PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Pyrethrins to Ziram --> Vernolate

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.


Publication Date: 9/95


The active ingredient vernolate is found in a variety of commercial herbicides. Some trade names for products containing vernolate include Reward, Surpass, and Vernam (1, 2, 3, 4).


Vernolate is registered in the U.S. for use on corn. Vernolate is a "general use" pesticide (GUP) with an EPA toxicity classification of III (slightly toxic). Check with specific state regulations for local restrictions which may apply. Products containing vernolate must bear the Signal Word "Caution" on their label (4).


Vernolate is a thiocarbamate compound used as a selective soil- incorporated herbicide. It is toxic to germinating broadleaf and grassy weeds. Vernolate is also used to control weeds in soybeans, peanuts and sweet potatoes (2, 3, 5, 8).



The acute oral LD50 for technical vernolate in rats ranged between 1,200 mg/kg and 1,900 mg/kg (1, 2, 4, 6). The oral LD50 for the formulated product Vernolate 6E is 1,800 mg/kg (3); and 1,200-1,470 mg/kg for the 7E formulation (4). The compound is considered moderately toxic by ingestion (6). A lethal dose by ingestion in rats was reported to be 1,200 mg/kg (6).

The acute dermal LD50 for vernolate in rabbits was greater than 1,955 mg/kg (1). The acute percutaneous LD50 was greater than 5,000 mg/kg. Vernolate is considered non-irritating to both the skin and eyes (2).

Repeated intracutaneous injections of vernolate in guinea pigs failed to reveal any indications that the compound is a sensitizing agent.


A dose of 80 mg/kg/day of vernolate for 51 weeks produced a significantly increased mortality in male rats due to hemorrhage. A dose of 20 mg/kg/day for 51 weeks produced an increase in blood clotting time (6). The highest dose without activity in 90-day feeding tests was 32 mg/kg body weight/day for rats (1, 3).

A 90-day sub-acute feeding study was conducted in dogs. A no-effect- level (NEL) was established in excess of 38 mg/kg/day (1, 3).

Reproductive Effects

In a two-generation reproduction study in rats exposed to technical Vernam, the levels tested were 0, 1, 5, and 25 mg/kg/day. The maternal no- observable-effect-level (NOEL) was 1 mg/kg/day. The maternal lowest-effect- level (LEL) was 5 mg/kg/day at which decreased body weight was noted. The reproduction NOEL was reported to be 25 mg/kg/day (HDT). The developmental toxicity NOEL was less than 1 mg/kg/day. An increased incidence of urinary tract variants was noted at this dose level (7).

Teratogenic Effects

In another developmental toxicity study, rabbits were exposed to technical Vernam. The levels tested by gavage in the New Zealand White strain from gestation days 6 to 21 were 0, 2, 20 and 200 mg/kg/day. The maternal NOEL was found to be greater than 200 mg/kg/day. The developmental toxicity NOEL was also greater than 200 mg/kg (7).

Mutagenic Effects

Technical Vernam (97.3%) when tested for lymphoma mutation potential, induced a positive responce in sister chromatid exchange under the activated (0.005-0.01 micro liters/ml) or the nonactivated (0.08-0.1 micro liters/ml) system (7).

Carcinogenic Effects

In a 24-month study of mice, no oncogenic/carcinogenic effects were observed at levels of vernolate as high as 100 mg/kg/day (6).

Organ Toxicity

No information currently available.

Fate in Humans and Animals

No information currently available.


Effects on Birds

Vernolate is relatively non-toxic to birds. The oral LC50 of technical vernolate in the bobwhite quail is 12,000 ppm for a 7-day feed treatment. The oral LC50 of vernolate 6E in bobwhite quail is 14,500 ppm for a comparable regimen (3).

No delayed neurotoxicity was observed in a study of hens (6, 7).

Effects on Aquatic Organisms

Vernolate is considered slightly toxic to fish.The LC50 for the active ingredient in rainbow trout (40-56 mm long) is 6.2 mg/l for 24 hours; 5.9 mg/l for 48 hours; and 4.3 mg/l for 96 hours (1, 4). The 96-hour LC50 for vernolate 6E in fingerling rainbow trout is 10.8 mg/l; and 9.6 mg/l for technical vernolate. Another study found the 96-hour LC50 for technical vernolate 6E in mosquito fish to be 14.5 ppm (3).

The EC50 (shell growth inhibition) of vernolate in oysters is greater than 1 ppm (maximum level tested) after a 96-hr exposure. The EC50 (loss of equilibrium or death) in brown shrimp (Penaeus aztecus) is greater than 1 ppm (maximum level tested) after 24 and 48-hour exposures (3).

The acute LC50 of vernolate in a juvenile estuarine species (Leiostomus xanthurus) is greater than 1 ppm (maximum level tested) after 24 and 48-hour exposures (3). The 96-hour LC50 of both technical vernolate and vernolate 6E for the three-spined stickleback (Gasterosteus aculeatus) is between 1 and 10 ppm (3).

Effects on Other Animals (Nontarget species)

No information currently available.


Breakdown of Chemical in Soil and Groundwater

Vernolate is adsorbed into dry soil but it can be removed by leaching. Microbial breakdown is the main mechanism by which vernolate is lost from soils. Vernolate is readily lost from the soil by volitalization when the soil surface is wet at the time of application and the herbicide is not incorporated immediately. At recommended rates of application, vernolate does not persist in soil and it should not leave residues that could injure subsequently planted sensitive crops. The half-life in moist loam soil at 21 to 27 degrees C (70 to 80 degrees F) is approximately 1.5 weeks (3). The half- life in clay soils is 10-12 days (1, 4). In soil, vernolate microbially decomposes to mercaptan, amine, carbon dioxide, and isopropanol (1).

Breakdown of Chemical in Surface Water

No information currently available.

Breakdown of Chemical in Vegetation

Vernolate's mechanism of action is not known. It inhibits growth in the meristematic region of the leaves of grasses (3). Vernolate is taken up by roots of soybean and peanut plants and translocated throughout the stems and leaves. It is rapidly metabolized by plants to CO2 and naturally occurring plant constituents (3). Vernolate has no other biological properties other than herbicidal (3). In plants, degradation involves carbon dioxide evolution (1).


Physical Properties:

CAS No.: 1929-77-7 (1)
Chemical name: S-propyl dipropylthio-carbamate (IUPAC); S-propyl dipropyl-carbamothioate (CA) (1, 3)
Chemical Class/Use: selective soil-herbicide (1)
Specific gravity: 0.954 20/20 (3)
Solubility in water: 90 mg/l at 20 degrees C (1, 3)
Solubility in other solvents: miscible with common organic solvents, e.g. xylene, methylisobutyl ketone, kerosene, etc. (1, 3)
Boiling point: 140 degrees C at 26.6 mbar; 150 degrees C at 40 mbar (1)
Flashpoint: 121 degrees C (3)
Vapor pressure: 1.39 Pa at 25 degrees C (2)


Drexel Chemical Co.
P. O. Box 9306
2487 Pennsylvania St.
Memphis, TN 38109
Telehone: 901-774-4370

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received: December, 1994


  1. The Agrochemicals Handbook. 1983. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Worthing, C. R. (ed.). 1983. The Pesticide Manual: A World Compendium. Seventh edition. Published by The British Crop Protection Council.
  3. Herbicide Handbook of the Weed Science Society of America. Sixth edition. 1989. Champaign, IL.
  4. Farm Chemicals Handbook. 1994. Meister Publishing Co. Willoughby, OH.
  5. Thomson, W. T. 1993. Agricultural Chemicals. Book II: Herbicides. Thomson Publications, Fresno, CA.
  6. OHS Database. 1994. Occupational Health Services, Inc. 1994. MSDS for Vernolate. OHS Inc., Secaucus, NJ.
  7. U.S. Environmental Protection Agency. 1993. Office of Pesticides. TOX Oneliners --Vernolate. May, 1993.
  8. Pesticide Management and Education. An on-line pesticide information database in CENET, Cornell Cooperative Extension Network. Cornell University, Ithaca, NY.