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Toxicity Effects

CAS Registry Number: 87-86-5

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 2.

Names 1

  • PCP
  • Pentachlorophenol
  • Pentachlorophenol (Transgenic Lecm)
  • Pentachlorophenol and By-products of Its Synthesis
  • Pentachlorophenol, Dowicide EC-7
  • Pentachlorophenol, purified
  • Pentachlorophenol, purified|PCP
  • Pentachlorophenol, technical
  • Phenol, Pentachloro-
  • Transgenic LECM (Pentachlorophenol)
  • Transgenic-Laboratory Of Environmental Carcinogenesis And Mutagenesis (Pentachlorophenol)

Human Toxicity Excerpts

  • BIOMONITORING: To determine whether pentachlorophenol (PCP) exposure had resulted in elevated serum dioxin levels twenty years after its use had ceased ... 94 former sawmill workers randomly selected from surviving members of a cohort enumerated for a mortality and cancer incidence study /were tested/ . After interviewing these individuals to collect demographic data and a comprehensive work history, they were divided into 71 PCP-exposed and 23 non-exposed individuals on the basis of job title and work tasks performed ... Age-adjusted dioxin levels /were compared/ in the exposed and non-exposed groups, examined the effect of PCP exposure duration and intensity, and compared congener profiles with those found in the commercial grade PCP used at the time. Mean levels in exposed workers were elevated when compared with the non-exposed, with levels of 1,2,3,6,7,8-HxCDD, 1,2,3,4,6,7,8-HpCDD and OCDD being two to three times higher. The congener profiles in serum were consistent with those in PCP solutions, and dioxin levels increased with both employment duration and estimated exposure intensity. Serum dioxin levels in former New Zealand sawmill workers remain elevated twenty years after exposure to PCP ceased, and reflect the pattern of past PCP exposure.[McLean D et al; Chemosphere 74 (7): 962-7 (2009). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: ... 9 deaths from chronic occupational exposure to PCP /were reported/. The major symptoms were hyperthermia, sweating, abdominal pain, dyspnea, and muscular spasms.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • CASE REPORTS: ... Poisonings in infants in a nursery PCP-treated diapers /were reported/. There were 20 cases of intoxication with 2 fatalities.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • CASE REPORTS: /In/ a case of intentional intoxication with PCP, the serum level of PCP was 150 ppm 5 hr after ingestion, and 28 ppm 2 wk later. PCP in the urine showed marked variation during forced diuresis (from 2.3 ppm to 8.6 ppm).[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • CASE REPORTS: A 32 year old white male was seen at a university dermatology clinic complaining of an acneform eruption of 6 months duration. The patient was part owner of a firm that constructed piers for small boat marinas. The lumber used was pretreated with pentachlorophenol. Within about 9 mo after beginning work, he noted a papular acneform eruption that occurred over the entire body. The eruption was characterized by multiple, small yellow/white papules. Areas most involved included the malar regions of the face, post auricular area, the trunk, buttocks, thighs, and lower legs. Some of papules were inflamed. A trephine punch biopsy of one of the papules showed a small epithelial lined cystic structure that communicated with the surface. The lining epithelium was composed of atrophic, but normal appearing, epidermis. Contained within the cyst was keratin-like material. The condition was diagnosed as chloracne. The patient's condition improved after 6 wk oral treatment with isoretinoin. The patient remained asymptomatic for the ensuing 2 yr of observation. The patient returned to work wearing appropriate protective clothing. A sample of pentachlorophenol used by the firm and samples of treated wood were analyzed for octachlorodibenzodioxin. Samples from the surface of the lumber contained about ten to 40 times the amount of octachlorodibenzodioxin as did the wood itself. The undiluted pentachlorophenol contained 1600 ppm octachlorodibenzodioxin.[Cole GW et al; Contact Dermatitis 15 (3): 164-8 (1986)] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: A 71-year-old Japanese man intentionally ingested 113 to 226 g of weed killer containing 12% PCP. Although he was treated with gastric aspiration and lavage within the next hour, a substantial amount of PCP must have already been absorbed, as indicated by the high serum level of 150 mg/L of PCP 5 hr after the incident. Forced diuresis with furosemide and mannitol substantially increased the urinary excretion of PCP. The serum level of the patient, who survived, decreased to 12 mg/L 27 days after the ingestion.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • CASE REPORTS: A case of a 33 yr old man who died following occupational exposure to pentachlorophenol is presented. Postmortem examination revealed cerebral edema and fatty degeneration of the viscera.[Gray RE et al; Arch Environ Health 40 (3): 161-4 (1988)] **PEER REVIEWED**
  • CASE REPORTS: A case of skin absorption was reported where a high PCP level in the urine was found after a worker had cleaned a paintbrush for only 10 min in a can that contained a 4% solution of PCP ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • CASE REPORTS: Five cases of pentachlorophenol poisoning, including 2 fatalities, occurred in two small wood preservative plants ... Fever, ... severe hyperpyrexia, ... increased anion gap, and renal insufficiency ... Pentachlorophenol may uncouple oxidative phosphorylation, resulting in a poisoning syndrome characterized by hyperpyrexia, diaphoresis, tachycardia, tachypnea, abdominal pain, nausea and even death.[Wood S et al; J Occup Med 25 (7): 527-530 (1983)] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: Pentachlorophenol (PCP) and its sodium salt are frequently used in wood preservatives. Little is known about the effects on man when being chronically exposed. Only vague skin symptoms, such as rashes, acne and cutaneous infections were described. We present two cases of pemphigus vulgaris with a known non-occupational chronic PCP exposure. The clinical course and the titer of pemphigus antibodies roughly correlate with the PCP levels in serum. In one case of chronic urticaria the exacerbations also run parallel to the PCP serum levels and increased anti-skin antibodies, without any manifestation of pemphigus vulgaris. The role of PCP as one of the causes provoking pemphigus vulgaris and chronic urticaria with raised anti-skin antibodies is discussed.[Lambert J et al; Acta Derm Venereol 66 (2): 170-2 (1986)] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: Repeated exposure to commercial (technical grade) pentachlorophenol preceded aplastic anemia in four patients and pure red cell aplasia in two. Two patients developed concomitant or subsequent Hodgkin's disease and acute leukemia ...[Roberts HJ; South Med J 76 (1): 45-8 (1983)] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: Three case reports of skin lesions associated with exposure to pentachlorophenol in wood preservatives were described. Since pentachlorophenol and its sodium salt are commonly used in wood preservatives, paints, and disinfectants due to their fungicidal, insecticidal, bactericidal, herbicidal, and molluscicidal properties, exposure can occur in both occupational and non-occupational settings. The cases described involved two males and one female, all of whom were caucasian. Serum pentachlorophenol levels were measured in each individual. In non-exposed individuals, normal levels did not exceed 15 ug/L. The first case was that of a 41 year old man diagnosed as having pemphigus vulgaris. Exposure was attributed to a bookcase which had been treated with pentachlorophenol. Serum levels of pentachlorophenol varied from 10 to 47 ug/L in this patient, and clinical improvement was associated with decreased serum levels. A 28 year old female also diagnosed as having pemphigus vulgaris. Exposure in this case was ascribed to rafters in her home which had been treated with pentachlorophenol. Serum pentachlorophenol levels ranged from 10.8 to 114 ug/L, and also tended to decline with periods of clinical improvement. The third case was that of a 35 year old male who suffered from urticaria. Exposure in this case occurred when the patient had treated wood framework. Serum pentachlorophenol levels varied from 20.9 to 96 ug/L in this individual.[Lambert J et al; Acta Dermato-Venerolog 66 (2): 170-2 (1986)] **PEER REVIEWED**
  • EPIDEMIOLOGY STUDIES: ... Surviving members of a cohort enumerated to study mortality in sawmill workers employed from 1970 to 1990 /were surveyed/. Estimates of historical exposure were based on job titles held, using the results of a PCP biomonitoring survey conducted in the 1980s. The survey involved interviews and clinical examinations, with interviewers and examiners blinded to exposure status. RESULTS: Of the 293 participants 177 had not been exposed, and of the 116 exposed all but 10% had low or short-term PCP exposure. Nevertheless, a number of significant associations between PCP exposure and the prevalence of various symptoms were observed including associations between: (i) exposure levels and self-reported tuberculosis, pleurisy or pneumonia (P < 0.01) and a deficit in cranial nerve function (P = 0.04); (ii) duration of employment and thyroid disorders (P = 0.04), and neuropsychological symptoms including often going back to check things (P = 0.04), low libido (P = 0.02) and heart palpitations (P = 0.02), and a strong dose-response trend for frequent mood changes without cause (P < 0.01); and (iii) cumulative exposure and frequent mood changes without cause (P = 0.02), low libido (P = 0.04), and in the overall number of neuropsychological symptoms reported (P = 0.03). PCP exposure was associated with a number of physical and neuropsychological health effects that persisted long after exposure had ceased.[McLean D et al; Am J Ind Med 52 (4): 271-81 (2009). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract
  • EPIDEMIOLOGY STUDIES: ... This study examined the relationship between exposure to potential thyroid hormone-disrupting toxicants and thyroid hormone status in pregnant Inuit women from Nunavik and their infants within the first year of life ... Thyroid hormone parameters [thyroid stimulating hormone (TSH), free thyroxine (fT(4)), total triiodothyronine (T(3)), thyroxine-binding globulin (TBG)] and concentrations of several contaminants [PCB-153, hydroxylated metabolites of PCBs (HO-PCBs), pentachlorophenol (PCP) and hexachlorobenzene (HCB)] /were measured/ in maternal plasma at delivery (n = 120), in umbilical cord plasma (n = 95), and in infant plasma at 7 months postpartum (n = 130). In pregnant women, ... a positive association /was found/ between HO-PCBs and T(3) concentrations (beta = 0.57, p = 0.02). In umbilical cord blood, PCB-153 concentrations were negatively associated with TBG levels (beta = -0.26, p = 0.01). In a subsample analysis, a negative relationship was also found between maternal PCP levels and cord fT(4) concentrations in neonates (beta = -0.59, p = 0.02). No association was observed between contaminants and thyroid hormones at 7 months of age. Overall, there is little evidence that the environmental contaminants analyzed in this study affect thyroid hormone status in Inuit mothers and their infants ...[Dallaire R et al; Environ Health Perspect 117 (6): 1014-20 (2009). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract Full text: PMC2702396
  • EPIDEMIOLOGY STUDIES: A longitudinal study was performed to examine whether chronic occupational exposure to pentachlorophenol or its compounds causes measurable alterations in the conduction velocity in peripheral nerves as an adverse effect. In total, the results of nerve conduction velocity determinations in 1980 and 1984 in 10 subjects (7 men, 3 women) who had been exposed for an average of 16 yr (range 4-24) were available. The concentrations of pentachlorophenol in the air at the workplace varied between 0.3 and 180 ug/cu m and were thus below the maximum allowed concn (MAK value) of 500 ug/cu m. The biological monitoring carried out showed the following results: pentachlorophenol in the serum: 38-1270 ug/L; pentachlorophenol in urine 8-1224 ug/L. Compared with the upper normal limits pentachlorophenol in the serum 150 ug/L, (pentachlorophenol in the urine 60 ug/L), distinct internal exposure to pentachlorophenol has resulted in some of the employees. Determinations of the nerve conduction velocity of motor and sensory nerve fibers (ulnar, median, peroneal, and sural nerve) were always in the normal range. A significant difference in the nerve conduction velocity for the period 1980-4 could not be detected. In addition, the correlation analyses did not show any hints of dose-effect relations.[Triebig G et al; Br J Ind Med 44 (9): 638-41 (1987)] **PEER REVIEWED** PubMed Abstract Full text: PMC1007890
  • EPIDEMIOLOGY STUDIES: Exposure to wood treated with PCP has been associated with an increased incidence of Hodgkin's Disease ... and non-Hodgkin's lymphoma ... There is epidemiological evidence that occupational exposure to mixtures of chlorophenols increases the risk of soft tissue sarcoma and lymphoma, but there is no clear dose-effect relationship. The major deficiency in all of these studies appears to be a lack of specific exposure data, with the ever-present problem of impurities[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • EPIDEMIOLOGY STUDIES: Several epidemiological studies from Sweden and the United States have associated soft tissue sarcomas with occupational exposure to PCP. Surveys from Finland and New Zealand have not confirmed this relationship. There are no conclusive reports of increased incidence of cancer in workers specifically exposed to PCP.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • EPIDEMIOLOGY STUDIES: The pregnancy outcomes in 43 women married to sawmill workers in Canada did not reveal any significant differences when compared with a control group ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • EPIDEMIOLOGY STUDIES: There are several published case reports, case-control studies, and cohort studies on the association of pentachlorophenol exposure with cancer risk in occupational settings. Associations between occupational exposure to pentachlorophenol and non-Hodgkin lymphoma, multiple myeloma, or soft tissue sarcoma (four studies summarized in a meta-analysis) have been reported. In a recent review of published studies of pentachlorophenol exposure and cancer risk, several points were made that are pertinent in the assessment of cancer risk in humans from pentachlorophenol exposure. Specifically, a large cohort study of sawmill workers from 14 mills in British Columbia, Canada that was updated ...showed that, in contrast to an earlier analysis ... /that/ reported only a weak association between total chlorophenol measures and non-Hodgkin lymphoma risk and no association with multiple myeloma, that similar or stronger associations were found for exposure and risk of non-Hodgkin lymphoma and multiple myeloma. In addition, the review... notes that both animal and human evidence suggests that contaminants of pentachlorophenol are an unlikely explanation for the carcinogenicity associated with pentachlorophenol, although from analysis of the 1989 National Toxicology Program study on pentachlorophenol, the technical grade of pentachlorophenol showed a slightly greater potency relative to commercial-grade pentachlorophenol, which contains lower levels of dioxin and furan congener contaminants.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.20 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • GENOTOXICITY: A cytogenetic study was performed on 20 healthy workers exposed to pentachlorophenol in concentrations ranging from 1.2 to 180 ug/cu m (maximum concentration at the workplace is 500 ug/cu m) for 3 to 34 years. Pentachlorophenol was determined in the blood plasma of all probands, yielding concentrations between 23 and 775 ug/L (Biological Tolerance Value is 1000 ug/L). In vitro pentachlorophenol up to 90 mg/L was added to phytohemagglutinin-stimulated lymphocytes of normal healthy donors without any effect on sister chromatid exchange or chromosomal aberrations, whereas a slow down of cell proliferation could be detected in the presence of 60 mg pentachlorophenol/L.[Ziemsen B et al; Int Arch Occup Environ Health 59: 413-7 (1987)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Chromosome analyses were carried out on peripheral lymphocytes from 22 male workers employed at a pentachlorophenol producing factory ... A small but significant increase in the frequency of dicentrics and acentrics was observed ...[Bauchinger M et al; Mutat Res 102 (1): 83-8 (1982)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Pentachlorophenol (PCP) is a substance whose widespread use, mainly in wood protection and pulp and paper mills, has led to a substantial environmental contamination. This in turn accounts for a significant exposure of the general human population, with rather high exposure levels being attained in occupational settings. Investigations on the genotoxic activity of PCP have given rise to divergent results which would seem to make an evaluation difficult. By grouping them into 3 categories a somewhat clearer picture, allowing finally an (admittedly tentative) assessment, can be obtained. PCP does seem to be at most a weak inducer of DNA damage: it produces neither DNA-strand breaks nor clear differential toxicity to bacteria in rec-assays in the absence of metabolic activation. Also in SCE induction no increase can be observed in vivo, while PCP is found marginally active in a single in vitro experiment. Metabolic activation, however, leads to prophage induction and to DNA strand breaks in human lymphocytes, presumably through the formation of oxygen radicals. A possible further exception in this area might be the positive results in the yeast recombination tests, although their inadequate reporting makes a full evaluation difficult. PCP does not seem to induce gene (point) mutations, as most bacterial assays, the Drosophila sex-linked recessive lethal test and in vitro assays with mammalian cells did not demonstrate any effects. Marginally positive results were obtained in the mammalian spot test in vivo and in one bacterial test; the positive result in the yeast assay for cycloheximide resistance is fraught somewhat with its questionable genetic basis. PCP does, however, induce chromosomal aberrations in mammalian cells in vitro and in lymphocytes of exposed persons in vivo. Those in vivo results that were unable to provide evidence of chromosomal damage are hampered either by methodological inadequacies or by too low exposure levels. The (rodent) metabolite tetrachlorohydroquinone might be a real genotoxic agent, capable of binding to DNA and producing DNA strand breaks; this activity is probably due to semiquinone radical formation and partly mediated through active oxygen species. Since this compound has not been tested in the common bacterial and mammalian mutagenicity assays, the few ancillary results on this substance cannot be used in a meaningful human risk assessment of PCP. Furthermore, this metabolite has only been produced by human liver microsomes in vitro, but has not been detected in exposed humans in vivo.[Seiler JP; Mutat Res 257 (1) 27-47 (1991)] **PEER REVIEWED**
  • HUMAN EXPOSURE STUDIES: Dust and mist concn greater than 1.0 mg/cu m resulted in painful irritation of upper respiratory tract in persons not previously exposed to pentachlorophenol. Violent sneezing and coughing accompanied exposure. Conditioned persons tolerated concn up to 2.4 mg/cu m.[USEPA; Ambient Water Quality Criteria Doc: Pentachlorophenol p.C-20 (1980) EPA 440/5-80-065] **PEER REVIEWED**
  • IMMUNOTOXICITY: Evaluation of lymphocyte phenotype frequencies, functional responses, serum immunoglobulin levels, and autoantibodies was completed for 38 individuals (ie, 10 families) who were exposed to pentachlorophenol in manufacturer treated log houses. Comparison of subjects with controls revealed that the exposed individuals had activated T cells, autoimmunity, functional immunosuppression, and B cell dysregulation. Autoimmunity was evidenced by elevation of TA1 phenotype frequencies and a 21% incidence of anti-smooth muscle antibody. Functional immunosuppression was evidenced by the significantly reduced responses to all mitogens tested and to allogeneic lymphocytes in the mixed lymphocyte culture test. There was a significant elevation of CD10, and an 18% increase or decrease in serum immunoglobulins was noted. A striking anomaly was the enhanced natural killer activity found in exposed females but not in males.[Mcconnachie PR, Zahalsky AC; Arch Environ Health 46 (4): 249-53 (1991)] **PEER REVIEWED** PubMed Abstract
  • IMMUNOTOXICITY: Immune parameters were examined in 188 patients who were exposed for more than 6 mo to pentachlorophenol containing pesticides. Blood levels of pentachlorophenol, lymphocyte populations, in vitro responses to mitogenic and allogenic stimulation, plasma neopterin levels, plasma cytokine and cytokine receptors were determined. Impaired in vitro lymphocyte stimulation responses were impaired in 65% of the patients ... Impaired lymphocyte stimulation incr significantly with levels of pentachlorophenol that exceeded 10 uL/L (p < 0.05). Patients who had high levels of pentachlorophenol and abnormal lymphocyte stimulation also had incr proportions of blood monocytes in blood (p < 0.05), as well as incr IL-8 serum levels (p < 0.02). Eleven patients had abnormal mitogen stimulation experienced decr CD4/CD8 ratios of < 1.0; 5 of these patients had decr CD4+ lymphocyte counts of < 500/uL, and 3 patients had incr plasma neopterin of >15 nmol/L. ... This indicates that incr levels of pentachlorophenol in blood can lead to severe T lymphocyte dysfunction.[Daniel V et al; 50 (4): 287 (1995)] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: /NRC Safe Drinking Water Committee/ ... noted that the toxicity of pentachlorophenol is increased by impurities contained in the technical product. For example, the No Observed Effect Level for pure pentachlorophenol is 3 mg/kg/day; however, the No Observed Effect Level for technical pentachlorophenol is 1 mg/kg/day, indicating increased toxicity due to impurities.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 396] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Although pentachlorophenol is highly toxic in its own right, some studies suggest that contaminants may be responsible for /SRP: some of the poisonous potential of/ the technical grade. Comparison of effects of technical versus purified PCP indicated that only technical grade produced chloracne, chick edema, hepatic porphyria, and incr relative liver wt. Technical grade was also much more active as liver enzyme inducer.[Doull, J., C.D.Klassen, and M.D. Amdur (eds.). Casarett and Doull's Toxicology. 3rd ed., New York: Macmillan Co., Inc., 1986., p. 561] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Individuals emptying bags of prilled (granular) or powder formulations of pentachlorophenol and of sodium pentachlorophenol are at an incr oncogenic risk.[USEPA; Wood Preservatives Position Doc 2/3: Creosote, Inorganic Arsenicals, Pentachlorophenol p.587 (1981) EPA 341-085/4643] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: The general population is exposed to PCP through the ingestion of drinking-water (0.01 - 0.1 ug/L) and food (up to 40 ug/kg in composite food samples). Apart from the daily dietary intake (0.1 - 6 ug/person per day) resulting from direct food contamination with PCP, continuous exposure to hexachlorobenzene and related compounds in food, which are biotransformed to PCP, may be another important source. In addition, because of its widespread use, the general population can be exposed to PCP in treated items such as textiles, leather, and paper products, and above all, through inhalation of indoor air contaminated with PCP. Generally, PCP concentrations of up to about 30 ug/cu m can be expected, for up to the first month, after indoor treatment of large surfaces; considerably higher levels (up to 160 ug/cu m) cannot be excluded under unfavourable conditions. In the long term, values of between 1 and 10 ug/cu m are typical PCP concentrations after extensive treatments, though higher levels, up to 25 ug/cu m, have been found in rooms treated one to several years earlier. For comparison, PCP indoor air levels in untreated houses are generally below 0.1 ug/cu m.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: The general population is more susceptible during hot weather.[Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: A common mode of pentachlorophenol exposure is inhalation and may cause irritation of the eyes, nose, and throat and deaths after acute significant inhalation. Dermal contact may cause erythema, pain, and exfoliation. Systemic toxicity is related to the ability of pentachlorophenol to uncouple oxidative phosphorylation. This may produce hyperthermia, sweating, hepatotoxicity, altered mental status, and seizures.[Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1530] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Acute poisoning is marked by weakness with changes in respiration, blood pressure, and urinary output. Also causes dermatitis, convulsions, and collapse. Chronic exposure can cause liver and kidney injury.[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Aplastic anemia and decreased hematocrit have been associated with PCP use ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Chloracne, skin pustular eruptions, eczema, rashes, inflammation of the skin, and subcutaneous lesions are common ... Low-grade infection or inflammation of the skin and subcutaneous tissue /were reported/.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Chronic exposure can cause: porphyria cutanea tarda, weight loss, increased basal metabolic rate, functional changes of the liver and kidneys. Insomnia and vertigo have also been reported.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Chronic exposure in workers resulted in elevated bilirubin and creatine phosphokinase. Higher prevalence of gamma mobility C-reactive protein in sera.[USEPA; Ambient Water Quality Criteria Doc: Pentachlorophenol p.C-23 (1980) EPA 440/5-80-065] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Functional changes in the kidneys (reduction in creatinine clearance and resorption of phosphorus) have been reported ... Kidney failure can occur after severe acute poisoning[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Hyperglycemia and glycosuria may occur in cases of acute poisoning ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Increasing anxiety and restlessness, together with an increased rate and depth of respiration, cyanosis, tachycardia, diarrhea, rise in body temperature, and, eventually, convulsions and coma are signs of more severe PCP poisoning. Death is due to cardiac arrest and victims usually show an immediate onset of marked rigor mortis.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Industrial hygiene experience shows that pentachlorophenol and its sodium salt are capable of inducing discomfort and local as well as systemic effects. Dusts are particularly irritating to the eyes and nose in concentrations greater than 1 mg/cu m. Some irritation of the nose may occur at 0.3 mg/cu m. /Previously exposed/ workers can tolerate up to 2.4 mg/cu m. Pentachlorophenol is highly poisonous with a wide range of acute action but no pronounced cumulative properties.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Ingestion causes incr then decr of resp, blood pressure, urinary output; fever; incr bowel action; motor weakness, collapse with convulsions and death. Causes lung, liver, kidney damage; contact dermatitis ... Dust causes sneezing.[The Merck Index. 10th ed. Rahway, New Jersey: Merck Co., Inc., 1983., p. 1021] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Most important effect of pentachlorophenol inhalation is acute poisoning centering in circulatory system with accompanying heart failure ... Dusts are particularly irritating to eyes and nose in concn greater than 1 mg/cu m. Some irritation of nose may occur at 0.3 mg/cu m ... Survivors of ... intoxication suffer ... visual damage and acute type of scotoma. Other damage incl acute inflammation of conjunctiva and characteristically shaped corneal opacity, corneal numbness, and slight mydriasis.[American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 461] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Symptoms of acute systemic poisoning are: headache, profuse sweating, depression, nausea, weakness, and sometimes fever; tachycardia, tachypnea, pain in the chest, thirst. Abdominal colic is frequent. Mental distress can occur, progressing to coma and occasionally convulsions; irritation of the skin, mucous membranes, and respiratory tract (including painful irritation of the nose and intense sneezing when pentachlorophenol is inhaled); contact dermatitis and chloracne.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Symptoms of overexposure include an increase followed by a decrease in respiration, blood pressure, and urinary output; fever; increase in bowel action; motor weakness; and collapse with convulsions and death.[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., p. 49-114] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: The survivors of pentachlorophenol intoxication suffer with impairments in autonomic function, circulation, visual damage, and an acute type of scotoma. Other damage included acute inflammation of the conjunctiva and characteristically shaped corneal opacity, corneal numbness, and slight mydriasis. Other symptoms involve excessive sweating, tachycardia, tachypnea, respiratory distress, hepatic enlargement, and metabolic acidosis.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**
  • SURVEILLANCE: ... The results of a 7-year study on 400 Hawaiians, many of whom had long-term, high-level exposure to PCP, /were reported/. Concen of PCP in blood-serum far exceeded the 1.05 mg/L reported /earlier/; workers treating wood in open-vats had a mean level of 3.78 mg PCP/L, pressure- tank workers 1.72 mg/L, and farmers and controls 0.25 and 0.32 mg/L, repectively. After considering data on 189 individuals of the total of 400, /it was/ concluded /that/ ... "despite high chronic exposures to PCP, individuals in the wood treatment group of workers had not undergone any serious health effects from this exposure. The only evidence of tangible health effects, part of which could have been caused by exposures to chemicals other than PCP, were the low-grade infections or inflammations of the skin and subcutaneous tissue, of the protective membrane of the eye, and of the mucous membrane of the upper respiratory tract. No specific long-term effects could be elicited in the exposed group".[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • SURVEILLANCE: A mortality study was conducted in a cohort of 2283 plywood mill workers employed for at least one year between 1945 and 1955 in this industry. There were 570 deaths in this cohort, which was only 74% of the number expected based on comparable US mortality figures. A statistically nonsignificant excess of deaths was observed for lymphatic and hematopoietic cancer excluding leukemia (standard mortality ratio (SRM)=156). The greatest excess was for multiple myeloma (SRM=333). The excess mortality due to lymphatic and hematopoietic cancer excluding leukemia was highest after 20 yr duration of employment and latency. The workers were potentially exposed to formaldehyde, but there were no deaths due to nasal cancer. A subcohort of 818 workers involved in drying or gluing operations and exposed to formaldehyde and pentachlorophenol was also studied. Based on small numbers, statistically nonsignificant increased risks of death from Hodgkin's disease (SRM=333) and lymphosarcoma (SRM=250) were observed.[Robinson CF et al; NIOSH; Plywood Mill Workers' Mortality Patterns 1945-77 (Revised) (1987)] **PEER REVIEWED**
  • SURVEILLANCE: A series of studies of chronically exposed workers has been conducted in Hawaii. The first involved workers in wood treatment plants and farmers or pest-control operators. Elevation of serum enzyme levels, ie, serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and lactic dehydrogenase, and low-grade infections or inflammations of the skin, eye, and respiratory tract were found in the exposed groups. In a /separate/ study, plasma protein levels were found to be elevated in exposed, as compared with unexposed, workers.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 388] **PEER REVIEWED**
  • SURVEILLANCE: Aplastic anemia, pure red cell aplasia, leukemia, lymphoma and other hematologic disorders have followed exposure to products containing the pesticide pentachlorophenol (PCP). Information in a 25 yr compilation of documented case reports is summarized, involving industrial and home exposure and accidental poisoning in a nursery. The potential hematologic, mutagenic and carcinogenic effects of PCP and its dioxin-dibenzofuran contaminants also are reviewed. Owing to widespread contamination of the environment by PCP products, and latent periods of up to several decades after exposure before these disorders become manifest clinically, it is necessary to consider their etiologic or contributory role.[Roberts HJ; J Fla Med Assoc 77 (2): 86-90 (1990)] **PEER REVIEWED** PubMed Abstract
  • SURVEILLANCE: Fatal poisoning of infants was traced to improper laundering of diapers and bedding with material containing Na-pentachlorophenate and other phenols.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • SURVEILLANCE: The occurrence of chloracne among pentachlorophenol (PCP) workers was evaluated, and the risk of chloracne among workers who had records of direct skin contact with PCP was assessed. The workers had been employed at a facility which had produced PCP from 1938 through 1978. Of the 926 hourly workers in the study cohort, 666 had medical records available and were employed in 1953 or later; 65 had a diagnosis of chloracne, of which 47 were thought to be associated with PCP. The increase in duration of exposure did not appear to be related to the increased risk of chloracne. Episodes of direct skin contact with PCP were reported throughout the history of the facility. The workers with independent records of direct skin exposure had overall a four fold increase in the risk of developing chloracne compared with workers who did not have records of direct skin contact. Eight of the 13 cases had only one episode of direct skin contact with PCP prior to the diagnosis of chloracne, three cases had two episodes, and two cases had three episodes. The interval between the latest episode of direct skin contact and the diagnosis of chloracne for these 13 cases ranged from about 7 wk to about 14 yr. Four of the 13 cases occurred within 6 mo of contact, four occurred between 1 and 2 yr after the skin contact. Two occurred between 2 and 3 yr after contact and three occurred more than 10 yr after exposure. The authors conclude that exposure to PCP contaminated with hexachlorinated, heptachlorinated, and octachlorinated dibenzo-p-dioxins and dibenzofurans was associated with the occurrence of chloracne.[O'Malley MA et al; American Journal of Industrial Medicine 17 (4): 411-21 (1990)] **PEER REVIEWED** PubMed Abstract
  • SURVEILLANCE: Urinary PCP was monitored in male volunteers exposed to Fungifen solution, which is a readily accessible pharmaceutical product containing 1% of PCP as active ingredient, and is recommended for the local treatment of interdigital mycoses. PCP absorbed readily through the skin and its elimination was slow. After the topical application of Fungifen, maximum levels of urine PCP ranged from 109 to 1290 ug/L. In a single case a peak value of 3200 ug/L was measured. At the same time, PCP could be detected in the saliva, too. Urinary preexposure levels (ranged around 10 ug/L) were reached within 75 and 90 days, respectively. Maximum urinary levels represent exposures corresponding to occupational ones, known from other studies. The toxicity of PCP as well as the health risk of the Fungifen use to the great masses of the people (including pregnant women and children) are discussed.[Gonczi C et al; Orv Hetil 132 (7): 361-3 (1991)] **PEER REVIEWED** PubMed Abstract
  • SURVEILLANCE: Workers (3 women, 15 men) in a pentachlorophenol processing factory, with a mean activity of processing pentachlorophenol for 12 yr were studied ... Pentachlorophenol levels in plasma ranged from 0.02-1.5 ug/L, median 0.25 ug/L, and in urine 13-1224 ug/L, median 112 ug/L or 11-2111 ug/g creatinine, median 111 ug/g creatinine ... Individual evaluation of the toxicological and neurophysiological results gave /indications/ that in some cases decreased nerve conduction velocity was caused by chronic exposure to pentachlorophenol.[Triebig G et al; Int Arch Occup Environ Health 48 (4): 357-68 (1981)] **PEER REVIEWED** PubMed Abstract

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Non-Human Toxicity Excerpts

  • ALTERNATIVE and IN VITRO TESTS: A study was designed to define the activity ranges of different chlorinated phenols in the series from monochlorophenol to pentachlorophenol in bacteria; to define the effect of these compounds on growth and viability parameters, correlating experimental findings with those obtained by enzymatic activities; and to define the relationships between toxicity and some physicochemical properties of these compounds. Escherichia coli was grown in the presence of test agents and assayed for growth and dehydrogenase and beta-galactosidase activities. Under these experimental conditions, the lag time to initiation of acclimation of growing cultures to phenol was 3 hours, while for chlorinated compounds it was about 2 hours longer. No effect of chlorine substituent number or concentration was seen. Toxicities of phenol, monochlorophenols, and polychlorophenols were differentiated by plotting specific growth rates, normalized to controls, against different concentrations. The validity of dehydrogenase activity in determining the toxicity of various phenol compounds by discriminating among different compounds was also demonstrated. Specific growth rate and dehydrogenase activity gave the best responses for quantitating toxicity and were compared for each phenol compound. The relative toxicity values showed that for both parameters the values obtained were lower than 10 for monochlorophenols and higher than 25 for polychlorinated phenols. A dependence of toxicity on phenol ionization constants was also noted.[Cenci G et al; Bull Environ Contam Toxicol 38 (5): 868-75 (1987)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: Chlorinated phenols represent a major component of hazardous oily and wood-preserving wastes that are widely distributed in chemical dumpsites throughout the United States. Pentachlorophenol has been reported to be highly embryolethal and embryotoxic in rats. However, data pertaining to the developmental toxicities of other important chlorophenols are limited. In this study, the toxicities of phenol, chlorophenol homologues and their isomers, selected phenyl acetates, anisoles, sodium phenates, and tetrachlorobenzoquinones (a total of 38 chemicals) were evaluated using cultures of Hydra attenuata. Developmental hazard index (A/D ratio) was determined for selected test chemicals (ie, those chemicals which resulted in an early toxic endpoint at the lowest whole-log concn in the adult hydra assay). These same chemicals were evaluated at equimolar concentration in postimplantation rat whole embryo culture. Hydra attenuata and whole embryo culture studies demonstrated a linear relationship between toxicity and the degree of chlorine substitution with pentachlorophenol > 2,3,4,5-tetrachlorophenol > 2,3,5-trichlorophenol > 3,5-dichlorophenol > 4-chlorophenol > phenol. The developmental hazard index A/D ratios from the Hydra attenuata assay were approximately 1 for all of the chemicals tested. Findings from the whole embryo culture assay indicated similar results based on growth, gross morphology, and DNA and protein content of embryos.[Mayura K et al; Toxicol Appl Pharmacol 108 (2): 253-66 (1991)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: In this investigation the effects of chlorophenols on rat liver mitochondrial respiratory parameters were determined and compared to the toxicities of those compounds in a variety of biological systems currently being used for toxicity testing. Mitochondrial fractions were exposed to six concentrations of five different chlorophenols in a semiclosed, 2 mL reaction vessel. Respiratory parameters were measured polarographically with an oxygen electrode and compared to control experiments. The toxicity of the chlorophenols, as measured by the concentration reducing the respiratory control ratio of the control to 50%, increased with increasing chloro substitution. The concentrations reducing the respiratory control ratio of the control to 50% ranged from 599 uM with 2 chlorophenol to 0.110 uM with pentachlorophenol. The RCR50 concentrations for the five chlorophenols were compared to six physicochemical parameters for the same chlorophenols; high degrees of correlation between the the concentrations reducing the respiratory control ratio of the control to 50% and the physicochemical parameters were found (r : 0.890). The highest correlation coefficient obtained was with the n-octanol/water partition coefficient (r = 0.991), indicating that the ability of chlorophenols to partition into the lipid mitochondrial membrane plays a significant role in eliciting its toxic effects. The concentrations reducing the respiratory control ratio of the control to 50% were also compared to nine currently existing short-term toxicity tests. High degrees of correlation were obtained with several of the tests, including algal, bacterial, and fish bioassays. This suggests that the uncoupling of oxidative phosphorylation may be the major mechanism by which chlorophenols cause toxicity to intact cells as well as more complex organisms. The use of mitochondrial respiratory parameters appears to offer a complementary approach as a short term toxicity test for this class of compounds. Further development and testing with a variety of other toxicants is suggested.[Shannon RD et al; Environ Toxicol Chem 10 (1): 57-66 (1991)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: The effect of pentachlorophenol (PCP) and its metabolite tetrachlorohydroquinone (TCH) were tested on growth, RNA, protein and ribosome syntheses, and ribosome content in yeast cells. Cells exposed to increasing concentrations of PCP show increasing inhibition to RNA and ribosome synthesis, and to cell growth. TCH causes a delay of the growth of the cell culture (prolongation of the lag phase) but does not cause inhibition. After treatment with TCH the maximum of the RNA synthesis was retarded, but subsequently reached nearly the same level as the untreated control cells. On ribosome synthesis and ribosome content, treatment with increasing concentrations of PCP, as well as of TCH, leads to a substantial decrease in ribosomal synthesis and, finally, total inhibition. Parallel to this, the content of free and membrane-bound ribosomes is diminished. PCP exhibits a stronger effect than TCH. The protein synthesis is only slightly reduced after treatment with PCP or TCH (with concentrations up to 20 ug/mL).[Ehrlich W et al; Ecotoxicol Environ Safety 13 (1): 7-12 (1987)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The effects of chlorophenols on the function and viability of rat hepatocytes were studied in vitro. Primary hepatocytes obtained from male Sprague Dawley rats were cultured and incubated with PCP, 2,3,4,5-tetrachlorophenol (TCP), 2,4,5-trichlorophenol (TrCP), 2,4-dichlorophenol (DCP), or 4-chlorophenol (chlorophenol) for 1 hr at concn of 0 to 1X10-3 M. The effects on phase I and phase II metabolism of 7-ethoxycoumarin (7EC) were assessed by determining the concentrations for inhibiting 7-ethoxycoumarin-deethylase activity and depleting intracellular ATP content by 50 percent. The cultures were assayed for leakage of lactate dehydrogenase (LDH) into the medium. The EC50s for inhibiting phase I 7EC metabolism were: PCP, 37.5 uM; TCP, 34.6 uM; TrCP, 36.4 uM; DCP, 87.8 uM; and clorophenol, 215.2 uM. The corresponding EC50s for phase II 7EC metabolism were 6.5, 22.8, 22.0, 30.9, and 48.4 uM, respectively. The EC50s for depleting cellular ATP were: PCP, 6.4 uM; TCP, 18.4 uM; TrCP, 25.9 uM; DCP, 185.8 uM; and chlorophenol, 1334.1 uM. None of the compounds caused a significant leakage of LDH into the medium. When compared with published values of their octanol/water partition coefficients, the log of the EC50s were linearly correlated with the log of their partition coefficients.[Aschmann C et al; Arch Toxicol 63 (2): 121-6 (1989)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The effects of pure and technical grade pentachlorophenol on primary cultured rat hepatocytes were compared to determine if contaminants of commercial preparations of pentachlorophenol increased its toxicity. Hepatocytes isolated from adult Sprague Dawley rats were incubated with analytical pentachlorophenol of 99 percent purity, technical grade pentachlorophenol, or its sodium salt (technical grade pentachlorophenol sodium salt), which contains only minor concentrations of technical impurities. Monooxygenase activity was markedly induced by technical grade pentachlorophenol in a concn dependent pattern, with a maximum response of approximately 14 fold seen at concentrations of 30 to 50 uM. Monooxygenase induction was much less marked after exposure to 50 uM technical grade pentachlorophenol sodium salt, only 2.7 fold, and was barely detectable after exposure to 50 uM analytical pentachlorophenol. Phase II metabolism of monooxygenase product was equally inhibited by pretreatment with any of the pentachlorophenol preparations. Cell membrane damage, assessed by leakage of lactate dehydrogenase into the culture medium, was also observed with all the pentachlorophenol preparations tested.[Wollesen C et al; Chemosphere 15 (9-12): 2125-8 (1986)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: The effects of pure and technical grade pentachlorophenol on primary cultured rat hepatocytes were compared to determine if contaminants of commercial preparations of pentachlorophenol increased its toxicity. Hepatocytes isolated from adult Sprague-Dawley rats were incubated with analytical /grade/ pentachlorophenol of 99% purity, technical grade pentachlorophenol, or its sodium salt, which contains only minor concentrations of technical impurities. Monooxygenase activity was markedly induced by technical grade pentachlorophenol in a concentration dependent pattern, with a maximum response of approximately 14 fold seen at concentrations of 30 to 50 uM. Monooxygenase induction was much less marked after exposure to 50 uM sodium salt of technical pentachlorophenol, only 2.7 fold, and was barely detectable after exposure to 50 uM 99% purity pentachlorophenol. Phase II metabolism of monooxygenase product was equally inhibited by pretreatment with any of the pentachlorophenol preparations. Cell membrane damage, assessed by leakage of LDH into the culture medium, was also observed with all the pentachlorophenol preparations tested.[Wollesen C et al; Chemosphere 15 (9-12): 2125-8 (1986)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: The suitability of ejaculated bovine spermatozoa as an in vitro model of the assessment of the cytotoxic potential of chemicals was evaluated using several endpoints: swimming activity, adenine nucleotide content, membrane integrity and oxygen consumption. A series of chlorophenols inhibited sperm motion (motility and velocity) in a concentration dependent manner. This could be determined quantitatively and reproducibly by means of videomicrography and automatic computer image analysis. The sperm immobilizing potency increased with increasing chlorination and was positively correlated with lipophilicity. Concentrations which reduced the percentage of moving sperm to 50% of controls ranged from 43 uM for pentachlorophenol to 1440 uM for 4-monochlorophenol. Determinations of adenine nucleotides and percentages of viable cells revealed qualitative differences between the action of pentachlorophenol and the lower chlorinated phenols. While the latter decreased the total adenine nucleotide contents and the percentage of unstained cells in parallel to motion inhibition, no such changes occurred after exposure to immobilizing concentrations of pentachlorophenol. Penta-, tetra-, and trichlorinated phenols stimulated cellular respiration, indicating their uncouping activity, at concentrations lower than those necessary for motion inhibition.[Seibert H et al; Cell Biol Toxicol 5 (3): 315-30 (1989)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: This study investigated impairment of oxidative phosphorylation in mitochondria isolated from the liver of hexachlorobenzene treated rats. Partial and reversible uncoupling of the phosphorylative process was found in liver mitochondria from rats dosed with hexachlorobenzene for 60 days. Pentachlorophenol, endogenously formed by hexachlorobenzene metabolism was detected in the mitochondria at a concn of 0.3-0.4 nmol/mg protein.[Trenti T et al; IARC Sci Pub 77: 329-31 (1986)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: This study investigated the extent of impairment in function parameters of liver mitochondria from rats treated for 60 days with hexachlorobenzene. A constant amount of mitochondrial uncoupling was found throughout the treatment period. At the same time a nearly constant amount of pentachlorophenol was detected in these mitochondria. In contrast, the level of mitochondrial porphyrins increased progressively. There was good correlation between the concentration of mitochondrial pentachlorophenol and the degree of uncoupling of oxidative phosphorylation.[Trenti T et al; IARC Sci Pub 77: 457-9 (1986)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: To evaluate the toxicities of 37 xenobiotics detected in drinking water, primary cultures of rat hepatocytes were treated with the xenobiotics at a concentration of 0.5 mM. The toxicities were assessed by four cellular markers: leakage of intracellular lactate dehydrogenase activity, glycogenolytic activity as a specific function of hepatocytes, intracellular glutathione content, and observations of cytopathic effects. The cytotoxic assay revealed that pesticides of xenobiotics used in the current study were the most toxic at muM levels, that phenolic compounds had potent toxicity for the cultured cells while benzoic compounds did not, and that 3 carbon compounds with substitution of hydrogen to bromine or chlorine at both positions 1 and 3 were highly toxic. The order of hepatotoxicity on the basis of IC50 was, 1,3-dichloro-2-propanone > pentachlorophenol : 1,2-dibromo-3-chloro-propane > hepatachlor > 2,4,6-trichlorophenol : 2,4,6-tribromophenol. Since lag times were observed for the expression of cytotoxicity by the pesticides, biotransformation appeared important for the toxicity. Currently the concentration of pesticides is very low in the environment, and therefore the possibility of causing an impact on human health is low. However, the long lifetime and high lipophilicity of pesticides give them the potential to become some of the greatest environmental toxicants.[Murayama J-I et al; Eisei Kagaku 36 (4): 267-76 (1990)] **PEER REVIEWED**
  • ENDOCRINE MODULATION: ... 12 environmentally relevant pesticides (11 herbicides and pentachlorophenol (PCP)) were tested for their endocrine disrupting potential in two in vitro assays. A recombinant yeast screen was used to detect receptor mediated (anti-) estrogenic and (anti-) androgenic activity (concn range: 0.01-1000 uM), and cultured Xenopus oocytes were used to measure effects on the ovulatory response and ovarian steroidogenesis (concn range: 0.00625-62.5 uM). Eleven pesticides were active in at least one assay ... The most common effects were antiestrogenic/ antiandrogenic activity in the yeast screen, and inhibition of ovulation in vitro, accompanied by decreased testosterone production. Estrogenic activity was never observed. The most potent compound identified in vitro (PCP) was tested for ED activity in vivo. A short-term exposure (6 days) of adult female Xenopus to low concn (0.1 or 1 ug/L; 0.375 or 3.75 nM) resulted in minor alterations in plasma hormone levels and toxic effects on the ovary. Changes in in vitro human chorionic gonadotropin (hCG) stimulated hormone production in ovarian follicles from exposed individuals was also observed ...[Orton F et al; Environ Sci Technol 43 (6): 2144-50 (2009). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract
  • ENDOCRINE MODULATION: A yeast (Saccharomyces cerevisiae)-based assay was developed and tested with steroids and chemicals (mostly pesticides). The induction of beta-galactosidase activity was strictly dependent on the presence of seabream (Sparus aurata) betaa estrogen receptor (sbERbetaa) and substances known to have estrogenic activity. 17beta-Estradiol (E(2)) and diethylstilbestrol (DES), both agonists, were most active and the antagonist tamoxifen (TAM) was 14-fold less active than E(2). Among the chemicals tested bisphenol-A was most active, followed by pentachlorophenol and naphthalene ...[Passos AL et al; Ecotoxicol Environ Saf 72 (5): 1529-37 (2009)] **PEER REVIEWED** PubMed Abstract
  • ENDOCRINE MODULATION: An investigation was conducted to examine the competition of various chlorinated phenol congeners with the thyroxine (T4) binding site of transthyretin (TTR). Specifically, attempts were made to determine whether the T4 binding site of TTR could be occupied by hydroxylated chlorinated aromatic compounds using chlorinated phenol congeners as model compounds in a competition assay with (125)I labeled T4. 2,3-Dichlorobenzene, 3,4,3',4'-tetrachlorobiphenyl, 4-hydroxybiphenyl, and phenol were inefficient competitors. The chlorinated phenols which were tested were all competitors for the T4 binding site of TTR. The most effective competitor was pentachlorophenol (PCP), following in decreasing order by trichlorophenols, dichlorophenols, and monochlorophenols. When the chlorine was present in both ortho positions to the hydroxyl group, the competitor was more efficient. The relative affinity of binding of PCP to TTR was twice that of T4. PCP mainly decreased the affinity constant while the binding capacity was not altered. This indicated a competitive type of inhibition. PCP competed successfully with T4 sites on albumin as well with a relative affinity of 0.25. The binding of T4 to thyroid binding globulin was much less affected by PCP interference. /Results suggest/ that a specific interaction of chlorophenols exists with the T4 binding site of TTR.[van den Berg KJ; Chemico-Biological Interactions 76 (1): 63-75 (1990)] **PEER REVIEWED** PubMed Abstract
  • ENDOCRINE MODULATION: Effects of administration of equimolar doses of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroxine and triiodothyronine levels in rats were studied. Furthermore, it was investigated whether the observed effects were related to the serum levels of hexachlorobenzene or pentachlorophenol. Rats received either corn oil (controls) or hexachlorobenzene, pentachlorophenol or tetrachlorohydroquinone in a single equimolar intraperitoneal dose of 0.056 mM/kg. Results indicated that hexachlorobenzene did not alter serum thyroxine and triiodothyronine levels for a period up to 96 hr after dosing. In contrast, pentachlorophenol and tetrachlorohydroquinone were both capable of reducing serum thyroxine levels with a maximum effect between 6 and 24 hr after exposure. Tetrachlorohydroquinone was more effective in repressing triiodothyronine than thyroxine blood levels. Dose response experiments were carried out in order to obtain insight into the sensitivity of the observed effects. Rats received different doses of pentachlorophenol or tetrachlorohydroquinone intraperitoneally. The reductions of thyroxine levels by pentachlorophenol were inversely related to serum pentachlorophenol levels in exposed animals, based on the toxicokinetics and dose response profiles. Furthermore, pentachlorophenol serum levels after hexachlorobenzene administration appeared too low to cause an effect.[Van Raaij J A GM et al; Toxicology 67 (1): 107-16 (1991)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: In feeding expt with Drosophila melanogaster, 7 mM pentachlorophenol failed to induce sex-linked recessive lethals in meiotic and postmeiotic stages of male germ cells. In lateral roots of Vicia faba seedlings treated with 43.5-174 mg/L ... there was incr in frequency of abnormal cell divisions (eg, stickiness and lagging of chromosomes and chromosome fragmentation); these abnormalities were more frequent during metaphase than in earlier stages and, in general, incr with incr concn.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 316 (1979)] **PEER REVIEWED**
  • GENOTOXICITY: It is shown that p-tetrachlorohydroquinone (TCH), the metabolite of the environmental chemical pentachlorophenol (PCP), is more toxic to cultured CHO cells than PCP, and that it causes DNA single-strand breaks and/or alkali-labile sites at concn of 2-10 ug/mL as demonstrated by the alkaline elution technique.[Ehrlich W; Mutat Res 244 (4): 299-302 (1990)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Phenol and the 19 isomers of chlorophenol were evaluated in the Microscreen Prophage Induction Assay to characterize the genotoxicity of these agents. Seven of the isomers induced prophage lambda in the presence of S9, with 2,3,4-trichlorophenol, 2,4,5-trichlorophenol, and 3,4,5-trichlorophenol being about ten times as potent as 2,3,6-trichlorophenol, 2,4,6-trichlorophenol, and pentachlorophenol. Medium potency was demonstrated by 2,3,4,5-tetrachlorophenol. Structurally, the more potent isomers had one or no chlorine atoms in the ortho position to the hydroxyl group. The less potent isomers had two chlorine atoms ortho to the hydroxyl group. None of the 20 compounds was mutagenic in Salmonella. However, the prophage induction results agreed with earlier results that most of these seven isomers were clastogenic, were associated with cancer and chromosomal aberrations in humans, and were carcinogenic in rodents. The /results/ suggest that the metabolism of the parent isomer to a chlorohydroquinone is an important step in the genotoxicity of these isomers. This chlorohydroquinone can form a chlorobenzosemiquinone in the presence of oxygen. Free radicals can then be produced that can cause DNA strand breaks, resulting in prophage induction in Escherichia coli or possibly the chromosomal aberrations associated with human exposure to chlorophenols.[DeMarini DM et al; Environ Mol Mutagen 15 (1): 1-9 (1990)] **PEER REVIEWED**
  • GENOTOXICITY: Proved negative in sex-linked level test in Drosophila ...[National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 753] **PEER REVIEWED**
  • GENOTOXICITY: The induction of mutation of the hypoxanthine-guanine phosphoribosyl transferase locus and cytotoxicities of 6 different chlorophenols (2,4- and 2,6-dichlorophenol, 2,4,5- and 2,4,6-trichlorophenol, 2,3,4,6-tetrachlorophenol and pentachlorophenol) were examined in V79 Chinese hamster cells without exogenous metabolic activation. The chlorophenols were cytotoxic to V79 cells, but fail to produce significant increases in the frequency of 6-thioguanine-resistant mutants.[Jansson K, Jansson V; Mutat Res 171 (2-3): 165-8 (1986)] **PEER REVIEWED** PubMed Abstract
  • IMMUNOTOXICITY: The effects of chronic dietary exposure to technical grade pentachlorophenol on humoral immune responses in mice were examined. Primary and secondary splenic antibody responses to the T-dependent antigen, sheep red blood cells, were examined in mice using the Hemolytic Antibody Isotope Release assay. To assess the direct effects of technical grade pentachlorophenol on B cells, the splenic plaque-forming cell response and serum antibody titers to the T-independent antigen, dinitrophenyl Ficoll, were examined. Technical grade pentachlorophenol exposure altered the kinetics and the magnitude of the humoral antibody responses to sheep red blood cells and dinitrophenyl Ficoll. Peak splenic antibody production and serum antibody responses were dose-dependently suppressed by technical grade pentachlorophenol exposure. IgM responses appeared to be more sensitive to technical grade pentachlorophenol induced suppression than the IgG response. Significant depresssion of the IgM anti-sheep red blood cells splenic hemolytic antibody isotope release response was apparent as early as 2 wk after initiation of technical grade pentachlorophenol exposure and persisted for at least 8 wk after terminination of technical grade pentachlorophenol feeding. Liver wt and serum lactate dehydrogenase and alanine aminotransferase levels were significantly elevated during technical grade pentachlorophenol exposure and returned to control levels after a 4-6 wk recovery period. The immunotoxic effect of pentachlorphenol on humoral immunity was observed only in animals exposed to technical grade pentachlorphenol known to be contaminated with significant levels of other chlorinated phenols as well as nonphenolic impurities including chlorinated dioxins, furans, and diphenyl ethers. Animals exposed to analytical grade pentachlorophenol did not exhibit depressed humoral immunity.[Kerkvliet NI et al; Fundam Appl Toxicol 2 (2): 90-9 (1982)] **PEER REVIEWED** PubMed Abstract
  • IMMUNOTOXICITY: The immunosuppressive effects produced by exposure to technical grade pentachlorophenol were compared with those produced by purified pentachlorophenol both in vitro and in vivo in mice. Female B6C3F1 mice were administered daily doses of 10, 30, or 100 mg/kg technical grade pentachlorophenol, or corn oil via gastric intubation for 14 days. Animals were sacrificed the day after the last dose, and antibody responses to multiple antigenic stimuli were measured in spleen cell suspensions from the mice. There were no differences in the antibody responses in the spleen cell suspensions from technical grade pentachlorophenol or purified pentachlorophenol treated animals as compared to controls. When mice were immunized with sheep erythrocytes on day 10 or 11 of the 14 day exposure period, there was a dose dependent suppression of the immunoglobulin-M antibody response to sheep erythrocytes in spleen cells from mice treated with technical grade pentachlorophenol. No changes were observed in the antibody responses of spleen cells from mice to purified pentachlorophenol which were immunized during exposure. When added directly to spleen cell cultures from untreated mice, both technical grade pentachlorophenoland purified pentachlorophenol suppressed the in vitro antibody responses and were cytotoxic to the spleen cells.[Holsapple MP et al; J Tox Environ Health 20 (3): 229-39 (1987)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: In addition to its systemic effects, PCP also induces more localized effects in test organisms. Both dermal and subcutaneous applications have produced swelling, skin damage, and occasionally hair loss in a variety of animals ... Localized effects on blood vessels may result in hyperemia or erythema.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: In rats, lethal doses induce an increased respiratory rate, a marked rise in temperature, tremors, and a loss of righting reflex. Asphyxial spasms and cessation of breathing occur just before cardiac arrest, which is in turn followed by a rapid, intense rigor morris.[International Program on Chemical Safety; Health and Safety Guide No. 19: Pentachlorophenol (1989). Available from, as of October 15, 2009: http://www.inchem.org/pages/hsg.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: It is generally agreed that the symptoms and signs of acute chlorophenol toxicity result from the effects of the chlorophenol molecule itself, rather than from the microcontaminants. Chlorophenol rapidly causes hyperthermia, profuse sweating and early death. These signs are not observed in animals exposed only to PCDD and PCDF.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Literature data on eye irritation classify technical pentachlorophenol as a moderate to severe eye irritant with irreversible corneal opacity, while data on dermal irritation classify pentachlorophenol technical as a mild dermal irritant.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.10 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: PCP, regardless of the route of administration, is the most acutely toxic of the chlorophenols tested in laboratory animal species. Oral LD50 values range between 27 and 205 mg/kg bw for a variety of species, regardless of the vehicle of administration and the grade of PCP ... Acute oral exposure of mice and rats to lethal doses of PCP ... results in an increase in respiratory rate, a marked rise in temperature (4-4.5 deg C), tremors or possibly convulsions, and a loss of the righting reflex. Asphyxial spasms and cessation of breathing usually occurs 0.5-2 min before cardiac arrest. A rapid and intense rigor mortis is observed within 3-5 min of death and approximately 45 min sooner than the onset of rigor mortis in rats given ether. Similar signs are observed with lethal exposure to PCP and its sodium salt, regardless of the route of administration.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: The acute oral median lethal dose of technical grade pentachlorophenol was investigated in developing Sprague Dawley rats from 10 to 134 days old. Signs of acute toxicity included ataxia developing about 15 min after dosing, followed by rapidly developing motor weakness, hyperpyrexia, and rapid breathing about 25 min after dosing. Most deaths occurred either between 20 min and 2 hr, or between 4 hr and 8 hr following dosing. Those animals who recovered had little salivation, rectal temperatures only 1 to 3 deg F above normal, and began to recover after 8 hr. Rats who were 10 to 20 days of age and not yet weaned and adult rats aged 70 to 134 days old formed the two most susceptible groups, far more susceptible than were juveniles aged 25 to 50 days, to the toxic effects of pentachlorophenol. The LD50 increased 4.4 times from postnatal day ten to postnatal day 25, plateaued from day 25 to 50, and decreased 2.8 times from day 50 to 134. The LD50 (mg/kg) ranged from 50 to 180 for preweaned rats, from 220 to 230 for juveniles (25-59 days old), and from 80 to 120 for adults (70-130 days old). The physiological reasons for the developmental susceptibility as evidenced in this study were not known.[St. Omer VEV, Gadusek F; Environ Toxicol Chem 6 (2): 147-9 (1987)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: The only acute inhalation toxicity value reported for Na-PCP is for rats; Na-PCP is at least 10 times more toxic via inhalation than by oral ingestion.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: The toxicity of polychlorinated aromatic compounds was studied. Polychlorinated aromatic compounds in corn oil were administered to adult male and female albino mice, NMRJ strain, orally or by intraperitoneal injection. The median lethal dose for pentachlorophenol was 3.85 mg/mouse by the oral route and 1.75 mg/mouse by ip injection, for pentachloroanisole the values were 9.50 and 8.40, for tetrachlorocatechol 9.50 and 4.80, for tetrachlorohydroquinone 11.0 and 0.85, and for tetrachlororesorcinol the median lethal doses were 22.0 and 10.5 mg/mouse, respectively. After oral administration, pentachlorophenol was found to be the most toxic compound. After intraperitoneal administration, tetrachlorohydroquinone was found to be the most toxic compound.[Renner G et al; Toxicological and Environmental Chemistry 11 (1): 37-50 (1986)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: /Pentachlorophenol/ ... (0, 5, 50, or 500 ppm) /was administered/ to Sprague-Dawley rats in the diet beginning with the rats own weaning through the weaning of their pups ... Significant effects /were observed/ on the immune system (as indicated by decreased antibody titers, decreased delayed hypersensitivity to oxazolone, and increased peritoneal macrophage numbers) and reduced ethylnitrosourea-induced transplacental carcinogenesis.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 392] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Carcinogenicity bioassays were conducted utilizing 0, 100, or 200 ppm technical grade pentachlorophenol or 0, 100, 200, or 600 ppm (Dowicide EC-7, a technical grade formulation) fed to groups of 50 male and 50 female /B6C3F1 mice. ... Mean body weights of mice exposed to technical-grade pentachlorophenol and EC-7 were comparable to those of controls until weeks 36-82. Thereafter, a 4%-22% dose-related decrease was observed in the mid and high dose mice exposed to EC-7 and in high dose mice exposed to technical-grade pentachlorophenol. Females were more affected than males. Feed consumption by exposed mice was similar to that by controls. The average daily doses of technical-grade pentachlorophenol were approximately 17-18 or 35 mg/kg compared with 17-18, 34-37, or 114-118 mg/kg of EC-7. Survival of mice did not appear to be affected by exposure to either technical-grade pentachlorophenol or EC-7 at the doses used in these studies. The incidences of hepatocellular adenomas and carcinomas were increased (dose related) in male and female mice exposed to either technical-grade pentachlorophenol or EC-7, although the increase was less marked in females exposed to technical-grade pentachlorophenol (adenomas or carcinomas, combined: technical-grade: male-- control, 7/32, 22%; low dose, 26/47, 55%; high dose, 37/48, 77%; female--3/33, 9%; 9/49, 18%; 9/50, 18%; EC-7: male--control, 6/35, 17%; low dose, 19/48, 40%; mid dose, 21/48, 44%; high dose, 34/49, 69%; female-- 1/34, 3%; 4/50, 8%; 6/49, 12%; 31/48, 65%). The incidences of pheochromocytomas in male mice were significantly greater than those in controls for both technical-grade pentachlorophenol (0/31; 10/45, 22%; 23/45, 51%) and EC-7 (1/34, 3%; 4/48, 8%; 21/48, 44%; 45/49, 92%). These neoplasms were also increased in female mice exposed to EC-7 at the highest dose (0/35; 2/49, 4%; 2/46, 4%; 38/49, 78%) but not in those exposed to technical-grade pentachlorophenol (2/33, 6%; 2/48, 4%; 1/49, 2%). Hyperplasia of the adrenal medulla was observed at increased incidences in mice that received either technical-grade pentachlorophenol (male: 1/31; 10/45; female: 0/33; 4/48; 2/49) or EC-7 (male: 1/34; 19/48; 13/48; 1/49; female: 2/35; 1/49; 5/46; 17/49). The incidences of hemangiosarcomas in the spleen and/or liver were significantly greater than those in controls for high dose female mice that received technical-grade pentachlorophenol (0/35; 3/50, 6%; 6/50, 12%) or EC-7 (0/35; 1/50, 2%; 3/50, 6%; 8/49, 16%). Compound-related nonneoplastic lesions occurred in the liver, spleen, and nose in mice exposed to either technical-grade pentachlorophenol or EC-7. The lesions in the liver included dose-related increased incidences of clear cell foci, chronic active inflammation, pigmentation, necrosis, cytomegaly, proliferation of hematopoietic cells, and bile duct hyperplasia. Increased amounts of extramedullary hematopoiesis of the splenic red pulp were observed at increased incidences in dosed male and high dose female mice that received technical-grade pentachlorophenol (male: 5/30; 15/23; 18/46; female: 2/33; 4/13; 11/47). Acute focal inflammation of the nasal mucosa and focal metaplasia of the olfactory epithelium were observed at increased incidences in high dose mice that received EC-7 (inflammation--male: 4/35; 1/13; 3/16; 47/49; female: 0/35; 0/14; 2/5; 46/48; focal metaplasia-- male: 2/35; 1/13; 2/16; 46/49; female: 1/35; 0/14; 2/5; 45/48) but not in mice exposed to technical-grade pentachlorophenol. ... Under the conditions of these two yr studies, there was clear evidence of carcinogenic activity for male B6C3F1 mice fed diets containing technical grade pentachlorophenol, as shown by increased incidences of adrenal medullary and hepatocellular neoplasms. There was some evidence of carcinogenic activity for female B6C3F1 mice exposed to technical grade pentachlorophenol, as shown by increased incidences of hemangiosarcomas and
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Groups of 18 male and ... female (C57BL/6XC3H/ANF)F1 mice and 18 male and female (C57BL/6XAKR)F1 mice received ... Dowcide-7 (impurities unspecified) ... /at/ 46.4 mg/kg bw in 0.5% gelatin at 7 days of age by stomach tube and same amt (not adjusted for incr bw) daily up to 4 wk of age; subsequently, the mice were fed 130 mg/kg diet until ... 78 wk of age at which time 16, 18, 17 & 16 mice were still alive in the 4 groups, respectively. Tumors developed in 3/18, 4/18, 3/17 and 2/18 male and female ... mice; these incidences were not significantly greater than in 79-90 necropsied mice of each sex and strain, which had either been untreated or had received gelatin only.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 309 (1979)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Groups of 18 male and 18 female (C57BL/6XC3H/ANF)F1 mice and 18 male & 18 female (C57BL/6XAKR)F1 mice ... Given single sc injections of 46.4 mg/kg bw ... (Dowcide-7; impurities unspecified) in corn oil at 28 days of age and were observed up to 78 wk of age, at which time 14, 18, 18 & 16 mice in the 4 groups, respectively were still alive. Neg control groups consisted of animals that were either untreated or received gelatin, corn oil or dimethylsulfoxide and comprised 141 males and 154 females of the first strain and 161 males and 157 females of the second strain. The incidences of hepatomas (4/17) in males of 1st strain was significantly incr ... over that in controls (9/141).[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 313 (1979)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: In a chronic toxicity study, pentachlorophenol (90.9% a.i.) was fed (gelatin capsules) to four beagle dogs/sex/dose at dose levels of 0, 1.5, 3.5, or 6.5 mg/kg/day for 52 weeks. At 6.5 mg/kg/day, one male and one female dog were sacrificed in extremis on days 247 and 305, respectively, due to significant clinical toxicity (significant weight loss, lethargy, marked dehydration, vomiting, icterus). Group mean body weight in surviving male dogs at the 6.5 mg/kg/day dose was decreased by 15% at week 13, and 21% at study termination. In females, a 19% decrease in group mean body weight was observed at week 13, and bodyweight remained significantly decreased until study termination. Decreased red cell count (16%), hemoglobin (9%), and hematocrit (8%), was observed in males at the 6.5 mg/kg/day dose at week 13. These decreases were also observed at week 26 and at necropsy. In females, significant decreases of 10-17% in these hematologic parameters were observed at 6.5 mg/kg/day from week 26 until study termination. Activities of alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase were significantly elevated for both sexes throughout the study at the 6.5 mg/kg/day dose. Gamma-glutamyltranspeptidase activity was increased in male dogs at week 13 by 45%. Absolute and relative liver weight in males and females was elevated by 32% and 49% over control at 6.5 mg/kg/day. Absolute and relative thyroid weight was also increased significantly in females at the 6.5 mg/kg/day dose. Gross stomach lesions consisting of multiple, raised mucosal foci were observed in increased incidence in all treated groups of male and female dogs with only one female control dog showing a similar lesion. Dark, discolored liver was also observed in increased incidence in male and female treated dogs, but a dose-response was observed only for males. Microscopically, increased incidence of lymphocytic mucosal inflammation was observed in the stomach of treated males and females. The lesion was presenting in all treated and control groups, but the severity of the lesion was increased, especially at the 3.5 and 6.5 mg/kg/day doses. The LOAEL for this study was determined to be 1.5 mg/kg/day, based on the liver effects observed in male and female dogs at this dose.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.16 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Male and female F344/N rats were exposed to pentachlorophenol (approximately 99% pure) in feed for ... 2 years. ... Groups of 50 male and 50 female rats were fed diets containing 200, 400, or 600 ppm pentachlorophenol (equivalent to average daily doses of approximately 10, 20, and 30 mg/kg) for 105 weeks. Stop-exposure groups of 60 male and 60 female rats received 1,000 ppm (equivalent to 60 mg/kg) in feed for 52 weeks, after which animals received un-dosed feed for the remainder of the 2-year study; 10 male and 10 female control and 1,000 ppm rats were evaluated at 7 months. In the 2-year study, survival of 600 and 1,000 ppm males was greater than that of the controls. Mean body weights of 400 and 600 ppm males and females were generally less than those of controls. When exposure to pentachlorophenol was discontinued at week 52, mean body weights of 1,000 ppm males and females were 17% and 22% lower than those of the respective controls; however, by the end of week 87, the mean body weights were similar to those of the controls. Generally, feed consumption by exposed groups was similar to that by the controls. At 2 years, the incidence of malignant mesothelioma originating from the tunica vaginalis was significantly greater in 1,000 ppm males than in the controls, and the incidence exceeded the historical control range. Nasal squamous cell carcinomas were present in one control male, three 200 ppm males, one 400 ppm male, and five 1,000 ppm males at 2 years, and the incidence in 1,000 ppm males exceeded the historical control range. At the 7-month interim evaluation, the incidences of centrilobular hepatocyte hypertrophy in 1,000 ppm males and females and hepatocyte cytoplasmic vacuolation in 1,000 ppm males was significantly greater than those in the controls. At 2 years, the incidences of several nonneoplastic liver lesions including hepatodiaphragmatic nodules and hepatocyte cystic degeneration in all exposed groups of males and basophilic foci in 1,000 ppm males were increased compared to the controls. ... Under the conditions of this 2-year feed study, there was no evidence of carcinogenic activity of pentachlorophenol in male or female F344/N rats fed diets containing 200, 400, or 600 ppm. There was some evidence of carcinogenic activity of pentachlorophenol in male F344/N rats given feed containing 1,000 ppm for 1 year followed by control feed for 1 year (stop-exposure study), based on increased incidences of mesothelioma and nasal squamous cell carcinoma. There was no evidence of carcinogenic activity of pentachlorophenol in female rats given feed containing 1,000 ppm for 1 year and maintained on control feed for 1 year. Stop-exposure males and females recovered from a transitory reduction in body weight gain by the end of the 2-year study, and males had increased survival compared to the controls.[DHHS/NTP; Toxicology and Carcinogenesis Studies of Pentachlorophenol (CAS No. 87-86-5) in F344/N Rats p.5 (1999) Technical Rpt Series No. 483 NIH Pub No. 99-3973] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Six groups of 27 male and ... female weanling Sprague-Dawley (Spartan substrain) rats ... given lab chow ... containing pentachlorophenol (sample XD-9108.002: pentachlorophenol 90.4%; tetrachlorophenol 10.4%; trichlorophenol less than 0.1%; hepta- & octachlorodibenzo-p-dioxins about 21 mg/kg; hexa- & heptachlorodibenzofurans about 5.2 mg/kg; & hexachlorobenzene 400 mg/kg) to provide ... levels of 0, 1, 3, 10 or 30 mg PCP/kg bw/day. Pentachlorophenol was dissolved in anisole and concn ... adjusted on a monthly basis to maintain designated dose levels ... Groups of 27 male and 27 female controls ... received lab chow containing anisole only. Female rats were maintained on test diets for 24 mo, but the male/s/ ... were taken off ... After 22 mo because of high mortality ... The total and individual tumor incidences by sites, times of appearance ... and avg numbers ... per animal (predominantly benign neoplasms) were not significantly different from those observed in control rats. The number of rats with tumors/those exam were, in males: 11/27 (controls), 13/26 (1 mg/kg), 13/27 (3 mg/kg), 12/27 (10 mg/kg), 11/27 (30 mg/kg); in females: 27/27 (controls), 26/27 (1 mg/kg), 25/27 (at all other doses).[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 313 (1979)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: ...Doses of 0, 5, 15, 30, and 50 mg/kg/day commercial grade (88.4% a.i.) or purified (>98% a.i.) pentachlorophenol prepared in corn oil were administered to groups of pregnant Sprague-Dawley rats on gestation days 6-15 inclusive. For purified pentachlorophenol, the number of rats per group was as follows: control, 33 rats; 5 mg/kg, 15 rats; 15 mg/kg, 18 rats; 30 mg/kg/, 20 rats; 50 mg/kg, 19 rats. For the commercial grade of pentachlorophenol: 5 mg/kg, 18 rats; 15 mg/kg, 17 rats; 30 mg/kg, 19 rats; 50 mg/kg, 15 rats. Additional groups of rats were administered 0 or 30 mg/kg/day pentachlorophenol (type of a.i. not specified) on days 8-11 or 12-15 of gestation. Maternal toxicity from purified pentachlorophenol was evidenced by decreased maternal weight gain at the 30 and 50 mg/kg dose groups for days 6-21 of gestation (74% decrease vs. control). For the commercial grade, weight gain was decreased 43% at the 50 mg/kg dose, and by 22% at the 30 mg/kg dose. Weight gain appeared more significantly affected by purified pentachlorophenol. No other significant signs of maternal toxicity were observed. Fetal incidence of resorption was significantly increased at 30 and 50 mg/kg purified and commercial grade pentachlorophenol. The report stated that the fetal and litter incidence was also significantly increased at 15 mg/kg commercial grade pentachlorophenol, but the fetal incidence (7 and 8% at control and 15 mg/kg/day) as well as the litter incidence (55 and 64% at control and 15 mg/kg/day) did not appear biologically meaningful. Fetal body weight was reported significantly decreased for commercial grade pentachlorophenol at 30 and 50 mg/kg/day and at 30 mg/kg/day for purified pentachlorophenol, but actual values were not reported. Crown-rump length was significantly decreased at 30 mg/kg/day purified pentachlorophenol. The litter incidence of subcutaneous edema, lumber spurs, and supernumerary, lumber or fused ribs was significantly increased at 30 and 50 mg/kg commercial grade pentachlorophenol, but the data did not indicate a dose-response, i.e. the number of litters affected with subcutaneous edema, rib and vertebral abnormalities were greater at 30 mg/kg than at 50 mg/kg for the commercial grade of pentachlorophenol and for the purified pentachlorophenol. The number of litters at the high dose of purified pentachlorophenol was also severely limited (only 2 litters at this dose). Resorptions were significantly increased when pentachlorophenol (both grades) was administered on gestation days 8-11, but not on gestation days 12-15. Based on the results of this study, the Maternal NOAEL can be considered as 15 mg/kg/day, based on body weight effects, for both grades of pentachlorophenol. The Developmental NOAEL would appear to differ according to grade of pentachlorophenol used. Limited data for purified pentachlorophenol at the 50 mg/kg/dose hampers evaluation of a NOAEL and LOAEL for this grade. For the commercial grade of pentachlorophenol, the NOAEL can be considered as 15 mg/kg/day, and the LOAEL as 30 mg/kg/day, based on decreased fetal body weight and crown-rump length. The responses observed at the low dose of commercial grade pentachlorophenol for fetal anomalies (i.e. lumber spurs, anomalous ribs, subcutaneous edema) do not show a dose-response pattern at the higher doses of pentachlorophenol, and are also limited by reduced number of litters at the high dose.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.12 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: A level of purified technical PCP of 30 mg/kg bw per day ..., as well as pure Na-PCP at 26 mg/kg bw per day ... fed to male and female rats for 62 days before mating, 15 days during mating, and to females during gestation and lactation, caused reductions in the numbers of offspring, neonatal body weight, neonatal survival, and growth of weanlings. The no-observed-adverse-effect level was 3 mg/kg bw per day. Male fertility did not appear to be affected in this study.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: A single 60 mg/kg bw oral dose of purified pentachlorophenol was given to pregnant Charles River CD strain rats on days 8, 9, 10, 11, 12, or 13 of gestation. Treatment on days 9 or 10 had the greatest effect on fetotoxicity.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 392] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: In a 2-generation reproduction study, Pentachlorophenol (88.9% a.i.) in corn oil was administered to 30 male and female Sprague-Dawley rats/sex/dose by gavage at dose levels of 0, 10, 30, and 60 mg/kg/day. P1 male and female rats were given the test material once daily at least 70 days prior to cohabitation and continuing through the day before sacrifice. F1 generation rats may have been exposed in utero during gestation and via maternal milk during the postpartum period. The day after weaning, F1 generation rats were administered the test material by gavage at the same dose levels as P1 rats and were continued until one day prior to sacrifice. F2 pups were exposed possibly indirectly during maternal gestation or via maternal milk. In addition to standard parameters, estrous cycling and sperm morphology and function were measured. At 60 mg/kg/day pentachlorophenol, body weight and body weight gain of P1 and F1 parental rats was significantly decreased from control over the period of treatment pre-mating. Gestational and lactational body weights of P1 and F1 female rats were also significantly decreased. Fertility index and number of litters were decreased in both generations at 60 mg/kg/day pentachlorophenol. Days to vaginal patency were significantly increased in P1 female pups, as was days to preputial separation in P1 male pups. Estrous cycling was not significantly affected in either P1 or F1 females, but in F1 males, the number of sperm observed with a broken flagellum was significantly increased at 60 mg/kg/day, and the average testicular spermatid count was significantly decreased at 60 mg/kg/day. Testis weight in F1 generation males was also decreased. Decreased brain weight (4-8%) and increased liver weight (20-33%) were observed in both P1 and F1 male and female rats at 60 mg/kg/day. Macroscopic pathology (enlarged liver) and microscopic pathology (centrilobular hypertrophy, subacute inflammation, single cell necrosis, pigment deposition) were observed in increased incidence at 60 mg/kg/day. The single cell necrosis and pigment deposition were considered related to treatment. Mean litter size, number of live pups, and viability index were significantly reduced in the P1 and F1 pups. Decreased weight of the liver, brain, spleen, and thymus were observed in F2 pups at 60 mg/kg/day. At 30 mg/kg/day, body weight and weight gain decreases of approximately 11% were observed in F1 female parental rats. Significant decreases in average testicular spermatid count and testis weight were observed in F1 male parental rats. Based on the data in this study, the Systemic NOAEL = 10 mg/kg/day for male and female parental rats. The Systemic LOAEL = 30 mg/kg/day for male and female rats, based on decreased body weight and weight gain in F1 generation parental rats, and adverse testicular effects in F1 male rats (decreased testis weight, decreased spermatid count). The reproductive NOAEL = 10 mg/kg/day in this study. The reproductive LOAEL = 30 mg/kg/day, based on decreased group mean litter weight.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.14 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: In a developmental toxicity study, inseminated New Zealand White rabbits (20 rabbits/dose) were administered pentachlorophenol by gavage at doses of 0, 7.5, 15, and 30 mg/kg/day on gestation days 6-18 inclusive. Cesarean section examinations were performed on all surviving does on gestation day 29, followed by external, visceral, and skeletal examination of all fetuses. There were no maternal deaths or signs of maternal toxicity at any dose level. Significantly reduced weight gain was observed in the high dose group on gestation days 6-9 (loss of 40 g vs. gain of 20 g in controls), and in the mid and high dose groups for gestation days 9-12 (gain of 20 g at the mid and high dose vs. gain of 50 g in controls). These changes were considered minimal as the differences in weight gain were equivalent to only 0.5-1% of mean body weight. A consistent reduction in mean food consumption (71-90% of control value on gestation days 9-12) was observed at the high dose. Weight gain was comparable for treated and control rabbits following the treatment interval. A slight but non-significant dose-related decrease in litter size was observed, corresponding to a decrease in implantations/litter for the treated does. There were no statistical differences in the number of treated litters vs. control when the incidences for all observations of external, visceral, and skeletal effects were combined. Although the incidence of affected litters was not statistically significant, a significantly greater (p<0.01) number of individual fetuses in the 15 mg/kg litters contained interfrontal ossification sites compared to controls. Based on the results of this study, the Maternal toxicity NOAEL = 15 mg/kg/day, and the Maternal toxicity LOAEL = 30 mg/kg/day, based on minimally reduced body weight gain and consistent reductions in food consumption during treatment. The Developmental toxicity NOAEL = 30 mg/kg/day; a Developmental toxicity LOAEL was not identified.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.14 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: In a developmental toxicity study, pregnant Crl: CD BR VAF/plus rats (25/dose) received oral administration of Pentachlorophenol (88.9%) at doses of 0, 10, 30 or 80 mg/kg/day during gestation days 6 through 15. For maternal toxicity, the NOAEL was 30 mg/kg/day and the LOAEL was 80 mg/kg/day based on reduced body weight gain during the dosing period (79% of control) and for the entire gestation period (88% of controls). Developmental toxicity observed at 80 mg/kg/day included: significant increase in the number of resorptions (mainly early) with a corroborative decrease in litter size; reduced mean fetal weights; significant increase in the number of fetuses with external, visceral and/or skeletal malformation/variations (hydrocephaly, diaphragmatic hernia, and dilation of the renal pelvis); and significant increase in the number of litters (22 of 23) that contained fetuses (6 of 22) with skeletal anomalies. The most common were vertebral structural variations and incomplete ossification. For developmental toxicity, the NOAEL was 30 mg/kg and the LOAEL was 80 mg/kg/day based on increased resorptions, reduced fetal weight and skeletal malformations/variations.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.12 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Na-PCP (> 98% pure) fed to female Wistar rats at 10, 30, or 60 mg/kg bw during days 8 - 19 of gestation led to statistically significant reductions in bw in females, decreased litter wt, and dramatic increases in fetal resorption and fetal death in the 2 highest dose groups ... No birth defects were observed in the control group or in the group fed 10 mg/kg bw; however, 3/31 pups examined from females in the 30 mg/kg bw group had major malformations (hare lip, umbilical hernia, exocephalus) and 60% had spine and rib malformations (supernumerary, fused, bifurcated, or short ribs). In addition, retardation of ossification and increased breadth of sagittal fissure were extensive in this group. No pups were born to females in the 60 mg/kg bw group. /It was/ concluded that 10 mg/kg bw was the no- observed-adverse-effect level for teratogenicity, fetotoxicity, and embryotoxicity in rats administered Na-PCP. Considering the linearity of the dose-response curve and the fact that 10 mg/kg body weight was the lowest dose administered, the no-observed- adverse-effect level reported in this study is not substantially different from that determined for PCP. /Na-PCP/[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Pentachlorophenol (PCP) was administered to /Wistar rat/ dams and their offspring via drinking water (6.6 mg/L) during gestation and lactation. Tissue samples were obtained from dams, 3-wk-old weanling pups, and 12-wk-old pups. Gene expressions of thyroid hormone receptor beta1 and synapsin I, factors that promote brain growth, was increased in the cerebral cortex of PCP-treated weanling females, whereas plasma concentrations of total thyroxine were decreased in dams and weanling pups, and plasma thyroid-stimulating hormone concentrations were higher in PCP-treated weanling males. PCP caused a decrease in plasma corticosterone concentrations in 12-wk-old female rats, but not in male rats or weanling females. PCP-treated male pups had significantly increased testis wt at 12 wk of age. No overt signs of toxicity were noted throughout this study ... PCP exposure during development causes thyroid function vulnerability, testicular hypertrophy in adults, and aberrations of brain gene expression.[Kawaguchi M et al; Endocrine 33 (3): 277-84 (2008). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Pentachlorophenol was embryotoxic and fetotoxic /to Sprague-Dawley rats/ at doses of commercial and pure pentachlorophenol of 15 mg/kg and above ... Delayed ossification of skull was observed after treatment with pure pentachlorophenol. Oral admin ... to hamsters on days 5-10 of gestation produced fetal death and/or resorptions at 5 mg/kg/day and above.[National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 753] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Pregnant Syrian golden hamsters given daily oral doses of pentachlorophenol (unspecified purity) ranging from 1.25 to 20 mg/kg from days 5 to 10 of gestation experienced an increase in fetal deaths and resorptions. The no effect level was 2.5 mg/kg/day.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 392] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Purified and commercial grades ... given orally to /Sprague-Dawley/ rats at doses ranging from 5-10 mg/kg bw/day at various intervals during days 6-15 of pregnancy. Signs of embryotoxicity and fetotoxicity, ... resorptions, sc edema, dilated ureters, and anomalies of skull, ribs, vertebrae, and sternebrae were observed at incidence which incr with dose. Early organogenesis ... most sensitive period. No-effect ... level of commercial grade was 5 mg/kg/bw/day; purified pentachlorophenol given at same ... level caused ... significant incr in incidence of delayed ossification of skull bones but no other effect on ... development. Ingestion of 3 mg/kg bw/day of commerically available purified grade had no effect on reproduction, neonatal growth, survival, or development.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 315 (1979)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Technical grade PCP administered to pregnant female rats from day 6 to day 15 of gestation did not have any effects on the mother or fetus at 5 mg/kg bw per day ... Fetal resorptions and delayed development of fetuses were observed at 15 mg/kg bw per day, and signs of maternal toxicity, based on weight loss, were observed at 35 mg/kg bw per day. Reports of delayed ossification of the skull, supernumerary, fused, or missing vertebrae and lumbar spurs are usually considered indicative of delayed development rather than teratogenicity, and are responsible for the differences of opinion between the early position of US EPA, that PCP is teratogenic ..., and most other reviews. Purified PCP induced effects similar to those of technical PCP; however, maternal toxicity and decreased fetal weights occurred at 30 mg/kg bw per day, and delayed fetal development was observed at the 5 mg/kg bw per day dose level, which had previously been found to be the no-observed- adverse-effect-level for technical grade PCP. More limited fetotoxic effects were observed in rats exposed to PCP.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The rat embryo was shown to be most susceptible to the toxic effect of pentachlorophenol during the early phases of organogenesis. Pentachlorophenol produced dose-related signs of fetotoxicity, including resorptions, subcutaneous edema, dilated ureters, and anomalies of the skull, ribs, vertebrae, when given orally to pregnant rats at doses ranging from 5 to 50 mg/kg bodyweight per day.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: The teratogenic activities of highly purified pentachlorophenol and pentachloroanisole, administered in the diet of Sprague Dawley rats of both sexes, at the rate of 4, 13 or 43 mg/kg and 4, 12 or 41 mg/kg/day, respectively, for a period of 181 days, were investigated. Pregnant females treated with pentachlorophenol ate more food than untreated controls. As compared to controls, dams treated with the highest doses of both compounds had a lower bw on day 0 of gestation and gained less weight during their pregnancy. Animals treated with the highest dose of pentachlorophenol gained less weight during pregnancy than controls. Embryonic deaths were recorded following treatment with pentachlorophenol at the rate of 43 mg/kg/day, while lower doses of the compound induced dose related reductions in body wt. At the rate of 13 mg/kg/day only, pentachlorophenol reduced the crown to rump length and increased the skeletal alterations of the fetus. Decreased numbers of corpora lutea and embryonic death were recorded following the administration of pentachlorophenol at the rate of 4 and 41 mg/kg/day. At the same dose pentachlorophenol reduced the body wt and the crown to rump length of male fetuses, while their female counterparts were not affected. Neither pentachlorophenol nor pentachloroanisole affected the soft tissue of the animals.[Welsh JJ et al; Food Chem Tox 25 (2): 163-72 (1987)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Neurotoxicity: In a six month toxicity study using B6C3F1 mice (25 male mice and 10 female mice per dose group), diets containing 200, 600, or 1800 technical grade pentachlorophenol ; 200, 600, or 1200 ppm EC-7; 200, 600, or 1200 ppm DP-2; or 200, 500, or 1500 ppm pure pentachlorophenol were administered. The mice in this study were separated in to subgroups for determination of effects on behavior, histopathology, hematology, and clinical chemistry. Behavioral studies included 10 mice per sex per dose group. Examination for the presence of autonomic signs, pinnal, corneal, and righting reflexes; spontaneous motor activity; acoustical startle response; visual placement response; grip strength; and rotarod testing were performed. There were no treatment-related neurobehavioral effects observed at 5 weeks except for those mice receiving technical grade pentachlorophenol, in which a dose-dependent decrease in motor activity and rotarod performance was reported. After 26 weeks exposure, an increase in both motor activity and startle response was observed in female mice. No consistent effects were observed in any of the other behavioral parameters measured for any of the four grades of pentachlorophenol.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.23 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Neurotoxicity: The effects of phenol and pentachlorophenol on axonal conduction and ganglionic transmission were studied in vitro. Desheathed sciatic nerves from toads (Caudiverbera caudiverbera) were incubated with up to 10 mM phenol, pentachlorophenol, or procaine (as a reference compound) for 20 minutes. The extent of axonal conduction block was determined by measuring the compound action potentials evoked by supramaximal stimulation. Desheathed sciatic nerve preparations were incubated with 0.3 to 3 mM pentachlorophenol for 20 min, following which the preparations were placed in fresh medium. Compound action potentials were measured for up to 60 min to assess the reversibility of the block. Sheathed or desheathed nerve preparations were incubated with 3 mM pentachlorophenol at pHs 7.0 and 9.0 to assess the effect of pH on the axonal block. Phenol, pentachlorophenol, and procaine induced axonal conduction block in a dose dependent manner. The doses for causing a 50% block were phenol 6.30 mM, pentachlorophenol 1.00 mM, and procaine 2.00 mM. The block was irreversible. Shifting the pH of the medium from 7.0 to 9.0 in the absence of pentachlorophenol caused a nonsignificant axonal conduction block. When pentachlorophenol was present the same pH change caused a significant decrease in the axonal block. The eighth ganglia from the paravertebral chain of C-caudiverbera spinal cords were incubated with 0.003 to 0.03 mM pentachlorophenol at pH 7.0 and 9.0. In some experiments 0.1 mM 3,4-diaminopyridine was present. The effects on synaptic transmission were assessed by measuring compound action potentials as before. Pentachlorophenol induced a synaptic transmission block that was dose dependent and irreversible. The pentachlorophenol induced block at pH 9.0 was significantly less than at pH 7.0. 3,4-Diaminopyridine antagonized the effect of pentachlorophenol.[Montoya GA et al; Compar Biochem Physiol 89C: 377-82 (1988)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Neurotoxicity: Wistar rats were administered pentachlorophenol (unknown purity) in drinking water at approximately 0, 12, 40, and 118 mg/kg/day for 90-120 days. In rats given 40 mg/kg for 90 days and 118 mg/kg/ for 120 days, degenerative changes in approximately 10% of A and B nerve fibers of the sciatic nerve were observed, as was discontinuation of the myelin sheath by complete separation in several concentric rings, and variable loss of neurotubules, neurofilaments, and other axoplasmic components. It is noted that the doses at which these effects occurred (267 and 800 mg/L) are in excess of the solubility of pentachlorophenol (20 mg/L at 30 deg C; 80 mg/L at 25 deg C).[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.23 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: In a 90-day dermal toxicity study pentachlorophenol (88.9% a.i.) was administered by dermal occlusion to groups of 10 male and female Sprague-Dawley rats for 6 hours/day, 5 days/week, at doses of 0, 100, 500, or 1000 mg/kg/day. No statistically significant differences in group mean body weight or weight gain were observed at any treatment level, nor were there any treatment related mortalities or clinical signs of toxicity. Dermal irritation consisting of erythema (grade 1-2) at 100 mg/kg/day and erythema (grade 1-4) at 500 and 1000 mg/kg/day was observed during weeks 2-5 of the study. The magnitude of the dermal irritation decreased after week 5. There was no dermal irritation observed in control rats. At the 500 and 1000 mg/kg/day dose levels, increased total white blood cell counts and absolute lymphocyte counts were observed in female rats. Decreased platelet count was observed at all dose levels in female rats. The hematological effects were ascribed to dermal irritation and not to systemic effects of the test chemical. Significant increases in alanine and aspartate aminotransferase activities were observed in male and female rats at the 500 and 1000 mg/kg/day dose levels, while increased cholesterol was observed at these dose levels in females only. Significant increases in absolute liver weight were observed at the 1000 mg/kg/day dose level for both males and females. The increase in liver weight was thought to be the result of enzyme induction. Kidney weights were increased at the 1000 mg/kg/day dose in males, and at the 500 and 1000 mg/kg/day dose levels in females. At necropsy, tan crusty areas, acanthosis of the epidermis, and chronic inflammation of the dermis was noted at the treatment site in all treatment groups of both sexes. An increased incidence of hepatocellular degeneration accompanied by chronic inflammation was observed at 500 and 1000 mg/kg/day in both males and females. Based on the results of this study, the Systemic LOAEL = 500 mg/kg/day (enzyme induction and minimal to mild hepatocellular degeneration and chronic inflammation in males and females), and the Systemic NOAEL = 100 mg/kg/day.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.11 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 12, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: The no observable effect level for fetal resorption in pregnant Sprague Dawley female rats was 5.8 mg/kg/day of commercial grade pentachlorophenol and 15 mg/kg/day of purified pentachlorophenol. Measurements were also taken on fetal body weight and crown rump length, both of which decreased with increasing dose. The no observable effect level for these parameters was 15 mg/kg/day for both commercial grade and purified pentachlorophenol.[USEPA; Wood Preservative Position Doc 2/3: p.248 (1981)] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: A ... case, in Canada, of the mortality of young pigs kept on a PCP-treated wooden floor was reported ... Although PCP residues of 310 ug/L were found in sow's milk samples, no PCP could be detected in the liver and stomach of the young pigs. However, ug/kg concn of the higher chlorinated dioxins were found in the skin and liver of the young pigs.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987)] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: A case of acute and lethal poisoning of baby pigs by PCP /is described in which/ the owners of a newly constructed farrowing house had exceeded the manufacturer's recommendation in treating the floor with a solution of PCP in used crankcase oil. All piglets died within one day after they had been moved into the farrowing house. The sow was moved outside where she recovered. No information was given concerning the PCP levels in the air or in the swine.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: Animals fed in troughs made of lumber treated with penta may salivate and have irritated oral mucosa. Vaporization or leaching of penta in pens, enclosures, homes, and barns has caused illness and death. Signs of poisoning include nervousness, rapid pulse and respiratory rate, weakness, muscle tremors, fever, and convulsions, followed by death. Chronic poisoning results in fatty liver, nephrosis, and weight loss. Additional problems reported when penta-contaminated shavings are used as bedding include "off flavors" in broilers, impaired immune response in chickens, and possibly decreased fertility in boars.[Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2429] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: In a 160 day study, cattle fed 20 mg/kg doses of technical pentachlorophenol for 42 days, followed by 15 mg/kg/day for the remainder of the study, had decreased wt gain, progressive anemia, and immune effects. Only minimal adverse effects were observed after exposure to analytical grade pentachlorophenol.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 390] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: Pesticide poisonings of livestock in the United Kingdom have been reviewed ... for the period 1977-80. Of 38 suspected PCP poisoning incidents, only 9 were confirmed as PCP intoxications. High PCP levels found in wood shavings and sawdust used as bedding or litter for cats and poultry apparently caused the death of animals.[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: Post mortem, acutely poisoned sheep /from oral drenching/ showed generalized congestion. Lymph nodes appeared enlarged and edematous. There were hemorrhages in epicardium and along aorta. Lung showed isolated areas of collapse and generalized congestion. Blood splashes were occasionally seen on diaphragm. Stomach, intestines, liver, and kidney sometimes showed mild congestion. Bladder invariably empty.[Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 132] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: The effect of pentachlorophenol on microsomal mixed function oxidases was studied in cattle. Four adult lactating Holstein cattle were fed 0.2 mg/kg technical grade pentachlorophenol for 75 to 84 days, followed by 2 mg/kg for 56 to 60 days. Twelve adult nonlaboratory Holstein cattle were administered 0, 0.1, 1.0, or 10.0 mg/kg purified pentachlorophenol for 95 days. The pentachlorophenol was administered directly into the rumen by way of a permanent cannula. Fifteen male calves were administered 1, 2, 10, or 20 mg/kg technical grade or purified pentachlorophenol from 5 to 43 days of age. The animals were observed for clinical signs of toxicity; they were killed at the end of the dosing period and the liver and lungs were removed and weighed. Liver and lung microsomes were prepared and assayed for benzo(a)pyrene-hydroxylase, ethoxycoumarin-O-deethylase, hexobarbital-hydroxylase, ethylmorphine-N-demethylase, aminopyrine-N-demethylase, cytochrome-P450(448), or cytochrome-b5. None of the adult cattle exhibited clinical signs of toxicity. Liver and lung weights were significantly elevated in cattle given technical grade pentachlorophenol. Liver and lung benzo(a)pyrene-hydroxylase was significantly increased in these animals. Purified pentachlorophenol had no effect on any enzyme activities. Toxic effects such as growth impairment and mortality were observed in calves fed 10 and 20 mg/kg pentachlorophenol. Liver weights were significantly increased. No toxic effects were seen in calves fed pure pentachlorophenol. Cytochrome-P450(448) and cytochrome-b5 were significantly increased by 10 mg/kg technical or pure pentachlorophenol. Technical grade pentachlorophenol at 1 and 10 mg/kg induced benzo(a)pyrene-hydroxylase and ethoxycoumarin-O-deethylase. The 10 mg/kg dose of purified pentachlorophenol also stimulated these enzymes. The /results suggest/ that pentachlorophenol induces organ enlargement and stimulates cytochrome-P450(448) and certain mixed function oxidases. Benzo(a)pyrene-hydroxylase is the most inducible enzyme. The effects observed with technical grade pentachlorophenol are attributed to chlorinated dioxin and furan impurities. Newborn cattle are more susceptible to the inducing properties of pentachlorophenol and its impurities than adults.[Shull LR et al; Pest Biochem Physiol 25 (1): 31-9 (1986)] **PEER REVIEWED**
  • VETERINARY CASE REPORTS: Toxicity of pentachlorophenol to sheep and calves has been examined ... Min acute lethal dose rate was found to be approx 120 and 140 mg/kg respectively in the 2 species ... Death occurred in 2 to 14 hr. Most prominent clinical sign was accelerated breathing ... which distinguished dosed animals from controls 1 to 2 hr after /oral/ drenching. Badly affected animals stood swaying, with head lowered, panted noisily, and made little attempt to move when approached. Salivation was observed in calves and coat felt damp. Recovery from this stage ... was rapid and complete. In fatal cases, complete collapse occurred, animals lying with legs limp and panting vigorously through open mouth. Asphyxial tremors, but no convulsions, set in just before death.[Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 132] **PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LD50 Guinea pig oral 100 mg/kg[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • LD50 Mouse dermal 261 mg/kg[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • LD50 Mouse ip 58 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • LD50 Mouse oral 117 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • LD50 Mouse sc 63 mg/kg[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • LD50 Rabbit oral 105 mg/kg[Meister RT, Sine C, MeisterPro Crop Protection Handbook 2009 (CD-ROM)] **PEER REVIEWED**
  • LD50 Rat dermal 96-330 mg/kg[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED**
  • LD50 Rat female oral 175 mg/kg[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1227] **PEER REVIEWED**
  • LD50 Rat ip 56 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • LD50 Rat male oral 146 mg/kg[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1227] **PEER REVIEWED**
  • LD50 Rat oral 210 mg/kg[Hartley, D. and H. Kidd (eds.). The Agrochemicals Handbook. 2nd ed. Lechworth, Herts, England: The Royal Society of Chemistry, 1987., p. A473] **PEER REVIEWED**
  • LD50 Rat oral 27 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • LD50 Rat sc 100 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2835] **PEER REVIEWED**
  • LD50 Sheep oral 120 mg/kg[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**

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Absorption, Distribution And Excretion

  • (14)C-PCP was admin to mice by sc or ip injection. Most of the activity (72-83%) was excreted in urine in 4 days; about half, in 24 hr; and only trace (0.05%), in expired air. High activity observed in gallbladder and its contents, wall of stomach fundus, contents of GI tract, and liver.[Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 287] **PEER REVIEWED**
  • 1. Interspecies variability in the metabolism of pentachlorophenol (PCP) was investigated by exposing rainbow trout, fathead minnows, sheepshead minnow, firemouth, and goldfish to water-borne (14)C-PCP for 64 hr. 2. The amounts of metabolites in bile and exposure water were species-dependent; all of the metabolites excreted into the water were sulfate conjugates while bile was enriched in glucuronide conjugates. 3. Biliary excretion accounted for less than 30% of the total PCP metabolites. 4. Biliary metabolites alone were a poor indication of the metabolites produced and of the major routes of elimination.[Stehly GR, Hayton WL; Xenobiotica 19 (1): 75-81 (1989)] **PEER REVIEWED** PubMed Abstract
  • A pilot study was conducted to determine the overall efficiency of transdermal penetration of pentachlorophenol and tetrachlorophenol applied to human cadaver skin. Two commercially available wood preservatives were tested, one diesel oil based and the other a water based product. To simulate human exposure conditions at the workplace, small doses were used. The objective was to document the portion of applied dose which permeated the skin and to examine the effect of vehicle or formulation on the relative and absolute absorption of the chlorinated compounds. The penetration of the diesel oil preparations was 62% for pentachlorophenol and 63% for tetrachlorophenol. In the case of the aqueous based preparation, penetration was 16% for sodium-pentachlorophenate and 33% for sodium tetrachlorophenate. The incomplete recovery of each compound may have been due in part to the irreversible binding or unfavorable partitioning of the chlorophenols which would be consistent with the lipophilic character of these compounds.[Horstman SW et al; J Environ Sci Health A24 (3): 229-42 (1989)] **PEER REVIEWED**
  • Enterohepatic circulation of pentachlorophenol occurs in monkeys and mice. In rats, it is found mainly in plasma protein; liver and kidney have highest tissue concn. Plasma half-lives at 10 mg/kg bw dose were about 15 hr in rats and 78 hr in Macaca mulatta monkeys.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 316 (1979)] **PEER REVIEWED**
  • PCP is rapidly eliminated by most animals. It is cleared from the plasma by distribution to the tissues and by excretion via the urine and the feces; the metabolites, when produced, are also excreted rapidly ... 99% of PCP in rat plasma is bound to protein. Human plasma has high binding capacity (96%) that could explain the long retention times in humans. After a single oral dose was given to volunteers, the maximum urinary excretion was reached 40 hr after ingestion and 37 hr after the maximum plasma level of PCP. This delay is due to a marked enterohepatic circulation. The elimination half-life of PCP from plasma was about 30 hr, while that for PCP and PCP glucuronide elimination in the urine was 33 and 13 hr, respectively ... In a further study, an elimination half-life of 17 days was calculated from measuring PCP in both urine and blood ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • PCP is readily absorbed by the gastrointestinal tract and reaches peak plasma levels in 4 hr. Absorption is faster when PCP is dissolved in alcohol.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • Pentachlorophenol has been detected in human blood plasma at levels of 15.69 to 15.86 ug/L in hemodialyzed patients and 15.0 ug/L in persons used as control. It also has been detected in urine, seminal fluid (20-70 ug/kg), and fingernails of non-occupationally exposed individuals. Pentachlorophenol was found in 85% of 416-418 samples of urine collected from general population ... Max level was 193 ug/L and mean level 6.3 ug/L ... Urine samples taken at 25 factories using pentachlorophenol ... showed that avg worker's exposure to pentachlorophenol in air was 0.013 mg/cu m, with max range of 0.004-1.000 mg/ cu m, and level in urine ranged from 0.12 to 9.68 mg/L.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 308 (1979)] **PEER REVIEWED**
  • Pentachlorophenol was given orally to ... volunteers at single doses of 3.9, 4.5, 9, and 18.8 mg. Daily urinary excretion of pentachlorophenol and pentachlorophenol conjugated to glucuronic acid was monitored using gas chromatography with electron capture detection. Based on first order elimination kinetics an elimination half-life of 20 days was derived. To eliminate interference by the uncontrolled absorption of pentachlorophenol from the environment 0.98 mg (13)C-pentachlorophenol was taken by one of the volunteers. Pentachlorophenol levels in urine and plasma were determined using mass spectrometry with negative chemical ionization. An elimination half-life of 17 days was found in both urine and blood. The collected data were used to calculate the clearance of pentachlorophenol: a value of 0.07 mL/min was found. The long elimination half-life of pentachlorophenol is explained by the low urinary clearance due to the high plasma protein binding (>96%) and the tubular reabsorption. The pH-dependency of the elimination of pentachlorophenol was investigated, and a distinct increase in the daily excretion was observed following alkalinization by oral administration of sodium bicarbonate. In order to elucidate the role of the enterohepatic circulation as a possible pool for pentachlorophenol in humans, the bile of cholelithiasis patients with postoperative T-drainage was investigated for pentachlorophenol and compared with the corresponding urine and plasma levels, but no accumulation of pentachlorophenol in the enterohepatic circulation could be observed. The daily elimination and plasma levels of pentachlorophenol in a group of individuals without a specific exposure were found to range from 10 to 48 ug/day and 19 to 36 ug/L, respectively.[Uhl S et al; Arch Toxicol 58 (3): 182-6 (1986)] **PEER REVIEWED** PubMed Abstract
  • Plasma and urinary pentachlorophenol was measured in 209 workers who had occupational exposure to wood preservatives containing this compound and 101 workers not exposed occupationally to pentachlorophenol. Workers were examined for chloracne and blood concentrations of bilirubin, gamma-glutamyltransferase, cholesterol and high-density lipoproteins were determined. All the occupationally exposed groups showed evidence of pentachlorophenol absorption; highest mean concentrations were found in timber treatment /workers/ (6.0 mmol/L for plasma and 274 nmol/mmol of creatinine for urine).[Jones RD et al; Hum Toxicol 5 (3): 189-94 (1986)] **PEER REVIEWED** PubMed Abstract
  • Rapid absorption of pentachlorophenol has been reported in rodents, monkeys, & humans following oral, dermal, or inhalation exposure. ... The major tissue deposits vary somewhat between species. In humans whose deaths were not related to pentachlorophenol exposure, the liver (containing pentachlorophenol residues of 0.067 ug/g), kidney, brain, spleen, & fat (0.013 ug/g) appeared to be major deposition sites. In the mouse, the gall bladder is a principal storage site. In the rat, it is the kidney.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 385] **PEER REVIEWED**
  • Since the ambient concentrations of PCP in the water of natural aquatic environments are usually less than 1 ug/L ..., /studies on Rainbow trout at low concn are/ of particular importance ... Realistic concn /were applied/ in exposing rainbow trout (Salmo gairdneri) to < 10 (control), 35, and 660 ng Na-PCP/L, and distinguished between PCP content in liver and gall bladder, the remaining tissues, and whole fish ... Rainbow trout accumulated PCP even when exposed to concn as low as 35 ng Na-PCP/L over prolonged periods. The percentage of PCP stored was highest in the liver and gall bladder. /Na-PCP/[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • Small amounts have been shown to cross the placenta.[Shepard, T.H. Catalog of Teratogenic Agents. 5th ed. Baltimore, MD: The Johns Hopkins University Press, 1986., p. 443] **PEER REVIEWED**
  • Some animal data indicate that there may be long-term accumulation and storage of small amounts of PCP in human beings. The fact that urine- or blood-PCP levels do not completely disappear in some occupationally exposed people, even after a long absence of exposure, seems to confirm this, though the biotransformation of hexachlorobenzene and related compounds provides an alternative explanation of this phenomenon. However, there is a lack of data concerning the long-term fate of low PCP levels in animals as well as in man. Furthermore, no data are available on the accumulation and effects of microcontaminants taken up by man together with PCP.[International Program on Chemical Safety; Health and Safety Guide No. 19: Pentachlorophenol (1989). Available from, as of October 15, 2009: http://www.inchem.org/pages/hsg.html] **PEER REVIEWED**
  • The PCP concentration in human urine has been widely used as an indicator of the PCP body burden, based on the fact that, in man, renal excretion of PCP is the major elimination route. Volunteers excreted 74% of the total dose in urine as PCP, and 12% as PCP glucuronide. About 4% of the total dose was eliminated in the feces. In samples taken from non-occupationally exposed people, two-thirds of the PCP detected in the urine was conjugated.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • The aim of the present study was to understand the placental transfer of polychlorinated biphenyls (PCBs), specific hydroxylated PCB metabolites (OH-PCBs), and pentachlorophenol (PCP) in blood serum, in a birth cohort from eastern Slovakia. During the period 2002-2004, cord blood specimens were collected in parallel with maternal specimens from women delivering in the two eastern Slovak districts of Michalovce and Svidnik/Stropkov. A total of 92 pairs of mother-cord specimens at delivery were selected for this study. 4-OH-CB107, 3-OH-CB153, 4-OH-CB146, 3'-OH-CB138, 4-OH-CB187, and 4'-OH-CB172 were quantified. The median concentrations of Sigma(17)PCBs, Sigma(6)OH-PCBs, and PCP in cord serum were 0.92, 0.33, and 0.69 ng/g wet wt, respectively, and highly correlated with the corresponding maternal serum levels (correlations were R(2) = 0.61, 0.78, and 0.82, respectively). The median cord to mother ratios of the Sigma(17)PCBs, Sigma(6)OH-PCBs, and PCP were 0.18, 0.75, and 1.10, respectively. The median ratio of the Sigma(6)OH-PCBs to the Sigma(17) PCBs in the cord serum was 0.38 from wet wt based concn, which was about four times higher than the ratio of these compounds in maternal serum (0.09). PCP was more abundant than any PCB or OH-PCB congener measured in cord serum. The higher cord to maternal ratios of OH-PCB metabolites as compared with the parent cmpd suggests either a higher placental transfer rate or greater metabolism in the fetus as compared with the maternal compartment. These findings are consistent with their preferential binding to TTR that can cross the placenta. The cord to maternal ratio varies by congener (e.g., 4-OH-CB107 = 0.58, 4-OH-CB146 = 0.74, 3'-OH-CB138 = 1.01).[Park JS et al; Chemosphere 70 (9): 1676-84 (2008). Available from, as of September 30, 2009:] **PEER REVIEWED** PubMed Abstract Full text: PMC2703177
  • The compounds are readily absorbed from the gastroenteric tract and from parenteral sites of injection. /Chlorophenols/[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1615] **PEER REVIEWED**
  • The dependence of bats in Britain on houses as roosts may result in them being exposed to pesticides used in remedial timber treatments. Pentachlorophenol and permethrin are used as a fungicide and a insecticide for timber treatment, respectively. The present study investigated toxicity and distribution in body tissues of these two pesticides in pipistrelle bats. Four groups of nine to ten bats were kept in separate outdoor flight enclosures and were provided with roost boxes treated with either pentachlorophenol only, permethrin, pentachlorophenol/permethrin mixture or solvent only (control). At the start of the experiment, mean (: standard error) pentachlorophenol and permethrin concentrations on the surface of wooden blocks that had been treated in the same way as roost boxes were 69.32 : 6.76 mg/g (n = 6) and 3.3 : 1.6 mg/g (n = 3), respectively. All bats exposed to pentachlorophenol and pentachlorophenol/permethrin treated boxes died within 24 and 120 hr, respectively; nine out of the ten controls survived the 32 day experimental period (p< 0.001; both groups compared with control). Bats exposed to permethrin treated boxes survived as well as controls. Mean (: standard error) carcass pentachlorophenol concentration (excluding deposits on fur) of bats exposed to pentachlorophenol and pentachlorophenol/permethrin treated boxes was 13.11 : 2.52 ug/g body wt (n = 20). Pentachlorophenol burdens on fur were positively correlated with total weight of Pentachlorophenol in the carcass (p< 0.001). Pentachlorophenol was present in fat depots, liver, kidney and the remainder of the body which, despite containing low pentachlorophenol concentrations, was the main pentachlorophenol reservoir (66.4 : 5.0% of carcass pentachlorophenol load; n = 20). Total pentachlorophenol in the carcass was significantly correlated with lipid weight (p< 0.005). Permethrin was not detectable in body washes and tissues of bats exposed to pentachlorophenol/permethrin mixture or permet.[Shore RF et al; Environ Pollut 73 (2): 101-18 (1991)] **PEER REVIEWED** PubMed Abstract
  • The excretion and conjugation of chlorophenols were studied in workers exposed to 2,4,6-tri-, 2,3,4,6-tetra-, and pentachlorophenolates, the main components of the chlorophenolate product manufactured by direct chlorination of phenol. The workers were exposed in two different saw mills in which sodium chlorophenolate was used for treatment of lumber during the warm season. Urine specimens were collected at the end of the treatment season as well as at the start of a new treatment period in the spring. Serum specimens were collected towards the end of the treatment period. Total and unconjugated chlorophenols were analyzed with a GC method. The maximal concentrations of urinary 2,4,6-tri-, 2,3,4,6-tetra- and pentachlorophenol at the end of the lumber-treatment period were 1-11.8, 3.4-17.3, and 0.2-0.9 umol/L, respectively, and the average apparent half-times calculated using a one compartment model were 18 hr, 4.3 days and 16 days, respectively. For 2,3,4,6-tetrachlorophenol, the data of some subjects showed a better fit with a two compartment model; the corresponding half-times were 5.3 and 26 days. During the continuous-exposure period the average serum levels of tetra- and pentachlorophenol were rather similar before and after the working day: 2.79 + or - 1.78 umol/L for tetrachlorophenol and 0.85 + or - 0.4 umol/L for pentachlorophenol. Renal clearance values for tetra- and pentachlorophenol were related to urine flow and indicated tubular reabsorption. At low concentrations, sulfate conjugation was dominant. With increasing chlorophenol concentrations the proportion of glucuronide conjugation was increased, especially for pentachlorophenol.[Pekari K et al; Int Arch Occup Environ Health 63 (1): 57-62 (1991)] **PEER REVIEWED** PubMed Abstract
  • Unless renal and liver functions are impaired, pentachlorophenol is rapidly eliminated from blood and tissues.[Morgan, D.P. Recognition and Management of Pesticide Poisonings. EPA 540/9-80-005. Washington, DC: U.S. Government Printing Office, Jan. 1982., p. 22] **PEER REVIEWED**
  • Urine from 230 Finnish sawmill workers exposed to a combination of 2,3,4,6-tetrachlorophenol (80%), 2,4,6-trichlorophenol (10-20%), and pentachlorophenol (5%), was analyzed for the sum of the three chemicals as chlorophenols. Samples were collected at the end of the work shift. Workers were divided into the following exposure groups according to work tasks: primarily skin exposure (n= 112), primarily respiratory tract exposure (n= 34), and equal exposure by both routes (n= 84). Air concentrations at the workplace and amount of time spent with skin contact were not studied. There was no control group; values were compared to the nonexposed Finnish population level of < 0.1 umol/l. Skin absorption was the most effective route of exposure as reflected by urinary chlorophenol concentrations. The median concentration in workers with skin absorption was 7.8 umol/l (range 0.1 to 210.9 umol/l) and was significantly different from that in workers with the respiratory tract as the main route of exposure (median concentration 0.9 umol/l; range 0.1 to 13.3 umol/l; p< 0.001) and from those with both routes of equal importance (1.4 umol/l; range 0.1 to 47.8 umol/l; p< 0.001). /Tri-, Tetra-, and Pentachlorophenols/[Lindroos L et al; Int Arch Occupat Environ Health 59 (5): 463-7 (1987)] **PEER REVIEWED**
  • Usually, the highest PCP levels can be found in the urine immediately after exposure. Consequently, the PCP concentrations in the tissues account for only a small fraction of the PCP dose. Experimental studies do not show a uniform distribution pattern of PCP, but indicate that very high levels can be found in the liver and kidneys. After chronic exposure, most PCP is absorbed by the central nervous system. In rats, the amount of PCP that crosses the placenta is very low. There is an indication that, due to enterohepatic circulation, conjugated PCP is transferred to the gall bladder and bile. Autopsies performed in people who have died from PCP intoxication show that PCP levels in the liver, kidneys, and lungs are often elevated. The high levels in the lungs might be caused by uptake of PCP by inhalation. In general, PCP levels in various tissues do not clearly indicate accumulation of PCP, because PCP levels in the blood are often similar to the levels in the tissues ...[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • When worker exposure to pentachlorophenol at wood treatment plant was measured over 5 month period, serum and urine levels ... were 348.4 to 3963 ug/L and 41.3 to 760 ug/L, respectively. Pentachlorophenol residues in workplace air were in the range of 5.1 to 15275.1 ng/cu m.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V20 309 (1979)] **PEER REVIEWED**

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Metabolism/Metabolites

  • ... Major metabolite of HCB /hexachlorobenzene/ ... .[The Royal Society of Chemistry. Foreign Compound Metabolism in Mammals. Volume 6: A Review of the Literature Published during 1978 and 1979. London: The Royal Society of Chemistry, 1981., p. 327] **PEER REVIEWED**
  • ... Most of pentachlorophenol transferred to hepatopancreas /in goldfish/ was detoxified by sulfate conjugation or by decomposition. Excretion ... was in form of conjugate identified as pentachlorophenylsulfate.[Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2. Washington, DC: U.S. Government Printing Office, 1978., p. 221] **PEER REVIEWED**
  • ...A 60% recovery in urine /was observed/ from i.v. or oral administration of 2.5 mg/kg pentachlorophenol, mainly as conjugated pentachlorophenol and conjugated tetrahydroquinone. ...While previous work in humans has shown the absence of formation of the tetrahydroquinone metabolite, newer published literature indicates formation of this metabolite both in vitro as well as in vivo.[USEPA/Office of Pesticide Programs; Pentachlorophenol-Toxicology Chapter for the Reregistration Eligibility Decision Document. p.25 Identification Number: EPA-HQ-OPP-2004-0402-0104 (August 2008). Available from, as of October 15, 2009: http://www.regulations.gov/search/Regs/home.html#home] **PEER REVIEWED**
  • Bacterial isolate, related to saprophytic coryneform bacteria, was able to metabolize pentachlorophenol as sole source of carbon and energy. Pentachlorophenol was rapidly metabolized to CO2. In cultures of Trichoderma virgatum, pentachlorophenol was methylated to form pentachloroanisole. Similarly, pentachloroanisole was formed from pentachlorophenol by Penicillium sp and Cephaloascus fragrans.[Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 288] **PEER REVIEWED**
  • Following single oral dose of pentachloro-(14)C-benzene (0.5 mg/kg) to Rhesus monkeys ... /7% was excreted/ as pentachlorophenol ... in urine.[The Royal Society of Chemistry. Foreign Compound Metabolism in Mammals. Volume 6: A Review of the Literature Published during 1978 and 1979. London: The Royal Society of Chemistry, 1981., p. 346] **PEER REVIEWED**
  • In animals, PCP is excreted unchanged and as metabolites which include tetrachlorhydroquinone and glucuronides. In man, PCP is eliminated both unchanged and as the glucuronide. In one study, tetrachlorhydroquinone was found in the urine of two spray-men who were occupationally exposed. This metabolic transformation was confirmed in liver homogenates in humans and rats.[IPCS; Poisons Information Monograph 405: Pentachlorophenol. (May 1989). Available from, as of October 9, 2009: http://www.inchem.org/pages/pims.html] **PEER REVIEWED**
  • Metabolites formed by the microbial transformation of PCP: pentachlorophenol acetate; 2,3,4,5-tetrachlorophenol; 2,3,5,6-tetrachlorophenol; 2,3,4,6-tetrachlorophenol; 2,4,5-trichlorophenol; 2,3,6-trichlorophenol; 2,3,4-trichlorophenol; 2,3,5-trichlorophenol; 2,4,6-trichlorophenol; 3,4-dichlorophenol; 3,5-dichlorophenol; 2,3,4,5-tetrachloroanisole (acetate); 2,3,5,6-tetrachloroanisole (acetate); 2,3,4,6-tetrachloroanisole (acetate); 2,3,5-trichloroanisole; 2,4,5-trichloroanisole; 3,4-dichloroanisole; 3,5-dichloroanisole; 3-chloroanisole; pentachloroanisole; tetrachlorocatechol (diacetate); tetrachlorohydroquinone; tetrachlororesorcinol (diacetate); tetrachlorohydroquinonedimethylether (diacetate); tetrachlorobenzoquinone; trichlorohydroxybenzoquinone; 2,3,6-trichlorohydroquinone; 2,6-dichlorohydroquinone; 2-chlorohydroquinone; tetrachloromuconic acid; beta-hydroxytrichloromuconic acid; (14)CO2; Cl- /From table/[WHO; Environmental Health Criteria 71: Pentachlorophenol (1987) http://www.inchem.org/pages/ehc.html] **PEER REVIEWED**
  • Pentachlorophenol ... is dechlorinated in vivo and in vitro in rat to tetra- and tri-chlorohydroquinone ... Dechlorination is mediated by liver-microsomal enzymes, and their activity is enhanced by pre-treatment with several well-known inducers of cytochrome P450 ... Pharmacokinetic study of single oral dosage (0.1 mg/kg) ... in human subjects ... revealed no metabolites were detected apart from glucuronide of PCP (about 12%).[The Royal Society of Chemistry. Foreign Compound Metabolism in Mammals. Volume 6: A Review of the Literature Published during 1978 and 1979. London: The Royal Society of Chemistry, 1981., p. 327] **PEER REVIEWED**
  • The metabolism of pentachlorophenol and its covalent binding to protein and DNA were tested in the microsomes of Wistar rats of both sexes pretreated with hexachlorobenzene, phenobarbital, 3-methylcholanthrene, or isosafrole. Pentachlorophenol when incubated with microsomes, was converted into tetrachloro-1,2-hydroquinone and tetrachloro-1,4-hydroquinone. Isosafrole increased the rate of conversion 7 times as compared to control microsomes, while hexachlorobenzene, pentachlorophenol and 3-methylcholanthrene increased the rate of conversion 2 to 3 times. The fact that pentachlorophenol and hexachlorobenzene accounted for the production of tetrachloro-1,4-hydroquinone and tetrachloro-1,2-hydroquinone in a ratio of about 2, as compared to a ratio of about 1.3 for 3-methylcholanthrene and isosafrole, and the fact that this ratio decreased with increasing concentrations of pentachlorophenol in microsomes from hexachlorobenzene treated rats, were indicative of the involvement of the various cytochrome p450 isoenzymes. The covalent binding of pentachlorophenol to protein was inhibited by ascorbic acid, with a subsequent increase in the production of tetrachlorohydroquinones. The rate of covalent protein binding was constant, regardless of variation in the rate of conversion observed in the mirosomes of rats treated with various inducers. DNA binding was conversion dependent and was lower than protein binding. The addition of DNA did not affect the formation of soluble metabolites.[Van Ommen B et al; Chemico-Biol Interact 60 (1): 1-11 (1986)] **PEER REVIEWED**
  • The metabolism of pentachlorophenol in animals and man was reviewed. Tetrachlorophenols, 2,3,5,6-tetrachloro-1,4-benzoquinone, 2,3,4-trichlorophenol, 2,3,5-trichloro-1,4-hydroquinone, and their glucuronide conjugates were found in animals and man. Also identified were pentachlorophenylacetate, pentachloroanisole, and pentachlorophenylsulfate. The biotransformation of pentachlorophenol in man and animals takes place by conjugation, hydrolytic dechlorination, and reductive dechlorination. Further species dependent reactions are oxidation and methylation. The reaction with glutathione results in the formation of conjugates and cleavage of glycine and glutamate gives cysteine conjugates. Acetylation of the amino group of the cysteinyl moiety in mammals gives mercapturic acids. The metabolic pathways leading to dechlorinated derivatives may be mediated by the reaction with glutathione as the presence of the N-acetyl-S-(pentachlorophenyl)cysteine would indicate. The results of metabolic in vivo studies on hexachlorobenzene, pentachloronitrobenzene, pentachlorobenzene, and pentachlorophenol indicate that one pathway stems from hexachlorobenzene and pentachloronitrobenzene via sulfur containing conjugates to thiophenolic derivatives and to chlorinated benzenes, primarily to pentachlorobenzene. Another pathway transforms pentachlorophenol to less chlorinated phenols. The authors state that pentachlorophenol is a metabolite of various environmental chemicals and is itself metabolized. Therefore there is no direct relationship between the level of pentachlorophenol in body fluids and the degree of exposure.[Renner G, Mucke W; Toxicological and Environmental Chemistry 11 (1): 9-29 (1986)] **PEER REVIEWED**
  • The metabolism of pentachlorophenol is generally similar in mammalian species. In rodents, more than 40% is excreted in urine unchanged. The remainder is excreted as tetrachlorohydroquinone and glucuronide conjugates of pentachlorophenol. In limited studies of humans, pentachlorophenol, tetrachlorohydroquinone, & pentachlorophenol glucuronide have been found in urine. In vivo retention of pentachlorophenol by lipid-containing tissues may be attributable to conjugation with fatty acids.[National Research Council. Drinking Water and Health, Volume 6. Washington, D.C.: National Academy Press, 1986., p. 385] **PEER REVIEWED**
  • The protoporphyrin enzyme peroxidase, detected in snails, catalyzed oxidation of pentachlorophenol to 2,2',3,3',5,5',6,6'-octachlorobiphenylquinone.[Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 287] **PEER REVIEWED**
  • Unchanged pentachlorophenol is excreted in the urine of rabbit, rat, mouse, and monkey. In addition to free pentachlorophenol, rats excrete tetrachloro-p-hydroquinone and trichloro-p-hydroquinone. ... Both metabolites as well as the parent cmpd are excreted free and as glucuronides.[Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 474] **PEER REVIEWED**

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Tsca Test Submissions

  • None found

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Footnotes

1 Source: the NTP's CEBS database.

2 Source: the National Library of Medicine's Hazardous Substance Database, 02/28/2017.

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