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E X T O X N E T
A Pesticide Information Project of Cooperative Extension
Offices of Cornell University, Oregon State University, the
University of Idaho, and the University of California at Davis
and the Institute for Environmental Toxicology, Michigan State
University. Major support and funding was provided by the
USDA/Extension Service/National Agricultural Pesticide Impact
EXTOXNET primary files maintained and archived at Oregon State
TRADE OR OTHER NAMES: Trade names
include AC 3422, Alkron, Alleron, Aphamite, Corothion, E-605, ENT
15108, Ethyl parathion, Etilon, Fosferno 50, Niran, Orthophos,
Panthion, Paramar, Paraphos, Parathene, Parawet, Phoskil,
Rhodiatox, Soprathion, Stathion and Thiophos. The common name
thiophos is used in the former USSR.
REGULATORY STATUS: Because of its high
toxicity and risks of exposure to agricultural workers and to
birds, and in response to the manufacturers' request, EPA in
January 1992 announced the cancellation of all uses of parathion
on fruit, nut and vegetable crops. The only uses retained are
those on alfalfa, barley, corn, cotton, sorghum, soybeans,
sunflowers and wheat. Further, to reduce exposure of agricultural
workers, parathion may be applied to these crops only by
commercially certified aerial applicators and treated crops may
not be harvested by hand. EPA intends to cancel all uses of
parathion in the near future (12, 13).
Parathion is one of the most acutely toxic pesticides registered
by the EPA. Because of its highly toxic nature, parathion is
classified as a Restricted Use Pesticide (RUP) (1, 3). RUPs may
be purchased and used only by certified applicators. Products
containing parathion must bear the signal word "Danger"
CHEMICAL CLASS: organophosphate
INTRODUCTION: Parathion is a broad
spectrum, organophosphate pesticide used to control many insects
and mites (5, 8). It has non-systemic, contact, stomach and
fumigant actions (5, 8). It has a wide range of applications on
many crops against numerous insect species (1). Parathion is
available in dust, emulsion concentrate, granular, ULV liquid,
and wettable powder formulations (3).
Parathion 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
- Acute Toxicity: Parathion is highly
toxic by all routes of exposure. Human fatalities have
been caused by ingestion, dermal adsorption, and
inhalation of parathion (2). As with all
organophosphates, parathion is readily absorbed through
the skin (1). Skin which has come in contact with this
material should be washed immediately with soap and water
and all contaminated clothing should be removed. Persons
with cardiovascular, liver or kidney diseases, glaucoma,
or central nervous system abnormalities may be at
increased risk from exposure to parathion. High
environmental temperatures or exposure of the chemical to
visible or UV light may increase its toxicity (11).
Parathion may cause thickening and roughening of the skin
(hyperkeratinization). It does not cause sensitization
(allergies). Parathion is not irritating to the eyes.
Splashing parathion into an eye may cause constriction of
the pupil, making it difficult to determine the path of
moving objects. Organophosphates are used to treat
diseases of the eye, like glaucoma. It is possible,
though, that they cause cataracts to form (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, 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 (12). 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 parathion is 2 to 30
mg/kg in rats, 5 to 25 mg/kg in mice, 8 to 32 mg/kg in
guinea pigs, 10 mg/kg in rabbits, 0.93 mg/kg in cats, and
3 to 5 mg/kg in dogs (2, 3, 11). The dermal LD50 in rats
is 6.8 to 50 mg/kg (2, 3), in mice is 19 mg/kg, in guinea
pigs is 45 mg/kg, and in rabbits is 15 mg/kg (11). The
lowest dosage with toxic effects (TDlo) in humans is 240
ug/kg (less than 0.1 ounce). 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
inhalation LC50 for parathion in rats is 84 mg/m3 (11).
- Chronic Toxicity: 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 (12). One study found that dietary doses of
50 ppm (about 2.5 mg/kg/day) produced toxic symptoms,
growth retardation and death in rats. In another feeding
study, dietary doses of 2.5 mg/kg/day for 2-years had no
effect on rats, while doses of 5 mg/kg/day produced only
slight signs of toxicity and growth retardation, but no
- Reproductive Effects: Once in the
bloodstream, parathion may cross the placenta (7, 11).
Repeated feedings to female rats before mating resulted
in adverse effects on the reproductive system (11). In
lab animals, such as rats and mice, several effects are
seen. Fewer pups are born to dams fed parathion. These
pups have reduced birth weight and do not tend to survive
as well as normal pups (IARC Monographs, 16).
- Teratogenic Effects: While parathion is
toxic to the fetus, it does not cause birth defects (2).
- Mutagenic Effects: Dietary doses of
parathion failed to produce dominant lethal effects in
- Carcinogenic Effects: Parathion is a
possible carcinogen (14).
- Organ Toxicity: Parathion primarily
affects the nervous system through inhibition of
cholinesterase, an enzyme required for proper nerve
functioning. In humans poisoned with parathion, an
increase in brain weight occurs. It is not understood why
this happens (Z. Rechtsmed 90 (3):173 - 189. 1983). Dogs
have changes in their livers (NRC Drinking Water and
Health 1977). Delayed neurotoxicity is not a problem with
parathion (Toxicol. 23 (4):267-279. 1982).
- Fate in Humans and Animals: Parathion is
readily absorbed into the bloodstream from the skin,
lungs or gut (7). The vapor pressure of parathion is so
low that breathing the vapor alone is not a likely source
of poisoning. Breathing dusts, or aerosols, may be
extremely dangerous (6). Parathion is rapidly distributed
through the body. The liver metabolizes parathion into
the active metabolite: paraoxon. It is paraoxon that
actually inhibits the cholinesterase. Paraoxon is further
metabolized to compounds such as paranitrophenol which is
readily excreted in the urine. Parathion may be stored in
fat. Unlike the organochlorine pesticides (DDT), the
organophosphates (parathion) are rapidly broken down once
they are mobilized from the fat stores (6).
- Effects on Birds: Parathion is extremely
toxic to birds (4) such as mallards, pigeons (5), quail,
sparrows and grouse (4). It is less toxic to pheasants
(5). The LD50 for parathion in bobwhite quail is 6 mg/kg
(3), 3 mg/kg in pigeons, and 2.1 mg/kg in ducks (Hdbk
Acute Tox. Chem. Fish & Aquatic Inverts. 1980).
(NIOSH RTECS Online File # 84/8406).
- Effects on Aquatic Organisms: Parathion
is moderately toxic to fish and aquatic invertebrates
(like crayfish, snails and worms) (5, 8, 16). The 96-hour
LC50 for parathion in fish in general is 1.43 mg/l (3).
The 96-hour LC50 in trout is 1.6 mg/l, 1.8 mg/l in
goldfish, 2.7 mg/l in catfish, 0.3 mg/l in mosquito fish,
and 0.02 mg/l in bluegill (Hdbk Acute Tox. Chem. Fish
& Aquatic Inverts. 1980). (NIOSH RTECS Online File #
- Effects on Other Animals (Non-target species):
The 24-hour LD50 for parathion in honeybees is 0.07 to
0.10 ug/bee when applied topically (3). The LD50 for
parathion in mule deer is 22-44 mg/kg (Hdbk Acute Tox.
Chem. Fish & Aquatic Inverts. 1980). (NIOSH RTECS
Online File # 84/8406). Some fat storage of parathion
does occur. However, upon release from fat storage,
parathion is rapidly broken down and eliminated.
Bioconcentration of parathion is low to moderate. There
is no evidence of bioaccumulation of parathion in cattle,
sheep or rabbits (10).
- Breakdown of Chemical in Soil and Groundwater:
Parathion has little or no potential for groundwater
contamination (3). It binds tightly to soil particles and
is degraded by biological and chemical processes within
several weeks. Degradation is faster in flooded soil.
Residues of parathion can persist for many years, but
usually remain in the upper 6 inches of soil.
Photodegradation may occur on soil surfaces (10).
Sunlight can convert parathion into the active metabolite
paraoxon, which is more toxic than parathion. The
breakdown of parathion in soil or water increases with
increasing (more alkaline) pH. Soil microorganisms,
sunlight, plants and water all break parathion down.
- Breakdown of Chemical in Water: In open
water, parathion will usually disappear within a week,
mainly by adsorption to suspended particles and bottom
sediments. Adsorbed parathion is subject to degradation
by microorganisms and chemical hydrolysis. The half-life
for photo-degradation of parathion in water is 1 to 10
days. Increasing the pH (alkalinity), increases the rate
of breakdown (10).
- Breakdown of Chemical in Vegetation:
Following spray applications, parathion residues on
foliage will decay with a half-life of 1 day, reaching
low levels in a week or two (10). In orange groves, the
half-life of parathion is as long as one month. Usually,
it is closer to one-two weeks. Most crops tolerate
parathion very well. Only at high application rates do
apples, cucumbers, and tomatoes suffer from parathion
PHYSICAL PROPERTIES AND GUIDELINES
Parathion hydrolyzes slowly at pH 7 or below, but is otherwise
stable at normal temperatures (3). At temperatures above 120
degrees C, parathion decomposes and may develop enough pressure
to cause containers to explode. Thermal decomposition may release
toxic gases such as diethylsulfide, sulfur dioxide, carbon
monoxide, carbon dioxide, phosphorus pentoxide, and nitrogen
oxides (3). Parathion poses a fire and explosion hazard in the
presence of strong oxidizers. It may attack plastics, rubber and
coatings (11). 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 (15).
Protective clothing must be worn when handling fenthion.
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.
The National Fire Protection Agency ratings for parathion
include: A. health: 4 = a few whiffs of the fumes could prove
fatal; normal fire fighting gear is inadequate to protect against
any exposure to the skin. B. flammability: 1 = solids which must
be preheated to burn, but which are combustible. It may be
dangerous to use water to extinguish burning parathion. C.
reactivity: 2 = normally unstable materials which will react
violently (with water). Also, it is potentially explosive when
mixed with water (18).
- Appearance: Pure parathion is a pale
yellow liquid with a faint odor of garlic at temperatures
above 6 degrees C. Technical parathion is a deep brown to
yellow liquid (2, 11).
- Chemical Name: O,O-diethyl
- CAS Number: 56-38-2
- Molecular Weight: 291.3
- Water Solubility: 12.4 mg/l at 25
degrees C (3); 24 ppm (11)
- Solubility in Other Solvents: Soluble in
alcohols, animal & vegetable oils, aromatic
hydrocarbons, esters, ethers, n-hexane, dichloromethane,
2-propanol, toluene and ketones. Insoluble in kerosene,
petroleum ether, or spray oil (2, 3, 11, 19).
- Melting Point: 43 degrees F (6 degrees
- Vapor Pressure: 8.9 x 10 to the minus 6
mm Hg at 20 degrees C (3); 4 x 10 to the minus 5 mm Hg at
20 degrees C (11)
- Partition Coefficient: 3.83
- Adsorption Coefficient: Not Available
- ADI: 0.004 mg/kg b.w.
- MCL: Not Available
- RfD: Not Available
- PEL: Not Available
- HA: Not Available
- TLV: Not Available
Crop Protection and Animal Health Div.
PO Box 4913
Kansas City MO 64120
(1) Meister, R.T. (ed.) 1987. Farm Chemicals Handbook.
Willoughby, OH: Meister Publishing Co.
(2) Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of
Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic
Press, Inc., NY.
(3) Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92.
Meister Publishing Company, Willoughby, OH.
(4) Tucker, Richard. 1970. Handbook of toxicity of pesticides
to wildlife. USDI Fish & Wildlife Service.
(5) Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council. Croydon,
(6) Hayes, Wayland, Jr. 1982. Pesticides studied in man.
Baltimore, MD: Williams & Wilkins.
(7) Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides:
chemistry, degradation, and mode of action. 2nd Ed. Vol. 1 &
2. New York: M. Dekker.
(8) Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals
handbook. Nottingham, England: Royal Society of Chemistry.
(9) U. S. Department of Agriculture, Soil Conservation
Service. 1990 (Nov.). SCS/ARS/CES Pesticide Properties Database:
Version 2.0 (Summary). USDA - Soil Conservation Service,
(10) Howard, P.H. (ed.). 1989. Handbook of Environmental Fate
and Exposure Data for Organic Chemicals, Vol. III: Pesticides.
Lewis Publishers, Chelsea, MI.
(11) Occupational Health Services, Inc. 1991 (Feb. 25). MSDS
for Parathion. OHS Inc., Secaucus, NJ.
(12) US Environmental Protection Agency. 1992 (Feb. 4). Ethyl
Parathion, Correction to the Amended Cancellation Order. OPP,
USEPA, Washington DC.
(13) _____. 1991 (Dec.). Notice of Voluntary Cancellation of
Parathion Registrations Except for Use on Field Crops. US EPA,
(14) Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985.
Pesticides and human health. New York: Springer-Verlag.
(15) Cheminova Agro A/S. 1991 (June 11). Material Safety Data
Sheet : Dimethoate. Cheminova, Lemvig, Denmark.
(16) TOXNET. 1985. National library of medicine's toxicology
data network. Hazardous Substances Databank. Public Health
Service. National Institute of Healtyh. U.S. Department of Health
and Human Services. Bethesda, MD: NLM.
(17) Gosselin, R.E. 1984. Clinical toxicology of commercial
products. 5th Ed. Baltimore, MD: Williams & Wilkins.
(18) National Fire Protection Association (NFPA). 1978. Fire
Protection Guide. Hazardous Materials.
(19) Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia
of chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
DISCLAIMER: The information in
this profile does not in any way replace or supersede the
information on the pesticide product label/ing or other
regulatory requirements. Please refer to the pesticide product