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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


Trade names for products containing this compound include Apl-Luster, TBZ, Mertect, Mycozol, Tecto and Thibenzole. The product is often used in combination with other fungicides and insecticides.


Thiabendazole is a systemic benzimidazole fungicide used to control fruit and vegetable diseases such as mold, rot, blight and stain. It is also active against storage diseases and Dutch Elm disease. In livestock, thiabendazole is also applied to treat roundworms. Thiabendazole is also used medicinally as a chelating agent to bind metals (2).



Thiabendazole is classified as a slightly toxic pesticide and carries the signal word CAUTION on the label. Effects of acute overexposure to the fungicide include dizziness, anorexia, nausea, and vomiting. Other symptoms such as itching, rash, chills, and headache occur less frequently. The symptoms are brief and are related to the dose level (8).

The rat oral LD50 is 3,100-3,600 mg/kg, mouse oral LD50 1,395-3,810 mg/kg and the rabbit oral LD50 is greater than 3,850 mg/kg. The lethal dose in sheep is 1,200 mg/kg. Thiabendazole is not a skin irritant or a sensitizer.


Rats force-fed 200 mg/kg/day or less showed little or no growth effects. At higher levels (400 mg/kg) there was growth suppression. Death occurred in a few days at 1,200 mg/kg and 30% mortality occurred within 30 days at 800 mg/kg. A decrease of active bone marrow at high doses was also noted (3). At doses somewhat below the LD50, mice had liver, spleen, and intestinal effects.

In dogs, high daily doses (200 mg/kg) for two years produced few effects other than occasional attacks of vomiting and persistent anemia. Sheep experience toxic depression and anorexia at very high doses (800-1,000 mg/kg). Studies on cattle, sheep, goats, swine, horses and zoo animals have shown few chronic symptoms at low doses (8).

Reproductive Effects

A three-generation study in rats showed no adverse effects on reproduction at 20-80 mg/kg. However, four times this rather low therapeutic dose produced serious pregnancy-related disorders (eclampsia) in sheep (3).

Mice studied for five generations showed no effects at 10 mg/kg, decreased weanling weights at 50 mg/kg, and decreased weanling weight and size at 250 mg/kg.

Teratogenic Effects

Pregnant rats fed low doses (about 25 mg/kg) produced offspring with no abnormalities, but when pregnant rats were fed higher doses (200 mg/kg) on the 11th day of pregnancy, their offspring had skeletal defects. When fed the same dose on the 12th day of pregnancy, the young had cleft palates, brain hernia and absence of tails.

Mutagenic Effects

Several studies with bacteria have failed to produce any chromosome changes or mutations due to thiabendazole. It appears that the compound is not mutagenic.

Carcinogenic Effects

A two-year feeding study with rats at levels of 10-160 mg/kg produced no cancer related effects attributable to thiabendazole. There is no evidence of carcinogenic effects in humans from exposure to thiabendazole.

Organ Toxicity

Dogs autopsied after a two-year feeding study had incomplete development of bone marrow, a wasting away of lymph tissue, and other abnormalities (2). Most dogs tested at around 100 mg/day for two years developed anemia. The dogs recovered at the end of the study (8).

Fate in Humans and Animals

Excretion of thiabendazole in the urine and feces is rapid in most species and is almost complete after 48 hours in rats and 96 hours in sheep. The excretion products are metabolites reaching peak levels in the blood stream one hour after administration to rats, one to two hours after in humans, and four hours after in cattle. These metabolites, are distributed throughout most body tissues in sheep but detectable in only a few tissues at low levels (less than 0.2 ppm) in 16 days and at very low levels (0.06 ppm or less) after 30 days.

Oral doses given cattle and sheep reached a peak concentration in the milk at 0.1 to 1.0% of the dose in 24 hours. When cattle were continuously fed a diet of 30 ppm, residues in the milk were 0.05 to 0.17 ppm. No evidence of bioaccumulation in animal tissues was found.


There is no evidence of toxicity or hazard to bobwhite quail from non- target applications. Thiabendazole is weakly toxic to fish. Earthworms are sensitive to the compound (LD50 = approx. 20 ug/worm), while bees are not (1, 3).


Thiabendazole binding to soil increases with increasing soil acidity. It is quite persistent. In one study, nine months following application, most of the residues (85-95%) were recovered from soil. It is not expected to leach readily from soil.

No metabolism was seen with potatoes or corn, but photoproducts were detected on sugar beet leaves (3). Total residues were 78% parent compound with the remaining 22% being benzimidazole, benzimidazole-2-carboxamide and unidentified products. Thiabendazole is readily absorbed by roots and translocated to all parts of a plant but predominantly to the leaf margins. It is non-toxic to plants when used as directed (1).


Exposure Guidelines:

ADI: 0.1 mg/kg/day (ppm) (EPA); 0.3 mg/kg/day (ppm) (WHO)
RfD: 0.1 mg/kg/day (OPP)

Physical Properties:

Common name: thiabendazole
CAS #: 148-79-8
Chemical name: 2-(4-thiazolyl)-1H-benzimidazole
Chemical class/use: benzimidazole fungicide
Solubility in water: 50 mg/l (pH 7.0)
Solubility in solvent: acetone, 0.42 g/100 g; ethanol, 0.21 g/100g; benzene, 0.023 g/100 g; chloroform, 0.008 g/100g
Melting Point: 304-305 degrees
Vapor Pressure: non-volatile at room temperature; 4 x 10-9 mm Hg


Merck Agvet
Division of Merck & Co., Inc.
PO Box 2000
Rahway, NJ 07065-0912
Telephone: 908/855-3800

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: December, 1992


  1. Hartley, D., and H. Kidd (ed/). 1991. The Agrochemicals Handbook. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Gosselin, R.E., R.P. Smith, H.C. Hodge. 1984. Clinical Toxicology of Commercial Products, Williams and Wilkins, Baltimore, MD.
  3. National Library of Medicine. 1992. Hazardous Substances Databank. TOXNET, Medlars Management Section, Bethesda, MD.
  4. Menzie, Calvin M. 1980. Metabolism of Pesticides, Update III. U. S. Dept of the Interior, Fish and Wildlife Service, Special Scientific Report, Wildlife No. 232.
  5. Worthing, Charles R. (ed.). 1983. The Pesticide Manual, A World Compendium. The British Crop Protection Council, The Ravenham Press Limited, Ravenham, Suffolk, England.
  6. Food and Drug Administration. 1986. The FDA Surveillance Index. Bureau of Foods, Dept of Commerce, National Technical Information Service, Springfield, VA.
  7. Menzie, Calvin M. 1978. Metabolism of Pesticides, Update II. U. S. Dept of the Interior, Fish and Wildlife Service, Special Scientific Report, Wildlife No. 212.
  8. Edwards, I. Ralph, Donald G. Ferry, and Wayne A. Temple. 1991. Fungicides and Related Compounds. In Handbook of Pesticide Toxicology, Volume 3 Classes of Pesticides. Wayland J. Hayes and Edward R. Laws, Editors. Academic Press, Inc. NY.