PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> Carbaryl to Dicrotophos --> Dicofol

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
Dicofol

Publication Date: 9/93

TRADE OR OTHER NAMES

Trade names include Acarin, Cekudifol, Decofol, Dicomite, Hifol, Kelthane, and Mitigan (1, 4).

REGULATORY STATUS

Products containing dicofol must bear the signal word "Warning" or "Caution," depending on the formulation (4).

INTRODUCTION

Dicofol is an organochlorine miticide used on a wide variety of fruit, vegetable, ornamental and field crops. It is produced as emulsifiable concentrate and wettable powder formulations (4). Dicofol has little effect on insects.

Dicofol is manufactured from DDT. In 1986, use of dicofol was temporarily canceled by the EPA because of concerns raised by high levels of DDT contamination (9). Modern manufacturing processes can produce technical grade dicofol which contains less than 0.1 % DDT. Dicofol causes hyperstimulation of nerve transmissions along nerve axons. This hyperstimulation is thought to be related to inhibition of ATPases in the central nervous system (3).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Dicofol is moderately toxic to practically nontoxic to humans and may be absorbed through ingestion, inhalation or skin contact. Symptoms of exposure have included nausea, dizziness, weakness and vomiting from ingestion or respiratory exposure, skin irritation or rash from dermal exposure, and conjunctivitis from eye contact. Poisoning may affect the liver, kidneys or the central nervous system. Overexposure by any route to chlorinated insecticides may cause nervousness and hyperactivity, headache, nausea, vomiting, unusual sensations and fatigue. Very severe cases may result in convulsions, coma, or death from respiratory failure (3, 5, 6).

When dicofol was fed to rats for 3 months at doses of 0, 0.05, 0.5, 5, 25 or 75 mg/kg/day, fewer than half of the animals survived at the 75 mg/kg/dose. Liver enzyme induction was observed at 75 mg/kg and above. Decreased body weights, decreased cortisone levels, and toxic changes in the liver, adrenal glands, and kidneys were noted at 25 mg/kg. The NOEL in this study was 0.5 mg/kg. Similar results were observed in a 3-month feeding study with mice. When dogs were fed 0, 0.25, 2.5, 7.5 or 25 mg/kg/day for 3 months, only 2 out of 12 survived at 1000 ppm. Poisoning symptoms and effects on the liver, heart and testes were observed at the 7.5 mg/kg dose. The NOEL in dogs was 0.25 mg/kg/day (3).

Dicofol is a moderate skin and eye irritant (6). Between 30 and 75% of the dicofol in an emulsifiable concentrate formulation applied to the skin of rats and rabbits was absorbed during a 6 hour contact period (3).

Dicofol is stored in fatty tissues. Intense activity or starvation may mobilize the pesticide, resulting in the reappearance of toxic symptoms long after actual exposure (5).

The oral LD50 for dicofol in rats is 575 to 960 mg/kg, in rabbits and guinea pigs is 1810 mg/kg, and in mice is 420 to 675 mg/kg. The dermal LD50 in rats is 1,000 to 5,000 mg/kg, and in rabbits is between 2,000 and 5,000 mg/kg. The inhalation LC50 in rats is greater than 5 mg/l for 4 hours (4, 5, 6).

CHRONIC TOXICITY

Prolonged or repeated exposure to dicofol can cause the same effects and symptoms as acute exposure (5). Prolonged or repeated skin contact can cause moderate skin irritation and/or sensitization of the skin (6).

Dicofol is a liver enzyme inducer belonging to the phenobarbitol class and having about the same potency as phenobarbitol in this regard. The primary effects observed after short or long term dietary exposure of laboratory animals to dicofol are liver enlargement and enzyme induction. At very high doses, toxic effects to the adrenal glands, kidneys, heart, testes, ovaries and urinary bladder have also been observed. The effects of dicofol on the liver have culminated in the production of liver tumors in male mice (3).

When dicofol was fed to dogs at 0.125, 0.75 or 4.5 mg/kg/day for one year, toxic effects on the liver were observed. The NOEL was 0.75 mg/kg/day. Long term dermal exposure of rats to dicofol formulated as an emulsifiable concentrate also produced toxic effects on the liver (3).

Reproductive Effects

Reproductive effects in rat offspring have been observed only at doses high enough to also cause toxic effects on the livers, ovaries and feeding behavior of the parents. Rats fed diets containing 0, 0.25, 1.71, 6.25 or 12.5 mg/kg/day through two generations exhibited adverse effects on the survival and/or growth of newborns at 6.25 and 12.5 mg/kg/day. The NOEL for reproductive effects in rats was 25 ppm (1.7 to 4.0 mg/kg/day) (3).

Teratogenic Effects

No teratogenic effects were observed when rats were given up to 25 mg/kg/day on days 6 through 15 of pregnancy and killed on day 20 for maternal and fetal examinations (3).

Mutagenic Effects

Five separate laboratory tests have shown that dicofol is not mutagenic (3, 6).

Carcinogenic Effects

EPA has determined that there is limited evidence that dicofol may cause cancer in laboratory animals, but that there is no evidence that it causes cancer in humans. No evidence of carcinogenicity was observed in when rats were fed up to 47 mg/kg/day for 78 weeks. A 2-year oncogenicity study in mice showed an increased incidence of liver tumors in male mice at dietary concentration levels of 13.2 and 26.4 mg/kg/day (6, 8).

Organ Toxicity

Chronic exposure to dicofol can cause damage to the kidney, liver and heart. In a 2-year dietary study with rats, liver growth, enzyme induction and other changes in the liver, adrenal gland and urinary bladder were observed at doses of 2.5 mg/kg and above. The NOEL was 5 ppm (0.22 to 0.27 mg/kg/day) in rats. Effects on the liver, kidney, and adrenals, and reduced body weights were observed at doses of 6.25 mg/kg/day and above in a 3-month dietary study with mice. The NOEL was 0.5 mg/kg/day in mice (6).

Fate in Humans and Animals

Dicofol is converted in rats to the metabolites 4,4'-dichloro- benzophenone and 4,4'-dechlorodicofol. Dicofol is stored in fat and, to a lesser degree in muscle. It is excreted in the feces (1, 10).

Studies of the metabolism of dicofol in rats, mice and rabbits have shown that ingested dicofol is rapidly absorbed, distributed primarily to fat, and readily eliminated, primarily via the bile in feces. Concentrations in fat are generally no more than 0.5 to 5 times the dietary feeding level. When mice were given a single oral dose of 25 mg/kg dicofol, approximately 60% of the dose was eliminated within 96 hours, 20% in the urine and 40% in the feces. Concentrations in body tissues peaked between 24 and 48 hours following dosing, with 10% of the dose found in fat, followed by the liver and other tissues. Levels in tissues other than fat declined sharply after the peak. When rats were given a single oral dose of 50 mg/kg of dicofol, all but 2% of the dose was eliminated within 192 hours, with peak concentrations in body tissues occurring between 24 and 48 hours after dosing (3).

Most people come in contact with dicofol after eating food tainted with the pesticide. It may be stored in the body's fat deposits. The body usually rids itself of dicofol (small amounts) in 3-4 days.

ECOLOGICAL EFFECTS

Effects on Birds

Dicofol is slightly toxic to birds. The 8-day dietary LC50 for bobwhite quail is 3010 ppm, 1,418 ppm for Japanese quail, and 2,126 ppm for ring-necked pheasant. Eggshell thinning and reduced offspring survival were noted in the mallard duck, American kestrel, ring dove and screech owl (6).

Effects on Aquatic Organisms

Dicofol is highly toxic to fish, aquatic invertebrates and algae. The 96-hour LC50 for rainbow trout is 0.12 mg/l, 0.37 mg/l for sheepshead minnow, 0.06 mg/l for mysid shrimp, 15 ug/l for shell oysters, and 75 ug/l for algae (6).

Effects on Other Animals (Nontarget species)

Dicofol is not toxic to bees (4).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Dicofol is practically insoluble in water and adsorbs very strongly to soil particles. It is therefore nearly immobile in soils and unlikely to infiltrate groundwater. Even in sandy soil, dicofol was not detected below the top 3 inches in standard soil column tests. It is possible for dicofol to enter surface waters when soil erosion occurs (7, 10).

Dicofol has a soil half-life of 60 days (7, 10). When Kelthane 35 was applied to a crop of strawberries at 7 lbs of active ingredient per acre, the half life for residues due to dicofol or its metabolites was 78 days (10). Dicofol may be susceptible to chemical breakdown in moist soils (2). It is subject to degradation by UV light. In a silty loam soil, its photodegradation half-life was 30 days. Under anaerobic soil conditions, the half-life for dicofol was 15.9 days (10).

Breakdown of Chemical in Water

Dicofol degrades in water or when exposed to UV light at pH levels above 7. Its half-life in solution at pH 5 is 47 to 85 days, and at pH 7 is 7 minutes to 99 hours. The primary hydrolytic degradate is dichlorobenzophenone (DCBP) (10). Because of its very high absorption coefficient (Koc), dicofol is expected to adsorb to sediment when released into open waters (2).

Breakdown of Chemical in Vegetation

In a number of studies, dicofol residues on treated plant tissues have been shown to remain unchanged for up to 2 years (10).

PHYSICAL PROPERTIES AND GUIDELINES

Pure dicofol is a white crystalline solid. Technical dicofol is a red-brown viscous liquid with an odor like fresh cut hay. Dicofol is stable under normal conditions, but temperatures above 100 degrees C (212 degrees F) should be avoided to prevent thermal decomposition (6, 3). Thermal decomposition products may include toxic and corrosive fumes of chlorides and toxic oxides of carbon. While dicofol may burn, it does not ignite readily. Containers may explode in the heat of fire. Dicofol is slowly corrosive to iron or mild steel (3, 5).

Occupational Exposure Limits:

No occupational exposure limits have been set by ACGIH, NIOSH, or OSHA. Rohm and Haas Company has established a the following dermal exposure limits: 0.1 mg/m3 TWA, and 0.3 mg/m3 STEL (6, 5).

Physical Properties:

CAS #: 115-32-2
Specific gravity: 1.45 (6)
H20 solubility: practically insoluble; 0.8 ppm at 25 degrees C (6).
Solubility in other solvents: soluble in most organic solvents (1).
Melting point: 78.5 - 79.5 degrees C for pure dicofol (1, 5); 50 degrees C (122 degrees F) for technical dicofol (6)
Boiling point: dicofol decomposes before boiling (6) 193 degrees C (3)
Decomposition temperature: > 100 degrees C (212 degrees F) (6).
Flashpoint: 193 degrees C (379 degrees F) open cup (6). 120 degrees F (49 degrees C) (5).
Vapor pressure: Negligible at room temperature; < 0.00001 mm Hg at 20 degrees C/68 degrees F (6), 3.9 x 10 to the minus 7 power mm Hg at 25 degrees C (3, 10)
Koc: 5868 (silt loam) to 8383 (sand) (10)
Chemical Class/Use: Organochlorine miticide

BASIC MANUFACTURER

Rohm and Haas Company
Agricultural Chemicals
Independence Mall West
Philadelphia PA 19105

Review by Basic Manufacturer:

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

REFERENCES

  1. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  2. Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers, Chelsea, MI.
  3. Hurt, S.S. 1991 (July 24). Dicofol: Toxicological evaluation of dicofol prepared for the WHO expert group on pesticide residues (Report No. 91R-1017). Toxicology Dept., Rohm and Haas Company, Spring House, PA.
  4. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  5. Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for dicofol. OHS Inc., Secaucus, NJ.
  6. Rohm and Haas Company. 1991 (Dec 11). Material Safety Data Sheet for Kelthane Technical B Miticide. Rohm and Haas, Philadelphia, PA.
  7. 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.
  8. US Environmental Protection Agency. 1991 (Oct. 4). Dicofol; Proposed revocation of food additive regulation; Proposed rule. Federal Register 56(193): 504666-68.
  9. US Environmental Protection Agency. 1986 (May 29). Dicofol; Intent to cancel registrations of pesticide products containing dicofol. Federal Register 51(103): 19508-525.
  10. Tillman, Anne. 1992. Residues, Environmental Fate and Metabolism Evaluation of Dicofol Prepared for the FAO Expert Group on Pesticide Residues (Rohm and Haas Report No. AMT 92-76). Rohm and Haas Co., Philadelphia, PA.