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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

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  13. Mobay Chemical Corporation. 1982 (Jan). Technical information: Baygon insecticide. Agricultural Chemicals Division. Kansas City, MO: Mobay Chemical Corporation.
  14. 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.
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  21. 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.
  22. 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.
  23. _____. 1984 (Dec.). User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
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  31. Occupational Health Services, Inc. 1991. MSDS for Methomyl. OHS Inc., Secaucus, NJ.