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The information in this profile may be out-of-date. It was last revised in 1996. EXTOXNET no longer updates this information, but it may be useful as a reference or resource.

Please visit the National Pesticide Information Center (NPIC) to find updated pesticide fact sheets. If you don't find a fact sheet related to your question, feel free to call 1-800-858-7378. NPIC is open five days a week from 8:00am to 12:00pm Pacific Time.

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E X T O X N E T

Extension Toxicology Network

Pesticide Information Profiles

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

EXTOXNET primary files maintained and archived at Oregon State University

Revised 9/95.

VERNOLATE

TRADE OR OTHER NAMES: The active ingredient vernolate is found in a variety of commercial herbicides. Some trade names for products containing vernolate include Reward, Surpass, and Vernam (46, 47, 48, 49).

REGULATORY STATUS: 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 (49).

INTRODUCTION: 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 (47, 48, 50, 53).

TOXICOLOGICAL EFFECTS

• Acute Toxicity: The acute oral LD50 for technical vernolate in rats ranged between 1,200 mg/kg and 1,900 mg/kg (46, 47, 49, 51). The oral LD50 for the formulated product Vernolate 6E is 1,800 mg/kg (48); and 1,200-1,470 mg/kg for the 7E formulation (49). The compound is considered moderately toxic by ingestion (51). A lethal dose by ingestion in rats was reported to be 1,200 mg/kg (51). The acute dermal LD50 for vernolate in rabbits was greater than 1,955 mg/kg (46). The acute percutaneous LD50 was greater than 5,000 mg/kg. Vernolate is considered non-irritating to both the skin and eyes (47). Repeated intracutaneous injections of vernolate in guinea pigs failed to reveal any indications that the compound is a sensitizing agent.
• Chronic Toxicity: 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 (51). The highest dose without activity in 90-day feeding tests was 32 mg/kg body weight/day for rats (46, 48). 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 (46, 48).
• 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 (52).
• 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 (52).
• 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 (52).

• 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 (51).
• Organ Toxicity: No information currently available.
• Fate in Humans and Animals: No information currently available.

ECOLOGICAL EFFECTS

• 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 (48). No delayed neurotoxicity was observed in a study of hens (51,52).
• 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 (46, 49). 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 (48). 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 (48). 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 (48). The 96-hour LC50 of both technical vernolate and vernolate 6E for the three-spined stickleback (Gasterosteus aculeatus) is between 1 and 10 ppm (48).
• Effects on Other Animals (Nontarget species): No information currently available.

ENVIRONMENTAL FATE

• 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 (48). The half-life in clay soils is 10-12 days (46, 49). In soil, vernolate microbially decomposes to mercaptan, amine, carbon dioxide, and isopropanol (46).
• 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 (48). 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 (48). Vernolate has no other biological properties other than herbicidal (48). In plants, degradation involves carbon dioxide evolution (46).

PHYSICAL PROPERTIES AND GUIDELINES

Physical Properties:

• Appearance: Clear liquid
• Chemical Name: S-propyl dipropylthio-carbamate (IUPAC); S-propyl dipropyl-carbamothioate (CA) (46, 48)
• CAS Number: 1929-77-7 (46)
• Molecular Weight: 203.3
• Water Solubility: 90 mg/l at 20 degrees C (46, 48)
• Solubility in Other Solvents: miscible with common organic solvents, e.g. xylene, methylisobutyl ketone, kerosene, etc. (46, 48)
• Melting Point: Not Available
• Vapor Pressure: 1.39 Pa at 25 degrees C (47)
• Partition Coefficient: 3.84 (20 degreees C)
• Adsorption Coefficient: Not Available

Exposure Guidelines:

• ADI: Not Available
• MCL: Not Available
• RfD: Not Available
• PEL: Not Available
• HA: Not Available
• TLV: Not Available

BASIC MANUFACTURER:

Drexel Chemical Co.
P. O. Box 9306
2487 Pennsylvania St.
Memphis, TN 38109

• Telehone: 901-774-4370

REFERENCES

References for the information in this PIP can be found in Reference List Number 4