|
Pentachlorophenol
CASRN 87-86-5
Contents
0086
Pentachlorophenol; CASRN 87-86-5
Health assessment information on a chemical substance is included in IRIS only
after a comprehensive review of chronic toxicity data by U.S. EPA health
scientists from several Program Offices and the Office of Research and
Development. The summaries presented in Sections I and II represent a
consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Pentachlorophenol
File On-Line 01/31/1987
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) on-line 02/01/1993
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 07/01/1993
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
Last Revised -- 02/01/1993
The oral Reference Dose (RfD) is based on the assumption that thresholds exist
for certain toxic effects such as cellular necrosis. It is expressed in units
of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily exposure to the human population
(including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime. Please refer to the Background
Document for an elaboration of these concepts. RfDs can also be derived for
the noncarcinogenic health effects of substances that are also carcinogens.
Therefore, it is essential to refer to other sources of information concerning
the carcinogenicity of this substance. If the U.S. EPA has evaluated this
substance for potential human carcinogenicity, a summary of that evaluation
will be contained in Section II of this file.
___I.A.1. ORAL RfD SUMMARY
Critical Effect Experimental Doses* UF MF RfD
-------------------- ----------------------- ----- --- ---------
Liver and kidney NOAEL: 3 mg/kg/day 100 1 3E-2
pathology mg/kg/day
LOAEL: 10 mg/kg/day
Rat Oral Chronic Study
Schwetz et al., 1978
*Conversion Factors: none
___I.A.2. PRINCIPAL AND SUPPORTING STUDIES (ORAL RfD)
Schwetz, B.A., J.F. Quast, P.A. Keelev, C.G. Humiston and R.J. Kociba. 1978.
Results of 2-year toxicity and reproduction studies on pentachlorophenol in
rats. In: Pentachlorophenol: Chemistry, Pharmacology and Environmental
Toxicology, K.R. Rao, Ed. Plenum Press, NY. p. 301.
Only one chronic study regarding oral exposure (Schwetz et al., 1978) was
located in the available literature. Twenty-five rats/sex were administered 1
of 3 doses in the diet. At the 30 mg/kg/day level of treatment, a reduced
rate of body weight gain and increased specific gravity of the urine were
observed in females. Pigmentation of the liver and kidneys was observed in
females exposed at 10 mg/kg/day or higher levels and in males exposed to 30
mg/kg/day. The 3 mg/kg/day level of exposure was reported as a chronic NOAEL.
A number of studies that have investigated the teratogenicity of orally
administered pentachlorophenol in rodents are available in the literature.
Although these studies (Larsen et al., 1975; Schwetz and Gehring, 1973;
Schwetz et al., 1978; Hinkle, 1973) did not reveal teratogenic effects, feto-
maternal toxicity was seen at 30 mg/kg/day (Schwetz and Gehring, 1973). Since
pentachlorophenol apparently does not cross the placental barrier, the
observed fetotoxicity may be a reflection of maternal toxicity (Larsen et al.,
1975). The NOAEL in these studies was concluded to be 3.0 mg/kg/day (U.S.
EPA, 1984), which is the same as for the chronic study reported earlier.
___I.A.3. UNCERTAINTY AND MODIFYING FACTORS (ORAL RfD)
UF -- The 100-fold factor accounts for the expected intra- and inter- species
variability to the toxicity of this chemical in lieu of specific data.
MF -- None
___I.A.4. ADDITIONAL COMMENTS (ORAL RfD)
None.
___I.A.5. CONFIDENCE IN THE ORAL RfD
Study -- High
Data Base -- Medium
RfD -- Medium
The confidence in the chosen study is rated high because a moderate number of
animals/sex were used in each of three doses, a comprehensive analysis of
parameters was conducted, and a reproductive study was also run. Confidence
in the supporting data base is rated medium because only one chronic study is
available. Other subchronic studies provide adequate but weaker supporting
data. The confidence in the RfD is medium. More chronic/reproductive studies
are needed to provide a higher confidence in the RfD.
___I.A.6. EPA DOCUMENTATION AND REVIEW OF THE ORAL RfD
U.S. EPA. 1984. Health Effects Assessment for Pentachlorophenol. Prepared
by the Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial
Response, Washington, DC.
Limited Peer Review and Agency-wide Internal Review, 1984.
U.S. EPA. 1985. Drinking Water Criteria Document for Pentachlorophenol.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking
Water, Washington, DC.
Two external peer reviews and an Agency internal review.
Agency Work Group Review -- 05/20/1985
Verification Date -- 05/20/1985
___I.A.7. EPA CONTACTS (ORAL RfD)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
Last Revised -- 07/01/1993
Section II provides information on three aspects of the carcinogenic
assessment for the substance in question; the weight-of-evidence judgment of
the likelihood that the substance is a human carcinogen, and quantitative
estimates of risk from oral exposure and from inhalation exposure. The
quantitative risk estimates are presented in three ways. The slope factor is
the result of application of a low-dose extrapolation procedure and is
presented as the risk per (mg/kg)/day. The unit risk is the quantitative
estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m
air breathed. The third form in which risk is presented is a drinking water
or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1
in 1,000,000. The rationale and methods used to develop the carcinogenicity
information in IRIS are described in The Risk Assessment Guidelines of 1986
(EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries
developed since the publication of EPA's more recent Proposed Guidelines for
Carcinogen Risk Assessment also utilize those Guidelines where indicated
(Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to
Section I of this IRIS file for information on long-term toxic effects other
than carcinogenicity.
__II.A. EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
___II.A.1. WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification -- B2; probable human carcinogen
Basis -- The classification is based on inadequate human data and sufficient
evidence of carcinogenicity in animals: statistically significant increases
in the incidences of multiple biologically significant tumor types
(hepatocellular adenomas and carcinomas, adrenal medulla pheochromocytomas and
malignant pheochromocytomas, and/or hemangiosarcomas and hemangiomas) in one
or both sexes of B6C3F1 mice using two different preparations of
pentachlorophenol (PeCP). In addition, a high incidence of two uncommon
tumors (adrenal medulla pheochromocytomas and hemangiomas/hemangiosarcomas)
was observed with both preparations. This classification is supported by
mutagenicity data, which provides some indication that PeCP has clastogenic
potential.
___II.A.2. HUMAN CARCINOGENICITY DATA
Inadequate. Gilbert et al. (1990) attempted to study the effects of
exposure to PeCP and other chemical preservatives among a cohort of 182 men
employed in the wood treating industry in Hawaii. The study included both
current and former workers who had experienced a minimum of 3 months of
continuous employment treating wood between 1960 and November 1981. The first
part of the study consisted of a cross-sectional clinical assessment of 88
workers (66 current, 22 former) and 58 nonexposed men employed in other
occupations. Significantly elevated levels of urinary PeCP were found among
the wood treaters but this was not related to any morbidity or mortality
endpoint.
In part two of the study, the authors attempted to compare the mortality
experience of the cohort with that expected in Hawaiian males of the same age.
Only deaths that occurred in Hawaii were ascertained. Six deaths were
observed compared with eight expected. Overall, the authors concluded that
their results do not suggest any clinically significant adverse health effects
nor any increased cancer morbidity or mortality from exposure to PeCP and
other wood preserving chemicals. These conclusions must be seriously
questioned based on the following: inadequate detail of selection for
participation, particularly among the 58 unexposed "controls"; only 50% of
eligible workers participated in the clinical portion which creates the
potential for selection bias; employment eligibility criteria were different
for current versus former workers; the clinical examiner was not blinded as to
the exposure status of participants which raises questions about the presence
of observation bias; the clinical data were presented and analyzed in a
nonstandard way; no details are given about methods used to compute mortality
"rates"; and, failure to ascertain deaths occurring outside of Hawaii. With
over 30% of the original cohort apparently lost to follow-up, the study is of
questionable validity. It cannot be used as evidence of no effect of the
exposures but instead must be viewed as uninformative.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. Two different 90% pure preparations of PeCP were tested in
2-year bioassays in B6C3Fl mice (NTP, 1989). Typical impurities present in
both preparations included tri- and tetrachlorophenol, hexachlorobenzene,
polychlorinated dibenzo-p-dioxins, and polychlorinated dibenzofurans.
Technical grade PeCP (TG-PeCP) is a composite that consisted of equal
proportions of product from Monsanto, Reichold and Vulcan. These specific
products are no longer being produced. The second 90% pure preparation of
PeCP, EC-7 PeCP, differed from TG-PeCP in the level and nature of impurities
present (e.g., EC-7 PeCP contained lower levels of dioxins and dibenzofurans).
TG-PeCP was administered daily in the feed at dose levels of 0, 100, and 200
ppm to groups of 50 male and 50 female B6C3F1 mice for 2 years. The average
doses of TG-PeCP were approximately 17-18 or 35 mg/kg for males and females,
respectively. Two groups of control mice (35/sex) were fed basal diets.
Survival of the mice did not appear to be affected by exposure to TG-PeCP at
any dose level tested. However, it should be noted that survival of the male
control mice (12/35) was low compared with historical control values. The
early deaths were found to be due to urinary tract infections resulting from
injuries sustained during fighting among the group-housed control male mice.
After month 16 of the study, the male mice were singly housed to reduce the
incidence of fighting and consequent high mortality. The incidences of
hepatocellular adenomas and/or carcinomas were significantly increased in male
mice exposed to TG-PeCP when compared with controls; the incidences were 7/32,
26/47 and 37/48 in control, low-dose and high-dose male mice, respectively.
The incidences of benign and malignant pheochromocytomas of the adrenal
medulla were also significantly greater in dosed male mice than in controls;
the incidences were 0/31 in controls, 10/45 in low-dose animals and 23/45 in
the high-dose animals. There was no significant increase in the numbers of
liver tumors or pheochromocytomas in female mice exposed to TG-PeCP. However,
the nonsignificant increase in liver tumors in TG-PeCP exposed females was
considered biologically significant. TG-PeCP- and EC-7 PeCP-exposed females
showed comparable responses in the 100- and 200-ppm dose groups with a marked
increase observed only at 600 ppm in the EC-7 PeCP females. The liver tumor
incidences for TG-PeCP exposed females was 3/33, 9/49 and 9/50, respectively.
Vascular tumors (hemangiomas and/or hemangiosarcomas) were observed in female
mice but not in male mice. Incidences of the hemangiosarcoma tumors were
statistically significantly increased when compared to controls and all were
malignant (0/30, 3/48, 6/46 in the control, low-dose and high-dose females,
respectively).
EC-7 PeCP was administered daily in the feed at dose levels of 0, 100,
200, and 600 ppm (NTP, 1989). The average daily doses of EC-7 PeCP were
approximately 17-18, 34-37, and 114-118 mg/kg, for the low-, mid-, and high-
dose groups, respectively. Two groups of control mice (35/sex) were fed basal
diets. Survival did not appear to be affected by exposure to EC-7 PeCP at any
of the dose levels tested. The incidences of hepatocellular adenomas and/or
carcinomas were significantly increased in dosed male mice exposed to EC-7
PeCP when compared with controls (6/35, 19/48, 21/48, 34/49 in the control,
low-, mid-, and high-dose males, respectively). The incidences of benign and
malignant pheochromocytomas of the adrenal medulla in males were also
significantly greater in treated males than in the controls (1/34, 4/48,
21/48, 45/49 in the control, low-, mid-, and high-dose males, respectively).
There was a significant increase in liver tumors (adenomas and/or carcinomas)
(1/34, 4/50, 6/49 and 31/48 in the control, low-, mid-, and high-dose females,
respectively) and benign and malignant pheochromocytomas in female mice
exposed to EC-7 PeCP at the high-dose only (0/35, 2/49, 2/46, 38/49 in the
control, low-, mid-, and high-dose females, respectively). Vascular tumors
(hemangiomas and/or hemangiosarcomas) were observed in female mice but not in
male mice. The incidence of these latter tumors was statistically
significantly elevated in the high-dose group when compared with controls and
all but one of the tumors was malignant (0/34, 1/50, 3/48, 9/47 in the
control, low-, mid-, and high-dose females, respectively).
In a study reported by BRL (1968) and Innes et al. (1969), 18 male and 18
female crossbred mice were administered 46.4 mg/kg EC-7 PeCP in gelatin by
gavage on days 7 through 28 after birth, followed by administration of 130 ppm
(17 mg/kg/day) EC-7 PeCP in the diet for 18 months. It is not possible to
ascertain whether the EC-7 PeCP used in this study is the same as the EC-7
used in the NTP (1989) study, since the level and nature of the impurities
present in the preparation were not reported by Innes or BRL. Groups of mice
from each strain served as negative or vehicle controls. Results indicated
that there was no difference between the incidence of tumors in the PeCP-
treated group and the control groups. Only tumor incidences were reported, so
it is not known what other toxic effects (if any) may have occurred. This
study is limited for drawing conclusions concerning the carcinogenicity of
PeCP, however, because only one dose level was used. Furthermore, an
insufficient number of animals (according to current guidelines) was studied.
In a chronic oral study on a different species conducted by Schwetz et al.
(1978), groups of 25 Sprague-Dawley rats/sex were fed diets of 0, 8, 23, 77,
or 231 ppm PeCP for 22 (for male) or 24 (for female) months (equivalent to l,
3, 10, or 30 mg PeCP/kg/day). The PeCP preparation used in this study was
reported to be 90% pure, and representative of the commercially available
Dowicide EC-7 PeCP used in the NTP (1989) study. Results from the experiment
indicated that in the high-dose group a reduced rate of body weight gain
(i.e., a 12% lower mean monthly body weight during the last 12 months of the
study) and an increased specific gravity of the urine were observed in
females. Pigmentation of the liver and kidneys was observed in females
exposed at 10 mg/kg/day or higher levels and in males exposed to 30 mg/kg/day.
There was no significant increase in tumor incidence as compared with
controls. A slight increase in pheochromocytomas of the adrenal medulla was
noted at the lower dose levels. Survival was reported to be unaffected by
treatment. Since the high dose (30 mg/kg/day) elicited signs of only mild
toxicity, NTP suggested that the MTD had been reached but not exceeded in this
study.
Catilina et al. (1981) also found no evidence of carcinogenicity in Wistar
rats following subcutaneous administration of purified and technical grades of
PeCP (6 mg/kg/dose). Test compounds were administered 3 times/week for 40
weeks followed by a 3-month post-treatment observation period. The use of
only one dose, the use of an inappropriate route of administration, the
relatively short exposure time, and excessive mortality limit the usefulness
of this study for drawing conclusions concerning the carcinogenicity of PeCP.
In another study, Boutwell and Bosch (1959) applied a 20% solution of
commercial grade PeCP in benzene to the shaved skin of Sutter mice twice
weekly for 13 weeks following an initial exposure with 0.3% DMBA in benzene.
Because of the dose level, frequency and duration of exposure in this study,
only limited conclusions concerning the effectiveness of PeCP as a complete
carcinogen can be made; these results, however, are sufficient to conclude
that PeCP was not a tumor promoter in this assay.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Results from cytogenetic studies provide evidence for the clastogenic
potential of PeCP. In cytogenicity studies with cultured CHO cells, TG-PeCP
produced an increase in chromosomal aberrations in the presence but not the
absence of S9 hepatic homogenate activation. Conversely, SCEs were induced
only in the absence of S9 hepatic homogenate (NTP, 1989).
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Oral Slope Factor -- 1.2E-1 per (mg/kg)/day
Drinking Water Unit Risk -- 3E-6 per (ug/L)
Extrapolation Method -- Linearized multistage procedure
Drinking Water Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 3E+l ug/L
E-5 (1 in 100,000) 3E+O ug/L
E-6 (1 in 1,000,000) 3E-l ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- hepatocellular adenoma/carcinoma, pheochromocytoma/malignant
pheochromocytoma, hemangiosarcoma/hemangioma (pooled incidence)
Test Animals -- mouse/B6C3F1, female
Route -- diet
Reference -- NTP, 1989
Human Equiv- Pooled Hepatocellular
Administered Dose alent Dose and Hemangiosarcoma
ppm (mg/kg)/day (mg/kg)/day Tumor Incidence
----- ----------- ----------- -------------------
Technical grade pentachlorophenol
0 0 0 5/31
100 17 1.4 12/48
200 35 2.7 15/46
Dowicide EC-7 pentachlorophenol
0 0 0 1/34
100 17 1.3 6/49
200 34 2.7 9/46
600 114 8.7 42/49
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
Two different pentachlorophenol preparations induced liver tumors,
pheochromocytomas and hemangiosarcomas in female mice and liver tumors and
pheochromocytomas in male mice. All three tumor types are considered related
to the administration of pentachlorophenol. The hemangiosarcomas, however,
are considered to be the tumor of greatest concern; the EPA Science Advisory
Board found that "these tumors were related to the administration of the
pentachlorophenol formulations tested, occurred in a dose-response manner in
the treated animals, and are morphologically related to known fatal human
cancers that are induced by xenobiotics." Hemangiosarcomas were found only in
female mice. To give preference to the data on hemangiosarcomas and because
some male groups experienced significant early loss, only the female mice are
used in the quantitative risk assessment.
In developing these estimates, benign and malignant tumors are combined;
the liver tumors and pheochromocytomas were mostly benign. The pooled
incidence counts animals with any of the three tumor types. Animals dying
before the first tumor was observed are not considered to be at risk and are
not included in the totals. Equivalent human doses are calculated using a
surface-area adjustment. There are no pharmacokinetic data on
pentachlorophenol. The slope factor is calculated as the geometric mean of
the slope factors for each pentachlorophenol preparation.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
For purposes of comparison, a slope factor of 0.05 can be derived from the
incidence of hemangiosarcomas alone. Also for comparison, a slope factor of
0.5 can be derived from the pooled incidence of liver tumors and
pheochromocytomas in male B6C3F1 mice.
The carcinogenicity assessment is based on results in a single animal
species.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
Not available.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- This assessment is not presented in any existing U.S. EPA
document.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 11/10/1987, 09/22/1988, 10/19/1988, 12/06/1989, 02/08/1990,
08/02/1990
Verification Date -- 08/02/1990
___II.D.3. U.S. EPA CONTACTS (CARCINOGENICITY ASSESSMENT)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_VI. BIBLIOGRAPHY
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
Last Revised -- 03/01/1991
__VI.A. ORAL RfD REFERENCES
Hinkle, D.K. 1973. Fetotoxic effects of pentachlorophenol in the Golden
Syrian Hamster. Toxicol. Appl. Pharmacol. 25: 445.
Larsen, R.V., G.S. Born, W.V. Kessler, S.M. Shaw and D.C. Van Sickle. 1975.
Placental transfer and teratology of pentachlorophenol in rats. Environ.
Lett. 10: 121-128.
Schwetz, B.A. and P.J. Gehring. 1973. The effect of tetrachlorophenol and
pentachlorophenol on rat embryonal and fetal development. Toxicol. Appl.
Pharmacol. 25: 455.
Schwetz, B.A., J.F. Quast, P.A. Keelev, C.G. Humiston and R.J. Kociba. 1978.
Results of 2-year toxicity and reproduction studies on pentachlorophenol in
rats. In: Pentachlorophenol: Chemistry, Pharmacology and Environmental
Toxicology, K.R. Rao, Ed. Plenum Press, NY. p. 301.
U.S. EPA. 1984. Health Effects Assessment for Pentachlorophenol. Prepared
by the Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial
Response, Washiington, DC.
U.S. EPA. 1985. Drinking Water Criteria Document for Pentachlorophenol.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking
Water, Washington, DC.
__VI.B. INHALATION RfC REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Boutwell, R.K. and D.K. Bosch. 1959. The tumor-promoting action of phenol
and related compounds for mouse skin. Cancer Res. 19: 413-424.
BRL (Bionetics Research Laboratories). 1968. Evaluation of the carcinogenic,
teratogenic and mutagenic activities of selected pesticides and industrial
chemicals, Vol. 1. Carcinogenic Study. Prepared for the National Cancer
Institute, Bethesda, MD. NTIS PB-223-159. p. 393.
Catilina, P., A. Chamoux, M.J. Catilina and J. Champeix. 1981. Study of the
pathogenic properties of substances used as wood protectives:
Pentachlorophenol. Arch. Mal. Prof. Med. Trav. Secur. Soc. 42(6): 334-337.
(Fre.)
Gilbert, F., C. Minn, R. Duncan and J. Wilkinson. 1990. Effects of
pentachlorophenol and other chemical preservatives on the health of wood-
treating workers in Hawaii. Arch. Environ. Contam. Toxicol. 19(4): 603-609.
Innes, J.R.M., B.M. Ulland, M.G. Valerio, et al. 1969. Bioassay of
pesticides and industrial chemicals for tumorigenicity in mice. A preliminary
note. J. Natl. Cancer Inst. 42: 1101-1114.
NTP (National Toxicology Program). 1989. Technical Report on the Toxicology
and Carcinogenesis Studies of Pentachlorophenol (CAS No. 87-86-5) in B6C3F1
mice (Feed Studies). NTP Tech. Report No. 349. NIH Publ. No. 89-2804.
Schwetz, B.A., J.F. Quast, P.A. Keeler, C.G. Humiston and R.J Kociba. 1978.
Results of two-year toxicity and reproduction studies on pentachlorophenol in
rats. In: Pentachlorophenol: Chemistry, Pharmacology and Environmental
Toxicology, K.R. Rao, Ed. Plenum Press, NY. p. 301-309.
_VII. REVISION HISTORY
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
03/01/1988 III.A. Health Advisory added
06/30/1988 I.A.6. Documentation year corrected
01/01/1990 II. Carcinogen assessment now under review
01/01/1990 VI. Bibliography on-line
04/01/1990 I.A.2. NOEL corrected to NOAEL in last sentence, 1st paragraph
07/01/1990 I.B. Inhalation RfC now under review
07/01/1990 IV.F.1. EPA contact changed
08/01/1990 III.A.10 Primary contact changed
03/01/1991 II. Carcinogenicity assessment on-line
03/01/1991 VI.C. Carcinogenicity references added
01/01/1992 I.A.7. Primary contact changed
01/01/1992 IV. Regulatory actions updated
02/01/1993 I.A.7. Minor text change
07/01/1993 II.D.3. Primary contact's phone number changed
VIII. SYNONYMS
Substance Name -- Pentachlorophenol
CASRN -- 87-86-5
Last Revised -- 01/31/1987
87-86-5
Chem-Tol
Chlorophen
Cryptogil OL
Dowcide 7
Dowicide EC-7
DP-2, technical
Durotox
EP 30
Fungifen
Glazd penta
Grundier arbezol
1-Hydroxy- 2,3,4,5,6-pentachlorobenzene
Lauxtol
Lauxtol A
Liroprem
NCI-C54933
NCI-C55378
NCI-C55389
NCI-C56655
PCP
Penchlorol
Penta
Pentachloorfenol
Pentachlorofenol
Pentachlorofenolo
Pentachlorophenate
Pentachlorophenol
2,3,4,5,6-Pentachlorophenol.
Pentachlorphenol
Pentaclorofenolo
Pentacon
Penta-Kil
Pentasol
Penwar
Peratox
Permacide
Permagard
Permasan
Permatox
Permatox dp-2
Permatox penta
Permite
Phenol, pentachloro-
Preventol P
Priltox
Santobrite
Santophen
Santophen 20
Sinituho
Term-i-trol
WLN: QR BG CG DG EG FG
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0086.HTM
|
