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
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis
Publishers, Chelsea, MI.
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.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for
dicofol. OHS Inc., Secaucus, NJ.
Rohm and Haas Company. 1991 (Dec 11). Material Safety Data Sheet
for Kelthane Technical B Miticide. Rohm and Haas, Philadelphia, PA.
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.
US Environmental Protection Agency. 1991 (Oct. 4). Dicofol;
Proposed revocation of food additive regulation; Proposed rule. Federal
Register 56(193): 504666-68.
US Environmental Protection Agency. 1986 (May 29). Dicofol;
Intent to cancel registrations of pesticide products containing dicofol.
Federal Register 51(103): 19508-525.
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.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
To Top
For more information relative to pesticides and their use, please contact the PMEP staff at:
Pesticide Safety Education Pgm.
5123 Comstock Hall
Cornell University
Ithaca, NY 14853-0901
(607) 255-1866 |
Pesticide Sales & Use Reporting Database Grp.
Cornell University
20 Thornwood Dr. #106
Ithaca, NY 14850
(607) 257-5706 |
|
 |
This site is supported, in part, by funding from the
 |
Questions regarding the development of this web site should be directed to the
PMEP Webmaster
