United States
Environmental Protection
Agencv
FINAL DRAFT
ICAO-CIN-R693
March, 1992
EPA Research and
Development
REPORTABLE QUANTITY DOCUMENT ON CHRONIC TOXICITY
FOR a-CRESOL
Prepared for
Office of Solid Waste
and Emergency Response
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
DRAFT: DO NOT CITE OR QUOTE
NOTICE
This document is a preliminary draft. It has not been formally
released by the U.S. Environmental Protection Agency and should not at this
stage be construed to represent Agency policy. It is being circulated for
comments on its technical accuracy and policy implications.

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DISCLAIMER
This report is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
ii

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PREFACE
This report describes the relevant studies used to derive the
reportable quantity for m-cresol. Reportable Quantity (RQ) documents are
prepared for the Office of Solid Waste and Emergency Response (OSWER) by the
Office of Health and Environmental Assessment (OHEA). They are intended to
provide health-related limits for emergency actions under Section 101 of the
Comprehensive Emergency Response, Compensation and Liability Act (CERCLA).
The RQ value of 1, 10, 100, 1000 or 5000 pounds is used to determine the
quantity of a hazarduous substance for which notification is required in the
event of a release as specified by CERCLA. This series of RQs is based upon
chronic toxicity, one of six primary criteria used to adjust RQs from their
statutory level of 1 pound. RQs were derived according to the procedures
described in Methodology and Guidelines for Ranking Chemicals Based on
Chronic Toxicity Data (U.S. EPA, 1984).
A previous derivation of an RQ is reported in two U.S. EPA (1983,
1985) documents. This information is included in this report. The original
references were not reviewed, but where necessary, are referred to for
comparison with the values derived from the new data.
The citations summarized in this document were obtained from online
literature searches in the following data bases: HSDB, RTECS, IRIS, TOXLINE
AND TOXLIT of the MEDLARS systems, and CA search of DIALOG. The searches
were performed using the CAS number for m-cresol.
The first draft of this document was prepared by RAO Enterprises, DBA
Integrated Laboratory Systems under contract #68-CO-0059. The document was
subsequently revised by the Environmental Criteria and Assessment Office
after review by the Human Health Assessment Group.
iii

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LIST OF ABBREVIATIONS
CS	Composite score
MED	Minimum effective dose
RQ	Reportable quantity
RVd	Dose-rating value
RVe	Effect-rating value
TAD	Transformed animal dose
iv

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m-CRESOL
(CAS No. 108-39-4)
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Species/Sex:
Route:
MED*:
Effect:
RVd:
RVe:
CS:
RQ:
Reference:
CD Rat/M&F
Oral (gavage)
59.8 mg/day
Behavioral changes including hyperactivity,
excessive urination, piloerection, lacrimation,
transient hypoactivity, salivation and diminished
respiration
2.83
8
22.68
100
U.S. EPA, 1987
~Equivalent human dose
v

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1. TOXICOLOGY
m-Cresol (CAS No. 108-39-4, molecular formula, C7HaO, molecular weight
of 108), is a solid at room temperature, with a melting point of 35°C and
a boiling point of 202°C. It has a phenol-like odor and is soluble in both
water and organic solvents. The compound is one of three closely related
isomers (with o- and p-cresols) that are used in industry, either singly or
in a mixture of the isomers, as chemical intermediates in the manufacture
of a wide range of products. For example, m-cresol, either pure or mixed
with p-cresol, is important in the production of some herbicides and
insecticides. In addition it finds a use as a precursor in the production
of certain antioxidants. Commercially produced mixtures of the cresols, of
which the m-isomer is the major component, are used as solvents for
synthetic resin coatings, such as wire enamels, metal degreasers and cutting
oils.
The toxic responses of animals to m-cresol appear to be focused on
sometimes transient neurochemical effects, of which certain behavioral
changes are the most obvious manifestation. Changes such as these are
described in more detail in the following section of this document. The
evidence relating m-cresol to any form of carcinogenic effect is extremely
sparse, although studies reviewed by the ATSDR (1990) have been identified
which showed that the cresols as a mixture had tumor promotional activity
in the PAH-initiated mouse skin painting system. The U.S. EPA (1991) has
assigned m-cresol to the weight-of-evidence classification C - a possible
human carcinogen. The classification was based upon the development of skin
papillomas in mouse initiation-promotion studies (Boutwell and Bosch, 1959;
Kaiser, 1967; Bock et al., 1971). Although cresols may have an effect on
the etiology of cancer development, these studies, without additional
evidence, are inadequate for the derivation of an RQ.
In the sections that follow, a summary of the nonneoplasmic chronic
toxicologic effects of m-cresol is provided,, in which the toxic effects of
m-cresol at the various effective dose levels are ascribed a rating value
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for the effect (RVe). The summary allows the derivation of the RQ for
chronic toxicity by the mathematical transformation of the human "minimum
effective dose" into a CS based on the value assigned to the chronic effects
observed at the different dose levels. The studies are then evaluated based
on the CSs derived from their various dose levels, and the study that has
the combination of rating values that gives the highest CS is the one that
is specified to form the basis of the derived RQ for chronic toxicity.
1.1. ORAL
In a study by U.S. EPA (1987), which was reviewed and evaluated in a
subsequent report by Rubenstein et al. (1991), 10 male and 10 female CD rats
per treatment group received corn oil solutions of n-cresol (0, 50, 150 or
450 mg/kg/day) by gavage once daily for 13 weeks (Table 1). The animals
were observed for mortality and clinical effects at least twice daily
throughout the study, and body weights and food consumption were recorded
weekly. On study days 2, 7, 14, 30, 60 and 90 the animals were observed for
signs of neurobehavioral toxicity.
Mean food consumption in female rats administered 450 mg/kg/day was
significantly (p<0.01) less than controls for study week 1 only. Reduced
food consumption for the male high-dose group was significant (p<0.05) only
in week 3. No treatment-related changes in body weight were evident. Signs
of neurobehavioral toxicity, such as salivation, occurred in all groups in
a dose-related manner, with an incidence of 8/20 at the 50 mg/kg/day dose
level. Hypoactivity and rapid respiration were present in a dose-related
manner in all treatment groups at all doses tested. Thus, a NOEL for
hypoactivity and rapid respiration was not determined. These symptoms were
more evident during the first few weeks of the study, but then diminished
by study termination. Thus, hypoactivity reached a peak by study week 5
(450 mg/kg/day dose level), but by week 13 only 1-4 animals were affected.
The observed effect of rapid respiration also reached a peak during study
week 5 (450 mg/kg/day dose level), although 8 animals/group still exhibited
rapid respiration at termination. Other behavioral responses at all dose
levels included hyperactivity, myoclonus, labored respiration, low body
posture, lacrimation, piloerection, urine wet abdomen and alopecia.
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TABLE 1
Oral (gavage) Toxicity Summary for m-Cresol Using the CO Rat'
Sex
Nuttier
at
Start
Purity
Dosage/
Exposure
tng/kg/day
Transformed Animal
Dose (TAD")
(mg/kg/day)
Response
Reference
H&F
80
NR
0, 50, 150 and 450
mg/kg/day for 13
weeks
50, 150 and 450
Changes in behavior,
e.g. hyperactivity,
urination,
piloerection,
lacrimation,
transient
hypoactivity,
salivation and
diminished
respiration
U.S. EPA, 1987
H&F
240
NR
0, 50, 150 and 450
mg/kg/day for 13
weeks
150 and 450
Behavioral changes:
lethargy, tremors,
and reduction in body
weight
Dietz et al., 1986
H&F
200
certified
0, 30, 175 and 450
mg/kg/day 5
days/week for 2
generations (F.,
F,) including
gestation for 10
weeks/ generation.
25.7, 150 and
385.7
Death, hypoactivity,
ataxia, lacrimation,
perioral wetness
BRRC, 1989
'This vehicle/physical state was corn oil.
"Reference body weight was 0.35 kg (U.S. EPA, 1980)
NR = Not reported

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Eleven males and 12 females from the control group and 19 males and
25 females from the treatment group were examined following necropsy. No
statistically significant differences from controls were observed in treated
groups for any organ weights, or any organ-to-body weight ratios. A single
incidence of an adenocarcinoma of the mammary gland in one 450 mg/kg/day
female was not considered to be treatment-related.
In an unpublished study by Dietz (1986), which was evaluated and
reviewed by Rubenstein et al. (1991), the oral toxicity of m-cresol in
Sprague-Dawley rats was generally restricted to doses of 450 mg/kg/day. In
the experiment, four groups of 30 male and 30 female rats were given 0, 50,
150 or 450 mg/kg/day m-cresol in corn oil once daily for 13 weeks. Animals
were dosed up to the day before routine necropsy in either test week 7 (10
animals/sex/dose) or test week 14 (all surviving animals). Body weights
were recorded on test day 1 and weekly thereafter, while food consumption
data were collected on a weekly basis.
Morbidity/mortality checks were performed twice daily, and moribund
animals were killed and necropsied. Body weight, food consumption, clinical
chemistry, hematology and organ weight data were analyzed by sex by the one-
way Analysis of Variance test with Dunnett's test employed if a significant
F ratio was found (p<0.05).
Only one animal died during the treatment period from causes that were
not apparent at necropsy. On occasions, lethargy and tremors were seen in
some high-dose males and females, but no other clinical signs of toxicity
were apparent. Reductions in body weight gains were seen for animals
administered 450 mg/kg/day and to a lesser extent 150 mg/kg/day (only males
were affected at the lower dose). Body weights were essentially unaffected
at the low-dose level. Neither hematology nor clinical chemistry parameters
appeared to be altered by m-cresol treatment. In addition, no treatment-
related ophthalmic lesions were observed, and organ weights did not appear
to be affected for treated rats. No necropsy changes were evident in
m-cresol receiving rats compared with controls.
In an unpublished report by Bushy Run Research Center (BRRC, 1988a),
25 timed-pregnant female rats/group were exposed to m-cresol by gavage on
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gestation days 6-15 at doses of 0, 30, 175 or 450 mg/kg/day in corn oil.
Clinical observations were taken daily; maternal body weights on gestation
days 0, 6, 11, 15 and 21 were recorded; and food consumption was measured
throughout gestation. On gestation day 21, sacrificed dams were evaluated
for body weight, liver and gravid uterine weights, number of corpora lutea,
and number and status of implantation sites. All live fetuses were
dissected from the uterus, counted, weighed, sexed and examined for external
malformations and variations, before being decapitated and examined for soft
tissue craniofacial malformations. Intact fetuses in each litter were
eviscerated and examined for skeletal malformations.
There were no signs of developmental toxicity in the fetuses at any
dose level. For example, there were no changes in viability, percent live
fetuses per litter or fetal weight. Forty-six litters in the control group
and 21-24 litters in each of the treatment groups were examined for signs
of fetal toxicity, as described. However, treated groups showed no
significant differences compared with controls in the incidence of
individual malformations, malformations by category, or of total
malformations, nor were there any differences among groups in the incidence
of individual external variations. As there was no evidence of
developmental effects in the fetuses at any dose level, no RQ for chronic
toxicity could be derived for m-cresol from this study.
In a parallel unpublished report by Bushy Run Research Center (BRRC,
1988b), m-cresol was administered to New Zealand White rabbits during
organogenesis with no resulting evidence of developmental toxicity.
Fourteen mated females/group were exposed to at-cresol by gavage on gestation
days 6-18 at doses of 0, 5, 50 or 100 mg/kg/day in corn oil. Clinical
observations were taken daily, maternal body weights on gestation days 0,
6, 12, 18, 24 and 29 were recorded, and food consumption was measured
throughout gestation (days 0-29). On gestation day 29, sacrificed does were
evaluated for body weight, liver and gravid uterine weights, number of
corpora lutea, and number and status of implantation sites. All live
fetuses were dissected from the uterus, counted, weighed, sexed, and
examined for visceral malformations and variations before being decapitated
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and examined for soft tissue craniofacial malformations. All other fetuses
in each litter (50% intact and 50% decapitated) were eviscerated and
examined for skeletal malformations and variations.
Twenty-four litters in the control group and 12-14 litters in each of
the treatment groups were examined. Treated groups showed no significant
differences among groups in the incidence of individual malformations,
malformations by category or of total malformations. Nor were there any
differences among groups in the incidence of individual external variations,
variations by category or of total variations. The number of live fetuses
per litter, the sex ratio, and the fetal weights were also unchanged
throughout the treatment groups. As before, because there is no evidence
of developmental effects in the fetuses at any dose level, no RQ for chronic
toxicity could be derived for m-cresol from this study.
In an unpublished 2-generation subchronic toxicity study (BRRC, 1989),
m-cresol was administered in corn oil by gavage to Sprague-Dawley rats, in
each dosage group, there were 25 male and 25 female rats of two generations,
designated F0 and Fx Doses of 0, 30, 175 or 450 mg/kg/day were
administered to male and females of the F0 generation, for 10 weeks, 5
days/week. Following the prebreeding period, the males and females were
randomly paired and allowed to mate for 3 weeks, to produce the Fx
generation. Dosing of females was continued daily during the mating,
gestation and lactation periods. Males were dosed daily during the mating
period and then sacrificed and necropsied.
At weaning, 25 Fj weanlings/sex/group were randomly selected to
produce the F2 generation and the rest discarded. After weaning of the Fx
pups, all F0 females were necropsied. Fx males and females were subjected
to the same dosing protocol as their parents. Thus the animals received the
compound for a prebreeding period of 11 weeks followed by mating, gestation
and lactation periods. All surviving Fz pups were examined externally, then
euthanized and examined histopathologically following necropsy at weaning.
The F0 and Fj generations were examined intermittently for weight
gain, food consumption, and twice daily for clinical and toxicologic signs.
However, no hematologic or clinical analyses were conducted in this study.
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There was an increase in mortality at the 450 mg/kg/day dose level
compared with controls in both males and females of the F0 and Fx
generation, during the prebreeding period and also in the gestation and
lactation periods (7 out of 25). In addition, there were two deaths in Fx
females receiving the 30 mg/kg/day dose, one during the mating period, and
one during gestation. However, at least one of these deaths was probably
not related to treatment. The number of F2 pup deaths increased at the 450
mg/kg/day dose level on lactation day 14, thereby reducing the pup
lactational index.
There were no treatment-related gross lesions of F2 pups that died
during lactation, or of Fj^ adults at scheduled sacrifice. Similarly, there
were no treatment-related histologic lesions in FL adults that survived to
sacrifice. All of the treatment-related gross and histologic lesions that
were noted for m-cresol were observed in F0 or FL parents that died before
scheduled sacrifice. Thus, the offspring of those high-dose adult rats that
survived through parturition displayed equivalent litter size, sex ratios,
pup body weights and weight gains when compared with controls.
Clinical signs of toxicity at 450 mg/kg/day included hypoactivity,
ataxia, twitches, tremors, prostration, unkempt appearance (males only),
urine stains, audible respiration, perinatal encrustation (FL females only)
and perioral wetness. These signs were observed in all F0 and FL parents
at the highest concentration. In addition, perioral wetness was also
observed in females of the Fj^ generation at 175 mg/kg/day.
Reduced body weight gains and reduced food consumption were apparent
during the 10 weeks of prebreeding, and in the 3 weeks of breeding in males
of the F0 generation at the 450 mg/kg/day dose level. Similar reductions
were observed in F0 females also, but only for the first week of the pre-
breeding and mating periods. There was no change in reproductive
parameters, including gestational lengths. Intermittent reductions in body
weight gain were apparent during the gestation and lactation periods for F0
and Fl females receiving the highest dose. Additionally, Fj^ female pup body
weight and weight gain were affected at the 30 and 450 mg/kg/day doses but
not at 175 mg/kg/day during lactational days 1 and 4.
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1.2.	INHALATION
No toxicologic studies were identified that examined the effects of
m-cresol by the inhalation route.
1.3.	DERIVATION OF THE RQ
Experimental conditions and the results of the studies described in .
this document are summarized in Table 1. Table 2 contains a summary of the
key studies and dosages selected for calculation of Composite Scores (CS).
The following section discusses the rationale for selection of the studies.
In this report RQs are derived from three studies (U.S. EPA, 1987;
Dietz, 1986; BRRC, 1989). An RQ could not be derived from the developmental
toxicity studies using rats and rabbits (BRRC, 1988a,b) because there were
no effects that provided evidence of developmental toxicity in the test
animals at any dose level used.
From the U.S. EPA (1987) study, the behavioral changes including
hyperactivity, urination and piloerection, and the transient hypoactivity,
salivation and diminished respiration observed at the 50 mg/kg/day dose
level were given an RVe of 8. This dose level allowed the calculation of
the MED of 59.8 mg/day, which is equivalent to an RVd of 2.83. These rating
values factored together gave a CS value of 22.68, which is indicative of
an RQ of 100. At the 150 mg/kg/day dose level these same symptoms,
manifested with slightly increased incidence, were again given an RVa of 8.
At this dose level the MED was calculated at 179.5 mg/day, which indicates
an RVd of 2.12. The product of these two rating values gave a CS of 16.96,
which indicates an RQ of 1000. The 450 mg/kg/day dose level produced
similar symptoms to those of the lower doses, and therefore was also given
an RVe of 8. The 450 mg/kg/day dose allowed the calculation of an MED of
538.6 mg/day, equivalent to an RVd of 1.40. The two rating values factored
together gave a CS of 11.20, equivalent to an RQ of 1000.
The Dietz (1986) subchronic study indicating reduction in body weight
gain in males at the 150 mg/kg/day dose level yielded an RVe of 4. The 150
mg/kg/day dose level allowed the calculation of an MED of 179.5 mg/day,
which is equivalent to an RVd of 2.12. The product of the two rating values
at this dose level gave a CS of 8.47, which indicates an RQ of 1000 (see
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TABLE 2
Gavage Composite Scores for Toxicity of m-Cresol Using the Rat
TAD
(mg/kg/day)
Hunan*'"
HED
(mg/day)
RV„
Effect
RV.
cs
RQ
Reference
50
59.8
2.83
Behavioral changes; hyper-
act ivity, urination,
piloerection, lacrimation,
etc.; transient hypoacti-
vity, salivation and dimin-
ished respiration
8
22.68
100
U.S. EPA, 1987
150
179.5
2.12
Reduction in body weight
4
8.47
1000
Dietz, 1986
450
538.6
1.4
Behavioral changes:
lethargy and tremors;
reduction in body weight
7
9.82
1000
Dietz, 1986
385.7
461.7
1.50
Death, hypoactivity,
ataxia, lacrimation, and
perioral wetness
10
15.03
1000
BRRC, 1989
'Calculation: Hunan HED (mg/day) ¦ TAD (mg/day) x (reference human body weight [70 kg]/animal body weight [kg])"'. This calculation
accounts for differences in body size and metabolic rate between hunan and animal models.
"An uncertainty factor of 10 was applied to reflect the derivation of the chronic HED from a subchronic study.

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Table 2). At the 450 mg/kg/day dose level, in addition to body weight gain,
the behavioral changes such as lethargy and tremors justified the choice of
an RVe of 7. The MED at this dose level was calculated at 538.6 mg/day,
which is equivalent to an RVd of 1.40. These two rating values factored
together gave a CS of 9.82, which again indicates an RQ of 1000.
In the BRRC (1988a,b) developmental toxicity studies, the Sprague-
Dawley rats and New Zealand rabbits displayed no evidence of fetal toxicity
at any of the treatment dose levels. Therefore, an RQ for chronic toxicity
could not be established from these studies.
In the 2-generation subchronic toxicity study using rats (BRRC, 1989),
RQs could be derived for two dose levels, 175 and 450 mg/kg/day. The TADs
at these dose levels were 150 and 385.7 mg/kg/day, respectively, taking into
account the change in the dosing regimen from 5 to 7 days/week almost
halfway through the schedule. The MEDs calculated at these levels were
179.54 and 461.69 mg/day, and the RVds were 2.12 and 1.5, respectively. The
RVa at 175 mg/kg/day was chosen to be 7 because of the appearance of
behavioral abnormalities such as hypoactivity, ataxia and perioral wetness.
The single death at this level did not represent a significant increase in
mortality compared with controls. The product of the RVe and the RVd gave
a CS of 14.83, equivalent to an RQ of 1000. The RV8 for the 450 mg/kg/day
dose level is 10 because of the number of deaths in F0 and Fj adults
compared with that in controls. The product of the rating values for effect
and dose at this dose level gave a CS of 15.03, again equivalent to an RQ
of 1000. From the studies summarized above, the highest CS arose from the
U.S. EPA (1987) study, at the 50 mg/kg/day dose level, with a value of
22.68, equivalent to an RQ of 100. This study is therefore specified as the
basis for derivation of the RQ for m-cresol.
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2. REFERENCES
ATSDR (Agency for Toxic Substances and Disease Registry). 1990.
Toxicological Profile for Cresol: o-Cresol, p-Cresol, /n-Cresol. Agency for
Toxic Substances and Disease Registry, Atlanta, GA, U.S. Public Health
Service, U.S. Department of Health and Human Services, Washington, DC.
Bock, F.G., A.P. Swain and R.L. Stedman. 1971. Composition studies on
tobacco. XLIV. Tumor-promoting activity of subfractions of the weak acid
fraction of cigarette smoke condensate. J. Natl. Cancer Inst. 47: 429-436.
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.
BRRC (Bushy Run Research Center). 1988a. Developmental Toxicity Evaluation
of o-, m-, and p-Cresol Administered by Gavage to Sprague-Dawley (CD) Rats.
Unpublished data submitted to U.S. EPA/OTS. Fiche no. OTS0517695.
BRRC (Bushy Run Research Center). 1988b. Developmental Toxicity Evaluation
of o-, m-, and p-Cresol Administered by Gavage to New Zealand White Rabbits.
Unpublished study submitted to U.S. EPA/OTS. Fiche no. OTS0517695.
BRRC (Bushy Run Research Center). 1989. Two-Generation Study of /n-Cresol
(CAS No. 108-39-4) Administered by Gavage to Sprague-Dawley (CD) Rats.
Unpublished study submitted to U.S. EPA/OTS.
Dietz, D. 1986. Subchronic Toxicity of meta Cresol in Sprague-Dawley Rats:
MBA Chemical No. 24. Prepared by Research Triangle Institute, Research
Triangle Park, NC for U.S. EPA, Office of Solid Waste, Washington, DC.
Study No. 5221.07.
Kaiser, H.E.
20: 614-616.
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1967. Cancer-promoting effects of phenols in tea. Cancer.
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Rubenstein, R., C.T. DeRosa, B.R. Sonawane, D.D. Dietz, J.W. Henck and R.A.
Faust. 1991. Subchronic oral toxicity studies with cresol isomers in rats.
Fund. Appl. Toxicol. (Manuscript in preparation)
U.S. EPA. 1980. Guidelines and Methodology Used in the Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45(231): 79347-79357.
U.S. EPA. 1983. Reportable Quantity Document for Cresol. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Solid Waste and
Emergency Response, Washington, DC.
U.S. EPA. 1984. Methodology and Guidelines for Ranking Chemicals Based on
Chronic Toxicity Data. Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of the Emergency and Remedial Response, Washington, DC.
U.S. EPA. 1985. Health and Environmental Effects Profile for Cresols.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste
and Emergency Response, Washington, DC.
U.S. EPA. 1987. Subchronic Neurotoxicity Study in Rats of ortho-, meta-,
and para-Cresol. Office of Solid Waste, U.S. Environmental Protection
Agency, Washington, DC.
U.S. EPA. 1991. Integrated Risk Information System (IRIS). Online.
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH.
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