Pentachlorophenol is used as an industrial wood preservative for utility poles, crossarms, fence posts, and other purposes (79%);for NaPCP (12%); and miscellaneous, including mill uses, consumer wood preserving formulations and herbicide intermediate (9%) (CMR, 1980). As a wood preservative, pentachlorophenol acts as both a fungicide and insecticide (Freiter, 1978). The miscellaneous mill uses primarily involve the application of pentachlorophenol as a slime reducer in paper and pulp milling and may constitute ∼6% of the total annual consumption of pentachlorophenol (Crosby et al., 1981). Sodium pentachlorophenate (NaPCP) is also used as an antifungal and antibacterial agent (Freiter, 1978). Pentachlorophenol also is used as a general herbicide (Martin and Worthing, 1977). Photolysis and microbial degradation are the important chemical removal mechanisms for pentachlorophenol in water. In surface waters, pentachlorophenol photolyzes rapidly (ECETOC, 1984; Wong and Crosby. 1981; Zepp et al., 1984); however, the photolytic rate decreases as the depth in water increases (Pignatello et al., 1983). Pentachlorophenol is readily biodegradable in the presence of accli-mated microorganisms; however, biodegradation in natural waters requires the presence of microbes that can become acclimated. A natural river water that had been receiving domestic and industrial effluents significantly biodegraded pentachlorophenol after a 15-day lag period, while an unpolluted natural river water was unable to biodegrade the compound (Banerjee et al., 1984). Even though pentachlorophenol is in ionized form in natural waters, sorption to organic particulate matter and sediments can occur (Schellenberg et al., 1984), with desorption contributing as a continuing source of pollution in a contaminated environment (Pierce and Victor, 1978). Experimentally determined BCFs have shown that pentachlorophenol can significantly accumulate in aquatic organisms (Gluth et al., 1985; Butte et al., 1985; Statham et al., 1976; Veith et al., 1979a,b; Ernst and Weber, 1978), which is consistent with its widespread detection in fish and other organisms. Direct photolysis may be an important environmental sink for pen tachlorophenol present in the atmosphere. The detection of pen tachlorophenol in snow and rain water (Paasivirta et al., 1985; Bevenue et al., 1972) suggests that removal from air by dissolution is possible. Soil degradation studies indicate that pentachlorophenol is biodegrad able; microbial decomposition is an important and potentially domin ant removal mechanism in soil (Baker et al., 1980; Baker and Mayfield, 1980; Edgehill and Finn, 1983; Kirsch and Etzel, 1973; Ahlborg and Thunberg, 1980). The degree to which pentachlorophenol leaches in soil is dependent on the type of soil. In soils of neutral pH, leaching may be significant, but in acidic soils, adsorption to soil generally increases (Callahan et al. , 1979; Sanborn et al. , 1977). The ionized form of pentachlorophenol may be susceptible to adsorption in some soils (Schellenberg et al., 1984). In laboratory soils, pen tachlorophenol decomposes faster in soils of high organic content as compared with low organic content, and faster when moisture content is high and the temperature is conducive to microbial activity. Half- lives are usually ∼2-4 weeks (Crosby et al., 1981). Monitoring studies have confirmed the widespread occurrence of pentachlorophenol in surface waters, groundwater, drinking water and industrial effluents (see Table 2). The U.S. EPA's National Urban Runoff Program and National Organic Monitoring Survey reported frequent detections in storm water runoff and public water supplies (Cole et al., 1984; Mello, 1978). Primary sources by which pen tachlorophenol may be emitted to environmental waters may be through its use in wood preservation and the associated effluents and its pesticidal applications. Pentachlorophenol can be emitted to the atmosphere by evaporation from treated wood or water surfaces, by releases from cooling towers using pentachlorophenol biocides or by incineration of treated wood (Skow et al., 1980; Crosby et al., 1981). Pentachlorophenol has been detected in ambient atmospheres (Caut reels et al., 1977), in snow and rain water (Paasivirta et al,. 1985; Bevenue et al., 1972) and in emissions from hazardous waste incinera tion (Oberg et al., 1985). The U.S. Food and Drug Administration's Total Diet Study (conducted between 1964 and 1977) found pen tachlorophenol residues in 91/4428 ready-to-eat food composites (See Tables 4 and 5). The average American dietary intake of pen tachlorophenol during 1965-1969 was estimated to range from <0.001-0.006 mg/day (Duggan and Corneliussen, 1972). The most likely source of pentachlorophenol contamination in many food prod ucts may be the exposure of the food to pentachlorophenol-treated wood materials such as storage containers (Dougherty, 1978). Acute toxicity data indicated that salmonids are more sensitive to the toxic effects of pentachlorophenol than other fish species, with LC50 values of 34-128 μ g/l for salmonids and 60-600 μ g/l for other species. More recent data showed that carp larvae, bluegills, channel catfish and knifefish also had LC50 values < 100 μ gl (see Table 10). The most sensitive marine fishes were pinfish larvae, the goby, Gobius minutus, and eggs and larvae of the flounder, Pleuronectes platessa, all with LC50 values <100 μ g/l (Adema and Vink, 1981). The most sensitive freshwater invertebrate species were the chironomid, Chironomus gr. thummi (Slooff, 1983) and the snail, Lymnaea luteola (Gupta et al., 1984). The most sensitive marine invertebrates were the Eastern oyster (Borthwick and Schimmel, 1978), larvae of the crusta ceans, Crangon crangon and Palaemon elegans (VanDijk et al. , 1977), and the copepod, Pseudodiaptomus coronatus (Hauch et al., 1980), all with LC50 values <200 μ g/l. In chronic toxicity tests, the lowest concentration reported to cause adverse effects was 1.8 μ g/l (NaPCP), which inhibited growth of sockeye salmon (Webb and Brett, 1973). The marine species tested displayed similar thresholds for chronic toxicity. Both acute and chronic toxicity increased at lower pH, probably because a lower pH favors the un-ionized form of pentachlorophenol, which is taken up more readily and is therefore more toxic than ionized pentachlorophenol (Kobayashi and Kishino, 1980; Spehar et al., 1985). Data concerning the effects of pentachlorophenol on aquatic plants were highly variable. Therefore, it was difficult to draw conclusions from these data. Pentachlorophenol did not appear to bioaccumulate in aquatic or ganisms to very high concentrations. BCFs for pentachlorophenol were <1000 for most species tested. The highest BCF was 3830 for the polychaete, Lanice conchilega (Ernst, 1979). Some species appear to have an inducible pentachlorophenol-detoxification mechanism, as evidenced in several experiments in which pentachlorophenol tissue levels peaked in 4-8 days and declined thereafter despite continued exposure (Pruitt et al., 1977; Trujillo et al., 1982). A study by Niimi and Cho (1983) indicated that uptake of waterborne pentachlorophenol from gills was much greater than uptake from food, indicating that bioconcentration of pentachlorophenol through the food chain is unlikely. Biomonitoring data of Lake Ontario fishes showed that similar pentachlorophenol levels were found in predators andforage species. Studies with experimental ecosystems have indicated that ecological effects may occur at pentachlorophenol levels as low as those causing chronic toxicity in sensitive species in single-species tests. The lowest concentration that caused adverse effects in these studies was 15.8 μ g/l, which caused a reduction in numbers of individuals and species in a marine benthic community (Tagatz et al., 1978). Pentachlorophenol is readily absorbed from the gastrointestinal tract of rats, mice, monkeys and humans (Braun et al. , 1977, 1978; Ahlborg et al., 1974; Braun and Sauerhoff, 1976). Peak plasma concentrations are reached within 12-24 hours after oral administration to monkeys (Braun and Sauerhoff, 1976), but 4-6 hours after oral administration to rats (Braun et al., 1977). After oral administration, the highest concentration of radioactivity was found in the liver and gastrointesti nal tract of monkeys (Braun et al., 1977). In rats and mice, tet rachlorohydroquinone was identified in the urine (Jakobson and Yllner, 1971; Braun et al., 1977; Ahlborg et al., 1974) as well as unmetabolized pentachlorophenol and glucuronide-conjugated pen tachlorophenol. Although Ahlborg et al. (1974) reported that oxidative dechlorination of pentachlorophenol occurs in humans, as evidenced by the presence of tetrachlorohydroquinone in the urine of workers occupationally exposed (probably by inhalation), analysis of human urine after ingestion of pentachlorophenol revealed the presence of conjugated pentachlorophenol and unmetabolized pentachlorophenol (Braun et al., 1978). The primary route of excretion after oral administrtation of all species studied is in the urine (Braun et al. , 1977, 1978; Ahlborg et al., 1974; Larsen et al., 1972; Braun and Sauerhoff, 1976). Although urinary excretion followed second-order kinetics in rats (Larsen et al., 1972; Braun et al., 1977) except in females receiving a single high dose (100 mg/kg) of pentachlorophenol, urinary excretion of pentachlorophenol in humans and monkeys followed first-order kinetics (Braun and Sauerhoff, 1976; Braun et al., 1978). Enterohepatic circulation played an importation role in the pharmacokinetics of pen tachlorophenol. The half-life of pentachlorophenol in the plasma is longer in female rats and monkeys than it is in male rats and monkeys (Braun et al. , 1978; Braun and Sauerhoff, 1976). Because many preparations of pentachlorophenol are contaminated with small but measurable amounts of highly toxic substances, such as dibenzodioxins, special attention must be paid to the composition of the pentachlorophenol solution tested. In studies where technical and purified pentachlorophenol have been evaluated (Schwetz et al., 1974; Goldstein et al., 1977; Kimbrough and Linder, 1978; Knudsen et al., 1974; Johnson et al., 1973; Kerkvliet et al., 1982), only the results of the experiments using purified pentachlorophenol were reported in detail. Oral exposure to pentachlorophenol was not carcinogenic in mice (BRL, 1968; Innes et al., 1969) or rats (Schwetz et al., 1977), regardless of the composition of the pentachlorophenol solution tested. Although there are a few studies that suggest pentachlorophenol may be mutagenic in B. subtilis (Waters et al., 1982; Shirasu, 1976), in yeast, Saccharomyces cerevisiae (Fahrig et al., 1977) and in mice, as evidenced by the coat-color spot test (Fahrig et al., 1977), no evidence of mutagenicity was reported in S. typhimurium (Anderson et al. , 1972; Simmon et al., 1977; Lemma and Ames, 1975; Moriya et al. , 1983; Waters et al., 1982; Buselmaier et al., 1973) or in E. coli (Simmon et al., 1977; Fahrig, 1974; Moriya et al., 1983; Waters et al., 1982) with or without metabolic activation. Three teratogenicitylreproductive toxicity studies (Schwetz et al., 1974, 1977; Courtney et al., 1976) indicate that pentachlorophenol is fetotoxic in rats at oral dose levels ≥5 mg/kg/day. At the highest dose tested (500 ppm) in a fourth teratogenicity/reproductive toxicity study (Exon and Koller, 1982), there was a statistically nonsignificant decrease in litter size. The lowest dose tested (5 mg/kg/day) by Schwetz et al. (1977) was the lowest dose at which any evidence offetotoxicity, as indicated by delayed ossification, was observed. No adverse fetal or reproductive effects were reported at ≤3 mg/kg/day (Schwetz et al., 1977; Exon and Koller, 1982). In subchronic and chronic toxicity studies, adverse effects occurred primarily in the liver (Kerkvliet et al., 1982; Johnson et al., 1973; Knudsen et al. , 1974; Goldstein et al. , 1977; Kimbrough and Linder, 1978; Schwetz et al., 1977), the kidney (Johnson et al., 1973; Kimbrough and Linder, 1978; Schwetz et al., 1977) and the immune system (Kerkvliet et al., 1982). Knudsen et al. (1974) reported increased liver weights in female rats and centrilobu lar vacuolization in male rats exposed to diets containing ≧50 ppm commercial pentachlorophenol, which contained 282 ppm dioxins. In the remaining studies, increased liver weight (Johnson et al., 1973) and increased pigmentation of hepatocytes (Schwetz et al., 1977) were observed at oral doses of≥10 mg/kg/day (∼90%), and SGPT levels significantly increased in rats ingesting 30 mg/kg/day pentachloro phenol (∼90%) for 2 years (Schwetz et al., 1977). Increased kidney weight unaccompanied by renal histopathology was reported in rats exposed to dietary concentration ≧20 ppm of pentachlorophenol (>99%) for 8 months (Kimbrough and Linder, 1978) and in rats ingesting 30 mg/kg/day (∼90%) for 90 days (Johnson et al., 1973). Increased pigmentation of the renal tubular epithelial cells was re ported in rats ingesting 10 or 30 mg/kg/day pentachlorophenol for 2 years (Schwetz et al., 1977). Although decreased immunocompetence was reported in mice exposed to dietary levels of 50 or 500 ppm of pentachlorophenol (>99%) for 34 weeks (Kerkvliet et al., 1982), the decrease was statistically significant only at the higher dose. An ADI of 0.03 mg/kg/day or 2.1 mg/day for a 70 kg human was derivedfrom the NOAEL of 3 mg/kg/day in rats in the chronic dietary study by Schwetz et al. (1977). An uncertainty factor of 100 was used. An RQ of 100 was derived based on the fetotoxic effects of pen tachlorophenol in rats in the study by Schwetz et al. (1974). Based on guidelines for carcinogen risk assessment (U.S. EPA, 1984b) and inadequate evidence for animal carcinogenicity or absence of human cancer data, pentachlorophenol is classified as Group D, meaning that it is not classified as a human carcinogen.
