E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
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University of California at Davis. Major support and funding was provided
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Pesticide
Information
Profile
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Dichlorvos
Publication Date: 9/93
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TRADE OR OTHER NAMES
Apavap, Benfos, Cekusan, Cypona, Derriban, Derribante Devikol,
Didivane, Duo-Kill, Duravos, Elastrel, Fly-Die, Fly-Fighter, Herkol,
Marvex, No-Pest, Prentox, Vaponite, Vapona, Verdican, Verdipor,
Verdisol. Trade names used outside of the U.S. include Doom, Nogos, and
Nuvan (2).
REGULATORY STATUS
A Special Review of dichlorvos was initiated in February 1988
because EPA determined that the registered uses of dichlorvos may pose a
risk of cancer as well as inadequate margins of safety for
cholinesterase inhibition and liver effects to exposed persons (12).
The Special Review was not complete as of March 1992 (10). Products
containing dichlorvos must bear the signal words "Danger-Poison" (2).
INTRODUCTION
Dichlorvos is used to control household, public health, and stored
product insects. It is effective against mushroom flies, aphids, spider
mites, caterpillars, thrips, and white flies in greenhouse, outdoor
fruit, and vegetable crops (2). Therapeutically, dichlorvos is used to
treat a variety of parasitic worm infections in dogs, livestock and
humans. Dichlorvos can be fed to livestock to control botfly larvae in
the manure. It acts against insects as both a contact and a stomach
poison (2). Dichlorvos is available in aerosol and soluble concentrate
formulations (2). It is used as a fumigant (2) and has been used to
make pet collars and pest strips (3).
Dichlorvos 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.
In 1955, it was discovered that crystalline trichlorfon, another
organophosphate pesticide, gave off a vapor which was capable of killing
insects. That vapor was dichlorvos, which has since been developed for
insect control in enclosed spaces (3).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Dichlorvos is highly toxic by inhalation, dermal absorption and
ingestion (9). Because dichlorvos is volatile, inhalation is the most
common route of exposure. As with all organophosphates, dichlorvos 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.
Acute illness from dichlorvos is limited to the effects of
cholinesterase inhibition. Compared to poisoning by other
organophosphates, dichlorvos causes a more rapid onset of symptoms,
which is often followed by a similarly rapid recovery (3). This occurs
because dichlorvos is rapidly metabolized and eliminated from the body.
Persons with reduced pulmonary (lung) function, convulsive disorders,
liver disorders, or recent exposure to cholinesterase inhibitors will be
at increased risk from exposure to dichlorvos. Alcoholic beverages may
enhance the toxic effects of dichlorvos. High environmental
temperatures or exposure of dichlorvos to visible or UV light may
enhance its toxicity (9).
Dichlorvos is mildly irritating to skin (9). Concentrates of
dichlorvos may cause burning sensations, or actual burns (6).
Dichlorvos can be very toxic if it is not immediately washed off, but
instead left on the skin long enough for it to become absorbed through
the skin and into the bloodstream. One man nearly died after spilling 4
ounces of a 3% oil solution of dichlorvos on his lap. He did not wash
it off. Another man only became nauseous and dizzy after spilling a
similar amount on his arm. He washed off the dichlorvos with soap and
water (6). Do not use organic solvents to remove dichlorvos from the
skin (DLA/DOD Hazardous Mat'ls Info. System #0014-29- 438-0000. 1982).
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, difficult or short 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 (9).
Some organophosphates may cause delayed symptoms beginning 1 to 4
weeks after an acute exposure which may or may not have produced
immediate symptoms. In such cases, numbness, tingling, weakness and
cramping may appear in the lower limbs and progress to incoordination
and paralysis. Improvement may occur over months or years, but some
residual impairment will remain (9).
The administration of slow-release formulations of dichlorvos to
domestic animals to treat for internal parasites has caused some
inhibition of cholinesterase and mild symptoms such as nausea or
diarrhea, but no serious signs of illness. Repeated, small doses
generally have no effect on treated animals. Doses of up to 4 mg/kg of
a slow release formulation, given to cows to reduce flies in their
feces, had no visibly adverse effects on the cows. Blood tests of these
cows indicated cholinesterase inhibition (3).
Dichlorvos is very volatile, meaning that it readily forms vapors
which may be inhaled. Inhalation is the most common way to be exposed
to dichlorvos. Low, repeated doses may be non-toxic. High doses of
dichlorvos may be very toxic, especially if inhalation exposure is
continuous (6). Dichlorvos produces irritating gases, such as
phosphorous and chlorine oxides, when heated (NIH/EPA 1984).
Eye protection should be worn when handling dichlorvos.
Application of 1.67 mg/kg in rabbits' eyes produced mild redness and
swelling, but no injury to the cornea (9). Dichlorvos may cause eye
burns. Organophosphates cause the pupils to constrict (pin point
pupils).
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 dichlorvos in mice is 61
to 175 mg/kg, 100 to 1090 mg/kg in dogs, 15 mg/kg in chickens, 25 to 80
mg/kg in rats, 157 mg/kg in pigs, and 11 to 12.5 mg/kg in rabbits (2, 6,
9). The dermal LD50 for dichlorvos in rats is 70.4 to 250 mg/kg, 206
mg/kg in mice, and 107 mg/kg in rabbits (2, 3, 6, 9).
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 4-hour LC50 for dichlorvos in
rats is 15 mg/m3, and 13 mg/m3 in mice (9).
CHRONIC TOXICITY
Feeding studies indicate that a dosage of dichlorvos very much
larger than doses which inhibit cholinesterase are needed to produce
illness. Rats tolerated dietary doses as high as 62.5 mg/kg/day for 90
days with no visible signs of illness, while a dietary level of 0.25
mg/kg/day for only 4 days produced a reduction in cholinesterase levels
(3).
Rats were exposed to air concentrations of 0, 0.05, 0.5 and 5 mg/m3
of dichlorvos over a 5 week period. Rats in the 0.5 and 5 mg/kg groups
exhibited significantly decreased cholinesterase activity in the plasma,
red blood cells, and brain. The NOEL for this study was 0.05 mg/m3. In
dogs fed dietary doses of 0.0095, 0.016, 0.16, 1.6 or 12.5 mg/kg/day for
2 years, decreased red blood cell cholinesterase activity, increased
liver weights and increased liver cell size occurred in the two highest
doses tested. The NOEL was 0.08 mg/kg/day (12). Chronic exposure to
dichlorvos will cause fluid to build up in the lungs (pulmonary edema)
(NIH/EPA; OHM/TADS 1984).
Repeated or prolonged exposure to organophosphates may result in
the same effects as acute exposure including the delayed symptoms.
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. An
influenza-like condition with headache, nausea, weakness, loss of
appetite, and malaise has also been reported (9).
Reproductive Effects
When male and female rats were given a diet containing 100 ppm (5
mg/kg/day) dichlorvos just before mating, and with this dosage continued
through pregnancy and lactation for females, there were no effects on
reproduction or on the survival or growth of the offspring, even though
severe cholinesterase inhibition occurred in the mothers and significant
inhibition occurred in the offspring. The same results were observed in
a 3-generation study with rats fed dietary levels up to (25 mg/kg/day)
(3). Once in the bloodstream, dichlorvos may cross the placenta (9).
Teratogenic Effects
A dose of 12 mg/kg was not teratogenic in rabbits and did not
interfere with reproduction in any way. There was no evidence of
teratogenicity when rats and rabbits were exposed to air concentrations
of up to 6.25 mg/m3 throughout pregnancy. Dichlorvos was not
teratogenic when given orally to rats (3).
Mutagenic Effects
Dichlorvos can bind to molecules such as DNA. For this reason,
there has been extensive testing of dichlorvos for mutagenicity.
Several studies reviewed by EPA have shown dichlorvos to be a mutagen
(12). Dichlorvos is reported positive in the Ames mutagenicity assay
(Mut. Res. 87:211 (1981); 76:169 (1980); 40 (1):19 (1976) and in other
tests involving bacterial or animal cell cultures. However no evidence
of mutagenicity has been found in tests performed on live animals. Its
lack of mutagenicity in live animals may be due to rapid metabolism and
excretion of dichlorvos (3).
Carcinogenic Effects
Dichlorvos has been classified as a possible human carcinogen by
EPA because of the results of tests on rats and mice (11). When
dichlorvos was administered by gavage to mice for 5 days per week for
103 weeks at doses of 10 or 20 mg/kg to males and 20 or 40 mg/kg to
females, there was an increased incidence of benign tumors in the lining
of the stomach at the high dose for both sexes. When rats given daily
doses of 0, 4 or 8 mg/kg for five days per week for 103 weeks, there was
an increased incidence of benign tumors of the pancreas and of leukemia
in male rats at both doses. At the highest dose, there was also an
increased incidence of benign lung tumors in males. In female rats,
there was an increase in the incidence of benign tumors of the mammary
gland (12). No tumors caused by dichlorvos were found in rats fed up
to 25 mg/kg/day for 2 years or in dogs fed up to 11 mg/kg/day for 2
years. No evidence of carcinogenicity was found when rats were exposed
to air containing up to 5 mg/m3 for 23 hours/day for 2 years (3). A few
tumors were found in the esophagus of mice given dichlorvos orally, even
though tumors of this kind are normally rare (9).
Organ Toxicity
Dichlorvos primarily affects the nervous system through
cholinesterase inhibition, by which there is a deactivation of
cholinesterase, an enzyme required for proper nerve functioning.
Dichlorvos causes fluid to accumulate in the lungs (6). Liver
enlargement has occurred in pigs maintained for long periods of time on
high doses (500 ppm) (3, 6). Dichlorvos caused adverse liver effects in
dogs (12). Lung hemorrhages may occur (14). Cholinesterase inhibition
may affect the nervous system. In mice, a single oral dose of 40
micrograms (ug)/kg caused changes in the testes. In male rats, repeated
doses caused abnormalities in the tissues of the lungs, heart, thyroid,
liver and kidneys (9).
Fate in Humans and Animals
Amongst the organophosphates, dichlorvos is remarkable for its
rapid metabolism and excretion by mammals. Dichlorvos was not detected
in the blood of rats, mice or people after exposure to atmospheric
concentrations of up to 17 times that normally reached for insect
control in homes. Exposure of rats to 11 mg/m3 (250 times the normal
exposure) for 4 hours was required before dichlorvos was detectable in
the rats. Even then, it was detected only in the kidneys. At 90 mg/m3
(2000 times normal exposure), dichlorvos was detected in most tissues of
the rat. Following exposure to 50 mg/m3, the half-life for dichlorvos
in the rat kidney was 13.5 minutes. The reason for this rapid
disappearance of dichlorvos is the presence of degrading enzymes in both
tissues and blood plasma. From the gastrointestinal tract, dichlorvos is
absorbed into the portal blood, rather than into the general
bloodstream. From the portal blood, it is moved to the liver where it
is rapidly detoxified. Thus poisoning by nonlethal doses of dichlorvos
is usually followed by rapid detoxification in the liver and recovery.
Rats given oral or dermal doses at the LD50 level either died within one
hour of dosing or recovered completely (3, 6).
Dichlorvos does not accumulate in body tissues and has not been
detected in the milk of cows or rats, even when the animals were given
doses high enough to produce symptoms of severe poisoning (3).
ECOLOGICAL EFFECTS
Effects on Birds
Dichlorvos is highly toxic to birds including ducks and pheasants
(4, 8). The LD50 for wild birds fed dichlorvos is 12 mg/kg (NIOSH RTECS
Online File #82/8110).
Effects on Aquatic Organisms
UV light makes dichlorvos more toxic to aquatic life by 5-150 times
(15). NIH/EPA found the grass shrimp to be more sensitive to dichlorvos
than the sand shrimp, hermit crab and mummichog (in that order) (1984).
For ocean-dwelling species they found: scud > Atlantic silverside >
striped killfish > striped mullet > bluehead > American eel > northern
puffer; where ">" indicates a greater sensitivity to dichlorvos. The
96-hour LC50 for dichlorvos in fathead minnow is 11.6 mg/l, 0.9 mg/l in
bluegill, 5.3 mg/l in mosquito fish, 0.004 ppm in sand shrimp, 3.7 ppm
in mummichogs, and 1.8 ppm/96 hours in American eels (NIH/EPA 1984).
The 24-hour LC50 for dichlorvos in bluegill sunfish is 1.0 mg/l (2).
Dichlorvos does not significantly bioaccumulate in fish (4).
Effects on Other Animals (Nontarget species)
Dichlorvos is toxic to bees (2).
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
Dichlorvos does not adsorb to soil particles and it is likely to
contaminate groundwater. When spilled on soil, dichlorvos leached into
the ground with 18 to 20% penetrating to a depth of 30 cm within 5 days.
In soil, dichlorvos is subject to hydrolysis and biodegradation.
Volatilization from moist soils is expected to be slow. Half-lives of 7
days were measured on clay, sandy-clay, and loose sandy soil (4).
Dichlorvos is rapidly broken down in the air and in damp media such
as soil. The pH of the media determines the rate of breakdown.
Alkaline soils, water, etc., show rapid breakdown, whereas acidic media
shows slow degradation. For instance, at a pH of 9.1 the half-life of
dichlorvos is about 4.5 hours. At a pH of 1 (very acidic), the half-
life is 50 hours (8). Dichlorvos is non-persistent.
Breakdown of Chemical in Water
In water dichlorvos remains in solution and does not adsorb to
sediments. It degrades primarily by hydrolysis, with a half-life of
approximately 4 days in lakes and rivers. This half-life will vary from
20 to 80 hours between pH 4 and pH 9. Hydrolysis is slow at pH 4 and
rapid at pH 9 (4, 5). Biodegradation may occur, especially under acidic
conditions which slow hydrolysis, or where populations of acclimated
micro-organisms exist, as in polluted waters. Volatilization from water
is expected to be slow. The volatilization half-life from river and
pond waters have been estimated at 57 and over 400 days respectively
(4).
Breakdown of Chemical in Vegetation
Except for cucumbers, roses, and some chrysanthemums, plants
tolerate dichlorvos very well (5).
PHYSICAL PROPERTIES AND GUIDELINES
Dichlorvos is a colorless to amber liquid with a mild chemical
odor. Dilute dichlorvos breaks down rapidly in the presence of
moisture. Concentrated forms are readily decomposed by strong acids and
bases (3). Dichlorvos is stable under normal temperatures and
pressures, but it may pose a moderate fire hazard if exposed to heat or
flame. It may hydrolyze on contact with moisture, and may decompose in
the presence of strong acids or bases (3, 9). Thermal decomposition of
dichlorvos will release toxic oxides of phosphorus and carbon, toxic and
corrosive chlorides and toxic phosgene gas. Dichlorvos is corrosive to
iron and steel. It may attack materials such as plastics, rubber and
coatings (9). Other metals (stainless steel, aluminum, nickel) are
resistant if no water is present.
Dichlorvos increases the effects of malathion (5). Alcoholic
beverages promote the absorption of dichlorvos into the bloodstream (8).
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 (13).
Protective clothing must be worn when handling dichlorvos. 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:
| 1 mg/m3 OSHA TWA (skin) (9) |
| 0.1 ppm (0.9 mg/m3) ACGIH TWA (skin) (9) |
| 1 mg/m3 NIOSH Recommended TWA (skin) (9) |
| Air concentrations of 200 mg/m3 are immediately dangerous to life or health (9). |
| PADI: | 8 x 10 to the minus 4 power mg/kg/day, based on a 2-year dog feeding study (12) |
Physical Properties
| CAS #: | 62-73-7 |
| Specific gravity: | 1.44 (60 degrees /60 degrees F) (2) |
| Solubility in water: | 1 g/100g at 25 degrees C (17) |
| Solubility: | Miscible in non-polar solvents such as dichloromethane, 2-propanol and toluene (2, 17). Soluble in ethanol, chloroform, acetone, and kerosene (1, 5). Miscible in alcohol and in aromatic and chlorinated hydrocarbon solvents. Solubility in kerosene and mineral oils is about 3% (3). |
| Boiling point: | 140 degrees C at 20 mm Hg (17); 117 degrees C at 11 mm Hg (2); 35 degrees C at 0.05 mm Hg (3); 183 degrees F (84 degrees C) (9) |
| Flash point: | >175 degrees F (>80 degrees C) (2, 16), practically non-flammable (17). |
| Vapor pressure: | 0.01 mm Hg at 30 degrees C (18) |
| Chemical class/use: | Organophosphate insecticide |
BASIC MANUFACTURER
Amvac Chemical Corp.
4100 E. Washington Blvd.
Los Angeles CA 90023
Review by Basic Manufacturer
Comments solicited: January, 1992.
Comments received: April, 1992.
REFERENCES
Farm Chemicals Handbook. Ed by R.T. Meister. Meister Publishing
Co., Willoughby, OH. 1987.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis
Publishers, Chelsea, MI.
The Pesticide Manual. 8th Ed. Ed. by C.R. Worthing. British Crop
Protection Council. 1987.
Pesticides Studied in Man. Wayland Hayes, Jr. Williams and
Wilkins, Baltimore, MD. 1982.
Herbicides. 2nd Ed. Vols. 1, 2. Kearney. 1975.
The Agrochemicals Handbook. The Royal Society of Chem. 1983.
Occupational Health Services, Inc. 1991 (May 15). MSDS for
Dichlorvos. OHS Inc., Secaucus, NJ.
US Environmental Protection Agency. 1992 (March). Status of
Pesticides in Reregistration and Special Review (H-7508W). Prevention,
Pesticides and Toxic Substances, US EPA, Washington, DC.
_____. 1991 (Feb. 13). Dichlorvos; Revocation of tolerance and
food additive regulation. Federal Register 56 (30): 5788-9.
_____. 1988 (Feb. 24). Dichlorvos; Initiation of Special Review.
Federal Register 53 (36): 5542-9.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Pesticides and Human Health. Hallenbeck & Cunningham-Burns.
Springer-Verlag.
TOXNET. 1985. National library of medicine's toxicology data
network. Hazardous Substances Databank. Public health Service.
National Institute of Health. U.S. Department of Health and Human
Services. Bethesda, MD: NLM.
National Fire Protection Association (NFPA). Fire Protection
Guide. Hazardous Materials. 1978.
Merck Index 9th Ed. 1976.
Handbook of Analytical Toxicology. Sunshine. 1969.
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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