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
|
Propoxur
Publication Date: 9/93
|
|
TRADE OR OTHER NAMES
Some trade names include Baygon, Bayer 39007, arprocarb, UNDEN, Suncide,
Sendran, Invisigard, Bay 9010, Bifex, Bolfo, Blattanex, Rhoden, Propogon,
Propyon, Sendra, Tendex and Undene.
REGULATORY STATUS
Propoxur is currently registered by the U. S. Environmental Protection
Agency (EPA) as a general use pesticide. General use pesticides may be
purchased and used by persons who are not certified pesticide applicators.
Check with specific state regulations for local restrictions which may apply.
Pesticide products containing Propoxur must bear the signal word, "Caution" or
"Danger."
INTRODUCTION
Propoxur is a non-systemic insecticide which was introduced in 1959 (25).
Propoxur is not used on food crops. It is used against mosquitoes in outdoor
areas, for flies in agricultural settings, for fleas and ticks on pets, as an
acaricide, on lawns and turf for ants, on flowering plants, and in private
dwellings and public buildings. It is also used as a molluscicide, a chemical
that kills snails. It is effective against cockroaches, aphids and
leafhoppers (27, 20). Propoxur is one of the chemicals that have, to a large
extent, replaced DDT in the control of black flies and mosquitoes (11). It is
a nonsystemic insecticide with contact and stomach action that has
longstanding residual poisonous, or toxic activity when it is in direct
contact with the target pest (27, 7). Many formulations are available
including ready-to-use liquids and aerosols, emulsifiable concentrates,
wettable powders, granular baits, dusts and impregnated pet collars and strips
(27).
Propoxur is one of a family of insecticides called carbamates. These
chemicals block the production and action of cholinesterase, an essential
nervous system enzyme. These materials quickly paralyze the nervous systems
of insects, gaining them a reputation of having a rapid "knockdown"
effect (8, 2).
Please refer to the Toxicology Information Brief on cholinesterase-inhibition
for a more detailed discussion of cholinesterase inhibition.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Propoxur is classified as highly toxic to humans. Carbamates can be
absorbed in a variety of ways: breathing, eating and/or skin contact (1).
During wide-scale spraying of propoxur in malarial control activities
conducted by the World Health Organization (WHO), only mild cases of poisoning
were noted. Applicators who used propoxur regularly showed a pronounced daily
fall in whole blood cholinesterase activity and a distinct recovery after
exposure stopped. No adverse cumulative effects on cholinesterase activity
were demonstrated (27, 20). Human adults have ingested single doses of 90 mg
of propoxur without apparent symptoms (4). A 42 year old male volunteer who
ingested 1.5 mg/kg of propoxur experienced cholinesterase inhibition symptoms
including nausea, vomiting, blurred vision, increased pulse rate and profuse
sweating, with full recovery 3 hours after the dose was taken (25, 28).
Volunteers fed 0.20 mg/kg every half hour for a total dose of 1.0 mg/kg were
symptomless, but blood tests showed that cholinesterase inhibition occurred
and peaked at greater than 50 percent (25, 28).
As with other carbamate compounds, propoxur's cholinesterase-inhibiting
effect is short-term and reversible (7). Symptoms of propoxur poisoning
include nausea, vomiting, abdominal cramps, sweating, diarrhea, excessive,
salivation, weakness, imbalance, blurring of vision, breathing difficulty,
increased blood pressure or 'hypertension' and lack of control of urine or
feces release, referred to as 'incontinence.' Death may result from
respiratory system failure associated with propoxur exposure (4). Complete
recovery from an acute poisoning by propoxur, with no long-term health
effects, is possible if exposure ceases and the victim has time to reform
their normal level of cholinesterase and to recover from symptoms (25, 7).
Carbamates generally are excreted rapidly and do not accumulate in
mammalian tissue. If exposure does not continue, cholinesterase inhibition
reverses rapidly. In non-fatal cases, the illness generally lasts less than
24 hours (31).
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 LD50 for propoxur in rats ranges from 83 mg/kg to 150 mg/kg
(28, 2, 7, 8). In rats, propoxur poisoning resulted in brain pattern and learning
ability changes at lower concentrations than those which caused
cholinesterase-inhibition and/or organ weight changes (20). The oral LD50 in
mice is 23.5 mg/kg (28), 40 mg/kg in guinea pigs (28, 16). Twelve-month old
male goats have an oral LD50 greater than 800 mg/kg (9). The oral LD50 for
technical propoxur in rats was 50 mg/kg for males and 104 mg/kg for females
(26).
Propoxur is reportedly less toxic when absorbed through the skin, than
when it is ingested (11). The dermal LD50 in rats is greater than 2,400 -
5,000 mg/kg in rats. In rabbits, the LD50 is 500 mg/kg (28, 8, 2). 500 mg of
technical Baygon dissolved in acetone did not cause skin irritation with 72
hours of application to the skin of rabbits. Tests show that propoxur is not
an eye irritant (28).
CHRONIC TOXICITY
Prolonged or repeated exposure to propoxur may cause symptoms similar to
acute effects. While permanent behavioral changes were reported in rats that
received propoxur repeatedly, no effect was seen in experimental rats exposed
to 7.5 mg/day for 28 days as a part of a chronic oral study (1, 4, 27).
Propoxur is very efficiently detoxified, or made into nonpoisonous forms,
thus making it possible for rats to tolerate daily doses approximately equal
to the LD50 of the insecticide for long periods, provided that the dose is
spread out over the entire day, rather than ingested all at once (25). A
three-month exposure of rats to dietary doses of 40 mg/kg did not affect
growth rate, cholinesterase levels, or food consumption (1, 27). In two-year
feeding trials, male and female rats receiving 250 mg active ingredient/kg of
body weight showed no ill effect. At 750 mg/kg, the liver weight of female
rats increased, otherwise there was no ill-effect (24).
Reproductive Effects
Propoxur had adverse effects on the newborn of female rats that were
given oral doses of 1,600 mg/kg between the sixth and 15th day of pregnancy,
and on the 15th day after birth (16). In female rats given a dietary dose of
300 mg/kg of propoxur as a part of a three-generation reproduction study,
reduced parental food consumption, growth, lactation, litter size, and growth
of the pups were observed. In the same study, dietary doses of 37.5 mg/kg did
not affect fertility, litter size or lactation. However, the size and growth
of litters was reduced, and food intake, growth, and lactation were depressed
in parents (25). Offspring of female rats fed 5 mg/kg of propoxur during
gestation and weaning exhibited reduced birth weight, retarded development of
some reflexes, and evidence of central nervous system impairment (25).
Teratogenic Effects
A growth reduction was observed in the offspring of pregnant rats given
doses of 50, 150 or 500 mg/kg of propoxur, but no teratogenic abnormalities
were observed. At 500 mg/kg there was a decrease in the number of fetuses
produced. In mice, dosages as high as 31 mg/kg of the herbicide caused some
embryotoxicity, or poisoning of embryos, but no teratogenic effects were
observed (25).
Mutagenic Effects
Propoxur did not cause mutations in six different types of bacteria (8).
A derivative of propoxur (N-nitroso) is mutagenic, however (5).
Carcinogenic Effects
No carcinogenic effects have been reported for propoxur.
Organ Toxicity
The autopsy of a human adult who died six hours after eating an unknown
quantity of UNDEN, a pesticide containing propoxur, showed swelling of the
brain with excess fluid, distended lungs, and increased blood in the
capillaries of internal organs (4). Dietary doses of 50 and 100 mg/kg of
propoxur in rats depressed cholinesterase activity of the brain and blood, and
also caused some cellular changes in the liver (25, 8).
Fate in Humans and Animals
Propoxur is broken down and excreted rapidly in urine (1, 14). In humans
given a single oral dose of 92.2 mg of Baygon, 38 percent of the dose was
excreted in urine over the next 24 hours, with most of it excreted in the
first 8 to 10 hours (28).
ECOLOGICAL EFFECTS
Harmful Effects on Birds
Birds feeding on propoxur-treated areas may be killed (19). The toxicity
of propoxur varies by type of bird. Its oral LD50 in chickens is 47 mg/kg, 4
mg/kg in wild birds, and 9,580 micrograms (ug)/kg (or approximately 10 mg/kg)
in ducks (16). The LC50 for Japanese quail is greater than 5,000 mg/kg (26).
The following list indicates the oral LD50s, for several bird species, of two
different formulations: (a) 97%, and (b) 98% technical propoxur:
| 4-6 month old female mallards | 11.9 mg/kg (b) |
| 3-5 month old male pheasants | 20 mg/kg (b) |
| 2 year old male California quail | 30 mg/kg (a) |
| male and female pigeons | 60.4 mg/kg (a) |
| male and female mourning doves | 4.20 mg/kg (a) |
| male and female house finches | 3.55 mg/kg (a) |
Acute symptoms of propoxur poisoning in birds include eye tearing,
salivation, muscle incoordination, diarrhea and trembling (21). Depending on
the type of bird, poisoning signs can appear within five minutes of exposure,
with deaths occurring between five and 45 minutes, or overnight. Symptoms in
survivors disappeared from 90 minutes to several days after treatment (9).
Species tested include mallard Canada goose, sharp-tailed grouse, quail and
pheasant (9).
Harmful Effects on Aquatic Organisms
Propoxur is toxic to fish, as well as other animals that eat fish (7).
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 48-hour LC50 for fathead minnows is 19 parts per
billion (ppb) (11). The 96-hour LC50 for rainbow trout is 13.6 mg/liter (26).
The oral LD50 for propoxur in bullfrogs was 595 mg/kg.
Effects on Other Animals (Nontarget species)
Propoxur is highly toxic to honey bees (24). The LD50 for bees is
greater than one ug/honey bee (10). Severe bee losses may be expected if
propoxur is used when bees are present either at treatment time or within a
day after treatment (15).
Propoxur is toxic to wildlife (13). The oral LD50 for propoxur in mule
deer is 100 to 350 mg/kg (9).
ENVIRONMENTAL FATE
The breakdown of propoxur in soil and water is accelerated by alkaline
conditions (19).
Breakdown of Chemical in Soil and Groundwater
Because it is both highly soluble in water (2,000 ug/ml) and has a
lengthy soil half-life (28 days), and does not adsorb strongly to soil
particle, propoxur has a high potential for groundwater penetration (28, 29, 30).
In one study, there was practically no loss of propoxur from a silt-loam
soil to which it was applied during a six-month period, but 25% of applied
Baygon was lost from sand in 100 days. In another study, propoxur was very
mobile in sandy loam, silt loam and silty clay soils. The rate of
biodegradation in soil increases in soils that have been previously exposed to
propoxur or other methylcarbamate pesticides (12, 30, 28).
Breakdown of Chemical in Water
Propoxur should not be applied to tidal marshes or estuaries and it
should be kept out of streams, lakes or ponds (13, 19). It hydrolyzes, or
breaks down in water, at a rate of 1.5%/day in a 1% aqueous solution, at a pH
of 7 (7). Water can be contaminated by cleaning of equipment, or disposal of
wastes, associated with propoxur (13).
Breakdown of Chemical in Vegetation
Propoxur is not poisonous to plants (24). Crop tolerance is good for
recommended areas of use, although some injury from higher use rates of
propoxur has been reported on chrysanthemums, carnations and hydrangeas (6).
Propoxur has systemic activity when it is applied to the soil, indicating
that it can enter the roots of a plant and travel to the leaves, where it can
then poison insects that feed on the leaves (19). It can have residual
activity of up to one month when applied to plant surfaces (6).
PHYSICAL PROPERTIES AND GUIDELINES
Pure propoxur is a white crystalline solid with a faint characteristic
odor (2, 11, 1). Technical propoxur is about 95% pure and is a white to cream
colored crystalline powder with a milk-phenol odor (25, 8). It is formulated
as emulsifiable concentrates, 50% wettable powder, baits, and 1 and 2% dusts
(2, 8). It is unstable in alkaline media, as it is hydrolyzed by strong
alkalis. It has a half-life of 40 minutes at pH 10 (25, 8). Propoxur is
dangerous if it is heated to decomposition, for it emits highly toxic fumes
(18). Skin contact, and inhalation of dusts or spray mists, should be avoided
(7). Applicators or mixers of propoxur should use the following protective
measures: wear overalls which have been cleaned daily; wear impervious shoes
and rubber gloves (mixers only); wash hands and face following each pump
charge (20).
Occupational Exposure Limits:
| TLV-TWA: | 0.5 mg/m3 (1, 3) |
Physical Properties:
| CAS #: | 114-26-1 |
| H20 solubility: | 2,000 mg/l at 20-25 degrees C (23); 1,750 ppm at 20 degrees C (2) |
| Solubility in other solvents: | soluble in organic polar solvents, readily soluble in acetone (1);
soluble in methanol, acetone, and many other organic solvents but only slightly soluble in cold hydrocarbons (8). |
| Melting Point: | 81 degrees C (2) |
| Vapor pressure: | 6.5 x 10 to the minus 6 mmHg at 20 degrees C (8); 1 x 10 to the minus 6 mmHg at 120 degrees C (24) |
| Bioconcentration factor: | 9 (calculated from water solubility by regression equations) (20) |
| Kow: | log Kow = 1.45 (22) |
| Koc: | 67 (calculated from water solubility by regression equations) (20) |
| Partitioning Model: | PCMC1 (mole fraction) 1.72 x 10 to the minus 4; PCMC2 (mg/l) 2,000; PCMC3 (mcm/l) 9,600 (23) |
| Chemical Class/Use: | methyl carbamate insecticide |
BASIC MANUFACTURER
Mobay Corporation
PO Box 64120
Kansas City, MO 64120
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received:
REFERENCES
American Conference of Governmental Industrial Hygienists, Inc. 1986.
Documentation of the threshold limit values and biological exposure indices.
Fifth edition. Cincinatti, OH: Publications Office, ACGIH.
Berg, G. L., ed. 1986. Farm Chemicals Handbook. Willoughby, Ohio:
Meister Publishing Co.
Dreisbach, R. H. 1983. Handbook of poisoning: Prevention, diagnosis
and treatment. Eleventh edition. Los Altos, CA: Lange Medical Publications.
Gosselin, R. E., et al., 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and
human health. NY: Springer-Verlag.
Harding, W. C. 1979. Pesticide profiles. Part one: Insecticides and
miticides. Bulletin 267. Cooperative Extension Service: University of
Maryland.
Hartley, D. and H. Kidd, eds. 1983. The Agrochemicals Handbook.
Nottingham, England: Royal Society of Chemistry.
Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD:
Williams and Wilkins.
Hudson, R. H., et al. 1984. Handbook of toxicity of pesticides to
wildlife. Second edition. United States Department of the Interior. Fish and
Wildlife Service. Resource Publication 153. Washington, DC: U.S. Government
Printing Office.
Kuhr, R. J. and H. W. Dorough. 1976. Carbamate insecticides:
Chemistry, biochemistry, and toxicology. Cleveland, OH: CRC Press, Inc.
McEwen, F. L. and G. R. Stephenson. 1979. The use and significance
of pesticides in the environment. NY: John Wiley and Sons, Inc.
Menzie, C. M. 1974. 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.
Mobay Chemical Corporation. 1982 (Jan). Technical information:
Baygon insecticide. Agricultural Chemicals Division. Kansas City, MO: Mobay
Chemical Corporation.
Morgan, D. P. 1982 (Jan). Recognition and management of pesticide
poisonings. Third edition. U. S. Environmental Protection Agency.
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). Cincinatti, OH:
NIOSH.
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. 1984. Dangerous properties of industrial materials.
Sixth edition. NY: VanNostrand Reinhold Co.
Thomson, W. T. 1985. Insecticides. Agricultural Chemicals, Book I.
Fresno, CA: Thomson Publications.
TOXNET. 1986. 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.
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. Environmental Protection Agency. 1986 (Jan). Estimating
pesticide sorption coefficients for soils and sediments. Richard E. Green and
Samuel W. Karickhoff. Environmental Research Laboratory. Office of Research
and Development. Athens, GA.
_____. 1984 (Dec.). User's manual for the pesticide root zone model
(PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
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.). 1991. Farm Chemicals Handbook '91. Meister
Publishing Company, Willoughby, OH.
USDA. 1992 (March). The biologic and economic assessment of propoxur.
NAPIAP, Extension Service, USDA, Washington, DC.
US EPA. 1988 (Aug.). (Baygon) Propoxur Health Advisory. Office of
Drinking Water, USEPA, Washington, DC.
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. MSDS for Methomyl. OHS
Inc., Secaucus, NJ.
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
|
|
 |
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
