Amsterdam:
Elsevier.
McEwen, F. L. and G. R. Stephenson. 1979. The use and significance
of pesticides in the environment. NY: John Wiley and Sons, Inc.
Melnikov, N. N. 1971. Chemistry of pesticides. New York: Springer-
Verlag, Inc.
Menzie, C. M. 1980. Metabolism of pesticides. Update III. U.S.
Department of the Interior. Fish and Wildlife Service. Special Scientific
Report. Wildlife No. 232. Washington, DC: U.S. Government Printing Office.
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.
National Institute for Occupational Safety and Health (NIOSH). 1986.
Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH:
NIOSH.
Occupational Health Services, Inc. 1986. Material safety data sheet
on mevinphos. Secaucus, NJ: OHS, Inc.
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.
Sax, N. I. 1979. Dangerous properties of industrial materials.
Sixth edition. NY: VanNostrand Reinhold Co.
Shell Chemical Company. 1972. Summary of basic data for mevinphos
insecticide. Technical data bulletin. San Ramon, CA: Shell.
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.
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.
U. S. Department of Transportation. 1983. 1984 Emergency response
guidebook. Guidebook for hazardous materials incidents. G-31. Washington, DC:
D.O.T.
U.S. Environmental Protection Agency. 1987 (Oct. 23). Subject:
Active ingredients subject to restricted use classification. Office of
Pesticide Programs, Registration Division. Washington, DC.
_____. 1986. Memorandum from Ferial S. Bishop. List of federally
restricted products. Registration Support and Emergency Response Branch (TS-
767). Washington, DC.
_____. 1985 (Oct. 31). EPA chemical profile: Mevinphos.
Washington, DC.
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.
Worthing, C. R., ed. 1983. The pesticide manual: A world
compendium. Croydon, England: The British Crop Protection Council.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
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.
Occupational Health Services, Inc. 1991 (May 2). MSDS for Mevinphos.
OHS Inc., Secaucus, NJ.
US Environmental Protection Agency. 1984 (March 28). Methyl 3-
[(Dimethoxyphosphinyl)Oxy] Butenoate, alpha and beta isomers; Proposed
tolerance. Federal Register 49 (61): 11854.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Wu, J., et. al. Metabolic fate of mevinphos in the lactating goat.
AMVAC Chemical Corp., City of Commerce, CA.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
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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