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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Malathion
Publication Date: 9/93
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TRADE OR OTHER NAME
Malathion is also known as carbophos, maldison and mercaptothion.
Trade names for products containing malathion include Celthion, Cythion,
Dielathion, Karbofos, Maltox, El 4049, Emmaton, Fyfanon and Exathion
among many others. Malathion may also be found in formulations with
many other pesticides.
INTRODUCTION
Malathion is a non-systemic, wide spectrum insecticide. It was one
of the earliest organophosphate insecticides developed (introduced in
1950). Malathion is suited for the control of sucking and chewing
insects on fruits and vegetables. Malathion is also used to control
mosquitoes, flies, household insects, animal parasites (ectoparasites)
and head and body lice.
Malathion is a general use pesticide.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Malathion is classified as slightly toxic and carries the signal
word CAUTION on the label. The acute effects of malathion depend on
product purity and the vehicle of administration (5). Thus the LD50 for
rats ranges from 480 to 10,700 mg/kg and from 775 to 3,321 mg/kg for
mice. Several other factors also affect the toxicity of the pesticide.
For example, the toxicity of malathion appeared to be strongly linked to
the amount of protein in the diet of laboratory rats (13). As protein
intake decreased, malathion was increasingly toxic to the rats.
Malathion has been shown to have different toxicities in male and female
rats (12) and humans due to metabolism, storage and excretion
differences between the sexes. For humans, the lowest dose at which
lethal effects have been observed was nearly three times higher for
males than for females. Acute symptoms in humans include nausea,
headache, tightness in the chest, and other symptoms typical of acetyl-
cholinesterase inhibition. Unconsciousness, convulsions, and a
"prolonged worsening illness" are also typical of malathion poisoning at
high doses (14).
There is one reported case of malathion poisoning of an infant who
exhibited severe signs of cholinesterase inhibition after exposure to an
aerosol bomb containing 0.5% malathion (3). Numerous other malathion
intoxication incidents have occurred among pesticide workers and with
small children through accidental exposure. Human exposures can occur
through ingestion, inhalation, and absorption through the skin.
As with many other organophosphate insecticides, malathion, at
relatively high doses (near the LC50) can act to suppress the immune
system in some animal species (16).
CHRONIC TOXICITY
Human volunteers fed very low doses of malathion for one and a half
months showed no significant effects on blood cholinesterase activity.
Rats fed diets containing 100-1,500 ppm of malathion in their food for
two years showed no symptoms apart from depressed cholinesterase
activity. When small amounts of the compound were administered for
eight weeks, rats showed no adverse effects on whole-blood
cholinesterase activity. Weanling male rats were twice as susceptible
to malathion as adults.
Reproductive and Teratogenic Effects
Several studies have documented developmental and reproductive
effects due to high doses of malathion in test animals (14). However,
malathion fed to rats at a low dosages caused no reproductive effects.
Malathion and its metabolites can cross the placenta of the goat
and depress cholinesterase activity of the fetus (6). Rats fed high
doses (240 mg/kg) showed no teratogenic effects, but similar doses (300
mg/kg) administered by stomach tube during pregnancy caused an increased
rate of newborn mortality. Chickens fed diets at low doses for two
years showed no adverse effects on egg hatching. There is no direct
evidence that malathion is teratogenic in mammals.
Mutagenic Effects
Malathion produced detectable mutations in three different types of
cultured human cells, including white blood cells and lymph cells. It
is possible that malathion could pose a mutagenic risk to humans
chronically exposed.
Carcinogenic Effects
Female mice fed approximately 1% diets of malathion for over three
years showed no significant increased tumor incidence. Female rats on
diets containing high concentrations of malathion for two years did not
develop tumors. Adrenal tumors developed in the males at low doses, but
not at the high doses (2), suggesting that malathion may not have been
the cause. Three of five studies that have investigated the
carcinogenicity of malathion have found that the compound does not
produce tumors in the test animals. The two other studies have been
determined to be unacceptible studies and the results discounted.
Additional studies are being requested by the EPA (17). While it seems
unlikely that the compound would pose a significant cancer risk to
humans exposed at low levels there is not enough data to draw definitive
conclusions.
Organ Toxicity
The pesticide has been shown to affect both the adrenal glands and
the liver of rats. It also has effects on blood clotting time in test
animals.
Fate in Humans and Animals
Malathion is rapidly and effectively absorbed by practically all
routes including the gastrointestinal tract, skin, mucous membranes, and
lungs.
In rats, 44% was excreted in the urine in eight hours and 83% after
24 hours. Of the remainder 6% appeared in feces, 3% was in expired air
and 8% remained in the gastrointestinal tract. Cows excreted malathion
less rapidly with 69% in the urine in four days, 8% in the feces and
0.2% in the milk.
Autopsy samples from one individual who had ingested large amounts
of malathion showed a substantial portion in the stomach and intestines,
a small amount in fat tissue and no detectable levels in the liver.
Malathion requires conversion to malaoxon to become an active
anticholinesterase agent. Most of the occupational evidence indicates a
low chronic toxicity for malathion. One important exception to this was
traced to impurities in the formulation of the pesticide (14).
ECOLOGICAL EFFECTS
Malathion is moderately toxic to birds and highly toxic to aquatic
invertebrates, the aquatic stages of amphibians and to honey bees.
Mallards have an LD50 of 1,485 mg/kg and chickens a LD50 of 948 mg/kg.
Bobwhite quail had an oral LC50 of 3,497 ppm and pheasants 2,639 ppm.
Ninety percent of the dose to birds was metabolized and excreted in 24
hours via urine (5).
Fish have a wide range of toxicities to malathion, extending from
very highly toxic for the walleye (96-hour LC50 64 ppb) to highly toxic
for brown trout (101 ppb) and the cutthroat trout (280 ppb), moderately
toxic for fathead minnows (8.6 ppm) and slightly toxic for goldfish
(10.7 ppm). Various aquatic invertebrates are sensitive, with EC50's in
the 1ppb to 1 ppm. Whole body analysis of pinfish showed the presence
of malathion, mono- and di-carboxylic acids but no malaoxon (7).
ENVIRONMENTAL FATE
Degradation in soil is rapid and related to the degree of soil
binding. Breakdown occurs by a combination of biological and non-
biological reaction with water. The average half-life for the compound
is six days (15). In raw river water, the half-life is less than one
week, whereas malathion remained stable in distilled water for three
weeks. Applied at 1 to 6 pounds/acre in log ponds for mosquito control,
it was effective for 2.5 to 6 weeks. In sterile seawater, the
degradation increases with increased salinity. The breakdown products
in water are mono- and di-carboxylic acids.
A field of kale was sprayed at 2.5 pounds per acre. After two
days, 18 ppm of the compound and its breakdown products were present.
After 15 days, only 1.2 ppm remained. If released to the atmosphere,
malathion will break down rapidly in sunlight. The half-life in air is
about 1.5 days (15). Malathion has been found in small concentrations
in several wells in California.
Residues were found mainly associated with areas of high lipid
content in the plant. Increased moisture content increased degradation.
The FDA Market Basket Survey (1965-1969) showed an average malathion
concentration in representative foods of 0.00013 ppm (5). The tolerance
on most food crops is 8 ppm.
Because of its very short half-life, malathion is not expected to
bioconcentrate in aquatic organisms (15). However, the brown shrimp
showed an average concentration of 869 and 959 times the ambient water
concentration in two separate samples.
Exposure Guidelines:
| NOEL: | rat: 5 mg/kg/day, based on erythrocyle cholinesterase
rat: 25 mg/kg/day, based on whole blood cholinesterase
human: 25 mg/kg/day, based on cholinesterase |
| DWEL: | 0.8 mg/l |
| HA: | 0.2 mg/l lifetime |
| TLV-TWA: | 15 mg/m3 |
| (NIOSH): | 10 mg/m3 (ACGIH) |
| ADI: | 0.2 mg/kg/day (WHO) |
| LEL: | 0.34 mg/kg/day (human) |
Physical Properties:
| CAS #: | 121-75-5 |
| Chemical name: | diethyl (dimethoxy phosphinothioyl) thiobutanedioate |
| Chemical class/use: | organophosphate insecticide |
| Solubility in water: | 130 mg/l |
| Solubility in other solvents: | light petroleum 35 g/100 g; miscible in most organic solvents |
| Melting Point: | 2.8-3.7 degrees C |
| Vapor Pressure: | 8 x 10 to the minus 6 power mm Hg |
| Partition Coefficient: | 2.89 (log) |
BASIC MANUFACTURER
Cheminova Agro A/S
Lemvig, Denmark
American Cyanamid Co.
One Cyanamid Plaza
Wayne, NJ 07470
Telephone: 201-831-3521
Review by Basic Manufacturer - Cheminova:
Comments solicited: November, 1992
Comments received: December, 1992
Review by Basic Manufacturer - American Cyanamid:
Comments solicited: November, 1992
Comments received: December, 1992
REFERENCES
Hartley, D., and H. Kidd, Editors (1986). The Agrochemicals
Handbook. The Royal Society of Chemistry, The University, Nottingham,
England.
National Cancer Institute (1978 and 1979). Bioassay of Malathion
for Possible Carcinogenicity, U.S. Department of Health, Education and
Welfare, Public Health Service, National Institutes of Health, Technical
Report Series 24 and 192.
Gosselin, R.E., R.P. Smith, H.C. Hodge (1984). Clinical Toxicology
of Commercial Products, Williams and Wilkins, Baltimore, MD.
Trabalka, J.R. and C.T. Garten, Jr. (No date). Development of
Predictive Models for Xenobiotic Bioaccumulation in Terrestrial
Ecosystems. Environmental Sciences Div Publication No. 2037, Oak Ridge
National Laboratory, Oak Ridge, TN.
National Research Council (1977). Drinking Water and Health,
Advisory Center on Toxicology, Assembly of Life Sciences. Safe Drinking
Water Committee, National Academy of Sciences, Washington, DC.
National Library of Medicine (1992). Hazardous Substances
Databank. TOXNET, Medlars Management Section, Bethesda, MD.
Menzie, Calvin M. (1980). Metabolism of Pesticides, Update III.
U. S. Dept of the Interior, Fish and Wildlife Service, Special
Scientific Report, Wildlife No. 232.
Eto, M. (1979). Organophosphorus Pesticides: Organic and
Biological Chemistry, pages 254-255, CRC Press, Inc., Boca Raton, FL.
National Institute for Occupational Safety and Health (1985-86)
Registry of Toxic Effects of Chemical Substances, U. S. Department of
Health and Human Services, Centers for Disease Control.
ICF Incorporated (1985). Superfund Public Health Evaluation
Manual - Draft. Office of Emergency and Remedial Response, Office of
Solid Waste and Emergency Response, U.S. EPA.
Menzie, Calvin M. (1974). Metabolism of Pesticides, an Update.
U.S. Department of the Interior, Fish and Wildlife Service, Special
Scientific Report, Wildlife No. 184.
Menzer, Robert E. (1987) Selection of Animal Models for Data
Interpretation. in Toxic Substances and Human Risk: Principles of Data
Interpretation. Robert G. Tardiff and Joseph V. Rodricks editors.
Plenum Press, NY.
Carlson, Gary P. (1987). Factors Modifying Toxicity. in Toxic
Substances and Human Risk: Principles of Data Interpretation. Robert G.
Tardiff and Joseph V. Rodricks editors. Plenum Press, NY.
Gallo, Michael A. and Nicholas J. Lawryk. (1991). Organic
Phosphorous Pesticides. in Handbook of Pesticide Toxicology; Volume 2
Classes of Pesticides. Wayland J. Hayes and Edward R. Laws editors.
Academic Press, Inc., NY.
Howard, Philip H. (1991). Handbook of environmental Fate and
Exposure Data for Organic Chemicals, Volume III, Pesticides. Lewis
Publishers. Chelsea, MI.
Dean, Jack H. and Michael J. Murray. 1991. Toxic Responses of the
Immune System. in Casarett and Doull's Toxicology, the Basic Science of
Poisons, Fourth Edition. Mary O. Amdur, John Doull, and Curtis Klaassen
editors. Pergamon Press, NY.
Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet
Database. Lewis Publishers. Chelsea, MI.
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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