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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


Pentachlorophenol is abbreviated as PCP. Product names include Dowicide EC-7, Penchlorol, Penta, Pentacon, Penwar, Priltox, Sinituho and Weedone.


Pentachlorophenol (PCP) is a chlorinated hydrocarbon insecticide and fungicide. It is used primarily to protect timber from fungal rot and wood- boring insects. PCP products are very toxic to plants and are used as preharvest defoliants and general herbicides. Their use as herbicides is currently restricted to nonagricultural uses along drainage ditches, driveways, and fencerows.

The results described in this profile are mostly from studies that were conducted using technical-grade PCP, because it is technical-grade PCP that people are exposed to when they use commercial PCP products.

Commercial (technical) grades of PCP commonly contain manufacturing by- products, such as dioxin (HxCDD), which can be more toxic than the PCP itself. Another contaminant in PCP is HCB (Hexachlorobenzene). The use of PCP is being phased out because of the discovery of these highly toxic contaminants (9). PCP is a Restricted Use Pesticide (RUP). Restricted Use Pesticides may be purchased and used only by certified applicators.

In 1988 the EPA announced further restrictions on the use of PCP as in the pulp and paper industry where it is used in paper coatings, sizing, adhesives and in inks. Registration for use in cooling towers and for certain oil well operations was also cancelled. The 1988 regulations also required compliance with dioxin (HxCDD) concentration limits in the final product.



PCP is a very toxic compound, and is labeled with a DANGER signal word. The exact dose required to produce illness in humans is not known. Skin penetration is the most dangerous route of exposure, but inhalation or ingestion of PCP may also cause toxicity. There are about 50 known cases of poisoning from PCP containing herbicides, molluscicides or wood preservatives, 30 of which have resulted in death. Immersion of a man's hand in a 0.4 percent PCP solution for 10 minutes caused pain and inflammation.

Acute exposure to PCP can cause elevated temperature, profuse sweating, dehydration, loss of appetite, decreased body weight, nausea, uncoordinated movement and coma. Some of the symptoms may be due to the impurities in the formulation rather than the pentachlorophenol itself (9).

The oral LD50 of PCP for rats is 25-200 mg/kg, depending on the product quality. The oral LD50 for mice and rabbits is 130 mg/kg (6).

The dermal LD50 is 105 mg/kg for rabbits, 96-320 mg/kg for rats, and 261 mg/kg for mice (6). Acute dermal exposure of dogs, rabbits, rat, and guinea pigs to high doses of PCP causes dry wrinkled skin and loss of hair from topically treated areas, high blood pressure and fevor, motor weakness, rapid digestion, and extensive damage to the cardiovascular system.

The inhalation LD50 for rats is between about 10 and 225 mg/kg, and the mouse inhalation LD50 is 355 mg/kg (6).


Animal experiments suggest that chronic exposure to pure pentachlorophenol may affect reproduction, induce birth defects, and cause acne and other skin diseases.

In humans, the most common exposure to PCP is inhalation in the workplace. Abdominal pain, nausea, fever, and respiratory irritation result from PCP exposure (6). Inhalation of PCP at occupational levels causes eye, skin, and throat irritation, while high levels may affect the circulatory system and cause heart failure. Survivors of toxic exposures may suffer visual and central nervous system damage. Persons regularly exposed to PCP tend to tolerate higher levels of PCP vapors than persons having little contact with these vapors.

Reproductive and Teratogenic Effects

PCP has adverse effects on reproduction in rats when administered orally during pregnancy at very high doses, near lethal levels. Embryo death increased in rats fed high levels of PCP during the sensitive period of pregnancy (6). In hamsters, oral administration of low doses of PCP during the sensitive period of pregnancy caused fetal deaths, and PCP was found in the blood and fat of the fetuses (6). No developmental effects were observed in rats fed high doses of PCP. While PCP is clearly toxic to the developing fetus it does not appear to cause any birth defects.

Prolonged exposure to PCP by humans may result in adverse reproductive effects that are associated with changes in the endocrine gland function and other changes in the body (immunological dysfunction). A number of women with histories of spontaneous abortion, unexplained infertility and menstrual disorders had elevated levels of pentachlorophenol and/or lindane in their blood (11). While this evidence suggests some relationship between reproductive problems and PCP and/or lindane, it does not prove that PCP or lindane were the direct cause of the problems (11).

Mutagenic Effects

Mutagenic effects have not been clearly demonstrated for PCP in laboratory test systems (6). At the most, PCP should be classified as weakly mutagenic. There is no evidence from epidemiological studies of occupationally exposed workers that PCP causes mutations.

Carcinogenic Effects

Clear evidence links PCP exposure with carcinogenic activity in test mice. Limited evidence links PCP with carcinogenicity in humans. One study links PCP with Hodgkin's disease on the basis of a single family's case history and with the occurrence of the disease in carpentry and lumber workers in the United Kingdom (7). The World Health Organization publication cautions against the any conclusions based on such limited data.

Organ Toxicity

The major targets of toxicity of PCP are the liver, kidneys and central nervous system, with toxic effects occurring at low doses. In both rats and monkeys, the liver and kidneys concentrated PCP the most. Immunotoxicity occurred in animals exposed to PCP, but not to those exposed to pure PCP, suggesting the effects were due to impurities. Pure PCP has little effect on the livers of rats. Doses of PCP produced greater liver effects than doses of pure PCP which were 25 times greater (2).

In two-year studies of rats fed high doses of PCP, life spans were not changed, but liver and kidney changes were observed (6).

PCP causes lung, liver, kidney damage and contact dermatitis in humans. Extended periods of exposure to PCP results in persistent chloracne and damage to the nervous system. About two dozen fatalities due to accidental exposure to PCP in industry have been reported. Autopsies revealed changes in the brain, heart, kidneys, lungs, and liver.

Fate in Humans and Animals

PCP is rapidly absorbed through the gastrointestinal tract following ingestion. If deposition in the tissues occurs, the major sites are the liver, kidneys, plasma protein, brain, spleen and fat; but accumulation is not common. Unless kidney and liver functions are impaired, PCP is rapidly eliminated from blood and tissues, and is excreted unchanged via the urine. Single doses of PCP have half-lives in blood of 15 hours in rats, 78 hours in monkeys, and 30-50 hours in humans (2).


PCP is acutely and chronically highly toxic to cold and warm water fish and moderately toxic to other freshwater and marine organisms. PCP concentrations detected in rivers, streams, or surface water systems, up to now, are below lethal levels. Lethal levels have been exceeded only during accidental spills.

Most wood treated with PCP solutions will "bleed." Bleeding refers to the movement of PCP solution from the interior to the surface of the wood. Whereas pure PCP can evaporate from the surface of the wood into the air, the impurities in the solutions may not. Because of its popular use as a wood preservative, the public could be exposed to low levels of PCP in outdoor wood structures of many kinds.

Cattle and other farm animals have ingested PCP by chewing and licking outdoor wood structures, or from being housed in wooden pens that were treated with PCP solutions. This has caused sickness and death in some of these animals. In late 1976, about 100 Michigan dairy farms had herd health problems due to contact with PCP-treated wood. However, pure PCP or contaminants were detected in the milk of only two herds.

Pure PCP is absorbed by aquatic organisms. Once absorbed by fish, pure PCP is rapidly excreted as is its metabolite, with a biological half-life of only 10 hours. Bioaccumulation may be significant. Several species of fish, invertebrates and algae have had levels of PCP that were significantly higher (up to 10,000 times) than the concentration in the surrounding waters (11). Biomagnification, that is the concentration of a compound as it passes up the food chain, has not been observed and is not expected to be an important source of exposure because PCP breaks down rapidly in living organisms (11).


PCP is strongly toxic to plants. Its uses as a pre-harvest defoliant and desiccant on such crops as alfalfa and clover illustrate its toxicity to green plants. Lettuce grown on soil containing PCP contained low levels of PCP residues.

After reaching soil, PCP is broken down by sunlight and bacteria (11), and can leave the upper soil layer by evaporation and leaching into groundwater. PCP degrades most rapidly in flooded or anaerobic (airless) soils. The degradation rate increases at higher temperatures and in the presence of organic matter in the soil. The half-life for bacterial degradation ranges from 15 to 48 days, in anaerobic and aerobic laboratory conditions respectively.

PCP is used in wood products that come in contact with water. PCP has been detected at very low levels in rivers and streams (0.01-16 ppb), surface water systems (1.3-12 ppb), and seawater (0.02-11 ppt) (3). The compound has also been found in ground water in California, Oregon and Minnesota at very low concentrations ranging from 0.06 ppt to 0.64 ppb (10). It has been detected in well water in Japan and in Canada also.

Once released into water, PCP may be degraded by sunlight or microorganisms or bind to sediments and suspended particles in water (3). It does not evaporate to a significant degree. In water, biodegradation occurs with a half-life ranging from hours to days. Most biodegradation occurs at the surface. PCP levels measured in the air of two towns were up to 0.93 and 7.8 ppt (7).


Pentachlorophenol is a chlorinated organic compound, a solid which varies in color from white to dark grayish brown, depending on the purity of the compound. The solid beads or flakes have a distinctive odor. This chemical is non-corrosive in the pure state, but degrades rubber when in oil solution.

Exposure Guidelines:

NOEL: 1 mg/kg/day (rat)
ADI: 0.003 mg/l
TOL: 857 mg/l (30 degrees C)
TLV: air
TWA: 0.5 mg/m3 (skin)
STEL: 1.5 mg/m3 (skin)
Drinking water
health advisory:
Drinking Water Equivalent Level: 1/05 mg/L (8)
RfD: 0.003 mg/l (EPA)

Physical Properties:

CAS #: 87-86-5
Solubility in water: 0.0014 g/100g (20 degrees C) 0.0018g/100g (25 degrees C); 20 ppm (30 degrees C)
Solubility in solvents: PCP is soluble in acetone, alcohols, ether, and hot benzene; it is slightly soluble in petroleum ether, carbon tetrachloride, and paraffins.
Melting point: 191 degrees C, anhydrous (2)
Boiling point: 309-310 degrees C
Vapor pressure: 1.7 x 10 to the minus 4 torr (20 degrees C)
log P: -3.77
Kow: 4900-141,300 (1, 3)
log Kow: 5.15 (4)
Koc: 3-4000
Kd: 1.82 x 10 to the minus 5
BCF: 273-4760 (calculated) (4)
H: 3.2 torr/M


Chapman Chemical
PO Box 9158
416 E. Brooks Rd.
Memphis, Tennessee 38109
Telephone 901-396-5151
Emergency 901-396-5151

Review by Basic Manufacturer:

Comments solicited: December, 1991
Comments received:


  1. Figge, K., J. Klahn and J. Koch. 1986. Ecotoxicol. Environ. Safety 11: 320-338.
  2. Mercier, M. 1981. Organochlorine pesticides. p. 170. Pergamon Press.
  3. Murray, H.E., L.E. Ray and C.S. Giam. 1981. Chemosphere 10: 1327-34.
  4. Saarikoski, J., R. Lindstrom, M. Tyynela and M. Viluskela. 1986. Ecotoxicol. Environ. Safety 11: 158-173.
  5. Spacie, A. and J.L. Hamelink. 1982. Environ. Toxicol. Chem. 1: 309- 320.
  6. Wagner, Sheldon L. 1983. Clinical Toxicology of Agricultural Chemicals. Noyes Data Corporation.
  7. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Human. 1979. Vol 20: 303-325.
  8. U.S. Environmental Protection Agency. Office of Drinking Water. Pentachlorophenol Health Advisory. Draft Report. March 1987.
  9. Ecobichon, Donald J. 1991. Toxic Effects of Pesticides. in Casarett and Doull's Toxicology. The Basic Science of Poisons. Third Edition. Curtis D. Klaassen, Mary O. Amdur, and John Doull editors. Macmillan Publishing Company, NY.
  10. Howard, Philip H. 1991. Handbook of Environmental Fate and exposure Data for Organic Chemicals. Volume III. Pesticides. Lewis Publishers, Chelsea, MI.
  11. U.S. Dept. of Health and Human Services. 1992. Toxicological Profile for Pentachlorophenol. Agency for Toxic Substance and Disease Registry. Draft.