540186050
U«iii<3d States
Environmental Protection
Agency
Office of Emergency and
Remedial Response
Washington DC 20460
Off'ce of Research and Development
Office of Health and Environmental
Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
Superfund
&EPA
HEALTH EFFECTS ASSESSMENT
FOR CRESOLS
2? n2?mow*- TWs document
should be retained in the EPA
Region 5 Library Collection
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EPA/540/1-86-050
September 1984
HEALTH EFFECTS ASSESSMENT
FOR CRESOLS
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, DC 20460
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DISCLAIMER
This report has been funded wholly or In part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. It has been subject to the Agency's peer and adminis-
trative review, and 1t has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with cresols.
All estimates of acceptable Intakes and carcinogenic potency presented In
this document should be considered as preliminary and reflect limited re-
sources allocated to this project. Pertinent toxlcologlc and environmental
data were located through on-Hne literature searches of the Chemical
Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The
basic literature searched supporting this document 1s current up to
September, 1984. Secondary sources of Information have also been relied
upon In the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The
following Office of Health and Environmental Assessment (OHEA) sources have
been extensively utilized:
U.S. EPA. 1982. Cresols: Hazard Assessment. Environmental
Criteria and Assessment Office, Cincinnati, OH. Internal draft.
U.S. EPA. 1983b. Reportable Quantity Document for Cresol.
Prepared by the Environmental Criteria and Assessment Office,
Cincinnati, OH, OHEA for the Office of Solid Waste and Emergency
Response, Washington, DC.
The Intent 1n these assessments Is to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited In
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the Interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemlcal(s) addressed.
Whenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer Is not the endpolnt of concern).
The first, the AIS or acceptable Intake subchronlc, 1s an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (I.e., for an Interval that
does not constitute a significant portion of the llfespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants 1n ambient air or water where lifetime exposure 1s
assumed. Animal data used for AIS estimates generally Include exposures
with durations of 30-90 days. Subchronlc human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
111
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The AIC, acceptable Intake chronic, 1s similar 1n concept to the ADI
(acceptable dally Intake). It Is an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the Hfespan [see U.S. EPA (1980) for a discussion of
this concept]. The AIC Is route specific and estimates acceptable exposure
for a given route with the Implicit assumption that exposure by other routes
1s Insignificant.
Composite scores (CSs) for noncardnogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development 1s explained 1n U.S. EPA (1983a).
For compounds for which there Is sufficient evidence of carclnogenlcHy,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980). Since cancer 1s a
process that Is not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-|*s have been computed based on oral
and Inhalation data 1f available.
1v
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ABSTRACT
In order to place the risk assessment 1n proper context, the reader 1s
referred to the preface of this document. The preface outlines limitations
applicable to all documents 1n this series as well as the appropriate Inter-
pretation and use of quantitative estimates.
Oral toxldty data for cresols were not located. Therefore, an oral AIC
could not be estimated. Inhalation exposure data were severely limited, but
an Inhalation AIC of 7.14 mg/day was estimated based on the TLV. This
estimate should be reviewed as additional data become available. A CS for
cresols of 21.2 based on data for bone marrow depression 1n rats exposed via
Inhalation was calculated.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball wasithe Project
Officer. The final documents In this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of Air Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
4.
5.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL
INHALATION
Page
, , , 1
, , , 3
. . . 3
3
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 4
3.1.
3.2.
3.3.
3.4.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation
OTHER RELEVANT DATA
WEIGHT OF EVIDENCE
REGULATORY STANDARDS AND CRITERIA
4
. . . 4
. . . 4
, , 6
. . . 6
. . . 6
. . . 6
. . . 6
6
6
. . . 8
8
. . . 8
. . . 8
. . . 8
. . . 8
. . . 8
. . . 8
. . . 8
. . . 9
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TABLE OF CONTENTS (cont.)
Page
6. RISK ASSESSMENT 10
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS) 10
6.1.1. Oral 10
6.1.2. Inhalation 10
6.2. ACCEPTABLE INTAKE CHRONIC (AIC) 10
6.2.1. Oral 10
6.2.2. Inhalation 10
6.3. CARCINOGENIC POTENCY (q^) 12
6.3.1. Oral 12
6.3.2. Inhalation 12
7. REFERENCES 13
APPENDIX: Summary Table for o-, m- and p-Cresol 17
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
AIC Acceptable Intake chronic
AIS Acceptable Intake subchronlc
BCF B1oconcentrat1on factor
CAS Chemical Abstract Service
CNS Central nervous system
CS Composite score
EKG Electrocardiogram
GI Gastrointestinal
LOAEL Lowest-observed-adverse-effect level
MED Minimum effective dose
RQ Reportable quantity
RV(j Dose-rating value
RVe Effect-rating value
TLV Threshold limit value
TWA Time-weighted average
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties of o-cresol (CAS No.
95-48-7), m-cresol (CAS No. 108-39-4) and p-cresol (CAS No. 106-44-5), and
the half-lives for the nonlsomer specific cresols are given 1n Table 1-1.
The half-life of cresols 1n aquatic media has been estimated from the
estimated half-life of 2 days for chlorocresols 1n river water (Zoeteman et
al., 1980). Since the half-life of the nonchlorlnated cresols 1s expected
to be shorter than the chlorinated cresols (Mabey et al., 1981), the
half-life for cresols has been estimated to be <2 days In river water.
An estimate for the half-life of cresols 1n soil could not be located 1n
the available literature. B1odegradat1on 1s likely to be the most signifi-
cant fate determining process for these chemicals 1n soils (Medvedev and
Darydov, 1972). Based on the physical and chemical parameters of cresols
(see Table 1-1), 1t 1s possible that these compounds may leach from soil to
groundwater, particularly from soils with low organic carbon content.
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TABLE 1-1
Selected Physical and Chemical Properties and Half-Lives for Cresols
Property
Chemical class:
Molecular weight:
pKa:
Vapor pressure,
mm Hg at 25°C:
Mater
solubility:
pKow:
BCF:
Half-lives of
nonlsomer specific
cresols 1n:
A1r:
Water:
o-Cresol m-Cresol
methylated methylated
phenol phenol
108.13 108.13
10.2 10.01
0.25 0.15
31,000 mg/a, 23,500 mg/9.
at 40°C at 20°C
1.95 1.95
9 9
-3.3 hours
<2 days
(estimated)
p-Cresol Reference
methylated NA
phenol
108.13 Verschueren,
1983
10.17 Weast, 1980
0.11 NIOSH, 1978
24,000 mg/8. Verchueren,
at 40°C 1983
1.95 SRI, 1978
9 Velth
et al., 1979
CupHt, 1980
NA
NA = Not applicable
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1. ORAL
Although specific oral absorption data for o-, m- and p-cresol were not
available, the likelihood that the cresols are absorbed from the GI tract
can be Inferred from acute oral toxldty data (Delchmann and KepHnger,
1981).
2.2. INHALATION
Although specific pulmonary absorption data for o-, m- and p-cresol were
not available, the likelihood that the cresols are absorbed from the lungs
can be Inferred from Inhalation toxldty data (Delchmann and KepHnger,
1981).
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. Pertinent data regarding the subchronlc oral toxldty of
o-, m- and p-cresol to humans and experimental animals could not be located
1n the available literature.
3.1.2. Inhalation. The subchronlc Inhalation studies with o-, m- and
p-cresol have been summarized by U.S. EPA (1982). The discussion of these
studies 1s taken, 1n part, from that document.
Uzhdav1n1 et al. (1972) exposed rats and guinea pigs to o-cresol by
Inhalation at a level of 9 mg/m3, 6 hours/day, 5 days/week, for 2 months,
and subsequently for 4 hours/day, 5 days/week, for 2 months. During the
exposure period, the mean concentration was 9.0+0.9 mg/m3. In the experi-
ment with the rats, the following parameters were measured or observed:
elementary conditioned defensive reflex, leukocyte levels 1n the peripheral
blood, leukold and erythrold elements 1n the bone marrow, and liver function
(measured Indirectly by hexobarbltal narcosis). In the experiments with
guinea pigs, blood counts and electrocardiograms were performed. All the
exposed rats had lost the defensive reflex by the end of the second month.
This parameter was also depressed 1n control rats, but at a slower rate.
The exposed male rats had a greater number of white blood cells 1n the
peripheral blood (~22,000/mm3) than did the controls (~14,000/mm3),
especially by the fourth month of exposure. One month after cessation of
exposure to cresol, the leukocyte count 1n the exposed rats had returned to
essentially control values. In the female rats, no effects on leukocyte
count were described. Bone marrow examination revealed that rats 1n the
experimental groups had a statistically significant decrease 1n the numbers
of elements 1n the erythrold series compared to controls, which was
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reflected 1n a statistically significant difference 1n the Ieuko1d-to-
erythrold ratio (1.3:1 1n exposed rats and 2.1:1 1n controls). The authors
suggested that cresol had an effect on the liver since the duration of
hexobarbltal narcosis was significantly greater In exposed rats than In
controls, 62.0+5.2 minutes versus 37.4+0.7 minutes. In exposed rats there
was a slight decrease 1n the reactivity of the pituitary-adrenal system, but
H was not stated how this was measured.
In guinea pigs, Inhalation exposure to o-cresol had no effect on the
Ieuko1d-to-erythro1d ratio 1n the bone marrow. There were some unspecified
changes 1n the hemoglobin concentration. The wave component of the QRS
complex of the electrocardiogram was slightly decreased 1n exposed guinea
pigs, but 1t was not Indicated when these measurements were taken. Though
the results from this study are difficult to evaluate because the data
presented are Incomplete and lacking In such Information as description of
exposure conditions, numbers of animals used, and control conditions, NIOSH
(1978) believes that the adverse effects found by Uzhdavlnl et al. (1972)
are meaningful since they are 1n general agreement with those reported by
Delchmann and Wltherup (1944) for acute toxldty experiments.
Kurlyandskly et al. (1975) exposed rats to a mixture of o-, m- and
p-cresol by Inhalation at a level of 0, 0.0052 or 0.05 mg/m3 for 90 days
(exposure Interval). No treatment-related effects were seen at the 0.0052
mg/m3 level; however, at the higher dose level, treatment-related effects
Included CNS excitation, denaturatlon of lung protein and decreased body
weight gain. Further details regarding the experimental protocol and
effects were not available in the summaries of this Russian study.
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3.2. CHRONIC
3.2.1. Oral. Pertinent data regarding the chronic oral toxldty of o-,
m- and p-cresol were not- located 1n the available literature.
3.2.2. Inhalation. Pertinent data regarding the chronic Inhalation
toxldty of o-, m- and p-cresol could not be located In the available
literature.
3.3. TERAT06ENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Several human case studies have reported the use of
Lysol®, a cresol-contalnlng solution, as an abortlfaclent (Vance, 1945;
Presley and Brown, 1956). In addition to abortion, Intravaglnal application
of Lysol® produces extensive hemolysls, erosion of blood vessels, kidney
tubular damage, liver necrosis and death (Vance, 1945; Presley and Brown,
1956).
Pertinent data regarding the teratogenldty of o-, m- and p-cresol In
experimental animals following oral exposure could not be located In the
available literature.
3.3.2. Inhalation. Pertinent data regarding the teratogenldty of o-,
m- and p-cresol following Inhalation exposure could not be located 1n the
available literature.
3.4. TOXICANT INTERACTIONS
All three cresol Isomers were Individually tested for tumor-promoting
activity on mouse skin (Boutwell and Bosch, 1959). The skin of female mice
was Initiated with dlmethylbenzanthracene followed by the application of two
drops of a 20% solution of the test cresol 6 times/week for 12 weeks. The
Incidence of papHlomas was 59, 50 and 35% for the o-, m- and p-cresol
Isomers, respectively. Using the same procedure, a 5.7% solution of the
m- and p-cresol Isomers was tested in a 20-week study (Boutwell and Bosch,
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1959). The Incidences of papHlomas were 24 and 29% for the m- and
p-1somers, respectively. None of the mice 1n this study developed skin
carcinomas. The tumor Incidence 1n an Initiated only control group was not
presented in the reviews of this study (Battelle, 1981; U.S. EPA, 1982).
Also, Kaiser (1967) and Bock et al. (1971) demonstrated promoting activity
1n tea and cigarette smoke condensate, both of which contain cresols.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. Pertinent data regarding the carcinogenic effects 1n humans
of oral exposure to o-, m- and p-cresol could not be located In the avail-
able literature.
4.1.2. Inhalation. Pertinent data regarding the carcinogenic effects 1n
humans of Inhalation exposure to o-, m- and p-cresol could not be located In
the available literature.
4.2. BIOASSAYS
4.2.1. Oral. Pertinent data regarding the carcinogenic effects 1n
experimental animals from oral exposure to o-, m- and p-cresol could not be
located in the available literature.
4.2.2. Inhalation. Pertinent data regarding the carcinogenic effects 1n
experimental animals from Inhalation exposure to o-, m- and p-cresol could
not be located 1n the available literature.
4.3. OTHER RELEVANT DATA
Pertinent data regarding the mutagenlcHy of o-, m- and p-cresol could
not be located 1n the available literature.
4.4. WEIGHT OF EVIDENCE
Applying the criteria proposed by the Carcinogen Assessment Group of the
U.S. EPA (Federal Register, 1984) for evaluating weight of evidence for the
cardnogenlclty of the cresols, data were not available regarding the
cardnogenlclty of the cresols In either humans or animals. The cresols
are, therefore, most appropriately classified as Group D (Not classified)
chemicals.
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5. REGULATORY STANDARDS AND CRITERIA
Based somewhat on the subchronlc Inhalation studies of Kurlyandskly et
al. (1975) and Uzhdav1n1 et al. (1972), NIOSH (1978) has recommended a
TLV-TWA of 10 mg/m3 for all Isomers of cresol. AC6IH (1983) recommended a
TLV-TWA of 22 mg/m3 (5 ppm) for all Isomers of cresol, based on analogy to
phenol. The Occupational Safety and Health Administration has set a stan-
dard of 22 mg/m3 (5 ppm) for all Isomers of cresol (Code of Federal Regu-
lations, 1981).
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. The lack of pertinent subchronlc oral toxldty data
precludes the derivation of an AIS for subchronlc exposure to o-, m- and
p-cresol.
6.1.2. Inhalation. At an exposure level of 9 mg o-cresol/m3, 6 hours/
day, 5 days/week for 2 months and then for 4 hours/day, 5 days/week for 2
subsequent months, exposed guinea pigs had unspecified changes 1n EKGs and
exposed rats had CNS effects and blood changes (Uzhdav1n1 et al., 1972).
Rats exposed to a mixture of the three cresol Isomers at a level of 0.05
mg/m3 for 90 days (exposure Interval) had CNS excitation, lung protein
denaturatlon and decreased body weight gain (Kurlyandskly et al., 1975).
The effects seen In these two Russian studies may represent a LOAEL; how-
ever, without any details regarding the severity or type of these changes,
It 1s Impossible to assert that a LOAEL was obtained. Therefore, It would
be Imprudent to use either of these studies to derive a value for an AIS
without further Information.
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. The lack of pertinent chronic oral toxldty data precludes
the derivation of an AIC for chronic exposure to o-, m- and p-cresol.
6.2.2. Inhalation. Chronic Inhalation toxldty data could not be located
In the available literature. For reasons discussed 1n Section 6.1.2., the
subchronlc Inhalation data from the Russian studies of Uzhdavlnl et al.
(1972) and Kurlyandskly et al. (1975) cannot be used to derive an AIC for
chronic Inhalation exposure to cresols.
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U.S. EPA (1982) derived a chronic Inhalation laterlm ADI from the TLV
for cresols, and the same approach will be followed here. NIOSH (1978)
evaluated the toxldty of cresols to determine a TLV to protect the health
of workers. The experiments of Uzhdavlnl et al. (1972) and Kurlyandskly et
al. (1975) were considered Inadequate as a result of the Incomplete presen-
tation of experimental design and the confusing presentation of results. It
was noted, however, that the effects reported were not Inconsistent with
effects observed following acute exposure. Since the exposure levels
reported by Uzhdavlnl et al. (1972) and Kurlyandskly et al. (1975) were
lower than the TLV of 22 mg/m3 (5 ppm) recommended by ACGIH (1979, 1983),
and the ACGIH (1979, 1983) TLV was based primarily by analogy to the toxic
effects of phenol, NIOSH (1978) recommended a TLV of 10 mg/m3. Because of
the limited Information on the chronic Inhalation toxldty of cresols, NIOSH
(1978) did not totally disregard the studies of Uzhdavlnl et al. (1972) and
Kurlyandskly et al. (1975), but did not give them the weight of an
adequately performed toxldty study.
Using the TLV of 10 mg/m3 recommended by NIOSH (1978) for cresols
(singly or as a mixture), a chronic Inhalation Interim AIC for humans can be
derived. The TLV of 10 mg/m3 1s adjusted to units of mg/kg/day by multi-
plying by an assumed human breathing volume of 10 mVday and 5/7 to
convert from a 5-day work week to continuous exposure. This gives a dose of
71.43 mg/day. An uncertainty factor of 10 1s applied to protect the more
sensitive Individuals of a population. This gives a chronic Inhalation AIC
of 7.143 mg/day.
Cresol has been subjected to RQ ranking based on chronic toxldty. Only
one CS was calculated and 1t was based on the effect of depression of eryth-
ropoelsls In the bone marrow of male rats exposed to o-cresol vapor at 9.0
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mg/m3, 6 hours/day, 5 days/week for 2 months and then for 4 hours/day, 5
days/week for an additional 2 months.' A human MED was calculated by expand-
ing to continuous exposure, assuming a human Inhalation rate of 20 mVday
and an absorption factor of 0.5, and by applying an uncertainty factor of 10
to extrapolate from subchronlc to chronic exposure. The human MED of 1.34
mg/day corresponds to an RV. of 5.31. An RV of 4 was chosen to repre-
sent the effect of bone marrow depression. A CS of 21.2, the product of
RVd and RVg, resulted. This 1s 1n agreement with U.S. EPA (1983b).
6.3. CARCINOGENIC POTENCY (q^)
6.3.1. Oral. The lack of cardnogenlclty data precludes the derivation
of a carcinogenic potency for oral exposure to cresols.
6.3.2. Inhalation. The lack of cardnogenlclty data precludes the
derivation of a carcinogenic potency for Inhalation exposure to cresols.
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7. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyg1en1sts). 1979.
Threshold Limit Values for Chemical Substances and Physical Agents 1n the
Workroom Environment with Intended Changes for 1980. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyg1en1sts). 1983.
Threshold Limit Values for Chemical Substances and Physical Agents 1n the
Workroom Environment with Intended Changes for 1984. Cincinnati, OH.
Battelle. 1981. Chemical Hazard Profile on Cresols (Cresyllc Add, Methyl-
phenol). Battelle Columbus Laboratories, Columbus, OH. (Cited 1n U.S. EPA,
1982)
Bock, F.G., A.P. Swain and R.L. Stedman. 1971. Composition studies on
tobacco. XLIV. Tumor-promoting activity of subfractlons of the weak acid
fraction of cigarette smoke condensate. J. Natl. Cancer Inst. 47: 429-436.
(Cited 1n U.S. EPA, 1982)
Boutwell, R.K. and O.K. Bosch. 1959. The tumor-promoting action of phenol
and related compounds for mouse skin. Cancer Res. 19: 413-424. (Cited 1n
U.S. EPA, 1982)
Code of Federal Regulations. 1981. OSHA Safety and Health Standards. 29
CFR 1910.1000.
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CupHt, L.T. 1980. Fate of Toxic and Hazardous Materials In the A1r Envi-
ronment. U.S. EPA, Environmental Sciences Research Laboratory, Office of
Research and Development, Research Triangle Park, NC. EPA 600/3-80-084.
NTIS PB80-221948.
Delchmann, W.B. and M.L. KepHnger. 1981. Phenols and phenolic compounds.
In.: Patty's Industrial Hygiene and Toxicology, G.D. Clayton and F.E.
Clayton, Ed., Vol. IIA, 3rd rev. ed. John Wiley and Sons, Inc., NY.
p. 2597-2601.
Delchmann, W.B. and S.. Wltherup. 1944. Phenol studies—VI. The acute and
comparative toxldty of phenol and o-, m-, and p-cresols for experimental
animals. J. Pharmacol. Exp. Ther. 80: 233-240. (Cited In NIOSH, 1978).
Federal Register, 1984. Environmental Protection Agency. Proposed
guidelines for carcinogenic risk assessment. Federal Register
49:46294-46299.
Kaiser, H.E. 1967. Cancer-promoting effects of phenols 1n tea. Cancer.
20: 614-616. (Cited In U.S. EPA, 1982, U.S. EPA, 1983b.)
Kurlyandskly, B.A., D.P. Partsef and A.R. Chernomorskly. 1975. Methods for
determination of mean dally MPC of tMcresol 1n the atmosphere. 61g. SanH.
5: 85-87. (Rus.) (Cited 1n NIOSH, 1978; U.S. EPA, 1982, U.S. EPA, 1983b.)
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Mabey, W.R., J.H. Smith, R.T. Podoll, et al. 1981. Aquatic Fate Process
Data for Organic Priority Pollutants. U.S. EPA, Monitoring and Data Support
Division, Office of Water Regulations and Standards, Washington, DC. EPA
440/4-81-014.
Medvedev, V.A. and V.D. Darydov. 1972. Transformation of Individual coal-
tar-chem1cal-1ndustry organic products 1n a chernozem soil. Pochvovedenle.
11: 22-28. (CA 78:70618s)
NIOSH (National Institute for Occupational Safety and Health). 1978.
Criteria for a Recommended Standard...Occupational Exposure to Cresol. U.S.
DHEW, PHS, CDC, Cincinnati, OH. p. 117. Publ. No. 78-133.
Presley, J.A. and W.E. Brown. 1956. Lysol-1nduced criminal abortion.
Obstet. Gynecol. 8: 368-370. (Cited 1n NIOSH, T978)
SRI (Stanford Research Institute) International. 1978. A study of Indus-
trial data on candidate chemicals for testing. U.S. EPA, Washington, DC.
EPA 560/5-78-002. NTIS PB-78-284950.
U.S. EPA. 1980. Guidelines and Methodology Used 1n the Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45:79347-79357.
U.S. EPA. 1982. Cresols: Hazard Assessment. Environmental Criteria and
Assessment Office, Cincinnati, OH. Internal draft.
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APPENDIX
Summary Table for o-, m- and p-Cresol
CD
I
Species
Inhalation
AIS
AIC humans
Maximum rats
composite
score
Oral
AIS
AIC
Experimental Effect
Dose/Exposure
10 mg/m3 TLV
9.0 mg/m3 bone
5 hours/day, marrow
5 days/week depression
for 4 months (RVe=4)
(RVd=5.3)
•
Acceptable Intake Reference
(AIS or AIC)
7.14 mg/day NIOSH, 1978
21.2 Uzhdavlnl
et al., 1972
NA
NA
NA = Not available
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