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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.


Publication Date: 9/93


Some trade names include Kerb, Propyzamide, RH-315 and Benzamide.


The U.S. Environmental Protection Agency (EPA) restricts the use of all pronamide formulations, except those in water-soluble packets, due to their oncogenicity, or potential to cause tumor growth (2). Restricted Use Pesticides (RUP) may be purchasedand used only by certified applicators. Check with specific state regulations for local restrictions which may apply (9). Products containing pronamide must bear the signal word "Caution" (16).


Pronamide is an herbicide used either before weeds emerge (preemergence), and/or after weeds come up (postemergence). It controls a wide range of annual and perennial grasses, as well as certain annual broadleaf weeds. Pronamide is usually incorporated into the soil by cultivation, irrigation, or rain immediately following application (14). The toxic action of this herbicide is selective, meaning that it kills specific target plants while sparing other, desirable plants. It is used primarily on lettuce and alfalfa crops, as well as on blueberries, ornamentals, fruit trees, forage legumes, and on fallow lands. It is available in wettable powder and granular formulations (11, 16).



Pronamide is classified by EPA as a slightly poisonous herbicide. Mixers and applicators are expected to receive the most exposure to this material through skin contact. To protect workers from potential eye and mucous membrane irritation, precautionary statements on manufacturing-use product labels warn: "Harmful if absorbed through the skin or inhaled. Causes moderate eye irritation. Avoid contact with the skin, eyes, or clothing. Avoid breathing dust" (11).

The dose of a chemical that causes death in one-half (50%) of test animals when it is given to them by mouth, is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for pronamide ranges from 5620 mg/kg in female rats, to 8,350 mg/kg in male rats. In dogs, its LD50 is 10,000 mg/kg (1). When applied to the skin of rabbits, it produced slight local irritation, but no systemic intoxication. The acute dermal toxicity of pronamide is greater than 3160 mg/kg (4, 11, 14).


When dogs were fed a diet containing approximately 0, 11, 34, or 100 mg/kg pronamide for 3 months, decreases in weight gain and food consumption, changes in blood chemistry, and increased liver weights were observed at 100 mg/kg. No adverse effects occurred at 34 mg/kg. In a similar study of rats fed 0, 0.5, 7.5, 22.5, 67.5 or 202.5 mg/kg/day for 3 months, liver weight changes occurred in females at 7.5 mg/kg/day (22).

In a 2-year feeding study with dogs, the addition of pronamide to the diet at doses of 0, 0.75, 2.5 or 7.5 mg/kg/day caused no adverse health effects at any of the doses tested. A NOAEL of 7.5 mg/kg/day, the highest dose tested, was established for this study (22).

The EPA has established a Lifetime Health Advisory (LHA) level of 50 micrograms per liter (ug/l) for pronamide in drinking water. This means that EPA believes that water containing pronamide 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. However, consumption of pronamide at high levels well above the LHA level over a long period of time has been shown to cause liver damage in animal studies (21).

Reproductive Effects

When pregnant rabbits were given doses of 0, 5, 20 or 80 mg/kg/day during days 7 to 19 of gestation (18 rabbits per dose), no effects on development or reproduction were observed at or below the 20 mg/kg dose. At 80 mg/kg, there was an increased incidence of liver lesions, one maternal death, five abortions, and a decrease in maternal weight gain (22). In a 3- generation rat reproduction study, no effects on reproduction were observed at 300 ppm (15 mg/kg/day), the highest dose tested (20, 22).

Teratogenic Effects

No teratogenic effects were found when doses as high as 15 mg/kg/day were administered to pregnant rabbits (22).

Mutagenic Effects

Several tests for mutagenicity involving bacterial or mammalian cell cultures, or live animals have been performed. All test results have been negative (22, 23).

Carcinogenic Effects

Pronamide is classified as a possible human carcinogen by the EPA (21). A material is classified as a possible human carcinogen when there is limited or uncertain evidence that it has caused cancer in animals receiving high doses of the chemical over the course of their lifetimes. Pronamide has caused tumors in male rats at dosages of 150 mg/kg and 300 mg/kg in the diet. Cancerous tumors, 'carcinomas,' of the liver, as well as an increased incidence of tumors in all organs, were induced in male mice fed 50 or 100 mg/kg of pronamide for 18 months (7, 19). In a 2-year rat feeding study, the NOEL was 15 mg/kg and no evidence of tumor formation was observed at feeding levels of 1.5, 5 or 15 mg/kg/day (20).

The EPA has concluded that this herbicide poses a limited oncogenic risk for applicators which can be reduced through the use of protective measures, such as protective clothing and water-soluble packaging (10).

Organ Toxicity

Consumption of pronamide at high levels well above the Lifetime Health Advisory level over a long period of time has been shown to cause liver damage in animal studies (21).

Fate in Humans and Animals

Pronamide is not readily absorbed into the bloodstream from the gastrointestinal tracts of rats and cows. After oral doses of radio labeled Kerb to rats, unmetabolized Kerb accounted for 54 ad 0.6% of the radioactivity recovered in feces and urine, respectively. Unmetabolized Kerb did not appear in the urine of a cow treated orally with radio labeled Kerb (22). Traces of pronamide were found in the milk of cows given feed that contained five ppm doses of formulation (7). Pronamide has a low potential for bioaccumulation in animal tissues (18).


Effects on Birds

Pronamide is practically non-toxic to birds. The LD50 for pronamide in Japanese quail is 8,700 mg/kg, and 20,000 mg/kg in mallard ducks (11). The lethal concentration fifty, or LC50, is a calculated concentration of a material in air or water which causes death in 50% of an experimental animal population exposed to it for a specified length of time. The 8-day dietary LC50 for Kerb Technical Herbicide in bobwhite quail and mallard ducks is greater than 10,000 ppm (23).

Effects on Fish

Pronamide is practically non-toxic to warmwater fish and slightly toxic to coldwater fish. The 96-hour LC50 for pronamide in bluegills is 100 mg/l, 72 mg/l in rainbow trout, 350 mg/l in goldfish, 204 mg/l in harlequin fish, and 150 mg/l in guppies. The 48-hour LC50 for Daphnia magna, a small freshwater crustacean, is greater than 5.6 mg/l (11, 16, 23).

Effects on Other Animals (Nontarget species)

Pronamide is practically nontoxic to mammals, but may be moderately toxic to aquatic invertebrates (11). Pronamide is non-toxic to honey bees (16).


Breakdown of Chemical in Soil and Groundwater

Pronamide is readily bound, or adsorbed, to organic matter in soil (Koc = 990 g/ml) (17). In most soil types, there is very little movement, or leaching, of pronamide through the ground with soil moisture (14). It is nearly insoluble in water (15 ug/ml) (17). However, the EPA does consider a pronamide metabolite (RH24,580) to be one of the pesticide compounds with greatest potential for leaching into groundwater (8). Leaching of most pronamide residues in soil occurs in loamy sands and in silt loams (7). It was not found in groundwater in a national groundwater survey (12).

Pronamide is inactivated by soil organic matter and will not be effective on muck, peat, or other high-organic content soils (10). Depending upon soil type and climatic conditions, persistence of pronamide varies from two to nine months. Residual activity is greater in sandy soils with low organic matter. Accumulation of the herbicide from repeated annual applications to the same soil does not appear problematic.

Chemical degradation may be the main route of disappearance from the soil. Photodecomposition at the soil surface can also occur (18). A moderate amount of pronamide breakdown is carried out by soil microorganisms. The herbicide is not active against common soil microorganisms. Some studies indicate that under very hot and dry conditions, pronamide turns into a gaseous form, through a process called volatilization (14). The dissipation half-life for pronamide is 1.5 to 13 weeks in soil (12). Increasing soil temperature, and to a lesser extent, soil moisture and pH increase the rate of pronamide degradation in soil (22).

Breakdown of Chemical in Water

In water bodies, pronamide is chemically stable at a neutral pH. It is slowly degraded chemically, by light, and by aquatic and muck organisms. Loss from volatilization is not significant (3, 18). Pronamide is thought to be stable because less than 10% was hydrolyzed, or broken down in water, over a four week period (12). It is stable to hydrolysis between pH 4.7 and 8.8 (11).

Breakdown of Chemical in Vegetation

Crops for which pronamide is not registered must not be planted in fields that have been given previous treatment with pronamide products (10). Pronamide primarily inhibits root development in germinating seeds or young seedlings. In perennial grasses, it interrupts both root and shoot growth. For pronamide to be effective, it has to move into the root zone of target weeds. Since it is taken up by the roots, pronamide needs to be carried into the root zone by rainfall, irrigation, or soil incorporation. Pronamide is readily translocated from the roots to other plant parts. Absorption of pronamide through plant leaves is minimal. Pronamide is metabolized slowly by both tolerant and sensitive plants (11, 14).


Pronamide is a white or off-white crystalline solid with a mild odor (14). It is relatively stable (11). It should be stored in a cool, dry place at temperatures between 0 and 50 degrees C. Under normal conditions, there should be little decomposition of this material (1). Water-soluble packets of this herbicide significantly reduce the risk of exposure for mixers (11).

Pronamide is noncorrosive under normal use conditions. It is stable under normal temperatures and pressures, but may pose a slight fire hazard if exposed to heat or flame. It poses a fire and explosion hazard in the presence of strong oxidizers. Thermal decomposition of pronamide will release toxic oxides of nitrogen and carbon and toxic and corrosive fumes of chlorides (19).

Pronamide should not be applied directly to water, nor should water be contaminated by the cleaning of equipment or disposal of wastes associated with this material (11). Protective clothing is recommended during the mixing, loading, or application of end-use products unless water-soluble packaging is used (11). Pronamide applications should not be allowed to drift into nontarget areas (14).

Occupational Exposure Limits:

No occupational exposure limits have been established for pronamide by OSHA, NIOSH or ACGIH (19).

Physical Properties:

CAS#: 23950-58-5
Specific gravity: 0.48 gm/cc (22)
H20 solubility: 1.5 mg/100 g at 25 degrees C (14)
Solubility in other solvents (at 25 degrees C): 33 ppm dimethyl sulfoxide; 15 ppm in methanol; 10 ppm in xylene and kerosene; 5 ppm in nitrobenzene and ethylene dichloride (11).
Melting point: 155-156 degrees C (309-313 degrees F) (11)
Boiling point: 321 degrees C (18)
Vapor pressure: 8.5 x 10 to the minus 5 mmHg at 25 degrees C (14)
Koc: 215, 218, 200, 990 (calc) (12)
Kd: 0.42-7.98; 0.5-19 (12)
Chemical Class/Use: Substituted benzamide; amide herbicide


Rohm and Haas Co.
Agricultural Chemicals
Independence Mall West
Philadelphia, PA 19105

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received:


  1. Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, Ohio: Meister Publishing Co.
  2. Cornell University. 1987. 1988 New York State pesticide recommendations. Forty-ninth annual conference. Nov. 9, 10, 11. Ithaca, NY.
  3. Federal Register. 48 FR 34033. July 27, 1983. U.S. Government Printing Office. Washington, DC.
  4. Gosselin, R. E. et al. 1984. Clinical toxicology of commercial products. Fifth edition. Baltimore, MD: Williams and Wilkins.
  5. 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.
  6. Rohm and Haas Company. 1985. Pronamide. Rohm and Haas Co., Philadelphia, PA.
  7. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Data Bank (HSDB). Public Health Service. National Institute of Health, U.S. Department of Health and Human Services. Bethesda, MD: NLM.
  8. USEPA. 1987 (Feb. 4). Environmental News. Office of Public Affairs (A-107). Washington, DC.
  9. _____. 1986. Memorandum from Ferial S. Bishop. List of federally restricted products. Registration Support and Emergency Response Branch (TS- 767). Washington, DC.
  10. _____. 1986.(Apr.). Guidance for reregistration of pesticide products containing pronamide as the active ingredient. Office of Pesticide Programs, Registration Division. Washington, DC.
  11. _____. 1986 (Apr.). Pesticide fact sheet for pronamide. Washington, DC.
  12. _____. 1984. Memorandum from Stuart Z. Cohen. List of potential groundwater contaminants. Office of Pesticides and Toxic Substances, Washington, DC.
  13. _____. 1979. Pronamide: Position document. Office of Pesticide Programs. Washington, DC.
  14. WSSA Herbicide Handbook Committee. Herbicide Handbook of the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL. 1989.
  15. Worthing, C. R., ed. 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.
  16. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  17. 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.
  18. Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers, Chelsea, MI.
  19. Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for Pronamide. OHS Inc., Secaucus, NJ.
  20. U.S. Environmental Protection Agency. 1988 (Jan. 6). Pesticide tolerance for 3,5-dichloro-N-(1,1-dimethyl-2-propynyl)benzamide. Federal Register, 53(3): 262-263.
  21. _____. 1989 (Jan.) Health Advisory Summary: Pronamide. US EPA, Washington, DC.
  22. _____. 1988 (Aug.). Health Advisory: Pronamide. Office of Drinking Water, US EPA, Washington, DC.
  23. Rohm and Haas. 1991 (Nov. 6). Product: Kerb Technical Herbicide (Key: 906750-0). Rohm and Haas Company, Philadelphia, PA.