Health Effects Assessment For Phenol

EPA-540/1-86-007
&EPA
Wimou
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EPA/540/1-86-007
September 1984
HEALTH EFFECTS ASSESSMENT
FOR PHENOL
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 Haste and Emergency Response
Washington, DC 20460
U.S. Environmental Protection Agency
Region V, Library
230 South Dearborn Street
Chicago, Illinois 60604
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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.
0,5. Environmental Protection AgetW.
11
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PREFACE

This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with phenol.
All estimates of acceptable Intakes and carcinogenic potency presented 1n
this document should be considered as preliminary and reflect limited
resources 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 1n 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. 1980b. Ambient Water Quality Criteria for Phenol.
Environmental Criteria and Assessment Office, Cincinnati, OH.
EPA-440/5-80-066. NTIS PB 81-117772.

U.S. EPA. 1985. Health and Environmental Effects Profile for
Phenol. 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 1s to suggest acceptable exposure levels
a 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 1s 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 Hfespan). 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 Is
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 1s 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 (1980a) for a discussion
of this concept]. The AIC 1s 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 (1983).

For compounds for which there 1s sufficient evidence of cardnogenldty,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980a). Since cancer 1s a
process that 1s 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.
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• ABSTRACT

In order to place the risk assessment evaluation 1n proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate Inter-
pretation and use of the quantitative estimates presented.

Only one applicable study was found which addressed the toxlcologlcal
consequences of orally administered phenol. From this subchronlc study an
AIS of 7 mg/day and an AIC of 7 mg/day were estimated based on the approach
suggested by U.S. EPA (1980b). This value 1s supported by descriptive
chronic studies. This acceptable Intake estimate should be reviewed when
adequate chronic data are available.

Inhalation exposure data are similarly limited. A number of subchronlc
animal studies were located, but all were of limited use for risk assessment
as discussed In the text. Based on the TLV and AIS of 13.6 mg/day and an
AIC of 1.4 mg/day have been estimated. A CS of 35 was calculated for the
effects (death and severe hlstopathologlcal lesions) observed 1n guinea pigs
exposed by Inhalation.

All of these estimates should be reviewed when additional data are
available.
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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 was the 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 A1r 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'Offlce
Cincinnati, OH
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TABLE OF CONTENTS

1.
2.

ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL
INHALATION
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
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
Page
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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 11

6.3. CARCINOGENIC POTENCY (q-|*) 11

6.3.1. Oral 11
6.3.2. Inhalation 11

7. REFERENCES 12

APPENDIX: Summary Table for Phenol 17
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ADI
AIC
AIS
CAS
CS
LOAEL
MED
NOAEL
ppm
RVd
RVe
STEL
TLV
TWA
LIST OF ABBREVIATIONS
Acceptable dally Intake
Acceptable Intake chronic
Acceptable Intake subchronlc
Chemical Abstract Service
Composite score
Lowest-observed-adverse-effect level
Minimum effective dose
No-observed-adverse-effect level
Parts per million
Dose-rating value
Effect-rating value
Short-term exposure limit
Threshold limit value
Time-weighted average
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties and environmental fate of
phenol (CAS No. 108-95-2) are summarized below.
Chemical class
Molecular weight
Vapor pressure

Water solubility

Octanol/water
partition coefficient
B1oconcentrat1on factor
Half-lives 1n air and water
monocycllc aromatic alcohol
94.11
0.341 mm Hg at 25°C (Mabey et al.,
1981)
9.3xlO~* mg/8. at 258C (Callahan
et al., 1979)
28.8 (Callahan et al., 1979)

2 (Kobayashl et al., 1979)
15 hours to 9 days (Hendry and
Kenley, 1979; Lee and Ryan, 1979;
Rubin and Alexander, 1983; Scott et
al., 1982)
Phenol will blodegrade completely 1n soil 1n 2-5 days (Baker and
Mayfleld, 1980; Ehrllch et al., 1982; Delflno and Dube, 1976). Because of
Us high water solubility and poor adsorption to soil, phenol Is expected to
have a high soil mobility. Despite the expected high soil mobility,
blodegradatlon 1s sufficiently rapid so that the probability of groundwater
contamination through leaching Is Insignificant (Ehrllch et al., 1982). In
spills or similar cases where high concentrations of phenol may destroy
degrading microblal populations, leaching 1s expected to occur (Ehrllch et
al., 1982; Delflno and Dube, 1976).
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1. ORAL
Pertinent data regarding the oral absorption of phenol could not be
located 1n the available literature.
2.2. INHALATION
Quantitative data regarding the absorption of phenol by Inhalation were
not located 1n the available literature; however, that phenol 1s 1n fact
absorbed by Inhalation can be Inferred from the following studies.
Delchmann et al. (1944) exposed 12 guinea pigs, 15 rats and 6 rabbits to
vapor containing 100-200 mg/m3 phenol 7 hours/day, 5 days/week. After 38
days of treatment, levels of free phenol (1.0 mg/100 ml) and conjugated
phenol (0.4 mg/100 ml) were found 1n the blood of the guinea pigs. After
37 and 88 days of treatment, levels of free phenol and conjugated phenol In
the blood of the treated rabbits were 0.5 mg/100 ml and 0.7 mg/100 ml,
respectively. Blood phenol concentrations were not reported for the rats. 1n
this study.
P1otrowsk1 (1971) exposed human volunteers (seven males, one female) to
vapors of phenol through facemasks (6-20 mg/m3) for 8 hours. Urine
samples taken every 2 hours revealed that 60-80X of the administered dose
was retained throughout the period of exposure, regardless of the level of
exposure. Furthermore, 99i8% of the Inhaled dose was excreted within 16
hours post-treatment.
Ohtsujl and Ikeda (1972) found free phenol and conjugated phenol 1n the
urine of workers exposed to 0-12.5 mg/m3 phenol (estimated from air
samples). Levels of phenol 1n the urine (unspecified 1n NIOSH, 1976),
however, were not dose-dependent. These studies Indicate that phenol Is
readily absorbed by Inhalation.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. In the only study located In the available literature, Dow
Chemical Co. (1976) exposed rats to either 50 or 100 mg/kg/day phenol by
gavage, 135 times for 6 months. Neither the numbers of rats nor the
Intervals between treatments were specified. Rats exposed to 50 mg/kg/ day
were reported to suffer "slight" kidney damage, the nature of which was
unspecified. Rats exposed to the higher level of treatment suffered "some"
unspecified liver and kidney damage. A LOAEL of 50 mg/kg/day can thus be
established on the basis of kidney damage, but this must be done with
caution, because of the lack of details 1n the U.S. EPA (1980b) document.
3.1.2. Inhalation. Three subchronlc Inhalation studies reported by NIOSH
(1976) are summarized 1n Table 3-1.
In the subchronlc study by Delchmann et al. (1944), guinea pigs, rats
and rabbits exhibited a wide range of sensitivities to 100 mg/ms phenol.
Of twelve treated guinea pigs, five died after only 28 days of exposure.
The others had weight loss, signs of paralysis and numerous pathological
changes. In contrast, rats given the same level of exposure for 74 days had
no external or Internal signs of toxldty. Pathological changes 1n the
absence of external signs of toxldty were reported for rabbits exposed to
phenol at a level of 100 mg/m3.
Rats, mice and monkeys exposed by Inhalation to phenol at a level of 19
mg/m3 for 8 hours/day, 5 days/week for 90 days, had no significant adverse
toxic effects when compared with control animals (Sandage, 1961).
In contrast, MukhHov (1964) observed adverse effects of exposure to
phenol 1n rats at the 0.11 mg/m3 and 5.2 mg/m3 levels of exposure. In
this study, however, rats were exposed continuously for 61 days, whereas 1n
the study by Sandage (1961), rats were exposed noncontlnuously for 90 days.

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TABLE 3-1
Subchronlc Exposure to Phenol by Inhalation
Species
Guinea pigs

Rabbits

Rats

Monkeys

Nice

Rats

No. of
Animals
12 treated,
no controls

6 treated.
no controls

IS treated.
no controls

SO treated.
SO controls

10 treated.
10 controls

100 treated.
100 controls
15

Dose
100-200 ng/M*
(26-52 ppm)

100-200 mg/m*
(26-52 ppm)

19 mg/m*
(5 ppm)

19 mg/m*
(5 pp»)
0.0. 0.01 mg/m*
(0.003 ppm).
0.11 mg/m*
(0.03 ppm).
5.2 mg/m*
(1.4 ppm)

Exposure
Period
7 hours/day,
5 days/week
for 28 days

7 hours/day.
5 days/week
for 88 days

7 hours/day.
5 days/week
for 74 days
8 hours/day.
5 days/week
for 90 days

continuous.
61 days

Effects Reference
1
Five deaths; weight loss, signs of Delchmann et al..
paralysis; pathological changes 1944
Included extensive necrosis of
the myocardium, acute lobular
pneumonia, vascular damage.
renal and hepatic damage.
No external signs of toxlclty;
pathological changes Included
lobular pneumonia, chronic
degeneration of pulmonary blood
vessels, liver and kidney damage.
No Internal or external signs
of toxlclty

No significant difference between Sandage. 1961
treated animals and their controls
with respect to kidney function or
hematologlcal or urologlcal variables.
There was a slight gain In body weight
for treated rats and monkeys and
Increased 'endurance* (as Indicated
In stress test) In mice.
No effects at 0.01 mg/m*; extensor Hukhltov. 1964
muscle chronaxy was significantly
different from controls at 0.11 mg/m*.
Blood chollnesterase activity was
slightly Increased at 0.11 mg/m*. but
no other effects were observed.
Animals treated at 5.2 mg/m* were
sluggish, exhibited lower rates of '
weight gain, had significantly In-
creased blood chollnesterase activity.
and had shortened extensor muscle
chronaxy and lengthened flexor muscle
chronaxy.
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Since phenol 1s known to be excreted rapidly and completely after treatment
has been withdrawn (99+8% of the Inhaled dose was excreted within 16 hours
post-treatment 1n human volunteers exposed for 8 hours to 6-20 mg/m3)
(Plotrowskl, 1971), perhaps the animals 1n the Sandage study had enough time
(2-day breaks between 5-day exposures) to "recover" between exposures.
The data provided by Sandage (1961) and Delchmann et al. (1944) cannot
be used In the derivation of an AIS, since dose-response relationships were
not established for a range of doses. The data by Mukhltov (1964) are not
suitable for use 1n quantitative risk assessment, since the period of
exposure was only 61 days.
3.2. CHRONIC
3.2.1. Oral. Heller and Purse!! (1938) exposed rats to phenol by drink-
Ing water at levels ranging from 0-12,000 ppm for either 1 year or two,
three or five generations. Growth, fecundity and general condition were the
variables analyzed throughout the period of treatment. These data are
summarized 1n Table 3-2. However, the lack of pathological examinations or
functional tests In this study precludes the use of these data 1n the
calculation of an AIC for human 1ngest1on of phenol.
3.2.2. Inhalation. Pertinent data regarding chronic exposure to phenol
by Inhalation could not be located 1n the available literature.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenlclty of orally
administered phenol could not be located 1n the available literature;
however, reproductive effects associated with 1ngest1on of phenol were
reported In the study by Heller and Pursell (1938) summarized In Table 3-2.
3.3.2. Inhalation. Pertinent data regarding the teratogenlclty of
Inhaled phenol could not be located 1n the available literature.
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TABLE 3-2

Chronic Oral Exposure of Rats to Phenol via Drinking Watera«D
Dose (ppcn)
Period of Exposure
Effects
0, 100, 500,
1000

3000, 5000

7000, 8000
10,000,
12,000
5 generations

3 generations

2 generations

1 year
<5000 ppm: no effect upon growth,
general health or fecundity

7000 ppm: stunted growth 1n young rats

>8000 ppm: numerous deaths of young
rats (numbers unspecified); abnormal
maternal care

12,000 ppm: no reproduction
1000-12,000 ppm: older rats died more
quickly than controls
aSource: Heller and Pursell, 1938

Numbers of animals were not reported 1n NIOSH, 1976.
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3.4. TOXICANT INTERACTIONS
Pertinent data regarding toxicant Interactions between phenol and other
compounds could not be located In the available literature; however. Chains
(1973) reported that phenol and nitrites could react to form p-n1trosophenol
under 1n vitro conditions.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. Data pertaining to the cardnogenlcHy of Ingested phenol
1n humans could not be located 1n the available literature.
4.1.2. Inhalation. Data pertaining to the carc1nogen1c1ty of Inhaled
phenol 1n humans could not be located 1n the available literature.
4.2. BIOASSAYS
4.2.1. Oral. Data pertaining to the carc1nogen1c1ty of orally adminis-
tered phenol 1n animals could not be located In the available literature.
4.2.2. Inhalation. Data pertaining to the carclnogenlcHy of Inhaled
phenol 1n animals could not be located 1n the available literature.
4.3. OTHER RELEVANT DATA
Phenol was reported to be mutagenlc to Escher1ch1a coll. but only at
concentrations of phenol (0.1-0.2%) that caused a reduction In survival
(0.5-1.7% survival) (Demerec et al., 1951). In an ^ vitro experiment,
phenol Induced mutation 1n gonads of Drosophlla (Hadorn and Nlggll, 1946).
Dickey et al. (1949) reported that phenol was not mutagenlc to Neurospora.
4.4. WEIGHT OF EVIDENCE
IARC has not evaluated the risk to humans associated with oral or
Inhalation exposure to phenol. Applying the criteria for overall weight of
evidence of cardnogenlcHy to humans proposed by the Carcinogen Assessment
Group of the U.S. EPA (Federal Register, 1984) no data are available
regarding cardnogenlcHy of phenol In humans or animals and the chemical Is
most appropriately designated a Group D - Not Classified chemical.
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5. REGULATORY STANDARDS'AND CRITERIA
Based on subchronlc animal studies (Delchman et al., 1944), the American
Conference of Governmental Industrial Hyg1en1sts estab- Ushed a TWA-TLV of
19 mg/m3 and a STEL of 10 mg/m3 (ACGIH, 1983). NIOSH (1976) recommended
a TWA-TLV for a 10-hour workday, 40-hour week of 20 mg/m3, and a 60
mg/m3 celling for a period of exposure not to exceed 15 minutes.
Based on the subchronlc study by Dow Chemical Co. (1976) (discussed In
Section 3.1.1. of this report), and using a safety factor of 500, the U.S.
EPA (1980b) calculated an Interim ADI of 0.1 mg/kg/day or 7.0 mg/man/day for
1ngest1on of phenol. From this Interim ADI, and assuming that 2.0 8.
water/day and 0.0065 kg fish/day (with a bloconcentratlon factor of 1.4) are
consumed by the standard 70 kg man, an Interim ADI for drinking water of 3.5
mg/a/day was calculated. However, since an organoleptlc threshold (taste)
of 0.3 mg/8. was reported, a criterion level for phenol 1n water of 0.3
mg/i was established.
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. Based on the rat study by Dow Chemical Co. (1976), a LOAEL
of 50 mg/kg/day was established (see Section 3.1.1.) for slight kidney
damage. Using this value and an uncertainty factor of 500 following the
judgement of U.S. EPA (1980b), an oral AIS of 7.0 mg/man/day Is derived for
1ngest1on of phenol.
6.1.2. Inhalation. As discussed 1n Section 3.1.2., the available sub-
chronic data are not suitable for use In quantitative risk assessment.
However, the TLV of 19 mg/m3 can be used to estimate an AIS. Applying an
uncertainty factor of 10 and expanding exposure to 7 days/week, the AIS In
mg/day for a 70 kg man would be 13.6.
U.S. EPA (1985) calculated a CS for the effects (death, severe signs of
toxldty and extensive hlstopathologlcal changes) observed 1n guinea pigs
exposed .to atmospheric phenol at 100 mg/m3 7 hours/day, 5 days/week for a
total of 29 exposures (Delchmann et al., 1944). A human MED of 20.8 mg/day
was calculated by expanding to continuous exposure, multiplying by 20 m3
the assumed dally Inhalation volume of humans and an assumed absorption
factor of 0.5. and dividing by an uncertainty factor of 10 to correct from
subchronlc to chronic data. This MED corresponds to an Rv^ of 3.5. The
effects observed are assigned an RV of 10. A CS of 35, the product of
RV., and RV , 1s derived.
d e
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. Only one chronic oral study was located 1n the available
literature. As discussed 1n Section 3.2.2., these Investigators (Heller and
Pursell, 1938) reported only external effects, such as growth rates, general
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condition, and fecundity. Calculation of an oral AIC from these data would
be Imprudent, since no pathological or functional analyses were performed.
Based on the precedent established by U.S. EPA (1980b), the value of 7
mg/day as calculated 1n Section 6.1.1. Is proposed as an Interim oral AIC.
This value should be reevaluated when adequate chronic data are available.
In a similar manner, dividing the subchronlc LOAEL for oral exposure
(Section 6.1.1.) by a factor of 10, and then calculating the CS as described
1n Section 6.1.1., yields a CS of 19 for chronic oral exposure to phenol.
6.2.2. Inhalation. Data pertaining to the chronic toxldty of Inhaled
phenol could not be located In the available literature, and, as discussed
1n Section 3.1.2., the available subchronlc data are not suitable for use 1n
quantitative risk assessment. An Inhalation AIC, however, can be calculated
from the TWA-TLV of 10 mg/m3 established by ACGIH (1983). Assuming a 70
kg man breathes a volume of 10 m9 air per 8-hour workday and works 5
days/week, 8 hours/day, the TLV of 19 mg/m3 Is multiplied by the product
of 10 mVday x 5-7 days/week to arrive at an Inhaled dose of 135.7 mg
phenol/man/day. Dividing this value by an uncertainty factor of 10 to
account for the range of sensitivities In the human population, and an
additional 10 because of animal data which Indicate continuous exposures may
have more severe consequences than discontinuous exposures which are similar
to occupational exposure situations, a AIC of 1.4 mg phenol/man/day can be
established.
Since the AIC was established from a TLV, a CS cannot be established.
6.3. CARCINOGENIC POTENCY (q *)
6.3.1. Oral. The lack of pertinent data regarding the cardnogenlcHy of
Ingested phenol precludes the assessment of carcinogenic risk.
6.3.2. Inhalation. The lack of pertinent data regarding the cardno-
genlcHy of Inhaled phenol precludes assessment of carcinogenic risk.

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7. REFERENCES

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 1983-1984. Cincinnati, OH.
p. 28.

Baker, M.D. and C.I. Mayfleld. 1980. M1crob1al and non-biological decompo-
sition of chlorophenols and phenols 1n soil. Water Air Soil Pollut. 13:
411-424.

Callahan, M.A., M.W. SUmak, N.W. Gabel, et al. 1979. Water-Related
Environmental Fate of 129 Priority Pollutants. Vol. II. Office of Water
Planning and Standards, Office of Water and Waste Management, U.S. EPA,
Washington, DC. EPA 440/4-79-029b.

Chains, B.C. 1973. Rapid nltrosatlon of phenols and Us Implications for
health hazards from dietary nitrites. Nature. 244: 466.

Delflno, J.J. and D.J. Oube. 1976. Persistent contamination of groundwater
by phenol. J. Environ. Sd. Health. All: 345-355.

Delchmann, W.B., K.V. KHzmUler and B.S. WHherup. 1944. Phenol studies.
VII. Chronic phenol poisoning, with special reference to the effects upon
experimental animals of the Inhalation of phenol vapor. Am. J. Clln.
Pathol. 14: 273-277. (Cited 1n NIOSH. 1976)
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Demerec, M., et al. 1951. A survey of chemicals for mutagenlc action on £_.
coll. Am. Natur. 85: 119. (CHed In U.S. EPA, 19805)

Dickey, F.H., G.H. Cleland and C. Lotz. 1949. The role of organic
peroxides 1n the Induction of mutations. Proc. Natl. Acad. Sc1. 35:
581-586. (CUed 1n U.S. EPA, 19805)

Dow Chemical Co. 1976. References and literature review pertaining to
toxlcologlcal properties of phenol. Toxlcol. Res. Lab. (Unpubl. manu-
script) (CHed 1n U.S. EPA, 19805)

Ehrllch, G.G., D.F. GoerhHz, E.M. Godsy and M.F. Hult. 1982. Degradation
of phenolic contaminants In groundwater by anaerobic bacteria: St. Louis
Park, Minnesota. Groundwater. 20: 703-710.

Federal Register. 1984. Environmental Protection Agency. Proposed
guidelines for carcinogenic risk assessment. Federal Register. 49:
46294-46299.

Hadorn, E. and H. N1ggl1. 1946. Mutations 1n Drosophlla after chemical
treatment of gonads 1_n vitro. Nature. 157: 162-163.

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APPENDIX

Summary Table for Phenol

Inhalation
AIS
AIC
Maximum
composite
score
Oral
AIS
AIC
Species Experimental
Dose/Exposure

human TLV = 19 mg/m»
human TLV = 19 mg/ma
guinea pig 100 mg/ma
7 hours/day,
5 days/week for
29 exposures
(RVd = 3.5)

rat LOAEL = 50
mg/kg/day
rat LOAEL = 50
mg/kg/day
Effect

none
none
death, severe
toxlclty and
hlstopatholo-
glcal lesions
(RVe = 10)

slight kidney
damage
slight kidney
damage
Acceptable Intake
(AIS or AIC)

13.6 mg/man/day
1.4 mg/man/day
35

7 mg/man/day
7 mg/man/day
Reference

ACGIH, 1983
ACGIH. 1983
Delchmann
et al.. 1944;
U.S. EPA, 1985
•
Dow Chemical
Co., 1976
Dow Chemical
Co., 1976
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