PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Metiram to Propoxur --> Propazine

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
Propazine

Publication Date: 9/93

TRADE OR OTHER NAMES

Some trade names include Gesamil, Milocep, Milogard, Primatol, Geigy 30028, Plantulin, Propazin, G-30028, Milo-Pro and Prozinex.

REGULATORY STATUS

Propazine is classified as a general use herbicide by the U.S. Environmental Protection Agency (EPA). Products containing propazine must bear the EPA signal word "Caution," indicating that it is slightly poisonous (1).

INTRODUCTION

Propazine is an herbicide used for control of broadleaf weeds and annual grasses in sweet sorghum (24). It is applied as a spray at the time of planting or immediately following planting, but prior to weed or sorghum emergence. It is also used as a postemergence selective herbicide on carrots, celery and fennel (20, 21). Propazine is available in wettable powder, liquid and water dispersible granular formulations (23).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Propazine is classified as a moderately toxic herbicide. Administration of lethal or near lethal doses to rats has caused symptoms of lethargy, muscular weakness, runny nose, emaciation, diarrhea, and labored breathing (22). It is mildly irritating to the skin, eyes, and upper respiratory tract (10). Contact dermatitis has been reported among workers manufacturing propazine (7). No cases of poisoning from human ingestion of this herbicide have been recorded (27). Skin and eye contact with propazine, as well as inhalation, should be avoided (20).

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 propazine in rats is 3,840 to greater than 7,000 mg/kg, in mice is 3,180 mg/kg, and in guinea pigs is 1,200 mg/kg (11, 23). Slight irritation was noted after propazine was applied to the skin of rabbits (1). Its dermal LD50 in rats is 10,200 mg/kg, and in rabbits is greater than 2,000 mg/kg (1, 24). Eye applications of 400 mg caused mild eye irritation in these animals (11). Symptoms of dizziness, cramping, and labored and irregular breathing were evident in mice given 5,000 mg/kg orally (20). Propazine has caused convulsions or coma, as well as liver and/or kidney damage in experimental animals (3).

CHRONIC TOXICITY

When given daily to rabbits for one to four months, oral doses of 500 mg/kg propazine were reported to cause a type of anemia (4). No gross signs of toxicity or pathologic changes were evident in rats that received daily doses of 250 mg/kg of propazine for 130 consecutive days. No clinical or physical toxic symptoms were observed in beagle dogs fed 1.25, 5, or 25 mg/kg of propazine formulation in 90-day feeding studies (20).

EPA has established a Lifetime Health Advisory (LHA) level for propazine in drinking water at 10 ug/l. EPA believes that water containing propazine at or below this level is acceptable for drinking every day over the course of one's lifetime, and does not pose any health concerns. Consumption of propazine at high levels well above the LHA level over a long period of time has caused decreased fetal weight gain and delayed fetal bone development in animal studies (24).

The National Academy of Science has established an Acceptable Daily Intake (ADI) of 0.0464 mg/kg/day for propazine (12, 24).

Reproductive Effects

There was an increase in the number of deaths of newborns produced by female rats that were given 5 mg/kg of propazine during 18 days of pregnancy (15). Consumption of propazine at high levels well above the Lifetime Health Advisory level over a long period of time has caused decreased fetal weight gain and delayed fetal bone development in animal studies (24). Maternal doses of 500 mg/kg/day resulted in maternal toxicity and developmental toxicity expressed as increased incidence of extra ribs, incomplete bone formation, and decreased fetal body weights (29). In a 3-generation study with rats fed 0, 0.15, 5 or 50 mg/kg/day, no effects on fertility, length of pregnancy, pup viability or pup survival were observed. At 50 mg/kg, pup body weights on day 21 of lactation were reduced, and there were pathological changes in organ weights in the 2nd and 3rd generation (29).

Teratogenic Effects

No teratogenic effects were observed in rats fed 500 mg/kg/ day, the highest dose tested (29).

Mutagenic Effects

Propazine has shown no mutagenic effects in tests conducted on human and rat liver cells and in live hamsters (24).

Carcinogenic Effects

No evidence of increased tumor frequency was detected in a 2-year study in mice fed doses up to 450 mg/kg of propazine each day. When rats were fed 0. 0.15, 5, or 50 mg/kg of propazine each day for 2 years, there was an increase in the incidence of mammary gland tumors at the highest dose level. EPA has classified propazine as a possible human carcinogen. This category includes substances for which there is limited evidence of carcinogenicity in animals in the absence of human data. Because propazine in drinking water may possibly increase the risk of cancer in humans, the Lifetime Health Advisory for propazine includes an additional margin of safety (24).

Organ Toxicity

Liver damage is one of the suspected effects of propazine (5). The functioning of certain liver processes was decreased in rats which were given 2,500 mg/kg propazine (4).

Fate in Humans and Animals

Triazines, the family of chemicals within which propazine is included, may disturb the metabolism of some of the B vitamins, thiamine (B1) and riboflavin (B2). They may also concentrate and accumulate in the fat of humans and animals (5). Propazine is readily absorbed and metabolized in the body (4). 72 hours after administration of single oral doses of radio-labeled propazine to rats, 66% of the dose was excreted in the urine and 23% was excreted in the feces. This indicates that 77% of the dose was absorbed into the bloodstream from the gastrointestinal tract. Eight days after the dosing, propazine or its metabolites were detected in the rats' lungs, spleen, heart, kidneys and brain (24).

ECOLOGICAL EFFECTS

Effects on Birds

Propazine is considered slightly toxic to non-toxic to birds (21). The eight-day dietary LC50 is greater than 10,000 ppm for both bobwhite quail and mallard ducks (20).

Effects on Aquatic Organisms

Propazine is slightly toxic to coldwater fish (29). The 96-hour LC50 is 18 ppm for rainbow trout and greater than 100 ppm for bluegill sunfish (6, 20).

Effects on Other Animals (Nontarget species)

Propazine is practically non-toxic to bees (6, 29).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Propazine does not adsorb as strongly to soil particles as other commercial triazine herbicides. In most soils, it binds only weakly to soil particles (Koc = 154 g/m), and, depending on soil temperature, moisture and pH, it can become unbound. Its movement with soil moisture is limited by partial adsorption to soil particles, as well as its low water solubility (20). One study found propazine to be mobile in sandy loam, loam, and clay loam soils. It was very mobile in loamy sand (29). Propazine is persistent, moderately mobile in most soils, and it is resistant to breakdown by hydrolysis, photolysis or biodegradation (29). For these reasons, propazine is one of the pesticide compounds considered by the EPA to have the greatest potential for leaching into groundwater (18). Leaching of propazine is most likely to occur where there is irrigation and/or high rainfall, or sandy soil (20).

A significant portion of the herbicide may be broken down by soil microbes. Several soil microorganisms utilize propazine as a source of energy or nitrogen. Photolysis and volatilization are not important factors in propazine degradation (20).

Propazine will persist longer in dry or cold conditions or other conditions which inhibit biological and chemical activity (20). When it was applied at 0.5 pounds/acre, propazine persisted for 11 to 24 weeks (13). Its soil half-life is 135 days (25).

Breakdown of Chemical in Water

Propazine is resistant to breakdown by hydrolysis. After 28 days, at pH 5, 60% of applied propazine remained unhydrolyzed; at pH 7, 92% remained; and at pH 9, 100% remained (24).

Propazine has been detected in drinking water in the United States (12). It has been found in 33 out of 1,097 surface water samples and in 15 out of 906 groundwater samples. Contaminated groundwater samples have been collected from eight states. The maximum concentration found in any sample was 13 ug/l (ppb) for surface water and 300 ug/l (ppb) for groundwater (24, 29).

Breakdown of Chemical in Vegetation

Propazine is absorbed principally through plant roots. After absorption, it is moved, or translocated, upward into the plant where it accumulates in the growing shoots and leaves of plants (20).

The breakdown of propazine in plants is assumed to be similar to the metabolism of two other herbicides, atrazine and simazine. Propazine accumulates and causes death in those plants that are unable to readily metabolize it into a nonpoisonous compound (20).

PHYSICAL PROPERTIES AND GUIDELINES

Propazine is a colorless crystalline solid (28). The technical material is more than 95% pure (7, 9). It is stable in neutral, slightly acid, or alkaline media, but it is hydrolyzed by stronger acids and alkalis (7). It is nonflammable and noncorrosive under normal use conditions, but may burn if exposed to heat or flame. Thermal decomposition may produce toxic oxides of carbon and nitrogen, and toxic and corrosive fumes of chlorides (20, 26).

Occupational Exposure Guidelines:

Occupational exposure limits for propazine have not been established by OSHA, ACGIH, or NIOSH (26).

Physical Properties:

CAS #: 139-40-2
Specific gravity: 1.162 (26)
H20 solubility: 8.6 ppm at 20 degrees C (1, 9, 20)
Solubility in other solvents: Difficult to dissolve in organic solvents (20, 22); 6.2 g/kg at 22 degrees C in benzene and toluene (21); 2.5 g/kg in carbon tetrachloride (21); 0.5 g/100 ml at 20 degrees C in diethyl ether (6)
Melting point: 212-214 degrees C (1, 7)
Vapor pressure: 2.9 x 10 to the minus 8 mm Hg at 20 degrees C (7); 3.4 x 10 to the minus 6 mm Hg at 50 degrees C (20)
Log Kow: 2.94 (16); 785 (8)
Chemical Class/Use: selective triazine herbicide

BASIC MANUFACTURER

Ciba-Geigy Corp.
Agricultural Division
P.O. Box 18300
Greensboro, NC 27419

Review by Basic Manufacturer:

Comments solicited: January, 1992
Comments received: April, 1992

REFERENCES

  1. Berg, G. L., ed. 1987. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing Company.
  2. Clayton, G. D. and F. E. Clayton, eds. 1981. Patty's industrial hygiene and toxicology. Third edition. Vol. 2: Toxicology. NY: John Wiley and Sons.
  3. Dreisbach, R. H. 1983. Handbook of poisoning: Prevention, diagnosis and treatment. Eleventh edition. Los Altos, CA: Lange Medical Publications.
  4. Gosselin, R. E., et al. 1984. Clinical toxicology of commercial products. Fifth edition. Baltimore, MD: Williams and Wilkins.
  5. Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and human health. N.Y.: Springer-Verlag.
  6. Hartley, D. and H. Kidd, eds. 1983. The Agrochemicals Handbook. Nottingham, England: Royal Society of Chemistry.
  7. Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD: Williams and Wilkins.
  8. Kenaga, E. E. and C. A. I. Goring. 1980. Relationship between water solubility, soil sorption, octanol-water partitioning and concentration of chemicals in biota. In J. G. Eaton, P. R. Parrish, and A. C. Hendriks (eds), Aquatic Toxicology. ASTM STP 707, pp 78. Philadelphia: Amer. Soc. Testing and Materials.
  9. Melnikov, N. N. 1971. Chemistry of pesticides. N.Y.: Springer- Verlag, Inc.
  10. 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.
  11. National Institute for Occupational Safety and Health (NIOSH). 1986. Registry of toxic effects of chemical substances (RTECS). Cincinatti, OH: NIOSH.
  12. National Research Council, Safe Drinking Water Committee. 1977. Drinking water and health. National Academy of Sciences, Washington, DC: National Academy of Sciences.
  13. 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.
  14. Rao, P. S. C., et al. 1983 (Sept.). Pesticides and their behavior in soil and water. Florida Cooperative Extension Service. Institute of Food and Agricultural Sciences, University of Florida. Soil science fact sheet adapted from: Herbicide injury, symptoms and diagnosis, Skroch and Sheets, eds. 1981 (Dec.). North Carolina Agricultural Extension Service. AG-85.
  15. Shepard, T. H. 1980. Catalogue of teratogenic agents. Third edition. Baltimore, MD: The Johns Hopkins University Press.
  16. Smith, C. N. 1981. Partition coefficients (Log Kow) for selected chemicals. In USEPA, 1984. User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  17. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Data bank. Public Health Service. National Institute of Health, U. S. Department of Health and Human Services. Bethesda, MD: NLM.
  18. U. S. Environmental Protection Agency. 1987. (Feb. 4). Environmental News. Office of Public Affairs (A-107). Washington, DC.
  19. Weed Science Society of America. 1983. Herbicide handbook. Fifth edition. Champaign, IL: WSSA, Herbicide Handbook Committee.
  20. Worthing, C. R., ed. 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.
  21. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  22. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  23. U.S. Environmental Protection Agency. 1988 (Aug.). Propazine: Health Advisory. Office of Drinking Water, US EPA, Washington, DC.
  24. USDA Soil Conservation Service. 1990 (Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0 (Summary). USDA - Soil Conservation Service, Syracuse, NY.
  25. Occupational Health Services, Inc. 1991 (Feb. 21). MSDS for propazine. OHS Inc., Secaucus, NJ.
  26. WSSA Herbicide Handbook Committee. Herbicide Handbook of the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL. 1989.
  27. U.S. Environmental Protection Agency. 1988 (Dec. 20 ). Pesticide Fact Sheet #189: Propazine. Office of Pesticides and Toxic Substances, Office of Pesticide Programs, USEPA, Washington, DC.
  28. U. S. Environmental Protection Agency. 1988 (Dec.) Guidance for the Reregistration of Pesticide Products Containing Propazine as the Active Ingredient. Office of Pesticides and Toxic Substances, USEPA, Washington, DC.