It must be noted that the issue of a Data Sheet for a particular pesticide does not imply endorsement of the pesticide by WHO or FAO for any particular use, or exclude its use for other purposes not stated. While the information provided is believed to be accurate according to data available at the time when the sheet was compiled, neither WHO nor FAO are responsible for any errors or omissions, or any consequences therefrom.

The issue of this document does not constitute formal publication. It should not be reviewed, abstracted or quoted without the agreement of the Food and Agriculture Organization of the United Nations or of the World Health Organization.

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Dicofol (BSI, ESA, ISO).

A persistent organochlorine acaricide of moderate mammalian toxicity. Dicofol is structurally similar to DDT. It accumulates in body fat to a plateau level related to absorption. It is cumulative in the environment. Dicofol was introduced commercially in 1955.

Pure dicofol is a colourless solid; m.p. 78.5-79.5 ºC, b.p. 180 ºC at 0.13 mbar. Technical product (95% pure) is brown viscous oil and is composed of 80-85% p,p’-dicofol and 15-20% o,p’-dicofol; density 1.45 at 25 ºC, specific gravity 1.135 at 20 ºC; stable  80 ºC; up to 18 impurities were reported. The purer form is generally >95% dicofol which contains less than 0.1% DDT related impurities (i.e. DDT, DDE and DDI).

Practically insoluble in water. Soluble in most aliphatic and aromatic solvents and most common organic solvents.

Stable to acids but not to alkaline media. Slightly corrosive to metals.

Negligible at room temperature.

"Kelthane AP", 18.5% wettable powder, "Kelthane 35" 35% wettable powder, Kelthane MF", 42% emulsifiable concentrate, "Kelthane EC", 18.5% emulsifiable concentrate. "Kelthane dust base", 30% flowable, 41%.

Non-systemic acaricide. In agriculture and horticulture, controls spider mites and soft-bodied mites in apples, cucumbers, tomatoes, hops, wines, lettuce and ornamentals.

Recommended for control of mites on a wide range of crops at concentrations ranging from 0.5 to 2 kg AI/ha.

It should not be used on permanent or temporary grass for grazing, silage, or hay intended for feed to dairy or slaughter animals. May cause damage if used on canaeti juniper, Chinese holly, eggplant or pears. Toxic to fish.

No recommended uses were reported.

No recommended uses were reported.

Dicofol is extensively absorbed from the gastrointestinal tract. The highest tissue concentrations were found in adipose tissue followed by the adrenal glands, thyroid and liver. The p,p’-dicofol isomer, the main component of technical dicofol, was more persistent in the body than the o,p’-isomer. Female rats tended to retain dicofol to a greater extent than males. Dicofol showed a similar pattern of distribution on elimination as DDT but it is more polar and therefore less persistent in the body. In adipose tissue the parent compound was predominant.

Produces stimulation of axonal transmission of nervous signals, believed to be related to inhibition of ATPases in the central nervous system (CNS). The signs of toxicity are consistent with CNS depression.

In rats, dicofol was excreted as polar metabolites primarily in the faeces, but with lesser amounts in the urine. Metabolism involved dechlorination and oxidation of the ethanol moiety and hydroxylation of the aromatic rings.

After a single intraperitoneal dose of 230 mg/kg b.w. to rats, dicofol and DCB were found to be stored in fat and skeletal muscle an excreted in faeces. Initial accumulation of dicofol and DCB was in the liver.

Technical dicofol is reported to be irritating to the skin but non-irritating to the eye. Technical dicofol produced delayed contact hypersensitivity in guinea pigs.

In a 13 week study in mice using dietary concentrations of 0. 10, 125, 250, 500 or 1000 mg/kg in the diet, the NOAEL was 10 mg/kg diet, equal to 2.1 mg/kg b.w./day, based on reduced body-weight, liver enlargement, and increased hepatic mixed function oxidase (MFO) activity. In another 13-week study in mice using dietary concentrations of 0, 250, 500, or 750 mg/kg, liver histopathology, including centrilobular hypertrophy and eosinophilia of heptocytes was observed at all dose levels.

In a 13-week study in rats at dietary concentrations of 0, 1, 10, 100, 500, or 1500 mg/kg diet, the NOAEL was 1 mg/kg diet, equal to 0.07 mg/kg b.w./day. Although the incidence and severity of thyroid follicular epithelial hypertrophy was increased in males at 10 mg/kg diet group and above, this thyroid effect was not found in a second 13-week study using dietary concentrations of 0, 50, 200, 1000 or 3000 mg/kg.

In a 13-week study in dogs using dietary concentrations of 0, 10, 100, 300, or 1000 mg/kg in the diet, the NOAEL was 10 mg/kg diet, equal to 0.29 mg/kg b.w./day. At 100 mg/kg diet, equal to 3.3 mg/kg b.w./day, cortisol response to ACTH was reduced.

A one-year dog study used dietary levels of 0, 5, 30, or 180 mg/kg was performed to better define the NOAEL. The NOAEL was 30 mg/kg diet, equal to 0.82 mg/kg b.w./day, based on liver changes and reduced cortisol response to ACTH at 180 mg/kg diet, equal to 5.7 mg/kg b.w./day.

In a 78-week carcinogenicity study in mice using time-weighted average concentrations of 260, or 530 mg/kg diet for males and 120 or 240 mg/kg diet for females, dicofol produced an increased incidence of liver adenomas and adenomas/carcinomas combined in male mice at 260 and 530 mg/kg diet, equivalent to 4 and 80 mg/kg b.w./day. Dicofol was not carcinogenic in female mice.

In a two-year study in rats using dietary concentrations of 0, 5, 50, or 250 mg/kg in the diet, the NOAEL was 5 mg/kg diet, equal to 0.22 mg/kg b.w./day, based on histopathological changes in the liver and vacuolation of adrenal cortical cells at 50 mg/kg diet, equal to 2.2 mg/kg b.w./day. No treatment-related changes in the thyroid or in the incidence of neoplasia were observed. There was no evidence of carcinogenicity in a 78-week carcinogenicity study in rats using time-weighted average concentrations of 470 or 940 mg/kg diet (24 or 47 mg/kg b.w./day) (for males and 380 or 760 mg/kg diet, equal to 19 or 38 mg/kg b.w./day for females. Dicofol was not carcinogenic in rats.

Carcinogenicity: For a carcinogenicity study in mice and rats see Section 2.1.6.

Teratogenicity: In a teratology study in rats using gavage doses of 0, 0.25, 2.5, or 25 mg/kg b.w./day, the NOAEL for maternal toxicity was 0.25 mg/kg b.w./day based on clinical signs of toxicity at 2.5 mg/kg b.w./day. The NOAEL for embryofoetal toxicity was 25 mg/kg b.w./day.

In a teratology study in rabbits using gavage doses of 0, 0.4, 4 or 40 mg/kg b.w./day, the NOAEL for maternal toxicity was 0.4 mg/kg b.w./day based on histopathological changes in the liver at 4 mg/kg b.w./day. The NOAEL for embryofoetal toxicity was 4 mg/kg b.w./day based on an increased incidence of abortion at 40 mg/kg b.w./day. Teratogenic effects were not found in these studies.

Reproduction: In a two-generation reproduction study in rats using dietary concentrations of 5, 25, 125, or 250 mg/kg in the diet, the NOAEL was 5 mg/kg in diet, equal to 0.5 mg/kg b.w./day, based on an increased incidence of ovarian stromal cell hypertrophy and hepatocellular changes at 25 mg/kg diet. Offspring viability was reduced at 125 and 250 mg/kg diet. The NOAEL for reproductive parameters was 25 mg/kg diet, equal to 2.1 mg/kg b.w./day.

Mutagenicity: Dicofol was found to be not genotoxic in various in vitro and in vivo mutagenicity tests.

Other: Dicofol was found to induce rat liver mixed function oxidase activity ranked after heptachlor, DDT chlorfenson and dieldrin.

The dicofol metabolite dichlorobenzilic acid (DCBA) was measured in the urine of 4 workers involved in the mixing/loading or application of dicofol to citrus crops for 10 consecutive days. Urine samples were obtained over 4 days beginning 6 days after exposure. Because of previous use of chlorobenzilate, pre-exposure DCBA excretion rates were not zero. Mean daily DCBA excretion was 19-42 μg/day over the exposure period. The variation correlated with the difference in estimated dermal dose (2.7 - 13 mg/day). The percent dermal dose excreted as DCBA was estimated to be 0.25%. The half-life for DCBA excretion in the urine was estimated to be seven days.

Single dose: No information.

Repeated dose: No information.

No published information.

In 1979, 78 incidences of Kelthane^R overexposure were reported by the US Environmental Protection Agency Pesticide Incident Monitoring System. Fourteen cases involved dicofol alone and 8 of these reported symptoms. One case involved dicofol ingestion (amount unspecified) leading to nausea, dizziness, and vomiting. Three cases involved inhalation exposure resulting in dizziness, weakness, and vomiting in two cases and sinus congestion in the third. Two cases involved dermal exposure (amount unspecified) resulting in skin irritation in one case and rash in the other.

In a case report, a 12-year old male was accidentally exposed to dicofol when he fell from a bicycle into a puddle of spilled undiluted dicofol formulation (470 g/litre). The skin was abraded and clothing contaminated. The patient had initial symptoms of nausea, dizziness, disorientation, confusion, lethargy and headache. The patient demonstrated horizontal nystagmus and impaired balance. These symptoms resolved within three weeks. Three weeks after the incident, serum dicofol levels were 1.1 μg/litre and adipose tissue levels were 0.153 μg/kg (analytical methods unspecified). No dicofol was detected in serum one week after the exposure. Following persistent emotional difficulties, the patient underwent a neuropsychological evaluation eight months after the exposure, which showed impairment of certain cognitive functions including auditory attention, immediate memory, and ability to selectively inhibit inappropriate responses. A pre-exposure neuropsychological analysis was unavailable for comparison.

No published information.

No published information.

0-0.002 mg/kg b.w.

Sublethal effects include effects on feeding moulting and motor control.

[For definition of categories see the "Introduction to data sheets".]

Formulations in Categories 3 and 4: Should be transported in clearly labelled rigid and leakproof containers, away from containers of food and drink.

Storage should be under lock and key and secure from access by unauthorized persons and children.

Formulations in Categories 3 and 4: Protective clothing (see section 4) should be used by all handling the compound. Adequate washing facilities should be available at all times during handling and should be close to the site of handling. Eating, drinking and smoking should be prohibited during and after handling before washing of hands and face.

All formulations: Containers may be decontaminated (for method see section 4.3). Decontaminated containers should not be used for food and drink. Containers that are not decontaminated should be burned or rushed and buried below topsoil. Care must be taken to avoid subsequent contamination of water sources.

Formulations in Categories 3 and 4: Pre-employment medical examinations of workers is desirable. Workers suffering from active hepatic or renal disease should be excluded from contact. Pre-employment and periodic medical examination for workers desirable, especially for those handling concentrates. Special account should be taken of the workers’ mental ability to comprehend and follow instructions. Training of workers in techniques to avoid contact is essential.

All formulations: Pilots and loaders should have special training in application methods and in recognition of early symptoms of poisoning, and they must wear suitable protective clothing. Flagmen should wear overalls, an impermeable brimmed hat, and be located well away from the dropping zone.

Formulations in categories 3 and 4 - Minimum cautionary statement:

Dicofol is an organochlorine compound. It is poisonous if swallowed. It may be absorbed through the skin. Avoid skin contact; wear hand protection, clean protective clothing and a face mask when handling concentrate. Wash thoroughly with soap and water after using. Keep the material out of reach of children and well away from foodstuffs, animal feed and their containers. If poisoning occurs, call a physician.

Maximum residue limits (in mg/kg) for dicofol have been recommended by the Joint FAO/WHO Meeting on Pesticide Residues:

TLV - No information. Closed systems with forced ventilation may be required to reduce as much as possible the exposure of workers to the chemical. Protective equipment for the skin and respiratory protection is advisable.

When opening the container and when mixing, protective impermeable boots, clean overalls, gloves and respirator should be worn. Mixing, if not mechanical, should always be carried out with a paddle of appropriate length. When spraying tall crops or during aerial application, a face mask should be worn, as well as an impermeable hood, clothing, boots, and gloves. The applicator should avoid working in spray mist and avoid contact with the mouth. All protective clothing should be washed immediately after use, including the insides of gloves. Splashes must be washed immediately from the skin, or eyes with large quantities of water. Before eating, drinking, or smoking, hands and other exposed skin should be washed.

Persons exposed to dicofol and associated with its application should wear protective clothing and observe the precautions described above in 4.1.3. under "Mixers and applicators".

With correct use in agriculture, the general population should not be exposed to hazardous amounts of dicofol.

The general population should be kept out of treated areas for at least one day.

Spillage of dicofol and its formulations should be removed by washing with large quantities of water. Residues in containers should be emptied in a diluted form into a deep pit, taking care to avoid ground waters. The empty container may be decontaminated by rinsing two or three times with water and scrubbing the sides. An additional rinse should be carried out with 5% sodium hydroxide solution which should remain in the container overnight. Impermeable gauntlets should be worn during this work, and a soakage pit should be provided for the rinsings. Decontaminated containers should not be used for food and drink. Spillage of dicofol and its formulations should be removed by washing with 5% sodium hydroxide solution and then rinsing with large quantities of water.

These may include headache, nausea, fatigue, general weakness.

Remove contaminated clothing and wash the affected skin with water and soap and flush the area with large quantities of water.

If swallowed, vomiting should be induced if the person is conscious. Patient should be calmed and kept in quiet, shaded area until medical help arrives.

Dicofol is an organochlorine insecticide of moderate toxicity. It is absorbed from the gastrointestinal tract and by inhalation. It may also be absorbed through the intact skin, more especially in the case of oil-based formulations. Its mode of action is by stimulation of the CNS. It is slowly metabolized and eliminated from the tissues and may accumulate in body fat.

Symptoms of poisoning may include headache, nausea and vomiting, weakness, dizziness and confusion, impaired balance and horizontal nystagmus.

Measurement of blood or fat levels of dicofol and DCB and urine levels of the same will confirm absorption of Dicofol but will not necessarily reflect the degree of poisoning. High levels of dicofol and its metabolites will be found in body fats, these levels may continue to increase after acute dosage, when symptoms of poisoning have abated. Treatment should never be deferred pending the results of a laboratory test.

If the pesticide has been ingested, rapid gastric lavage should be performed. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with water. There is no specific antidote and treatment is symptomatic.

Possible development of neuropsychological disturbances.

No information available.

No information available.

Product analysis by HPLC. Residues determined by GLC.

CIPAC Handbook, 988 D, 67; AOAC Methods, 1990, 986. 06 (For HPLC).

Horwitz W, ed. (1980), Official Methods of Analysis of the Association of Official Analytical Chemists, 13th edition. Washington, D.C., Association of Official Analytical Chemists, pp.104-5.

Pestic Anal Man (1979), 201-A, 201-G, 201-J (for GLC).

Markus JR and Puma B, eds. (1973), Pesticide Residues, Pesticide Reg. Sec. 120.163 Washington D.C., U.S. Food and Drug Administration.

Rothman AM (1980), High performance liquid chromatographic analysis of dicofol acaricide. J Assoc Off Anal Chem, 63:1296-1299.

Impairment of some enzyme activities: liver monoamine oxidase, lipase, carbonic anhydrase).

IARC (1983), Dicofol. In: Miscellaneous Pesticides. Lyon, International Agency for Research on Cancer. pp.87-101. (IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans, Vol. 30).

WHO (1993), Pesticides Residues in Food - 1992 Evaluations, Part II - Toxicology. World Health Organization document WHO/PCS/93.34.

The Pesticide Manual, A World Compendium (10th edition 1994), Tomlin, C., ed., British Crop Protection Council, 20 Bridport Road, Thornton Heath, CR4 7QG, U.K.

    See Also:
       Toxicological Abbreviations
       Dicofol (ICSC)
       Dicofol (FAO/PL:1968/M/9/1)
       Dicofol (AGP:1970/M/12/1)
       Dicofol (WHO Pesticide Residues Series 4)
       Dicofol (Pesticide residues in food: 1992 evaluations Part II Toxicology)
       Dicofol (IARC Summary & Evaluation, Volume 30, 1983)