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

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
Terbacil

Publication Date: 3/94

TRADE OR OTHER NAMES

Some trade names include Sinbar, Compound 732, DuPont 732 and Geonter.

REGULATORY STATUS

Terbacil is registered by the U.S. Environmental Protection Agency (EPA) as a general use herbicide. The EPA requires the signal word "Caution" on containers of formulated terbacil (19). Check with specific state regulations for local restrictions that apply.

INTRODUCTION

Terbacil is a selective herbicide, an agricultural chemical used for control of both annual weeds and perennial grasses, in sugarcane, apples, alfalfa, peaches, pecans, and mints (16). It is sprayed on soil surfaces preferably just before, or otherwise during, the period of active weed growth. It should not be used on sandy or gravelly soils. Terbacil works in plants by interfering with photosynthesis, the process by which plants derive energy from the sun (13). It is part of a family of chemicals called substituted uracils. Terbacil is available in wettable powder formulations (19).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Terbacil has low acute toxicity in humans (16). Clinical signs of poisoning in rats included initial weight loss, pallor, prostration and rapid breathing. In dogs, a single dose of 5 mg/kg caused repeated vomiting (21).

Terbacil may irritate the skin, eyes, and mucous membranes of the nose and throat. Breathing of its dust or spray mist should be avoided (3). During the manufacturing of this herbicide, human exposure is limited due to normal control measures. However, during mixing and application of this herbicide, industrial and agricultural workers are exposed to the wettable powders and aqueous emulsions. The two primary routes of exposure are (a) respiratory, that is, inhalation of dusts and sprays and (b) skin contact with dusts, emulsions, or sprays (2). Respiratory exposure could be minimized by wearing an approved respirator. Skin and/or eye exposures could be minimized with the use of gloves, goggles, and other protective clothing during terbacil handling (16). Terbacil is not a skin sensitizer (22).

Terbacil is of low toxicity to animals. The lethal dose fifty, or LD50, is the amount of a chemical that is deadly to one-half of experimental animals exposed to it. When it is given by mouth, the oral LD50 of terbacil for rats is 5,000 to 7,500 milligrams per kilogram (mg/kg) (5, 8). Signs of acute terbacil poisoning in rats include weight loss, paleness, lack of movement and rapid respiration. Six out of six male rats survived ten daily doses of 1,000 mg/kg (17). The dermal LD50 in rabbits is greater than 5,000 mg/kg (the maximum feasible dose). These rabbits did not show clinical signs of toxicity, nor any obvious gross changes caused by disease. No skin irritation and only mild eye irritation was seen in rabbits at this dose (2, 17). Similarly, there was no skin irritation or sensitization in terbacil-treated guinea pigs (17). Dogs that are given five grams per kilogram (g/kg) of terbacil exhibit vomiting and a lack of eye pupil responsiveness (2).

CHRONIC TOXICITY

No evidence of toxicity was seen in two-year feeding studies of rats fed doses as high as 12.5 mg/kg or in dogs fed doses as high as 6.25 mg/kg of terbacil. At 125 to 500 mg/kg there was a lower rate of weight gain, liver enlargement and other liver changes in rats. The high dose produced a slight increase in liver weight in dogs (2).

The EPA has established a Lifetime Health Advisory (LHA) level of 90 micrograms per liter (ug/l) for terbacil in drinking water. This means that EPA believes that water containing terbacil 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 terbacil at high levels well above the LHA level over a long period of time has been shown to cause liver damage, reduced fetal weight, and disturbances in fetal development in laboratory animals (23).

Reproductive Effects

There were no adverse effects on lactation, fertility, birth rate, pup survival, or any other aspect of reproduction in rats fed 2.5 and 12.5 mg/kg/day of terbacil for 3-generations (2).

The average number of live fetuses per litter and the average final maternal body weight were significantly lowered in the 103 and 391 mg/kg/day dosage groups (24).

Teratogenic Effects

Terbacil was not teratogenic when tested on rats and rabbits (22). When doses of 0, 30, 200, or 600 mg/kg/day were administered by gavage to pregnant rabbits on days 7 to 19 of gestation, adverse effects on the fetuses appeared only at the highest dose tested. This dose also produced maternal toxicity and increased maternal mortality. No adverse effects on the mothers or the pups were observed at lower doses. The NOAEL for this study was 200 mg/kg/day. In another study, pregnant rats were fed doses of 0, 23, 103, or 391 mg/kg/day on days 6 to 15 of gestation. Abnormalities occurred in the renal pelvis, and ureter dilation was found in pups from all the treatment groups.

Mutagenic Effects

Terbacil was not mutagenic in several screening tests (2, 22).

Carcinogenic Effects

EPA has determined that terbacil does not increase the risk of cancer in humans (23). No evidence of carcinogenicity was found in rats fed 2.5, 12.5, 125 or 500 mg/kg/day of terbacil for two years nor in dogs fed as much as 250 mg/kg/day for 2.5, 62.5 or 250 mg/kg (2). When mice were fed dietary doses of 0, 2.5, 62.5 or 250 mg/kg for 2 years, no increased incidence of cancer was found (24).

Organ Toxicity

Various liver changes have been seen in experimental rats exposed to high doses of terbacil (2).

Fate in Humans and Animals

In general, the uracil herbicides, the chemical class in which terbacil is included, are rapidly excreted in urine by mammals (9). This may account for their reportedly low toxicity (4). When given in the feed of lactating cows at five and 30 ppm, terbacil was excreted in the milk at levels up to 0.03 and 0.08 ppm, respectively. No herbicide was detected in the cows' urine and feces (9).

ECOLOGICAL EFFECTS

Effects on Birds

Terbacil is slightly toxic to birds (19). The eight-day LD50 for terbacil is more than 56,000 ppm for Peking ducklings and greater than 31,450 ppm for pheasant chicks (17). The LD50 for terbacil in quail is greater than 2,250 mg/kg (22).

Effects on Aquatic Organisms

Terbacil is not toxic to fish (19). The median tolerance limit (TLM) is the concentration of a chemical that will kill 50% of exposed organisms in a given time period. The 48-hour TLM of terbacil in sunfish is 86 ppm (2). The LC50 for terbacil in bluegill sunfish is 102.9 ppm (practically non-toxic) and 46.2 (slightly toxic) in rainbow trout. Terbacil is slightly toxic to freshwater invertebrates, with an LC50 of 65 ppm in Daphnia, a small freshwater crustacean. The LC50 for terbacil in marine oysters is greater than 4.9 ppm (moderately toxic) and 49 ppm (slightly toxic) in shrimp (22). Terbacil does not bioaccumulate in bluegill sunfish (24).

A study on grass shrimp with an 84.7% formulated terbacil product was sufficient to characterize the herbicide as slightly toxic to marine invertebrates. Estuarine and marine organisms may be exposed to terbacil due to its use as a sugarcane herbicide (16). The 48-hour TLM of terbacil in fiddler crabs is 1,000 ppm (2).

Effects on Other Animals (Nontarget species)

Terbacil is not toxic to bees and can be used around bees with minimal injury (3, 7)

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

In most soil types, terbacil has a relatively low tendency to be adsorbed to soil particles (Koc = 55 g/ml). It also is highly soluble in water and highly persistent in soils. Soil half-lives of 120 days or 2 to 5 months have been reported. This information indicates that terbacil is likely to be moderately mobile in soil and can potentially pollute groundwater (4, 14, 17, 20, 24). It should not be used on sandy or gravelly soils that have less than 1% organic matter, particularly if the water table is near the soil surface (12, 16). A potential exists for residues of terbacil to contaminate groundwater beneath sandy soils treated with terbacil, particularly when deep tillage is used (14). When used in orchards, terbacil accumulates and moves, or 'leaches,' in soils, with most movement occurring in coarse textured soils (13). Leaching may be slower in soils that are finer textured and/or have higher organic matter content (16). Terbacil was not detected in a national groundwater survey conducted by EPA (15).

In moist soils, terbacil is subject to microbial degradation. However, data suggest that recommended rates of terbacil use may result in its persistence for more than one growing season (13). Data from field dissipation studies showed that terbacil persistence in soil varied with application rate, rainfall, soil type, and mobility (16). In topsoil, 50% of terbacil and its breakdown products still remained five to seven months after application (3). The soil half-life of radio-labeled terbacil was 5 to 6 months when 4 lb/acre were applied to the surface of a silt loam soil (17). Terbacil was extremely persistent, with soil half-lives of 520 day under aerobic conditions and 178 days under anaerobic conditions (22).

Breakdown of Chemical in Water

Contamination of surface waters near terbacil-treated areas, and subsequent exposure of humans and nontarget organisms, is possible due to terbacil's mobility in soil and its high water solubility (16). Terbacil is stable to hydrolysis and photo degrades slowly in water (22). Terbacil should be kept out of lakes, streams, and ponds. Water can be contaminated by inappropriate cleaning of equipment or disposal of wastes (1).

Breakdown of Chemical in Vegetation

At normal application rates, terbacil has residual phytotoxicity in treated soils for one to two years (16). Terbacil residues were phytotoxic to oats planted three years after a previous application of the herbicide (6). In alfalfa, 12% of terbacil plus its metabolites are still found six to eight months after application (3). Since treated cover crops contain residues of terbacil, there is a general restriction against the grazing or feeding of livestock on treated orchard cover crops (16).

Terbacil is most readily absorbed through the root system of plants to which it is applied. Less is absorbed through the leaves and stems of plants. Studies of sugarcane plants indicate that terbacil is moved, or 'translocated,' upward into the leaves after absorption by the roots (17).

PHYSICAL PROPERTIES AND GUIDELINES

Terbacil is a white, crystalline, odorless solid which is noncorrosive and nonflammable (2, 18). Terbacil is stable under normal temperatures and pressures, but may pose a slight fire hazard if exposed to heat or flame (21). It is stable in water, aqueous bases and common solvents, but poses a fire and explosion hazard in the presence of strong oxidizers. Thermal decomposition products may include toxic oxides of nitrogen and carbon and toxic and corrosive fumes of chlorides (2, 21).

Technical terbacil is 95% pure active material. Terbacil formulations are compatible with most herbicides with which they might be mixed (13, 17). It should be stored in a cool, dry place. The active ingredient is non-volatile and will remain chemically stable under normal storage conditions (1, 17). Keep terbacil out of reach of children and do not contaminate water, feed, or food by its storage or disposal. Empty terbacil containers should be disposed of or buried away from water supplies in accordance with federal, state and local regulations. Open dumping is prohibited (17).

Protective clothing is required, along with good sanitary practices, when terbacil is used (1). Care should be taken to prevent drifting terbacil over neighboring crops (3). Due to residues of terbacil contained in cover crops, grazing or feeding of livestock with such crops is restricted in pecan, apple, pear, and peach orchards, as well as in citrus groves (16).

Exposure Guidelines:

No occupational exposure limits have been established for terbacil by OSHA, NIOSH or ACGIH (21).

TWA (8-hour): 10 mg/m3 (2)
NOEL: 50 ppm in dog; 250 ppm in rat (in chronic feeding studies) (16)
ADI: 0.0125 mg/kg/day (16)
MPI (Maximum Permissible Daily Intake): 0.75 mg/day (based on 60 kg. body weight (16)

Physical Properties:

CAS #: 5902-51-2
Specific gravity: 1.34 (25/25 degrees C) (21)
H20 solubility: 710 ppm at 25 degrees C (17)
Solubility in other solvents: Barely soluble in mineral oils and aliphatic hydrocarbons.
Slightly soluble in methyl isobutyl ketone, butyl acetate and xylene.
Readily soluble in cyclohexanone, dimethylformamide, xylene and strong aqueous alkalis (3, 19).
Solubility at 25 degrees C: Dimethylformamide - 252,000 ppm; Cyclohexanone - 180,000 ppm; Methyl isobutyl ketone - 121,000 ppm; Butyl acetate - 88,000 xylene - 61,000 ppm (17)
Melting Point: 175-177 degrees C (347-351 degrees F) (17)
Boiling point: Terbacil is a solid at room temperature (22)
Vapor pressure: 4.7 x 10 to the minus 7 mmHg at 29.5 degrees C ; 5.4 x 10 to the minus 6 mmHg at 54 degrees C (17)
Kow: log Kow = 1.89 (11); 78 (14)
Koc: 55 g/ml (20)
Kd: 46 (10)
Chemical Class/Use: Substituted uracil herbicide

BASIC MANUFACTURER

Du Pont Agricultural Products
Walker's Mill, Barley Mill Plaza
PO Box 80038
Wilmington, DE 19880-0038

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: November, 1992

REFERENCES

  1. Berg, G. L. (ed.). 1986. Farm Chemicals Handbook. Willoughby, Ohio: Meister Publishing Co.
  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. Hartley, D. and H. Kidd (eds.). 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  4. McEwen, F. L. and G. R. Stephenson. 1979. The use and significance of pesticides in the environment. NY: John Wiley and Sons, Inc.
  5. Melnikov, N. N. 1971. Chemistry of pesticides. New York: Springer- Verlag, Inc.
  6. Menzie, C. M. 1980. Metabolism of pesticides. Update III. U.S. Dept. of the Interior. Fish and Wildlife Service. Special Scientific Report - Wildlife No. 232. Washington, DC: United State Government Printing Office.
  7. 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.
  8. National Institute for Occupational Safety and Health (NIOSH). 1981- 1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH: NIOSH.
  9. Paulson, G. D. 1975. Metabolic fates of herbicides in animals. NY: Springer-Verlag.
  10. 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.
  11. Smith, C. N. 1981. Partition coefficients (Log Kow) for selected chemicals. In U.S. EPA, 1984. User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  12. Thomson, W. T. 1983. Herbicides. Agricultural Chemicals, Book II. Fresno, CA: Thomson Publications.
  13. TOXNET. 1975-1986. 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.
  14. 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.
  15. _____. 1984 (December). User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  16. _____. 1982 (May). Terbacil - Registration standard. Office of Pesticide Programs, Registration Division. Washington, DC.
  17. WSSA Herbicide Handbook Committee. 1989. Herbicide Handbook of the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL.
  18. Worthing, C. R. (ed.). 1983. The pesticide manual: A world compendium. The British Crop Protection Council. Croydon, England.
  19. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  20. 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.
  21. Occupational Health Services, Inc. 1991 (Feb. 21). MSDS for Terbacil. OHS Inc., Secaucus, NJ.
  22. U.S. Environmental Protection Agency. 1989 (Aug.) Pesticide Fact Sheet Number 206: Terbacil. Office of Pesticides and Toxic Substances, Office of Pesticide Programs, US EPA, Washington, DC.
  23. US EPA. Jan. 1989. Health Advisory Summary: Tebacil. US EPA, Washington, DC.
  24. _____. 1988 (August). Terbacil: Health Advisory. Office of Drinking Water, US EPA, Washington, DC.