TECHNICAL REPORT DATA
                            (fttttf rt»d /ntovctioni on the rtvent before completing!
^. REPORT NO.

  EPA/600/8-89/095
4. TITLE AND SUBTITLE
                             a.
  Updated Health Effects Assessment for Phenol
             3. RECIPIENT'S ACCESSION NO
               PB90-142472/AS
                                                           6. REPORT DATE
                                                           •. PERFORMING ORGANIZATION CODE
'. AUTHOR(S)
                                                           I. PERFORMING ORGANIZATION REPORT NO
B. PERFORMING ORGANIZATION NAME AND ADDRESS
                                                           10. PROGRAM ELEMENT NO.
                                                           11. CONTRACT /GRANTNO.
12. SPONSORING AGENCY NAME AND ADDRESS
                                                           13. TYPE OF REPORT AND PERIOD COVERED
 Environmental Criteria  and Assessment Office
 Office of Research  and  Development
 U.S. Environmental  Protection Agency
 Cincinnati. OH  45268	
             14. SPONSORING AGENCY CODE
                EPA/600/22
IS SUPPLEMENTARY NOTES
16. ABSTRACT
   This report  summarizes and evaluates information relevant to a preliminary interim
 assessment of  adverse health effects associated with specific chemicals or  compounds.
 The Office of  Emergency and Remedial Response (Superfund) uses these, documents in
 preparing cost-benefit analyses under Executive Order J2991 for decision-making under
 CERCLA.  All estimates of acceptable intakes  and carcinogenic potency presented in
 this document  should be considered as preliminary and reflect limited resources
 allocated to this project.  The intent in  these assessments is to suggest acceptable
 exposure levels  whenever sufficient data are  available.  The interim values presented
 reflect the relative degree of hazard associated with exposure or risk to the
 chemical(s) addressed.  Whenever possible,  two categories of values have been
 estimated for  systemic toxicants (toxicants for which cancer is not the endpoint of
 concern).  The first, RfD$ or subchronic reference dose, is an estimate of  an exposure
 level that would not be expected to cause  adverse effects when exposure occurs during
 a limited time interval.  The RfD 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 lifespan.   For compounds for which  there is sufficient .evidence of
 carcinogenicity,  qj*s have been computed,  if  appropriate, based on oral and
 inhalation data  if available.
                               KEY WORDS AND DOCUMENT ANALYSIS
                  DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS  C. COSATI Field/Group
11. DISTRIBUTION STATEMENT
  Public
                                              19. SECURITY CLASS (THuKtponi

                                                Unclassified
                                                                         21. NO. Of PAGES
                                              20. SECURITY CLASS fThij jMft)
                                                Unclassified
                           22. PRICE
 PA F«n» 2220-1 (>•*. 4-77)   PRCVIOUI EDITION i» OMOLKTC

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                                            EPA/600/8-89/095
                                            3uly, 1989
          HEALTH EFFECTS ASSESSMENT
                 FOR PHENOL
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
      OFFICE OF RESEARCH AND DEVELOPMENT
    U.S. ENVIRONMENTAL PROTECTION AGENCY
            CINCINNATI, OH  45268

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                                  DISCLAIMER

    This  document  has  been  reviewed  1n  accordance with  the U.S.  Environ-
mental  Protection  Agency's   peer   and administrative  review  policies  and
approved  for  publication.   Mention of  trade names  or commercial  products
does not constitute endorsement or  recommendation for use.
                                      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  In
this  document  should  be  considered  as  preliminary  and  reflect  limited
resources  allocated  to  this  project.   Pertinent  toxlcologlc   and  environ-
mental data were located  through  on-Hne  literature searches  of the TOXLINE,
CANCERLINE  and  the  CHEMFATE/DATALOG  data  bases.   The  basic  literature
searched  supporting  this  document  Is  current  up  to  May 1987.   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.   1980a.    Ambient  Water  Quality  Criteria  Document  for
    Phenol.  Prepared by  the Office  of  Health and Environmental Assess-
    ment,  Environmental  Criteria  and Assessment  Office,  Cincinnati,  OH
    for  the  Office of Water Regulations and Standards,  Washington,  DC.
    EPA-440/5-80-066.  NTIS PB 81-117772.

    U.S.  EPA.   1987.   Health  and  Environmental  Effects  Profile  for
    Phenol.  Prepared by  the Office  of  Health and Environmental Assess-
    ment,  Environmental  Criteria  and Assessment  Office,  Cincinnati,  OH
    for  the  Office of  Solid  Waste and Emergency  Response,  Washington,
    DC.  EPA/600/X-87/121.  NTIS PB 89-132112/AS.

    U.S.   EPA.   1988.    Integrated   Risk   Information   System  {IRIS).
    Reference  dose   (RfD)   for   oral   exposure  for  phenol.    Online.
    (Verification  date  11/16/88).   Office  of Health and  Environmental
    Assessment,    Environmental    Criteria    and   Assessment    Office,
    Cincinnati, OH.

    The  Intent In  these  assessments  Is  to  suggest acceptable  exposure levels
for   noncardnogens   and  risk  cancer   potency  estimates  for  carcinogens
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.
Nevertheless,  the   Interim  values presented  reflect  the relative  degree  of
hazard or  risk associated with exposure to the chemical(s) addressed.

    Whenever  possible,   two  categories  of  values  have  been   estimated  for
systemic  toxicants  (toxicants  for  which  cancer  Is not  the  endpolnt  of
concern).  The  first, RfD$ (formerly AIS)  or subchronlc  reference dose,  Is
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).
                                      111

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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   RFD$   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.   These
values  are   developed  for  both   Inhalation   (RfD$i)  and   oral   (RfOgo)
exposures.

    The  RfD   (formerly  AIC)  1s  similar  In concept  and  addresses  chronic
exposure.  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 llfespan  [see  U.S. EPA  (1980b)  for a discussion of  this concept].   The
RfD  1s route-specific  and  estimates  acceptable  exposure for either  oral
(RfDg)  or Inhalation   (RfDj)  with  the   Implicit  assumption  that  exposure
by other routes Is Insignificant.

    Composite  scores  (CSs)  for  noncardnogens have also  been  calculated
where  data  permitted.   These  values  are  used for  Identifying  reportable
quantities and  the  methodology for  their development  Is  explained  In  U.S.
EPA (1984).

    For compounds for  which there  Is sufficient evidence of  cardnogenlcHy
     and  RfD values are not derived.  For  a  discussion of  risk  assessment
methodology for  carcinogens  refer  to  U.S.  EPA  (1980b).   Since cancer  1s  a
process that  Is  not  characterized  by  a  threshold, any  exposure  contributes
an Increment  of  risk.   For  carcinogens,  q^*s  have been computed,  1f  appro-
priate, based on oral and Inhalation  data  If available.
                                      1v

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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  that  addressed  the  toxlcologlcal
consequences  of   orally  administered  phenol.    From this  chronic   study  an
RfDso  of  42  mg/day  and an  RfDn, of  42  mg/day were estimated  based  on the
approach  suggested  by  U.S.   EPA   (1987).    This  value  Is  supported  by
descriptive  chronic  and  subchronlc  studies.   These   estimates  should  be
reviewed when adequate chronic data are available.

    Inhalation  exposure data   are  more  limited.    A  number of  subchronlc
animal studies were  located,  but all were  Inadequate for risk  assessment  as
discussed  1n  the text.   An RfDgj  and RfDj; were  not  derived.   A  CS of  44
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   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 the following:

    Judith Olsen and Erma Durden
    Environmental Criteria and Assessment Office
    Cincinnati, OH

Technical  support  services  for  the document  series  was provided  by  the
following:

    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.
6.




ENVIRONMENTAL CHEMISTRY AND FATE. . 	
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1. ORAL 	
2.2. INHALATION 	
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 	
3.1. SUBCHRONIC 	 ,
3.1.1. Oral 	 ,
3.1.2. Inhalation 	 ,
3.2. CHRONIC 	 ,
3.2.1. Oral 	
3.2.2. Inhalation 	 ,
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS 	
3.3.1. Oral 	
3.3.2. Inhalation 	
3.4. TOXICANT INTERACTIONS 	
CARCINOGENICITY 	
4.1. HUMAN DATA 	
4.2. BIOASSAYS 	
4.2.1. Oral 	
4.2.2. Inhalation 	
4.3. OTHER RELEVANT DATA 	
4.4. WEIGHT OF EVIDENCE 	
REGULATORY STANDARDS AND CRITERIA 	
RISK ASSESSMENT 	
6.1. SUBCHRONIC REFERENCE DOSE (RfDs) 	
6.1.1. Oral (RfDso) 	
6.1.2. Inhalation (RfDcr) 	
Page
1
, , . 3
. . . 3
. . . 3
4
, , 4
. . . 4
4
. . . 8
. . . 8
. . . 10
. . . 10
, . . 10
. . . 11
. . . 11
. . . 12
. . . 12
. . . 12
. . . 12
. . . 13
, . . 13
. . . 13
. . . 15
. . . 16
, . . 16
. . . 16
. . . 16
       V11

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                           TABLE  OF  CONTENTS  (cont.)

                                                                        Page

     6.2.   REFERENCE DOSE (RfD)	   16

            6.2.1.   Oral (RfD0)	   16
            6.2.2.   Inhalation (RfDj) 	   17

     6.3.   CARCINOGENIC POTENCY (q-\*)	   17

 7.  REFERENCES	  .   18

APPENDIX: Summary Table for Phenol	   25

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                             LIST OF  ABBREVIATIONS
ADI                     Acceptable dally Intake
CAS                     Chemical Abstract Service
CS                      Composite score
OMBA                    Dimethyl benzanthracene
LOAEL                   Lowest-observed-adverse-effect level
MED                     Minimum effective dose
NOAEL                   No-observed-adverse-effect level
ppm                     Parts per million
RfD                     Reference dose
RfDj                    Inhalation reference dose
RfDg                    Oral reference dose
RFDgi                   Subchronlc Inhalation reference dose
RfD$o                   Subchronlc oral reference dose
RV,j                     Dose-rating value
RVe                     Effect-rating value
STEL                    Short-term exposure limit
TLV                     Threshold limit value
TWA                     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                 monocycllc aromatic alcohol

       Molecular weight               94.11

       Vapor pressure                 0.341 mm Hg at 25°C
                                      (Mabey et a!., 1981)

       Water solubility               9.3x10* mg/l at 25°C
                                      (Callahan et al..  1979)

       Density                        1.072 (Dow Chemical Co.,  1976)

       Log Kow:                       1.46 (Hansch and Leo,  1985)

       Log Koc:                       16.2-91 (U.S. EPA, 1987)

       B1oconcentrat1on factor        2 (Kobayash! et al., 1979)

       Half-life 1n
         A1r:                         7-15 hours (Atkinson,  1985;  NLM,  1987)

         Water:                       
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    The  primary  removal  process  for  phenol  1n  water  Is  blodegradatlon.
Degradation will  be faster  In  freshwater systems  than  In estuarlne  waters
and faster  under  aerobic  conditions than anaerobic  conditions.   Photooxlda-
tlon may  also be an  Important  removal mechanism  In humlc waters  where  the
concentration of alkylperoxy radicals 1s significant (NLM,  1987).
    In  air,  phenol  1s  expected  to  react   with  photochemically  generated
hydroxyl  radicals.   Because of  the  lack of  data  on direct  photolysis,  the
atmospheric half-life  reported  above Is for  reaction with  hydroxyl radicals
only.   The  relatively high water solubility of  phenol  suggests  that signifi-
cant amounts  of  this compound would  also be  removed from  the  atmosphere In
precipitation (NLM,  1987).
0007H                               -2-                              07/24/87

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           2.   ABSORPTION  FACTORS  IN  HUMANS  AND  EXPERIMENTAL  ANIMALS
2.1.   ORAL
    Delchmann and  KepHnger  (1981)  reported that phenol  Is  readily  absorbed
following  oral   administration.   Humphrey  et  al.   (1980)   Investigated  the
disappearance of  a 40  mg/kg dose of  14C-phenol from  the  jji  s 11u  Isolated
small  Intestine  of  Sprague-Dawley  rats.   Disappearance  of  radioactivity
appeared to  follow first  order  kinetics with a  half-time of 5.5^0.5 minutes
and a rate constant for Intestinal absorption of 0.127*0.003 m1n-1.
2.2.   INHALATION
    P1otrowsk1  (1971)  exposed  human  volunteers   (seven males, one  female)  to
vapors of  phenol  through facemasks  (6-20  mg/m3) for 8  hours.   By  measuring
respiratory  volume and  the concentration of  phenol  1n  Inspired  and expired
air,  1t was  estimated that 60-80% of  the  Inhaled dose  was  retained  through-
out the period of exposure, regardless  of the Inspired concentration.
    Ohtsujl and  Ikeda  (1972)  found  free phenol  and  conjugated  phenol  1n the
urine of workers  exposed  to  0.0  (7), 0.6 (7),  4.2 (4),  -7.8  (8), 8.8  (8), 9.6
(8)  and  12.5  mg/m3   (7   subjects)  phenol  (estimated   from  air  samples).
Levels of  total phenols  1n  the  urine  varied proportionally  with  the  levels
of  phenol  In  the  atmosphere.   The authors  compared  the  amount of  phenol
Inhaled/hour  with  the  amount  excreted/hour  and  concluded  that phenol  1s
readily absorbed by Inhalation.
0007H                               -3-                              06/20/89

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                3.   TOXICITY  IN HUMANS  AND  EXPERIMENTAL ANIMALS
3.1.   SUBCHRONIC
3.1.1.   Oral.  Subchronlc and chronic  oral  toxIcHy data are  summarized  In
Table  3-1.   In an  unpublished study  conducted by  Dow  Chemical Co.  (1945,
1976)  phenol  was  administered by gavage  (vehicle  not specified) to  rats  at
10,  100 and  200  mg/kg/day   1n  20  dally  doses.   Slight  liver  and  kidney
effects were  reported at  the highest  dose  only.   Subsequently, a total  of
135 doses of  50 and 100 mg/kg/day phenol  was administered by gavage  to  rats
5  days/week  over  a  6-month  period.  At  the  high  dose,  slight liver  and
moderate kidney damage was  observed;  at  the low dose,  only  slight  kidney
damage  was  reported.  A  LOAEL  of 50  mg/kg/day (TWA =  35.7 mg/kg/day)  was
established on the basis of kidney damage (U.S.  EPA,  1988).
    A  90-day  range finding  study  was  conducted by  NCI  (1980)   to  determine
the concentration  of  phenol  to be used  1n F344 rats and  B6C3F1 mice for  a
2-year  cardnogenesls  bloassay.   The  compound  was  administered  1n drinking
water at five concentrations: 0, 100,  300, 1000, 3000 and  10,000 ppm  (0,  19,
57,  190,  570  and  1900  mg/kg bw/day)  (Table 3-1).  Decreased weight  gain
resulting from  rejection of water was  reported  1n both  sexes of both  species
at the highest dose level.  No other  effects  were observed.
    Two  additional  subchronlc  oral  studies  were  mentioned  In  U.S.   EPA
(1987); however, these studies were  available only as English abstracts  from
the foreign literature, details were poorly presented and  the quality of  the
studies was uncertain.
3.1.2.   Inhalation.  Three  subchronlc  Inhalation studies  reported  by NIOSH
(1976) are summarized 1n Table 3-2.
    In  the  subchronlc study  by  Delchmann  et al.  (1944),  guinea pigs,  rats
and  rabbits  exhibited a  wide range  of  sensitivities  to 100 mg/m3 phenol.


0007H                               -4-                              07/21/89

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0007H
-7-
06/20/89

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This dose corresponds to 9.92, 13.27 and  0.44  mg/kg  bw/day phenol  for guinea
pigs,  rats  and  rabbits,  respectively,  assuming U.S.  EPA (1986)  reference
values for  animal  weight  and breathing  rate.   Of 12 treated guinea  pigs,  5
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  toxlclty
were reported for rabbits  exposed to  phenol  at  a  level of 5.48 mg/kg  bw/day.
    Rats, mice  and  monkeys exposed  by  Inhalation  to   phenol  at  levels  of
1.44, 2.94 and 1.53  mg/kg  bw/day respectively, 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,  Mukhltov  (1964)  observed  adverse  effects  of  exposure  to
phenol In rats  at the 0.009 and  0.409  mg/kg bw/day levels of exposure.   In
this study, however,  rats  were  exposed  continuously for 61 days,  whereas  In
the study by Sandage (1961), rats were exposed  noncontlnuously for  90 days.
3.2.   CHRONIC
3.2.1.   Oral.   Four  studies  regarding  the  chronic  toxldty  resulting  from
oral  exposure  to  phenol were  located 1n  the  available literature  and  were
summarized  In  Table  3-1.   In the  NCI   (1980) bloassay (Section  4.2.1.),  a
treatment-related  Increase  In  the Incidence of  chronic kidney  Inflammation
was  reported  1n  high-dose  male and  female rats.   The Incidences  1n  males
were  37/50,  37/50 and  48/52 for  the  control, low  and high doses,  respec-
tively.   The  Incidences  1n  females were  7/50, 13/50,  and 28/50   for  the
control,  low and  high doses,  respectively.   Statistical  significance was not
reported by the  authors, but  the  Fisher  Exact  test  (U.S. EPA, 1987)  revealed
highly   significant   differences   for  the  Incidence   In  high-dose  males
(p=0.00191) and for the Incidence In high-dose females (p=0.00001).

0007H                               -8-                              07/21/89

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    Heller and  Pursell  (1938) administered  phenol  In the  drinking  water  of
rats at  0-12,000 ppm  (0,  14, 70,  140,  420,  700,  980,  1120,  1400  and 1680
mg/kg bw/day) for 1 year or  2,  3 or 5 generations (see Table 3-1).  The lack
of pathological examinations  or  functional  tests  1n  this study precludes the
use  of  these  data  1n  the  calculation  of  an RfDQ  for human  Ingestlon  of
phenol.
    Delchmann and Oesper (1940)  administered six  concentrations of phenol  In
the  drinking water  of rats  for  12 months  (see Table 3-1).   A decreased
weight gain at the two highest dose levels was the only effect reported.
    A teratologlc study of phenol effect was  performed  In  timed-pregnant  CD
rats (NTP,  1983).   Phenol  was administered In distilled water  by gavage  at
0, 30, 60 and 120 mg/kg/day  on  gestation days 6-15.   Groups of 20-22 females
per  dose were  weighed,  observed for signs of  toxlclty  and  sacrificed  on
gestation  day  20.    No  signs   of   maternal   toxlclty   or  any  dose-related
clinical  symptoms   were  observed.   There  were  no   significant  differences
between  treatment   groups  1n  the  number  of  Implantation  sites  or  In  the
number  of  live fetuses   per  litter.   There was  a  small but  significant
Increase  In  the  number  of  prelmplantatlon losses  between  the  30 and  60
mg/kg/day groups  and the  untreated controls  but  not for  the  120 mg/kg/day
group.  However,  since  Implantation takes  place  before  the first treatment,
which  Is  to gestation day 6, no relationship between  phenol  treatment  and
the  number  of  Implantation  sites could  be determined.   A detailed terato-
loglc  examination,  conducted at  sacrifice  on  gestation day  20,  revealed  a
highly  significant  reduction In  fetal   body weight  1n  the   120  mg/kg/day
group.   A   NOAEL   without  maternal  toxlclty  was   determined   to  be  60
mg/kg/day.   These data  were  also  described by 3ones-Pr1ce et  al. (1983a,b)
and are more fully detailed 1n Section 3.3.1.


0007H                               -9-                              07/21/89

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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.   The  teratogenldty  of  phenol  was  Investigated  by  Jones-
Price  et  al.  (1983a,b)  in  both   Sprague-Dawley   CD  rats  and  CD-I  mice.
Phenol, In distilled water (0, 30,  60 or  120 mg/kg/day), was administered by
gavage to timed-pregnant rats  (23/group)  on gestation days 6-15  (Jones-Price
et al.,  1983a).  The animals  were sacrificed  on  day 20  of  gestation.   No
signs  of  maternal toxlclty  were observed.  A  significant Increase  1n  the
proportion of  Utters  with  resorptlon  sites was observed at  the 30 and 60
mg/kg/day  doses,   (p<0.05  and  p<0.01,  respectively),  but not  at  the  120
mg/kg/day level.  The number of  Implantations was significantly  Increased In
the low and medium dose  groups,  however,  and no  differences were observed In
the percentage  of resorptlons per  Utter.   The number  of live  fetuses per
Utter,  sex  ratio of  the Utters,  the percentage of  affected fetuses  per
Utter and the  proportion  of lifters  with dead or  malformed fetuses did not
differ among  treated groups, but average  fetal body weight per  litter showed
a significant dose-related (p<0.001) decrease.   There was  also  a significant
(p<0.01)  difference  between  the  controls  and  the  high-dose  group.   No
structural teratogenlc  effects  resulting  from  administration  of  phenol were
reported.
    Phenol (0,  70, 140  and  280 mg/kg/day) was  administered by gavage  In  a
concurrent study   (Jones-Price  et  al.,  1983b)  to  timed-pregnant CD-I  mice
(31-36/group) on gestation days  6-15.  The dams were  sacrificed  on day 17 of
gestation.   Weight  loss,  tremors, ataxla,  lethargy and  Irritability  were
reported  In high-dose dams.  Other  Indications of maternal toxldty  Included
0007H                               -10-                             07/21/89

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Increased mortality  1n  the high-dose group  (11  vs.  0 In other  groups),  and
statistically significant  dose-related  trends for decreased  body  weight  and
gravid  uterine  weight  that  were   significantly   (p<0.01)   lower   In  the
high-dose group  compared with the  controls.   Numbers of  Implantation  sites
per dam,  fetal   viability  or  structural  abnormalities of  fetuses were  not
significantly different  among groups.   Dose-related decreases  (p<0.001  for
trend) 1n mean  fetal body weight  per Utter were reported;  a significantly
lower (p<0.001)  body  weight  was  reported 1n  the  highest  dose group  compared
with  controls.   The Incidence of  cleft palate  was  0/308,  1/290, 1/280  and
8/214  for   the   0,  70,  140   and  280  mg/kg/day  dose  groups,  respectively;
however,   the differences  were  not  statistically   significant.   The  fetal
effects  occurred at  doses  that  also produced maternal  toxlclty, and  were
probably secondary  to  the maternal  stress.   Reproductive  effects   In  rats
associated  with  Ingestlon  of  phenol  1n rats  were  reported  1n  the  drinking
water study by   Heller  and Pursell (1938)  and are  summarized  In  Table 3-1.
Growth of  offspring was retarded  at >980  mg/kg bw/day; Impaired mothering
and neonated death  occurred  at >1120 mg/kg bw/day;  offspring dying  at  birth
occurred at 1400 mg/kg bw/day; and  there  was no reproduction at  1680  mg/kg
bw/day.
3.3.2.   Inhalation.    Pertinent   data   regarding   the   developmental  or
reproductive toxlclty  of  Inhaled  phenol  were not  located  In the available
literature.
3.4.   TOXICANT  INTERACTIONS
    Pertinent data  regarding  toxicant Interactions  between phenol and  other
compounds were   not  located   In  the  available  literature;  however,  Chains
(1973) reported  that phenol and nitrites could  react to  form  p-nltrosophenol
under 1n vitro conditions.
0007H                               -11-                             07/21/89

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                             4.  CARCINOGENICITY
4.1.   HUMAN DATA
    Data  pertaining  to  the  cardnogenldty  of  phenol  1n humans  were  not
located 1n the available literature.
4.2.   BIOASSAYS
4.2.1.   Oral.  An NCI  (1980) bloassay of phenol was  conducted to test F344
rats and  B6C3F1  mice for possible cardnogenldty.  Phenol was  administered
1n  the  drinking  water  to groups of  50 male  and 50 female rats and  50 male
and 50  female  mice  at concentrations  of 0,  2500 and 5000  ppm  for  103 weeks.
A  dose-related decrease  1n  weight  gain was  reported  1n treated  animals,
which  was attributed   to  decreased  water  consumption.   No  other  clinical
signs  were observed.   Survival was  comparable among  control  and  treated
groups.   Statistically  significant  Increased  Incidences  of  leukemlas   or
lymphomas were  reported In low-dose male rats  compared with  controls.   The
Incidences  1n  high-dose males  were  also higher but  were not  significantly
different  from matched controls.  In  low-dose  male rats,  the  Incidence  of
Interstitial  cell  tumors  of the  testls was  Increased  when  compared with
controls.   Low-dose  male  rats  also had  a  significant  Incidence  of  C-cell
carcinomas  In  the  thyroid  and  pheochromocytomas  In  the   adrenals.    No
Increased  Incidences  of tumors  were  reported  1n female  rats or  1n  female or
male  mice.   Based  on  the high spontaneous  tumor  rate observed  In  matched
controls  and   the  lack  of  a positive  effect  In   the  high-dose groups  the
association  between  phenol  and  cancer  Is  not   clearly established.   NCI
(1980)  concludes  that  phenol  Is  not carcinogenic  under conditions  of  this
bloassay.   It  was   suggested   by  the  reviewers,   however,  that  phenol   be
considered  for  retestlng because of the  equivocal results obtained  In  male
rats.
0007H                               -12-                             06/20/89

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4.2.2.   Inhalation.   Data   pertaining  to  the  cardnogenlclty  of   Inhaled
phenol In animals were not located In the available literature.
4.3.   OTHER RELEVANT DATA
    Phenol was  reported  to  be mutagenlc  to Escherlchla  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  \i± vitro  experiment,
phenol Induced  mutation  In  gonads of  Drosophlla (Hadorn and Nlggll,  1946).
Dickey et al. (1949) reported that phenol was not mutagenlc to Neurospora.
    Negative  results  were reported  with  and without  S-9 In an  assay  using
hlstldlne  auxotrophs  of  Salmonella   typhlmurlum   (Pool   and   Lin,   1982).
Haworth et al.  (1983)  and Florin et al.  (1980)  reported  that phenol  did not
exhibit mutagenlc activity   In  similar  tests  using the  same strains of  £.
typhlmurlum  that  were used  by Pool and  L1n (1982).   Gocke et  al.  (1981),
however,   reported mutagenlc  activity  In  one strain  of S.  typhlmurlum  with
S-9, which was evaluated by  the above Investigators with negative results.
    Boutwell  and  Bosch  (1959)  Investigated  the tumor-promoting ability  of
phenol In  skin  painting experiments with  several  strains of mice and  using
DMBA  as  an Initiator.  Phenol  appeared to  be a weak  complete  carcinogen  In
these  studies.   Phenol  apparently Initiated and promoted  the development  of
skin  papHlomas  and carcinomas,  particularly 1n a  strain of  mice  selected
for  sensitivity  to  DMBA  Initiation   and  croton  oil  promotion.   Similar
results were obtained by Salaman and Glendennlng (1957) 1n strain "S"  mice.
4.4.   WEIGHT OF EVIDENCE
    IARC  has  not  evaluated  the risk to humans  associated  with  oral  or  Inha-
lation exposure to  phenol.   Phenol was  administered  In the drinking  water  of
mice  and  rats  for  2  years  at  levels  of  2500  and 5000  ppm  (NCI,  1980).
0007H                               -13-                             06/20/89

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Statistically  significant  Increased Incidences  of  pheochromocytomas of  the
adrenal medulla, C-cell  carcinoma  of  the thyroid and  leukemlas  or  lymphomas
were reported  1n  male rats at  2500 ppm but  not  at 5000 ppm.   No  Increased
tumor  Incidences were observed  1n  female rats or female and male mice.   NCI
(1980)  concluded  that phenol was  not  carcinogenic  under  the conditions  of
the  bloassay and  It was suggested  that  phenol be  considered  for  retestlng.
Applying  the  U.S.  EPA   (1986)  criteria  for  overall weight  of  evidence  of
cardnogenlclty to  humans,  data  are  Inadequate and  the  chemical  is  most
appropriately  designated a  Group  D  -  Not  Classified  chemical.   This  Is
consistent with the analysis by U.S. EPA  (1987).
0007H                               -H-                             07/21/89

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                     5.   REGULATORY  STANDARDS  AND  CRITERIA

    Based  on  subchronlc  animal  studies  (Delchmann  et  al.,  1944),  the
American  Conference  of  Governmental   Industrial  Hyglenlsts  established  a
TWA-TLV  of  5  ppm  (19  mg/m3)   and  a  STEL  of  10  ppm  (38  mg/m3)  (ACGIH,
1986a,b).  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.   The OSHA (1985) occupational  permissible  exposure limit
for  phenol  1s also  5 ppm  (19  mg/m3).    The  Public  Health Service  drinking
water standard for phenols Is 1.0 vg/l (U.S. DHEW, 1962).
    Based  on  the subchronlc  study  by  Dow Chemical  Co.  (1976) and using  a
safety factor of  500,  the U.S.   EPA (1980a) calculated  an  Interim  ADI  of 0.1
mg/kg/day or 7.0 mg/man/day  for  Ingestlon of  phenol.   From this Interim ADI,
and  assuming  that   2.0  I  water/day  and  0.0065  kg  fish/day   (with a  bio-
concentration  factor  of  2.0) are consumed by the reference  70 kg man,  an
Interim  ADI  for drinking   water  of  3.5  mg/l  was  calculated.   Since  an
organoleptlc  threshold   (taste)  of  0.3  mg/l   was   reported,  however,   a
criterion level for  phenol 1n water  of 0.3 mg/l was established.
0007H                               -15-                             07/21/89

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                             6.  RISK ASSESSMENT
6.1.   SUBCHRONIC REFERENCE DOSE (RfD$)
6.1.1.   Oral  (RfDso).   Based  on  the  rat study  by NTP  (1983),  a NOAEL  of
60  mg/kg/day was established  (see Section  3.1.1.) for  reduced  fetal  body
weight.  U.S.  EPA  (1988) verified a  chronic  RfO  based upon this  same  study
because the  exposure was considered to be  chronic  for  the fetus.   They  chose
a  composite  uncertainty  factor  (UF)  of  100  (10  for  Intraspecles,  10  for
Interspecles).   Medium  confidence  Is placed  1n  this RfDSQ.   Analysis  of
the data regarding the oral toxldty of  phenol  1s  expanded In Section  6.2.1.
6.1.2.   Inhalation   (RfDSI).    As   discussed   1n  Section   3.1.2.,    the
available  subchronlc  data  are not  suitable  for  use  1n quantitative  risk
assessment.
    U.S. EPA (1987) 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).   The  resulting exposure
corresponded  to 4.96  mg/kg/day.    A  chronic  human MED  of  5.6  mg/day  was
calculated,  which   Is  equivalent  to  an  RV.  of  4.4.   An  RV  of  10  was
chosen  to  represent mortality,  the most  severe   effect.   A CS  of  44,  the
product  of  RV.  and RV , results   In  an  RQ  of  10.  The  complete  derivation
of this value 1s presented In U.S.  EPA (1987).
6.2.   REFERENCE DOSE  (RfO)
6.2.1.   Oral  (RfDQ).    As  discussed  In  Section   3.2.1.  and  summarized  In
Table  3-1,  four chronic oral  studies were located In  the  literature.   Data
from  both  the  Heller  and  Pursell (1938)  and Delchmann and  Oesper  (1940)
studies  presented no pathological  or  functional evaluation  and  therefore are
0007H                               -16-                             07/21/89

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unsuitable  for  use  In   risk  assessment.   Based  on  a  verified  analysis
presented by  the U.S. EPA  (1987b),  the LOAEL of  50 mg/kg/day  from  the  Dow
Chemical  Co.   (1945)  study  was  used  as a  basis  for  a  chronic oral  RfD.
Further  review  Indicated  that  a  teratologlc  study  using   rats  would  be
preferable because  the exposure  was  considered to  be chronic  for the fetus.
The LOAEL for  reduced fetal body  weight was determined to be 120 mg/kg/day
and  the  NOAEL  was  60 mg/kg/day.   Applying  an  uncertainty  factor  of  100
results  In  an  RfOQ of 0.6 mg/kg/day  or  42  mg/day  for a 70 kg man  (U.S.
EPA, 1988).   Confidence In this value was rated medium.
6.2.2.   Inhalation  (RfD,).   Data  pertaining  to  the  chronic  toxlclty  of
Inhaled  phenol  were  not  located   1n   the  available  literature,  and,   as
discussed In Section  3.1.2.,  the available subchronlc  data are  not  suitable
for  use  1n  quantitative  risk  assessment.   An   RfD,,  therefore,  Is  not
calculated.
6.3.   CARCINOGENIC POTENCY (q^)
    The  lack  of pertinent  data  regarding  the  carc1nogen1c1ty  of  phenol
precludes the assessment of carcinogenic risk.
0007H                               -17-                             07/21/89

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                                7.  REFERENCES

ACGIH  (American  Conference of  Governmental  Industrial Hyg1en1sts).   1986a.
Threshold Limit  Values  for Chemical  Substances and  Physical  Agents  In  the
Workroom Environment  with Intended Changes  for 1986-1987.  Cincinnati,  OH.
p. 26.

ACGIH  (American  Conference of  Governmental  Industrial Hyglenlsts).   1986b.
Documentation of the Threshold  Limit  Values  and Biological  Exposure Indices,
5th ed.  Cincinnati, OH.  p.  469-471.

Atkinson, R.   1985.   Kinetics and mechanisms  of the gas phase  reactions  of
the  hydroxyl  radical with  organic compounds  under atmospheric  conditions.
Chem. Rev.   85: 69-201.

Baker, M.D. and  C.I. Mayfleld.   1980.   M1crob1al and non-biological decompo-
sition of  chlorophenols and  phenols  1n soil.   Water  A1r Soil  Pollut.   13:
411-424.

Boutwell, R.K. and  K.O.  Bosch.   1959.  The  tumor-promoting action  of  phenol
and  related compounds for  mouse skin.  Cancer  Res.  19:  413-424.   (Cited  In
U.S. EPA, 1987)

Callahan,  M.A.,   M.W.   Sllmak,   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.


0007H                               -18-                             07/21/89

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

Delchmann, W.B. and  M.L.  Kepllnger.  1981.  Industrial toxicology.   Phenols
and phenolic  compounds.   Iin:  Patty's  Industrial Hygiene and Toxicology,  3rd
rev. ed., Vol. 2A,  G.O.  Clayton and F.E.  Clayton, Ed.  John Wiley  and  Sons,
Inc., NY.  p. 2567-2676.

Delchmann, W.  and  P. Oesper.   1940.   Ingestlon of phenol  -- Effects on  the
albino rat.   Ind.  Med.  9: 296.  (Cited In U.S.  EPA,  1987)

Delchmann, W.B., K.V.  Kltzmlller  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.  0.  Clln.
Pathol.  14: 273-277.  (Cited 1n NIOSH, 1976)

Delflno, 0.0.  and D.O. Dube.   1976.   Persistent contamination of  groundwater
by phenol.  0. Environ. Scl.  Health.  All: 345-355.

Demerec, M., et al.   1951.  A  survey  of  chemicals  for mutagenlc action  on £.
coll.  Am. Natur.   85: 119.  (Cited In U.S. EPA, 1980a)

Dickey,  F.H.,  G.H.   Cleland   and   C.  Lotz.    1949.   The   role   of  organic
peroxides  In  the  Induction  of  mutations.   Proc.  Natl.   Acad.   Scl.    35:
581-586.  (Cited  In U.S.  EPA,  1980a)
0007H                               -19-                             07/21/89

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Dow  Chemical   Co.   1945.   The  toxldty  of  phenol.    Blochem.  Res.  Lab.
(Unpublished report  by E.M.  Adams,  4/12/45).   (CHed  In U.S. EPA, 1987)

Dow  Chemical  Co.   1976.    References  and  literature  review  pertaining  to
toxlcologlcal   properties  of  phenol.   Toxlcol.  Res.  Lab.   (Unpubl.  manu-
script)  (Cited 1n  U.S.  EPA, 1980a)

Ehrllch, G.G., D.F. Goerhltz, 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.

Florin,  I.,  L. Rutberg,  M. Curvall and  C.R. Enzell.   1980.   Screening  of
tobacco   smoke  constituents   for   mutagenlclty  using  the   Ames   test.
Toxicology.  15(3):  219-232.  (CUed In  U.S.  EPA, 1987)

Gocke,  E.,  M.T. King,  K.  Eckhardt and  D.  Wild.   1981.  Mutagenlclty  of
cosmetics  Ingredients  licensed  by  the  European  communities.   Mutat.  Res.
90(2): 91-109.  (CHed In  U.S.  EPA,  1987)

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

Hansch,  C.  and A.J.  Leo.  1985.   Medchem Project.   Issue no.  26.  Pomona
College.  Claremont, CA.

Haworth,  S.,   T.  Lawler,  K.  Mortelmans,  W.  Speck  and  B.  Zelger.   1983.
Salmonella mutagenlclty  test  results for  250 chemicals.  Environ. Mutagen.
Suppl.  1: 3-142.   (Cited  In U.S. EPA,  1987)

0007H                               -20-                            07/21/89

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Heller, V.G.  and L.  Purse!!.   1938.  Phenol-contaminated  waters  and their
physiological  action.   J.  Pharmacol.  Exp.  Ther.   63:  99-107.   (CHed 1fi
NIOSH, 1976)

Humphrey,   M.3.,  C.W.  Filer,   D.J.  Jeffery,  P.P. Langley  and  G.A.  Wadds.
1980.  The availability of carfecllUn and Us phenol moiety  In  rat and  dog.
Xenoblotlca.  10(10): 771-778.   (CHed  In  U.S.  EPA, 1987)

Jones-Price, C.,  T.A. Ledoux,  F.R.  Reel, P.M.  Fisher  and L.  Langhoff-Paschke.
1983a.  Teratologlc  evaluation of  phenol  (CAS  No.   108-95-2)   1n  CD rats.
NTIS  PB83-247726,  120 p.   Gov. Rep.  Announce. Index  (U.S.)  1983.   83(25):
6247.

Jones-Price, C.,  T.A.  Ledoux,  J.R.  Reel,  L.  Langhoff-Paschke, M.C. Maur and
C.A. Klmmel.  1983b.  Teratologlc  evaluation of phenol (CAS No.  108-95-2) in
CD-I mice.  September 18,  1980 to  January  12,  1981.  ~NTIS PB85-104451, 99 p.

Kobayashl.  K., H.  Akltake and K.  Manabe.   1979.   Relation between toxlclty
and accumulation  of  various chlorophenols  In goldfish.  Bull. Jap. Soc.  Scl.
Fish.  45: 173-175.

Mabey, W.R.,  J.H.  Smith,   R.T.  Podoll,  et al.   1981.   Aquatic  Fate  Process
Data  for  Organic  Priority Pollutants.   Monitoring  and Data Support Dlv.,
Office of  Water  Regulations and  Standards,  U.S. EPA,  Washington,  DC.   EPA
440/4_81-014.
0007H                               -21-                            07/21/89

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MukhHov, B.  1964.  The effect of low phenol concentrations  of  the  organism
of man or animals and their hygienic evaluation,  in:  USSR  Literature  on  AVr
Pollution  and  Related  Occupational  Diseases  —  A   Survey,  Vol.  9, B.S.
Levlne, Trans.  U.S. Dept. of Commerce,  p. 185-199.   NTIS  64-11574.   (Cited
1n NIOSH, 1976)

NCI  (National  Cancer  Institute).   1980.   Carclnogenesls  Testing  Program.
Bloassay  of  phenol  for  possible carc1nogen1c1ty.   Report,  NCI-CG-TR-203,
DHHS/PUB/NIH80-1759,  NTP-80-15;   NTIS   PB80-217946,   119  p.    Gov.   Rep.
Announce. Index  (U.S.)  1980,  80(25),  5298.

NIOSH  (National  Institute  for   Occupational  Safety   and   Health).    1976.
Criteria for  a  Recommended Standard...Occupational Exposure  to Phenol.  U.S.
DHEW, PHS, CDC,  Rockvllle,  MD.

NLM  (National Library  of Medicine).   1987.   Hazardous Substance  Data  Base.
Report No. 113.   Online.

NTP  (National Toxicology  Program).   1983.   Teratologlc evaluation of  phenol
1n  CD  rats  and  mice.   Report   prepared  by  Research  Triangle  Institute,
Research  Triangle  Park, NC.  NTIS  PB83-247726.   Gov.  Rep.   Announce.  Index.
83(25): 6247.

Ohtsujl,  H.  and   M.   Ikeda.    1972.   Quantitative   relationship  between
atmospheric  phenol  vapour  and phenol  In  the  urine of  employees  1n  Bake!He
factories.  Br.  J.  Ind. Med.  29:  70-73.   (CUed In NIOSH, 1976)
0007H                               -22-                             07/21/89

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OSHA  (Occupational  Safety  and  Health  Administration).   1985.   OSHA  Occu-
pational Standards  -  Permissible Exposure  Limits.   Code of  Federal  Regula-
tions.  29 CFR 1910.1000.

Plotrowskl,  O.K.   1971.  Evaluation  of exposure  to phenol.  Absorption  of
phenol  vapour  In  the  lungs and  through  the skin and excretion of  phenol  In
urine.  Br. J. Ind.  Med.  28:  172-178.

Pool,  B.L.  and  P.Z.  L1n.   1982.  Mutagenlclty  testing  In the  Salmonella
typhlmurlum assay of phenolic  compounds  and phenolic fractions  obtained from
smokehouse  condensates.  Food  Chem.  Toxlcol.   20(4):  383-391.    (Cited  In
U.S. EPA, 1987a)

Salaman, M.H. and O.M.  Glendennlng.   1957.   Tumor  promotion  In  mouse  skin  by
scleroslng agents.  Br.  J. Can.  11: 434-444.  (Cited 1n U.S. EPA,  1987)

Sandage, C.   1961.  Tolerance  criteria  for  continuous  Inhalation  exposure  to
toxic   material.    ASO   Technical  Report   61-519   (I).   Midwest   Research
Institute, Kansas City,  MO.  p. 1-29.   (CHed 1n NIOSH, 1976)

U.S.  DHEW  (Department  of  Health,  Education  and  Welfare).  1962.   Public
Health  Service  Drinking Water  Standards.   Consumer Protection and Environ-
mental  Health  Service,  Environmental  Control Administration, Rockville, MD.
p. 51.
0007H                               -23-                             07/21/89

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U.S. EPA.   1980a.   Ambient Water QualHy  Criteria  for Phenol.  Prepared  by
the  Office  of Health  and Environmental  Assessment,   Environmental  Criteria
and  Assessment  Office,  Cincinnati,  OH  for the  Office of Water  Regulations
and Standards, Washington, DC.   EPA-440/5-80-066.  NTIS PB81-117772.

U.S. EPA.   1980b.   Guidelines  and  Methodology  Used   In  the Preparation  of
Health  Effects   Assessment  Chapters  of  the   Consent  Decree  Water  QualHy
Criteria.  Federal  Register.   45(231):  79347-79357.

U.S. EPA.   1984.   Methodology  and  Guidelines  for Ranking Chemicals  Based  on
Chronic Tox1c1ty Data.   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.

U.S.  EPA.   1986.    Guidelines  for   Carcinogen   Risk   Assessment.    Federal
Register.  51(185): 33992-34003.

U.S.  EPA.   1987.   Health  and  Environmental  Effects Profile  for  Phenol.
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.   EPA/600/X-87/121.    NTIS  PB89-
132112/AS.

U.S. EPA.   1988.   Integrated Risk Information  System  (IRIS).   Reference dose
(RfD)  for oral exposure for phenol.   Online.   (Verification  date  11/16/88.)
Office  of Health  and  Environmental  Assessment,  Environmental  Criteria  and
Assessment Office,  Cincinnati,  OH.


0007H                               -24-                             08/14/89

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                                                                     07/24/89

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