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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 Zinc ethylenebisdithiocarbamate (EBDC), Chem Zineb, Devizeb, Discon-Z, Dithane Z-78, Lodaco, Mancozan, Parazate, Parzate, Tiezene, Zebtox, Ziden, Zinosan, Aspor, Dipher, Hexathane, Kypzin and Lonacol.


Zineb is registered as a general use pesticide by the U.S. Environmental Protection Agency (EPA). In July 1987, the Environmental Protection Agency announced the initiation of a special review of the ethylene bisdithiocarbamates (EBDCs), a class of chemicals to which zineb belongs. This Special Review was initiated because of concerns raised by laboratory tests on rats and mice. The EPA was concerned about a) potential effects on the general population from dietary exposure to residues left on food crops and b) potential occupational health risks to workers who handle and/or apply EBDC pesticides. As part of the Special Review, EPA reviewed data from market basket surveys and concluded that actual levels of EBDC residues on produce purchased by consumers are too low to affect human health. The EPA concluded its Special Review in April, 1992 with new label requirements for protective clothing to be worn by industrial and agricultural workers, and with the establishment of a 24-hour reentry period for agricultural workers. Many home garden uses of EBDCs have been canceled because the EPA has assumed that home users of these pesticides do not wear protective clothing during application (26). Toxicity data reviewed by the EPA as part of their Special Review of EBDCs are included in this document under "Toxicological Effects."

A preharvest interval of 5 to 40 days, depending on the crop, is required after application of zineb (24).


The EBDCs are fungicides used to prevent crop damage in the field and to protect harvested crops from deterioration in storage or transport (27). Zineb is used to protect fruit and vegetable crops from a wide range of foliar and other diseases. It is available in the U.S. as wettable powder and dust formulations. Zineb can be formed by combining nabam and zinc sulfate in the spray tank (22, 23).



Zineb is slightly to moderately toxic when ingested (4, 22, 25). Following a single large dose of zineb, rats and mice exhibited incoordination, hyperactivity followed by inactivity, loss of muscle tone and loss of hair (7, 22, 25). Sheep died within three weeks of being given oral doses of 500 mg/kg of zineb.

In spray or dust forms, the EBDCs are moderately irritating to the skin and to respiratory mucous membranes. poisoning from this class of chemicals include itching, scratchy throat, sneezing, coughing, inflammation of the nose or throat and bronchitis (10, 25, 29). Early symptoms from exposure of humans to inhalation of zineb include tiredness, dizziness and weakness. More severe symptoms include headache, nausea, fatigue, slurred speech, convulsions and unconsciousness (25). There is no evidence of 'neurotoxicity,' that is nerve tissue destruction or behavioral change, from the EBDCs (29). However, EBDCs are partially chemically broken down, or metabolized, to carbon disulfide, a neurotoxin capable of damaging nerve tissue (7). EBDC residues in or on foods convert readily to ETU during commercial processing or home cooking (27).

Zineb is a skin and eye irritant and a dermal sensitizer. Cross sensitization with maneb and mancozeb may occur (25). Mucous membrane irritation has also been reported in humans (6). Absorption of large amounts of zineb through the skin can lead to the same acute symptoms caused by inhalation exposure (25).

The oral LD50 for zineb in rats is 1,850 to 8,900 mg/kg, for mice is 7,600 to 8,200 to 8,900 mg/kg, and 4,450 mg/kg for rabbits. The LClo (inhalation) in rats is 800 mg/m3/4 hours. The dermal LD50 in rats is over 2,500 mg/kg, the highest dose that it is possible to administer (2, 11, 22, 23, 25).


The survival, growth, and blood chemistry of dogs were not affected by dietary levels up to 250 mg/kg for one year. However, thyroid size and weight increases were observed at this dose level. No effects on the thyroid were detected at 100 mg/kg (9, 22). In a two year study of rats fed 500 mg/kg, diminished growth, kidney pathology, and increased thyroid weight and size were observed (22). Sheep showed no adverse effects from dosages of 100 and 250 mg/kg/day for 19 weeks (22).

Occupational exposure to inhalation of zineb can lead to changes in liver enzymes, moderate anemia and other blood changes, increased incidence of poisoning symptoms during pregnancy, and chromosomal changes in the lymphocytes (25). Liver functioning was affected in workers exposed to zineb. Moderate anemia and other blood changes were also reported in 150 workers exposed to zineb in a chemical plant (9). A five-month study of zineb showed that concentrations of 20 and 200 mg/m3 caused a decrease in the activity of cholinesterase, an essential enzyme of the nervous system. A maximum permissible working air concentration of 0.5 mg/m3 is recommended by some researchers (4).

Repeated or prolonged dermal exposure may cause dermatitis or conjunctivitis (25). Farm workers who were repeatedly exposed to zineb, in fields sprayed with 0.5% suspension of the fungicide, reported severe and extensive contact dermatitis (19).

Ethylene bisdithiocarbamate pesticides (EBDCs), which include zineb, are generally considered to have low short-term mammalian toxicity. A major toxicological concern, however, is ethylenethiourea (ETU), an industrial contaminant and a breakdown product of zineb and other EBDC pesticides. In addition to having the potential to cause goiter, a condition in which the thyroid gland is enlarged, this metabolite has produced birth defects and cancer in experimental animals. ETU has been classified as a probable human carcinogen by the EPA (26). ETU can be produced when EBDCs are used on stored produce, and also when fruit or vegetables with residues of these fungicides are cooked (30).

Conversion of EBDCs into ETU can occur inside of spray tanks, during cooking of produce or processing of crops bearing EBDC residues, or as EBDCs are metabolized within the body. Residues of the EBDCs and of ETU can readily be removed from produce by washing or peeling.

Disulfiram is an EBDC which is used in the treatment of alcoholics to produce an intolerance to alcohol. Ingestion of disulfiram and alcohol together causes symptoms of nausea, vomiting, headache, excessive sweating and chills. Other EBDC compounds may cause similar symptoms when combined with alcohol (22).

Reproductive Effects

It is advisable that pregnant women avoid exposure to zineb, as it can damage the fetus, as well as cause adverse reproductive system effects (7, 9). A single intraperitoneal injection of four mg of zineb in mice, during the second half of pregnancy, resulted in abortions and weak offspring. Oral doses of zineb, at a rate of 100 mg/kg/day for two months or more, produced sterility, resorption of fetuses, abnormal tails in offspring (9, 25).

After oral ingestion, similar concentrations of ETU, a metabolite of zineb, were found in both maternal and fetal tissues of rats. In pregnant rats fed 5.0 mg/kg/day, the lowest dose tested, developmental toxicity was observed in the form of delayed hardening of the skull bones in offspring.

Teratogenic Effects

Zineb is metabolized, or broken down chemically, to ethylene thiourea (ETU), a chemical which can cause abnormal fetal development (7). Offspring of rats given a near lethal oral dose of 2,000 mg/kg/day of zineb on days 11 or 13 of pregnancy, showed a high incidence of skeletal malformations, as well as defects in the closing of the neural tube, an embryonic tube that eventually develops into the brain and spinal cord (12). A single oral dose of 8,000 mg/kg to rats on day 11 of gestation produced numerous deformities in the offspring (22). Teratogenic tendencies were also seen when pregnant mice were given intraperitoneal injections of 150 mg/kg. The teratogenic no- observable effect level (NOEL) in rats was found to be 1,000 mg/kg for zineb administered in single, daily oral doses (4).

ETU, the primary metabolite of zineb and other EBDC pesticides, has been shown to be teratogenic in hamsters, but not in mice (26).

Mutagenic Effects

One of zineb's metabolites, ETU, is known to cause mutations (7).

Carcinogenic Effects

Liver and thyroid cancer, goiter, mutagenesis, and the development of deformities, or 'teratogenesis,' can be caused by ETU, a chemical metabolite of zineb (7).

Available data clearly show that low doses of zineb are not carcinogenic. Very high doses have caused tumors in some test animals. In two strains of mice, the maximum tolerated lifetime dose of zineb did not cause tumors. Oral doses of 3,500 mg/kg/week for 6 weeks caused one of two mice strains tested to develop benign lung tumors after three weeks (22). Two rat feeding studies showed no evidence of tumor formation (23).

All of the EBDC pesticides can be degraded or metabolized into ethylene thiourea (ETU), which has been classified as a probable human carcinogen by the EPA (26, 27). Liver and thyroid cancer can be produced by ETU (7). Marked increases in the incidence of liver tumors were observed in mice fed 32.3 mg/kg of ETU daily for 80 weeks. Rats fed 8.75 or 17.5 mg/kg daily for 18 months developed malignant thyroid tumors. In rats fed ETU at doses of 0.1, 1.25, 6.25, 12.5 or 25 mg/kg/day ppm for nearly 2 years, a dose related increase in thyroid tumors was observed at the 12.5 and 25 mg/kg doses. Female mice fed doses of 16.7 or 50 mg/kg/day ETU for up to 2 years exhibited 58 and 96% incidence of malignant liver tumors, respectively. In this same study, there was also a significant increase in the incidence of thyroid tumors at the 50 mg/kg dose level (26).

Organ Toxicity

Inhalation exposure to zineb may decrease the size of the bronchial passages (9). Zineb appears to be harmful to the thyroid, liver and various muscles. Liver and kidney injury was observed in autopsies done on sheep that died after a three-week exposure to oral doses of 500 mg/kg zineb (9).

Several studies of the effects of EBDCs on test animals have shown rapid reduction in the uptake of iodine and swelling of the thyroid (i.e. goiter). In one study, a marked reduction of iodine uptake was measured 24-hours after administration of a large dose of maneb, another EBDC fungicide. A 90-day study of the effects of ETU, a common metabolite of the EBDCs on rat thyroids revealed a NOEL of 5 ppm (0.25 mg/kg/day) (22, 24, 29).

Fate in Humans and Animals

Approximately 68 to 74% of ingested material was recovered unchanged in the feces, after administration at various dietary levels. It is estimated that only 11 to 17% of an oral dose of zineb was absorbed into the body from the gastrointestinal tract of the rat (9, 22). In general, the EBDC compounds are so rapidly metabolized and excreted from the body, that blood detection is difficult. There are, however, ways of detecting ethylene thiourea in urine (10).

The ethylene bisdithiocarbamates break down in mammalian tissues into ethylenethiourea, the metabolite which has caused goiter and cancer in laboratory animals (9, 26).


Zineb is closely related to another fungicide, maneb, as they are both in the same chemical class, ethylene-bis-dithiocarbamates (EBDCs). EBDCs are noted for their environmental instability. In other words, they are readily degraded in the environment and in mammalian tissue, into a variety of breakdown byproducts, called 'degradates' or 'metabolites.' When heat is applied to these chemicals, some of them are converted directly into ethylene. Ethylene traces, or 'residues,' are commonly found on spinach and oranges. Both cooking and naturally-occurring environmental processes can cause EBDCs to break down in this way. Eleven to 26% of the original compound is believed to be broken down by cooking to ethylenethiourea (ETU). ETU is a teratogen, a chemical that has the potential to cause deformities in unborn offspring (19). Based on this potentially harmful quality of zineb's chemical class, extra care must be taken to both protect harvesters in treated fields, and to remove fungicidal residues from harvested crops (10).

Zineb varies in its toxicity to animals, birds, and fish; it is more toxic to fish than it is to birds.

Effects on Birds

Zineb is practically non-toxic to birds. The oral LD50 for zineb in mallards and young pheasants is greater than 2,000 mg/kg (14).

Effects on Aquatic Organisms

The threshold value for perch-or the amount that these fish can tolerate before toxicological effects appear-is 2 mg/l (or 2 ppm). For roach it is six to eight mg/l (8).

Effects on Other Animals (Nontarget species)

Zineb is non-toxic to bees (1, 8, 23). Little or no reduction in the numbers of beneficial predatory and parasitic arthropods was seen when zineb was used in Nova Scotian orchards at recommended dosages. Mites appear to be sensitive to zineb (11).


The EBDCs are generally unstable in the presence of moisture, oxygen, and in biological systems (28). They rapidly degrade to ETU. This rapid degradation lowers the need for concern about the environmental fate of EBDCs and focuses such concern on ETU. The EPA has either called for or is currently reviewing data on the behavior of ETU in the environment (9, 19, 24).

Breakdown of Chemical in Soil and Groundwater

Zineb is subject to chemical breakdown (hydrolysis) and does not persist in soil. It adsorbs strongly to soil particles and is usually does not move below the upper layer of soil. For this reason, zineb is unlikely to contaminate groundwater. Its bioactive half-life in the field is 16 days. Within 4 months after a field planted with alfalfa was sprayed, 99.7% of the applied zineb was lost (11, 20, 24). Results of an EPA review indicate that zineb and/or its breakdown products have the potential to leach into groundwater (15).

ETU, a metabolite of zineb, has been detected at 16 ppb in only one out of 1,295 drinking water wells tested (26).

Breakdown of Chemical in Water

Zineb is practically insoluble in water (4). It is unstable in water and hydrolyzes rapidly, producing ETU and other metabolites (24).

Breakdown of Chemical in Vegetation

Zineb is generally not poisonous to plants, except in zinc-sensitive varieties, such as tobacco and cucurbits. Pears have been slightly injured by this fungicide in a few cases (13). Ethylene thiourea (ETU) is the major zineb metabolite in plants (8).


Zineb is a light-colored powder or crystal (4, 9, 23). It decomposes when exposed to light, heat, and moisture (24, 21). Zineb should be stored in a cool, dry place. Prolonged storage can contribute to its instability, if conditions are not appropriate. Zineb does not ignite readily, but poses a slight fire hazard when exposed to heat and flame (25). It should be kept away from strong oxidizers, excessive heat, flames and sparks. Thermal decomposition may release toxic oxides of nitrogen and sulfur. Zineb is noncorrosive in the dry state, but in the presence of moisture, zineb is corrosive to iron and copper (8, 25). It is not compatible with alkaline or mercury compounds, although it is compatible with other fungicides and insecticides (13). Zineb containers should not be reused (1).

Occupational Exposure Limits:

Occupational exposure limits for zineb have not been established by OSHA, ACGIH or NIOSH (25).

Physical Properties:

CAS #: 12122-67-7
H20 solubility: practically insoluble in water (23); 10 mg/liter at room temperature (8)
Solubility in other solvents: soluble in carbon disulfide, slightly soluble in pyridine (21, 23); practically insoluble in common organic solvents (8, 23)
Melting point: Zineb decomposes before melting (21, 23)
Vapor pressure: Negligible at room temperature (21); Less than 10 minus 7 mbar at 20 degrees C (8)
Kow: log Kow: 1.78 (18)
Degradation rate constant (days-1): 0.0512 (18)
Chemical Class/Use: ethylene bisdithio-carbamate fungicide


Rhone Poulenc Ag. Co.
PO Box 12014
2 T.W. Alexander Dr.
Research Triangle Park, NC 27709

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received:


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  2. Berg, G. L. (ed.). 1986. Farm chemicals handbook. Willoughby, OH: Meister Publishing Co.
  3. Pesticide Management and Education. An on-line pesticide information database in CENET, Cornell Cooperative Extension Network. Cornell University, Ithaca, NY.
  4. 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.
  5. Cornell University. 1987. 1988 New York State pesticide recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11. Ithaca, NY.
  6. Gosselin, R. E., et al. 1984. Clinical toxicology of commercial products. Fifth edition. Baltimore, MD: Williams and Wilkins.
  7. Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and human health. NY: Springer-Verlag.
  8. Hartley, D. and H. Kidd (eds.). 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD: Williams and Wilkins.
  10. Morgan, D. P. 1982 (Jan.). Recognition and management of pesticide poisonings. Third edition. U.S. Environmental Protection Agency. Washington, DC: U.S. Government Printing Office.
  11. Pimentel, D. 1971 (June). Ecological effects of pesticides on nontarget species. Executive Office of the President's Office of Science and Technology. Washington, DC: U.S. Government Printing Office.
  12. Shepard, T.H. 1986. Catalog of teratogenic agents. Fifth edition. Baltimore, MD: The Johns Hopkins University Press.
  13. Thomson, W.T. 1985. Agricultural chemicals. Book IV. Fungicides. Fresno, CA: Thomson Publications.
  14. Tucker, R. and D.G. Crabtree. 1970. Handbook of toxicity of pesticides to wildlife. USDA Fish and Wildlife Service. Bureau of Sport Fisheries and Wildlife.
  15. U.S. Environmental Protection Agency. 1988. Memorandum from E.F. Tinsworth, Dir., Special Review and Reregistration Division. Office of Pesticides and Toxic Substances. "Data call-in for small-scale retrospective ground-water monitoring."
  16. ______. 1987 (May 13). Memorandum from E. Neil Pelletier. Status of EBDC fungicide registrations. Office of Pesticides and Toxic Substances. Science Support Branch. Benefits and Use Division (TS-768-C). Washington, DC. Photocopy.
  17. ______. 1986 (June). Pesticides fact book. (A-107/86-003). Office of Public Affairs. Washington, DC.
  18. ______. 1984 (Dec.). User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  19. Wagner, S.L. 1983. Clinical toxicology of agricultural chemicals. Environmental Health Sciences Center. Oregon State University. NJ: Noyes Data Corporation.
  20. Witt, J. M. (ed.). 1985. Chemistry, biochemistry, and toxicology of pesticides. Proceedings of an Extension Service Short Course at Oregon State University. Pest Control Education Program. Eugene, OR.
  21. Worthing, C.R. (ed.). 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.
  22. Hayes, W.J. and E.R. Laws (eds.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  23. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  24. Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers, Chelsea, MI.
  25. Occupational Health Services, Inc. 1991 (21 Feb.). MSDS for Zineb. OHS Inc., Secaucus, NJ.
  26. U.S. Environmental Protection Agency. 1992 (March 2). Ethylene bisdithiocarbamates (EBDCs); Notice of intent to cancel and conclusion of Special Review. Federal Register 57(41):7434-7530. US GAO, Washington, DC.
  27. U.S. Environmental Protection Agency. 1988 (Oct.). Guidance for the Registration of Pesticide Products Containing Maneb as the Active Ingredient. Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  28. U.S. Environmental Protection Agency. 1988 (Oct.). Guidance for the Reregistration of Pesticide Products Containing Metiram as the Active Ingredient. Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  29. Morgan, D.P. 1982 (Jan.). Recognition and management of pesticide poisonings. Third edition. Washington, DC: U.S. Environmental Protection Agency. U.S. Government Printing Office.
  30. McEwen, F.L. and G.R. Stephenson. 1979. The use and significance of pesticides in the environment. NY: John Wiley and Sons, Inc.