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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


Arathane, Caprane, Capryl, Cekucap 25 WP, Crotonate, Crotothane, DCPC, Dikar (a mixture of dinocap and mancozeb), DNOPC, Ezenosan, Iscothane, Karathane, Mildane, Mildex.


In 1985, the U.S. Environmental Protection Agency (EPA) initiated a Special Review of all pesticide products containing dinocap as an active ingredient. This was initiated because of lab results on rabbits indicating its potential to produce birth defects and chronic reproductive effects (2, 13). Upon completion of the Special Review in February 1990, EPA required a variety of measures to reduce risks of exposure to acceptable levels for mixers/loaders and applicators:
  1. wearing of protective suits, goggles or face shield, and chemical resistant gloves and boots during mixing and loading;

  2. the use of enclosed vehicles for application whenever possible. When use of enclosed vehicles is not possible, applicators must wear protective suits, goggles or face shield, and chemical resistant gloves and boots;

  3. wearing of protective hood or wide brim hat during mist blower or air blast applications;

  4. wearing of protective suit and equipment by applicators when leaving application vehicle or while repairing equipment. Chemical- resistant gloves when leaving the application vehicle for any reason;

  5. following application, applicators must remove all contaminated protective equipment, clothing and shoes, and shower with soap and water;

  6. teratogenicity warning statements on product labels (12, 23).

Products containing dinocap must bear the signal word "Caution" (20). Check with specific state regulations for local restrictions that may apply, and follow product label instructions carefully.


Dinocap was first registered in the late 1950s and has been used as a contact fungicide to control fungus and, to a lesser extent, as an acaricide for control of ticks and mites. It is applied to foliage for control of powdery mildew on fruit, vegetable, nursery, and ornamental crops, and to limit mite populations on apple trees. Apples are the major use site, accounting for over 90% of use (15). Dinocap may be applied from early spring to late summer (2). It is available as dust, liquid concentrate, and wettable powder formulations (20).



Dinocap is moderately toxic by ingestion and slightly toxic by dermal absorption (22). It poses the highest threat to humans through oral and inhalation exposure. It is irritating to the skin, eyes, and mucous membranes lining the nose, throat and lungs (9). Dermal contact is the most common route of exposure (15). Alcoholics and persons with kidney or liver diseases may be at increased risk from exposure to dinocap. Hot environments may enhance both the absorption and the toxicity of dinocap (22).

Dinocap is included in a class of compounds which cause the following symptoms upon acute exposure: fatigue, weakness, nausea, vomiting, headaches, flushed skin, exhaustion, abdominal pain, loss of appetite, weight loss, fever, excessive sweating, rapid breathing and heart beats, shortness of breath, thirst, dehydration, heat stroke, and convulsions. Dermal exposure can cause skin inflammation, flushing and yellow staining, diarrhea, dizziness, and excitement. Hair can be stained yellow by dinocap exposure. This kind of exposure can bring on headaches and heat sensitivity. Inhalation of dinocap can cause tightness in the chest and fluid retention in the lungs, a condition called pulmonary edema. In addition to causing conjunctivitis and yellow staining of the white portion of the eye, eye contact with the insecticide can also cause sweating, rapid heartbeat, thirst, imbalance, vomiting and weakness. Death from exposure to dinocap may be due to overheating, or failure of the respiratory system or of the blood circulation system (4, 17). Symptoms may appear immediately upon exposure or may suddenly appear at any time within 2 days after the cessation of exposure (22).

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for dinocap in rats is 980 mg/kg, 2,000 mg/kg in male rabbits, 53 mg/kg in mice, and 100 mg/kg in dogs (3, 6, 7, 19, 20). The dermal LD50 for dinocap on rabbits is 9,400 mg/kg (22).


In addition to the symptoms of acute exposure, prolonged or repeated exposure may cause weight loss, cataract formation, and liver or kidney damage (22). Greenhouse workers developed liver function abnormalities in association with exposure to the fungicide. The severity of the abnormalities varied with the length of work exposure (11). Prolonged skin exposure may lead to dermatitis or allergies. Prolonged eye contact may result in permanent injury (22).

At a dietary dose of 25 mg/kg/day of dinocap, dogs showed decreased appetite and drastic weight loss, followed by death within six weeks. At dietary doses of 6.25 and 25 mg/kg/day, cell death occurred in the liver (7). No weight loss occurred in dogs given 50 mg/kg of dinocap in a 1-year feeding study. Cataracts were produced in white Peking ducks at this same dose level (18). Rat growth and survival were reduced with a dietary level of 125 mg/kg/day of dinocap. Spleen enlargement occurred in male rats receiving 125 mg/kg/day of the fungicide. Only male rats showed growth retardation in a 2-year study (7). Degenerative changes and cell death were seen in the livers, kidneys and stomachs of rabbits given oral doses of 30 or 150 mg/kg of dinocap for 90 days (11).

Reproductive Effects

When pregnant rabbits were given dermal doses of 25, 50 or 100 mg/kg/day, developmental toxicity in the form of reduced fetal weight was observed at the highest dose. The developmental NOEL for this study was 50 mg/kg/day (23). There were decreased growth rates and reduced survival of offspring in the second generation of rats given dietary doses of 104 to 126 mg/kg/day (11, 19).

Teratogenic Effects

EPA has determined that dinocap has caused birth defects in animals and poses a teratogenic risk to humans (23). It is teratogenic at doses lower than those which cause toxic effects in pregnant mothers (19). Pregnant women should avoid exposure to dinocap. Exposure, especially by inhalation or dermal absorption, may put unborn offspring at significant risk of birth defects (2).

Fetal growth retardation, cleft palate, and abnormal rib formations were seen in mice exposed to dinocap during organogenesis, the organ- forming period of pregnancy. Fetal growth was inhibited at 5 mg/kg/day. Malformations were seen at 20 mg/kg/day and higher (16). Birth defects were observed in the offspring of rabbits given oral or dermal doses of dinocap during pregnancy. These included abnormalities of the neural tube, spine, and skull, at 3 mg/kg/day (13, 23). No birth defects were discovered in rabbits given dermal doses up to and including those that cause severe skin irritation and obvious maternal poisoning (Rohm and Haas Company, 1985). Following dermal applications of 100 mg/kg/day to animals, reduced fetal weight and an increased occurrence of skull malformations were observed (13).

Mutagenic Effects

No information found.

Carcinogenic Effects

Dinocap did not cause tumor development in mice that were fed the highest tolerated dose of the fungicide (7).

Organ Toxicity

Dinocap may increase the metabolic rate and cause adverse effects to the nervous system, liver and kidneys (22). Gastrointestinal, liver, and central nervous system changes would be expected with prolonged or increased exposure to dinocap (17). Degenerative changes and cell death occurred in the liver, kidneys and stomach of rabbits given oral doses of 30 or 150 mg/kg of dinocap for 90 days. The composition of blood and urine also changed (11).

Acute poisoning signs, degenerative changes, and cell deterioration were more obvious in the stomachs than in the livers and kidneys of experimental rats and rabbits. Degeneration of these organs took place after changes occurred in the functioning of cells within the organs (11). Spleen enlargement occurred in male rats that were given a 2,500 ppm dietary level of the material (7). Liver damage occurred in dogs given dietary doses of 250 and 1000 ppm for 6 weeks (19).

Fate in Humans and Animals

Residues of dinocap are expected to be found in urine and blood (17).


Effects on Birds

Dinocap is highly toxic to birds (20). Ducks fed 50 ppm of this fungicide developed cataracts (17).

Effects on Aquatic Organisms

Dinocap is slightly toxic to fish (1, 6). The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it. At 13 degrees C, 78% technical dinocap has an LC50 of 15 micrograms per liter (ug/l) in rainbow trout. Its LC50 in goldfish is 33 ug/l at 18 degrees C (11). This fungicide should not be applied directly to water due to its toxicity to fish (15).

Effects on Other Animals (Nontarget species)

Dinocap is nontoxic to bees and other beneficial insects (6, 5, 1). It does not usually interfere with IPM programs that use predatory insects for biological control of mites (13). The potential hazard of this fungicide to endangered species is low (15). Biological magnification of dinocap is unlikely (5).


Breakdown of Chemical in Soil and Groundwater

Dinocap adsorbs weakly to soil particles. It therefore has a moderate potential to contaminate groundwater (21). Dinocap is more readily bound to soils that have large amounts of clay or organic matter. It is subject to microbial degradation and to a small amount of photodegradation (15).

Breakdown of Chemical in Water

Dinocap is almost insoluble in water (6). The cleaning of dinocap application equipment or disposal of related wastes should not be done near/in water bodies, as this can cause contamination (15).

Breakdown of Chemical in Vegetation

Dinocap is readily absorbed and translocated by treated plants. It builds up in the growing shoots and leaf tips. Since this material penetrates foliage rapidly, it is not likely to be washed off by rain (15). There is good crop tolerance to dinocap for the recommended use areas (6). However, dinocap can be toxic to plants if it is applied in hot weather (13). The approximate trace, or 'residual,' period of dinocap in plants is 1 to 2 weeks (5). The edible portion of treated fruits or vegetables should be washed or wiped before they are used (10).


Dinocap is dark reddish-brown liquid (14). The technical product is about 80% pure (1). Dinocap poses a moderate fire hazard if exposed to heat or flame. Its vapors are heavier than air and may travel considerable distances to a source of ignition and flash back. Heating of dinocap for more than 48 hours at temperatures above 90 degrees F (32 degrees C) may result in explosive decomposition. Thermal decomposition may release toxic oxides of carbon and nitrogen. Dinocap may pose a fire and explosion hazard in the presence of strong oxidizers (22).

Dinocap should not be used or combined with oil or materials with petroleum-solvent bases (5). It is incompatible with alkaline preparations, lime sulfur, inorganic acids, amines, alkanolamines, caustic materials, halogenated compounds, and iron (6, 17). The fungicide should not be applied when temperatures are above 90 degrees F (10). Containers must be kept from freezing during storage (8). Inappropriate storage or disposal of this material can contaminate water, food, or feed.

Dinocap treated areas should not be entered without protective clothing until sprays have dried. Any unprotected persons must vacate areas being treated (14). Inhalation of dinocap vapors, dust, and spray mist should be avoided. Skin, eyes, and hair should be also protected from contact with this material (6). Dinocap treated areas should not be grazed (10).

Exposure Guidelines:

No occupational exposure limits for dinocap have been established by OSHA, NIOSH or ACGIH.

0.2 mg/m3 Rohm and Haas Recommended TWA (22)

0.6 mg/m3 Rohm and Haas Recommended STEL (22)

NOEL: 0.5 mg/kg/day for oral exposure (2); 50 mg/kg/day for dermal exposure (14)

Physical Properties:

CAS #: 39300-45-3
Specific gravity: 1.10 (22)
H20 solubility: practically insoluble in water (14); 4 ug/ml (21).
Solubility in other solvents: soluble in most organic solvents such as benzene and ether (17)
Boiling point: 138-140 degrees C (280-284 degrees C) at 0.05 mmHg (18, 22)
Flash point: 190 degrees F (88 degrees C) (22)
Vapor pressure: very low (6); 4.0 x 10 to the minus 8 power (21).
Koc: 630 g/ml (21)
pH: 3 - 5 (22)
Viscosity: 500 - 1000 CPS at 20 degrees C (22)
Chemical Class/Use: dinitrophenolic compound used as a protective fungicide and acaricide (10)


Rohm and Haas Co.
Agricultural Chemicals
Independence Mall West
Philadelphia, PA, 19105

Review by Basic Manufacturer:

Comments solicited: November, 1992.
Comments received:


  1. Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, OH: Meister Publishing Company.
  2. Federal Register. 50 FR 1119. Jan. 9, 1985. U. S. Government Printing Office. Washington, DC.
  3. Gosselin, R. E., et al. 1976. Clinical toxicology of commercial products. Fourth edition. Baltimore, MD: Williams and Wilkins.
  4. Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and human health. NY: Springer-Verlag.
  5. Harding, W. C. 1979. Pesticide profiles. Part one: Insecticides and miticides. Bulletin 267. Cooperative Extension Service, University of Maryland.
  6. Hartley, D.. and H. Kidd, eds. 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  7. Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD: Williams and Wilkins.
  8. Rohm and Haas Company. 1985 (May 6). Personal correspondence from Kay L. McCarthy. Agricultural Chemicals Registration and Regulatory Affairs Department. (Doc. #2842H). Philadelphia, PA.
  9. Sax, N. I. 1984. Dangerous properties of industrial materials. Sixth edition. NY: VanNostrand Reinhold Co.
  10. Thomson, W. T. 1985. Fungicides. Agricultural Chemicals, Book IV. Fresno, CA: Thomson Publications.
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  12. U.S. Environmental Protection Agency. 1990 (Feb.). Suspended, Canceled, and Restricted Pesticides. Pesticides and Toxic Substances, US EPA, Washington, DC.
  13. _____. 1986 (Oct.). Dinocap: Special review; technical support document. Office of Pesticide Programs. Washington, DC.
  14. _____. 1986 (Oct. 30). Pesticide fact sheet number 65.1: Dinocap. Office of Pesticide Programs. Washington, DC.
  15. _____. 1978 (June 30). Pesticide fact sheet number 65: Dinocap. Office of Pesticide Programs. Washington, DC.
  16. U. S. Health Effects Research Lab. 1986 (Aug.). Postnatal alterations in development resulting from prenatal exposure to pesticides. Research Triangle Park, NC.
  17. Wagner, S. L. 1983. Clinical toxicology of agricultural chemicals. Environmental Health Sciences Center. Oregon State University. NJ: Noyes Data Corporation.
  18. Worthing, C. R., ed. 1983. The pesticide manual: a world compendium. Croydon, England: The British Crop Protection Council.
  19. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  20. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  21. 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.
  22. Occupational Health Services, Inc. 1992 (June 4). MSDS for Dinocap. OHS Inc., Secaucus, NJ.
  23. U.S. Environmental Protection Agency. 1989 (Feb. 6). Dinocap: Notice of intent to cancel registrations; Conclusion of Special Review. Federal Register 54 (23): 5908-20.