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.
| |
Pesticide
Information
Profile
|
Parathion
Publication Date: 9/93
|
|
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" (3).
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 topic.
TOXICOLOGICAL EFFECTS
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 deaths (2).
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
mice (2).
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).
ECOLOGICAL EFFECTS
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 # 84/8406).
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).
ENVIRONMENTAL FATE
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 usage (8).
PHYSICAL PROPERTIES AND GUIDELINES
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). 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).
Exposure Guidelines:
Air concentrations of 20 mg/m3 or higher are immediately dangerous to life or
health (11).
| OSHA TWA (skin): | 0.1 mg/m3 (11) |
| ACGIH TWA (skin): | 0.1 mg/m3 (11) |
| NIOSH Recommended TWA (skin): | 0.05 mg/m3 (11) |
| Odor threshold: | 0.04 ppm (11) |
Physical Properties:
| CAS #: | 56-38-2 |
| Specific gravity: | 1.26 (3) |
| Viscosity: | 15.30 CPS at 25 degrees C (11) |
| Solubility in water: | 12.4 mg/l at 25 degrees C (3); 24 ppm (11) |
| Solubility: | 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). |
| Boiling point: | 375 degrees C (707 degrees F) at 760 mm Hg (19) |
| Melting point: | 43 degrees F (6 degrees C) (11) |
| Flash point: | 174 degrees C, decomposes rapidly above 120 degrees C (3); >200 degrees F (>93 degrees C) (11) |
| 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) |
| Oil: | water partition coefficient: |
| Chemical class/use: | organophosphate insecticide |
BASIC MANUFACTURER
Miles, Inc.
Crop Protection and Animal Health Div.
PO Box 4913
Kansas City MO 64120
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received:
REFERENCES
Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby, OH:
Meister Publishing Co.
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.
Tucker, Richard. 1970. Handbook of toxicity of pesticides to
wildlife. USDI Fish & Wildlife Service.
Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council. Croydon, England.
Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore, MD:
Williams & Wilkins.
Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides: chemistry,
degradation, and mode of action. 2nd Ed. Vol. 1 & 2. New York: M. Dekker.
Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
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.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers,
Chelsea, MI.
Occupational Health Services, Inc. 1991 (Feb. 25). MSDS for
Parathion. OHS Inc., Secaucus, NJ.
US Environmental Protection Agency. 1992 (Feb. 4). Ethyl Parathion,
Correction to the Amended Cancellation Order. OPP, USEPA, Washington DC.
_____. 1991 (Dec.). Notice of Voluntary Cancellation of Parathion
Registrations Except for Use on Field Crops. US EPA, Washington, DC.
Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and human
health. New York: Springer-Verlag.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
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.
Gosselin, R.E. 1984. Clinical toxicology of commercial products.
5th Ed. Baltimore, MD: Williams & Wilkins.
National Fire Protection Association (NFPA). 1978. Fire Protection
Guide. Hazardous Materials.
Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of
chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
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.
To Top
For more information relative to pesticides and their use in New York State, please contact the PMEP staff at:
| |
5123 Comstock Hall
Cornell University
Ithaca, NY 14853-0901
(607) 255-1866
|
PLEASE NOTE: If you are not in New York State, you must contact the appropriate
agency for your area.
|
 |
This site is supported, in part, by funding from the
 |
Questions regarding the development of this web site should be directed to the
PMEP Webmaster
