Toxicity Profiles
Condensed Toxicity Summary for PENTACHLOROPHENOL
NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
SEPTEMBER 1994
Prepared by: Robert A. Young, Ph.D., D.A.B.T., Chemical Hazard Evaluation and Communication Program, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee.
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Pentachlorophenol, a man-made organic biocide, is often contaminated with other toxic organic chemicals such as chlorinated phenols, dioxins, and dibenzofurans (Williams, 1982; U.S. Air Force, 1989; ATSDR, 1992).
Pentachlorophenol is readily absorbed following oral or inhalation exposure and is widely and rapidly distributed throughout the body (Wagner et al., 1991; ATSDR, 1992; Jorens and Schepens, 1993). Human and animal studies have provided evidence indicating that pentachlorophenol is metabolized to various conjugated metabolites. Both the parent compound and the conjugates are excreted in the urine (Braun et al., 1979).
Assessing the potential toxicity of technical (commercial) grade pentachlorophenol is complicated by the presence of the toxic impurities that are usually present, and the effects resulting from occupational exposure are often difficult to attribute to a specific route of exposure (Jorens and Schepens, 1993). The effects in humans following acute oral exposure include increased heart and respiratory rates, elevated temperature, increased basal metabolic rate, and death (29 and 401 mg/kg) (RTECS, 1989).
Human fatalities and toxic effects including tachycardia, jaundice, and other hematologic alterations have been reported for acute and subchronic occupational (e.g., sawmill workers, herbicide sprayers) inhalation exposures to pentachlorophenol. Upper respiratory tract inflammation and bronchitis were reported for sawmill workers chronically exposed to pentachlorophenol (Baader and Bauer, 1951; Menon et al., 1958; ATSDR, 1992). However, dose-terms for these exposures were not available, and concurrent exposures to other chemicals make definitive assessments impossible.
Data regarding the dermal exposure of humans to pentachlorophenol are anecdotal or equivocal, lack dose terms, and are compromised by concurrent exposures to other chemicals including the known contaminants in technical-grade pentachlorophenol. Acute exposure to 0.4% pentachlorophenol produced localized irritation (Bevenue et al., 1967), and subchronic exposures have caused chloracne (Baader and Bauer, 1951; O'Malley et al., 1990) and possibly renal damage (ATSDR, 1992). Dermal lesions including pemphigus and chronic urticaria have been reported for humans chronically exposed to pentachlorophenol-treated wood (Lambert et al., 1986). There currently are no definitive data regarding reproductive toxicity in humans exposed to pentachlorophenol.
Acute oral exposure of animals to pentachlorophenol affects the liver, kidneys, cardiovascular system, and the peripheral and central nervous system. Oral LD50 values for laboratory animals range from 27 to 230 mg/kg (Borzelleca et al., 1985; U.S. Air Force, 1989; ATSDR, 1992). Definitive data regarding the effects of subchronic or chronic oral exposure of humans to pentachlorophenol are not available. However, subchronic exposure (1 to 8 months) of rats to pentachlorophenol at doses ranging from 5 to 40 mg/kg/day has produced cardiovascular, hematotoxic, renal, hepatic, and immunologic responses (Schwetz et al., 1974, 1978; U.S. Air Force, 1989; ATSDR, 1992). Evidence of reproductive/developmental toxicity (increased resorptions, embryolethality, embryotoxicity, and teratogenicity) have also been observed in rats given pentachlorophenol during gestation (Larsen et al., 1974, 1976; Schwetz et al., 1978).
Because the most significant acute toxic effect of pentachlorophenol is elevated metabolism, a specific target organ or tissue is difficult to identify. However, for subchronic and chronic exposures, toxicity data indicate that the liver, kidney, and cardiovascular system are targets for some of the toxic effects of pentachlorophenol.
Both the chronic and subchronic RfDs for pentachlorophenol are 3.00E-02 mg/kg/day based on a NOAEL of 3 mg/kg/day and a LOAEL of 10 mg/kg/day for histopathologic findings in the liver and kidneys of rats given pentachlorophenol in the diet for 2 years (EPA, 1994; Schwetz et al., 1978).
The RfC for pentachlorophenol is under review (EPA, 1994a).
Based upon increased incidences of hepatocellular adenomas and carcinomas, adrenal medulla pheochromocytomas, malignant pheochromocytomas, and hemangiosarcomas/hemangiomas in mice, pentachlorophenol is classified by the EPA as a probable human carcinogen (Weight of Evidence Category B2) and has an oral slope factor of 1.2E-01 (mg/kg/day)-1 and an oral unit risk of 3.0E-06 (g/L)-1 (EPA, 1994). The potential carcinogenicity of pentachlorophenol following inhalation exposure has not been evaluated.
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