EPA-540/1-86-024
                      Agency
Office of Emergency and
Remedial Response
Washington DC 20460
Off'ce of Research and Development
Office of Health and Environmental
-Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
                      Superfund
oEPA
                       HEALTH EFFECTS ASSESSMENT
                       FOR COAL TARS

-------
                                           EPA/540/1-86-024
                                           September 1984
       HEALTH  EFFECTS  ASSESSMENT
              FOR COAL  TARS
    U.S. Environmental Protection  Agency
     Office of Research and Development
Office of Health  and  Environmental Assessment
Environmental Criteria and Assessment  Office
            Cincinnati,  OH  45268
    U.S. Environmental Protection  Agency
  Office of  Emergency  and Remedial Response
Office of Solid Waste and  Emergency  Response
            Washington, DC  20460

-------
                                  DISCLAIMER

    This  report  has  been  funded  wholly  or  1n  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.
                                      11

-------
                                    PREFACE


    This report  summarizes  and evaluates Information relevant  to  a prelimi-
nary Interim assessment of adverse  health effects  associated  with  coal tars.
All estimates  of  acceptable  Intakes and  carcinogenic  potency  presented  1n
this document  should be  considered as   preliminary  and reflect limited  re-
sources allocated  to this project.  Pertinent  toxlcologlc  and  environmental
data  were  located  through   on-Hne literature   searches  of  the  Chemical
Abstracts,  TOXLINE,   CANCERLINE  and  the CHEMFATE/DATALOG  data bases.   The
basic   literature  searched   supporting   this   document  1s   current  up  to
September,  1984.   Secondary  sources of  Information have  also been  relied
upon  In the  preparation  of  this  report  and  represent  large-scale  health
assessment  efforts  that   entail   extensive  peer  and  Agency  review.   The
following Office  of  Health  and Environmental Assessment  (OHEA)  sources  have
been extensively utilized:

    U.S.  EPA.   1982a.  Carcinogen  Assessment  of  Coke Oven  Emissions.
    Office  of  Health and  Environmental  Assessment,   Office  of  Research
    and  Development,  Washington,   DC.    EPA   600/6-82-003.    NTIS  PB
    83-129551.

    U.S.  EPA.   1982b.  Coal  Tars Health Effects  Assessment.   Environ-
    mental  Criteria  and   Assessment Office,   Cincinnati,  OH.   p. 10.
    Internal draft.

    The Intent  1n  these assessments  1s  to suggest  acceptable exposure levels
whenever sufficient  data  were available.  Values  were  not  derived or larger
uncertainty  factors  were employed  when  the  variable  data  were  limited  1n
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 chemical{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  llfespan).   This  type  of
exposure  estimate has not  been  extensively used  or rigorously defined,  as
previous  risk  assessment  efforts  have  been  primarily  directed  towards
exposures from toxicants  1n  ambient air or water  where lifetime exposure 1s
assumed.   Animal  data  used  for  AIS estimates generally  Include exposures
with  durations of 30-90  days.   Subchronlc  human  data  are  rarely  available.
Reported  exposures  are usually from chronic  occupational  exposure  situations
or  from reports of acute accidental  exposure.
                                      111

-------
    The  AIC,  acceptable  Intake  chronic,   Is  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 (1980)  for  a discussion of
this concept].  The AIC Is route specific and  estimates  acceptable exposure
for a  given  route with  the Implicit  assumption that exposure  by other routes
Is 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  cardnogenlcHy,
AIS  and  AIC  values  are  not  derived.   For a  discussion  of risk  assessment
methodology  for  carcinogens   refer  to  U.S.  EPA  (1980).    Since cancer 1s  a
process  that  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 If available.
                                      1v

-------
                                   ABSTRACT


    In order  to  place the risk  assessment 1n proper context, the  reader  Is
referred to the  preface  of  this  document.  The preface  outlines  limitations
applicable to all documents of this  serves  as  well  as  the appropriate Inter-
pretation and use of the quantitative numbers.

    There are  extensive  data  which  Indicated  that coal  tars  and coal  tar
components are  carcinogenic  1n  experimental  animals.   Human data  Indicate
that  Industrial  exposure mixtures  containing coal  tar  volatHes  are  asso-
ciated with excess cancer risk.

    U.S. EPA (1982a)  has  used  ep1dem1olog1cal  data  to  develop a  quantitative
risk  assessment  for  coke oven workers,  expressed  as an  Incremental  risk  of
3.2   (mg/kg/day)"1.    Although   coal  tar  volatHes  are  present  as  major
constituents  1n  coke oven emissions  1t  1s  probable that differences  exist
between  the  composition  of  the  oven  emissions  and   potential   exposure
mixtures from  coal  tar  products  following  the distillation   process.   It  1s
felt  that  despite   these  reservations,  exposures  should  be  substantially
similar and  that  the coke oven data  can  be used  to estimate  risk associated
with coal tar exposure.

-------
                               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.   Or.  Christopher  DeRosa and  Karen
Blackburn were the Technical Project Monitors  and  Helen Ball  was-,the Project
Officer.  The final documents  1n  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 Haste
         Office of Toxic Substances
         Office of Drinking Hater

Editorial review for the document series was provided by:

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

Technical support services for the document series  was provided by:

    Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
    Environmental Criteria and Assessment Office
    Cincinnati, OH
                                      v1

-------
TABLE OF CONTENTS

1.
2.


3.










4.








5.


ENVIRONMENTAL CHEMISTRY AND FATE 	
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . .
2.1.
2.2.
ORAL 	
INHALATION 	
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
.... 1
.... 3
.... 3
.... 3
.... 4
.... 4
.... 4
. . . . 4
	 5
	 5
	 5
	 6
	 6
	 6
	 6
	 7
	 7
	 7
	 7
	 8
	 8
	 8
	 12
	 13
	 14

-------
                          TABLE OF CONTENTS  (cont.)

                                                                        Page

 6.   RISK ASSESSMENT	    15

     6.1.   ACCEPTABLE INTAKE SUBCHRONIC (AIS) 	    15
     6.2.   ACCEPTABLE INTAKE CHRONIC (AIC)	    15
     6.3.   CARCINOGENIC POTENCY (q-j*)	    15

            6.3.1.    Oral	    15
            6.3.2.    Inhalation	    15

 7.   REFERENCES	    20

APPENDIX: Summary Table for  Coal Tars	    25
                                     V111

-------
                             LIST OF ABBREVIATIONS





AOI                     Acceptable  dally Intake



AIC                     Acceptable  Intake chronic



AIS                     Acceptable  Intake subchronlc



BaP                     Benzo(a)pyrene



CTPV                    Coal  tar  pitch volatHes



CS                      Composite score



DNA                     Deoxyrlbonuclelc add



PAH                     Polycycllc  aromatic  hydrocarbons



TWA                     Time-weighted  average
                                      1x

-------
                     1.   ENVIRONMENTAL CHEMISTRY AND FATE

    Coal tar  is  a black, viscous  liquid  or sem1sol1d  substance  obtained  by
the destructive  distillation of  bHumlnonus coal  as  in  the production  of
coke.    Typically,  one ton  of  coal in  a  coke  oven  may yield -27.5-34  I  of
coal  tar   (U.S.   EPA,  1982a).    The  physical  properties  of coal  tar  vary
substantially.   The  specific gravity of  coal  tar may  vary from  1.18-1.23
(Hawley, 1981).   Coal  tar  is soluble 1n  ether, benzene and chloroform, and
1s  partially  soluble  in ethanol,  acetone   and  methanol  and only  slightly
soluble in water  (Hawley,  1981).   The typical constituents  of United States
coke  oven-derived coal  tar are  the following:   benzene,   0.12%;  toluene,
0.25%;  o-xylene,  0.04%;  m-xylene,  0.07%;  p-xylene,  0.03%;  ethylbenzene,
0.02%;  styrene,   0.02%;   phenol,  0.61%;  o-cresol,  0.25%;   m-cresol,  0.45%;
p-cresol,   0.27%;  xylenols,  0.36%;  high  boiling  tar acids,  0.83%;  naphtha,
0.97%,  naphthalene,  8.8%;  1-methylnaphthalene,  0.65%;  2-methylnaphthalene,
1.23%;  acenaphthene,  1.05%;  fluorene,   0.64%;  anthracene,  0.75%;  phenan-
threne, 2.66%;  carbazole,  0.6%;  tar  bases,  2.08%;  and  medium  soft  pitch,
63.5%  (McNeil,  1983).   The pitch  contains  four,   five,  six and  seven-ring
PAHs and their methylated derivatives (McNeil,  1983).   The coal  tar obtained
through destructive  distillation  of  coal  1s  usually  subjected to  further
distillation.   The  distillation  of  coke  oven  tar  produces the  following
fractions: light  oil, phenolic  oil,  naphthalene  oil,  wash  oil,  light anthra-
cene oil,  heavy anthracene  oil  and medium soft pitch (McNeil, 1983).
    The exposure  of  undistilled  coal  tar  to the ambient atmosphere  is likely
to  contaminate  the  atmosphere  primarily  with  volatile  compounds  such  as
monocyclic  and  PAHs,  phenolic  compounds and  heterocycllc   compounds.   The
fate and transport of these compounds in  the atmosphere may be determined by
                                      -1-

-------
their chemical  and  photochemical  reactivity and  physical  removal  mechanisms
(dry  and  wet deposition)  1n the atmosphere.   In general,  the fate  of  the
most  relevant  compounds will  be very  similar  to  the fate  of PAHs  1n  the
atmosphere.
    In aquatic  systems,  coal  tar  constituents  will partition  Into  two frac-
tions: one  very  small  fraction  will be solublUzed 1n  the  water  and stay as
the  mobile phase,  and  the  other  very  large   fraction  will  precipitate  as
sediment  1n  water.   The  solublUzed  fraction   containing  different  chemical
constituents may  undergo chemical and microbiological  reactions,  and evapo-
rative and  sorptlve processes 1n aquatic  media.   The  Insoluble part In  the
sediment 1s expected to have a very long lifetime.
    In soils, coal  tar may partition Itself Into  three  fractions.   Volatile
constituents In coal tar may  enter  the  atmosphere as  a vapor or partially 1n
the  partlculate  phase.  A  second fraction of  coal  tar constituents  may  be
solublUzed  by   rainwater.    This  solublUzed  part,   consisting  of  several
chemicals, may  undergo physical  and chemical  processes In  soil.  The third
and  very  large  fraction  that may  consist  of  the nonvolatile  and  Insoluble
part of coal tar may persist In  soil for a long period of time.
                                      -2-

-------
           2.  ABSORPTION  FACTORS  IN  HUMANS AND  EXPERIMENTAL MAMMALS



2.1.    ORAL



    Pertinent  data  regarding  the  quantitative  absorption   of  coal  tars



following  exposure by  the  oral  route  were not  located  1n  the  available



literature.



2.2.    INHALATION



    Pertinent  data  regarding  the  quantitative  absorption   of  coal  tars



following exposure by the  Inhalation route were not  located  1n the available



literature.
                                     -3-

-------
                3.  TOXICITY  IN  HUMANS AND  EXPERIMENTAL  ANIMALS
3.1.   SUBCHRONIC
3.1.1.   Oral.   Pertinent  data  regarding  the  subchronlc  oral   toxldty  of
coal tars were not located In the available literature.
3.1.2.   Inhalation.    Klnkead   (1973)  prepared  an  aerosol  of  coal  tar  In
which the  solids  previously  had been removed by  centrlfugatlon.   He exposed
female Sprague-Dawley yearling  rats  (64),  male  (32)  and female  (32) Sprague-
Dawley weanling  rats,  male  ICR  mice (50), and  male  CAF-1  mice  (50) continu-
ously for  90  days  at  concentrations  of  0.2,  2.0  and  10 mg/m3.   In  addi-
tion, 80  yearling female Sprague-Dawley rats,  9  weanling  rats of  each sex,
25  male  CAF-1 mice,   25  male ICR mice,  24 female New  Zealand white rabbits
and 100 male  Syrian golden hamsters  were exposed  continuously for 90 days at
20  mg/m3.   Greater   than  95%  of  the  aerosol   droplets  were  <5  ym  in
diameter.
    Considerable  mortality   among  exposed animals  was  encountered  in  this
study, which  the authors attributed to  debilitation  causing  greater suscep-
tibility  to  infections.  However,  cumulative  animal  mortality  was  propor-
tional to  exposure concentration.   In all  species tested,  there  was a marked
effect of  exposure on  body weight  growth curves.   Animals either  lost weight
(mice, hamsters,  rabbits) or grew at a  slower  rate  than nonexposed controls
(rats).    Even the lowest  exposure  concentration,  0.2  mg/m3, produced some
adverse effects  on body weight  gain, with the  most  striking effect observed
in  male  CAF-1  mice whose body  weight decreased from 30 g to 25  g during the
90  days   in  the  0.2  mg/m3   group.   Following  the  termination  of  exposure,
the inhibitory effect  of coal tar  aerosol  on growth  was still evident for at
least 7 months in most species.
                                      -4-

-------
    Klnkead (1973) conducted  a  subsequent study, described by  McConnell  and
Specht (1973),  employing  a coal tar  1n  which the solid  particles  and  light
oil  fractions  were  retained In  the  experimental  aerosol.   Sprague-Oawley
rats,  New  Zealand  white  rabbits,  JAX   mice,   and  Syrian  golden  hamsters
(numbers   not  specified)  were exposed  continuously for  90  days to  the  coal
tar  aerosol  at a  concentration of  10 mg/m3.   In addition,  150   CF-1  mice
were  exposed   to  the  aerosol  and  serially  sacrificed   for  hlstopathologlc
analysis.  Among exposed  rats and  hamsters, McConnell and  Specht  (1973)  de-
scribed  three  significant  lesions  occurring at  the termination  of  exposure.
These were  phagocytlzed coal  tar  pigment In alveolar  macrophages  and 1n the
peMbronchlal   lymphold  tissue;  hepatic  and renal hemoslderosls, which  dis-
appeared  by 100 days  postexposure;  and mild central  lobular  necrosis In the
liver.   Among  mice sacrificed 99 days  postexposure, moderate  pigmentation of
alveolar  macrophages  was  observed  1n  14/15  CF-1 mice, but  1n   only  1/13
exposed  JAX mice.
3.2.   CHRONIC
3.2.1.    Oral.  Pertinent  data  regarding the chronic  oral  toxldty  of  coal
tars were not  located 1n the available literature.
3.2.2.    Inhalation.   MacEwen et  al.  (1976)  prepared a  composite  coal  tar
mixture  from multiple  coking ovens around  the greater PHtsburg area.   Coal
tar  samples  were  blended  together  with  a  20% by  volume   amount of  BTX
(benzene,  toluene, xylene) fraction of coke oven  distillate.   This material
was  believed  to be  more representative of  that  Inhaled  by  workers  on top of
coke  ovens.    Female  (75)  ICR-KF-1  mice,  female  (50)  CAF-1-JAX mice,  male
(40)  and female (40) weanling Sprague-Oawley  rats,  New Zealand white rabbits
(18),  and male (5)  and female  (9)  Macaca mulatta monkeys were  exposed  to a
coal  tar aerosol  at 10 mg/m3,  6 hours  dally,  5 days/week, for 18 months.
                                      -5-

-------
Animals  were  held  for  an  additional 6-month  observation period  following
termination  of   exposure.   Development  of  skin  tumors   1n  mice  precluded
assessment  of  other  systemic  effects.   A  significant  Inhibition  of  body
growth rate  was  observed  for both  male  and female  rats  after 4 months  and
for  rabbits  by  the  end of  the 1st  month.   Monkeys  showed  no  significant
Inhibition of growth  rate.   In  this study, 16/18  test  rabbits  and  6 control
rabbits died during the test period.
3.3.   TERATOGENICITY AND  OTHER  REPRODUCTIVE  EFFECTS
3.3.1.   Oral.    Pertinent  data  regarding  the  teratogenldty  of  coal  tars
following oral  exposure were not located  In the  available  literature.
3.3.2.   Inhalation.   Pertinent  data regarding  the teratogenldty  of coal
tars  following  Inhalation  exposure  were  not  located   1n   the   available
literature.
3.4.   TOXICANT INTERACTIONS
    Pertinent quantatlve  data regarding  the  Interactions  of  coal  tars with
other compounds  were  not located 1n  the available literature.
                                     -6-

-------
                             4.  CARCINOGENICITY
4.1.   HUMAN DATA
4.1.1.   Oral.   Pertinent  data  regarding  the  cardnogenldty  of  orally
administered coal tars were not located 1n the available literature.
4.1.2.   Inhalation.   Studies  of workers  exposed to  "tarry  fumes"  1n  the
coal  gas  (Doll  et  al.  1972,  Kawai et  al.,  1967),  steel  (Redmond et  al.,
1972) and  aluminum reduction  Industries  (G1bbs  and Horowitz,  1979;  Mllham,
1979) have supported an  occupational association  with  lung,  skin and hemato-
poletlc cancers.   Tarry  fumes, however, were  not coal tar per  se.   Only  1n
the studies of roofers (Hammond  et  al.,  1976)  and coke oven workers  (Redmond
et al., 1979) was exposure specifically to coal  tars  or coal tar volatlles.
    Hammond et al.  (1976)  observed  Increases  In  both  lung  and skin cancer  1n
roofers with >20 years of  work  experience,  and  Increases  1n skin cancer  1n  a
group with  9-19 years  of work  experience.  A  single measurement  reported
that workers  Inhaled  BaP,  a  polyaromatlc hydrocarbon  1n coal  tar,  at  levels
ranging  from  undetectable  to   153  yg  during  a 7-hour  work  shift.   The
corresponding levels of coal  tar were not reported.
    Redmond et  al.  (1979), in  a  final  report of  an  extensive epidemlologlc
study  of  coke  oven workers,  summarized  the  results  of  interim  reports  by
Lloyd (1971),  Redmond  et al.  (1972, 1976)  and Mazumdar et  al.  (1975).   Coke
oven workers  (2552 employed  1n  Allegheny  County) with >5  years  of  exposure
had  an increased  relative  risk of  lung  cancer  (2.63)   and  kidney  cancer
(3.55).  Mazumdar  et  al.  (1975) calculated cumulative exposures  to  CTPV for
the  subgroups  of the  cohort  and suggested that  exposures <200  mg/mVmonth
would  not  result  1n   an  Increased  risk  of cancer.   Using  CTPV  estimates,
there was  a  dose-related  Increase  1n  lung cancer  among  nonwhlte  workers,
while  for  white workers,  the  Increased risk  appeared  not  to  be  related  to
                                     -7-

-------
CTPV.   The  Increased  rate/1000  of  lung  cancer 1n  nonwhHe  males was  4.0,
12.9,  24.9  and 54.6  for  groups  exposed  to  <199,  200-499, 500-699 and  >700
mg/m3-month.   In  addition,  Redmond  et al.  (1976)  reported  that side  oven
workers also  had  an  Increase  In  risk of  cancer,  although  these  workers  are
exposed  to  much  lower   levels   of   CTPV.   In  10  plants  studied  outside
Allegheny  county,  there   was  no  difference   between  the  races,  although
similar excesses  1n risk  of lung  cancer  were  reported.   The  excess  risk of
kidney cancer was not apparent  1n the non-Allegheny county plants.
4.2.   BIOASSAYS
4.2.1.   Oral.   Pertinent  data  regarding  the  cardnogenldty  of   orally
administered coal tar  to  experimental  animals  were not  located 1n the avail-
able literature.
4.2.2.   Inhalation.   The   first   experimental   demonstration   of   cancer
produced by Inhalation of  coke  oven-derived  material  was by  Morton  et  al.
(1963).  They  used  the same coal  tar sample,  taken from a coke  oven,  that
had  previously  been reported to  produce  tumors  on the  skin of mice (Morton,
1961).  The tar was  characterized as  having a BaP  content of  0.71%,  a  high
"tar add"  content  (5.1%), and  a  low content  of  benzene Insolubles  (2.74%)
1n  comparison  with  other  coal tars.   Among  33 C3H  mice  Inhaling  a  coal  tar
aerosol  at  300  mg/m3 for  a  total  of 40-100 hours over a  13-  to  35-week
period, 5 developed squamous cell  tumors  In  the periphery of the lung during
the  36-week  postexposure observation  period.  One of  the  tumors  was  an
Invasive squamous cell carcinoma.   The control mice were killed  at  82 weeks
of age and  none of  the 30 animals had tumors of the  lung.
     Since  the  development of  cancers  by  the  Inhalation  of  xenoblotlcs  was,
at  that  time,  a rarely observed phenomenon  1n experimental  animals,  further
Inhalation  studies  were  pursued.  Tye and  Stemmer  (1967)  employed  two  coke
                                      -8-

-------
oven-derived tars  1n  their study.  The  first  was a  tar  sample of  the  same
composition as that used  In  previous  studies,  as  described  by  Horton  et al.
(1963).  The second coal  tar was  high  In  toluene-Insoluble  material  (17.8%),
low  1n tar adds  (1.4%)   and  had a  BaP content  of  1.1%.   Both tars  were
separated  Into phenolic  and  nonphenollc  fractions,  and  various combinations
were used  to  produce  aerosols  for Inhalation exposure  to male  C3H/HeJ mice.
Groups  of   50  mice were  exposed  for  2  hours,  three  times  weekly,  for  55
weeks.   The concentration of  coal  tar aerosol was  200 mg/m3  for  the first
8  weeks  and  120  mg/m3 for  the  remaining 47  weeks.  Animals  were  examined
after  spontaneous  death  or  after  scheduled  intervals.   During  the  study,
three  mice  from each  group were  killed at 4  weeks, five mice from each group
were killed at 31  weeks  and all  surviving animals were killed  at 55  weeks.
Their  findings Included the  observation  of  increases in squamous metaplasia,
intrabronchial and  alveolar  adenomas,  and adenocardnomas.   The most  promi-
nent  lesions  1n  exposed animals were  Intrabronchial  adenoma and adenocarci-
noma.  None of the control animals developed  lung tumors.   The authors con-
cluded that the presence  of  phenols  in the coal  tar exerted a cocardnogenic
effect  together  with  polynuclear  aromatic  hydrocarbons, possibly caused by
an  irritant effect.   No  direct  evidence was  provided, however,  to explain
the  role of the  phenolic   fraction in  tumor  development,  and the  tumorigenlc
potential  of the phenolic  fraction alone was not assessed.
     In  later  studies,  Kinkead  (1973)   exposed   mice,  rats,   hamsters  and
rabbits  to a  coke oven-derived coal tar  aerosol  at 20, 10,  2  and 0.2 mg/m3
continuously  for  90  days  and  observed  them until  death.   The aerosol  con-
sisted of  a benzene  extract of  coal  tar from which  the  solids were removed
by  centrlfugatlon,  and before  generating the aerosol,  the  added benzene and
the  light  oil fractions  were  also removed.   Several  types  of  tumors  devel-
oped in  the exposed  animals,  as  described  by McDonnell  and Specht (1973).

                                      -9-

-------
An Independent analysis of the pathologic  data  from this  study was conducted
by the National  Institute  for  Occupational Safety  and  Health  (NIOSH,  1978),
and  the  findings are  summarized  in Table  4-1.   No data were  available  for
the  20 mg/m3  concentration.   From  the  NIOSH  (1978) analysis  of  the Kinkead
(1973) data,  it was  concluded  that  the  coal  tar  aerosol  produced a  dose-
related incidence of  lung  tumors  1n mice.  In  addition,  the  Increased  Inci-
dence  of  splenic  lymphosarcomas  1n  mice and  lung tumors  in  rats  was  also
felt  to  be related  to the  coal  tar exposure.   There is  some disagreement
between  the  exposure  data  of Kinkead  (1973)  and  the pathologic  report  in
NIOSH  (1978).   Kinkead  (1973)  stated that rabbits  and  hamsters were exposed
only  at   20   mg/m3,  while  the  NIOSH  (1978)   report  gives  data   for  these
species at  lower exposure concentrations.  These conflicting  points make  it
unclear  as  to  whether  the animals  examined  in  NIOSH  (1978)   were  the  same
animals  exposed by  Kinkead  (1973)  and   examined  by  McConnell   and  Specht
(1973).
    A  follow-up long-term study  reported by MacEwen  and  Vernot  (1976)  and
MacEwen  et  al.  (1976)  involved  the  exposure  of  female ICR   CF-1  (75)  and
CAF-1  JAX (50)  mice, male  (40) and female (40)  weanling Sprague-Oawley rats,
18  New Zealand  albino  female rabbits,  and male (5)  and  female  (9)  Macaca
mulatta  monkeys to  a  coke  oven-derived coal  tar  aerosol.   Animals  were
exposed  to  a chamber  concentration of  10 mg/m3,  6  hours  dally,  for  up  to
18 months.  Hlstopathologic  data  for mice and  rats have  been  reported.   The
rabbits and monkeys were  not  sacrificed and examined 1n this  study, but were
maintained for  long-term, postexposure observation.
     Various  tumors  were  found  In  mice,  although  principally alveolargenic
carcinomas of the  lung were  observed (26/61  in  ICR CF-1 mice and 27/50  1n
CAF-1  JAX mice  as  compared with  3/68 and 8/48  1n the respective controls).
                                     -10-

-------
                                  TABLE 4-1

      Tumors from Exposure to Airborne Coal Tar 1n Four Animal Species3
Tumor Incidence (%)
Spec1esb
Mice





Rats




Hamsters





Rabbits





Tumor
skin
lung
spleen
kidney
liver
urocyst
skin
lung
spleen
kidney
liver
skin
lung
spleen
kidney
liver
adrenals
skin
lung
spleen
kidney
liver
urocyst
0.00 mg/m3
3
30
5
1
9
0
10
4
8
1
1
0.7
0.6
0.7
2
0.6
27
0
0
0
0
0
0
0.20 mg/m3
1
39
20
3
4
0
6
3
4
0
0
0
3
0
1
0
0
0
0
0
0
0
0
2.00 mg/m3
1
58
5
0
11
3
3
10
4
0
0
0
0
0
0
0
57
0
0
0
0
0
0
10.00 mg/m3
6
77
14
0
0
0
0
18
8
6
3
4
4
4
0
2
17
12
0
0
0
0
0
aSource: NIOSH, 1978

bResults are  based on  data  from a  total  of  63 rabbits,  376  hamsters,  498
 rats and 563 mice.
                                     -11-

-------
The Incidence  of  squamous cell carcinomas  1n the lungs of  exposed  rats was
100% 1n  males  and 82%  1n  females.   None of the control rats  developed lung
tumors.
4.3.   OTHER RELEVANT DATA
    Horton  (1961)  demonstrated  that twice weekly dermal application  of coal
tar to  the  shaved skin of mice resulted  1n  Increases  In  dermal  tumors.  The
latency  period  ranged  from 7-15 months  depending on the  source  of  the tar.
Human case  reports  dating back to  1885  (NIOSH,  1978)  have also  supported an
association  between  occupational  exposure  to  coal  tars and  the  development
of skin cancer.
    Although coal  tar  contains Individual  components,  primarily  PAHs,  which
have been  extensively  evaluated and  found  to be mutagenic  (F1shbe1n,  1976;
U.S. EPA, 1982a),  few  data  are  available concerning  the mutagenlcity of coal
tar mixtures  as a whole.   Brat et al.  (1982)  tested roofing tar  pot  emis-
sions for  genotoxicity  1n  a  number  of  systems  using mammalian  cells.   No
details  were  given concerning  sample collection methods  or  sample  composi-
tion.   The  tar emission  samples  gave  positive  results in  a  HPC/DNA repair
assay using primary hepatocyte cultures,  but not the  ARL/H6PRT  mutagenesis
assay.    Coke oven  emissions  were  also  tested  1n the  DNA repair assay and
yielded  greater DNA  repair  activity than the tar  sample  (106 grains/nucleus
vs. 37.7 grains/nucleus) when both were tested at doses of 10"1 mg/mS,.
    More  extensive data  are  available  concerning  the mutagenlcity  of coke
oven emission;  these  are reviewed  1n  U.S.  EPA  (1982a).   Extracts  of coke
oven door  emissions  have been  shown  to be  mutagenic  1n  bacteria.   Extracts
of  samples  from  coke  oven  collecting mains  have  been shown  to  cause  muta-
tions  in  bacteria  and  mammalian  cells   in  culture.   These  studies  are
                                     -12-

-------
relevant to coal tars In that a  large  proportion  of the Identified mutagenlc
compounds  1n  coke  oven emissions  are  PAHs,  presumably from coal  tar  vola-
tilization.
    BaP  1s  the marker  PAH  which has  been  most extensively monitored.   BaP
was detected  1n  "air contaminated with  coal  tar  pitch fumes"  at  a  level  of
400   ng/1000   m3   (1800   pg/g   partlculates)    (Sawlckl   et   al.,   1965).
Worker-exposure concentrations of  BaP  1n coal  and  pitch coking  plants  have
been  measured  as  0.3-35 mg/1000  m3 (Fishbein,  1976).   Emissions  from  coke
ovens  In  the  USSR  have   been   reported   to   contain  120-1700  yg  BaP/g
partlculates (von Lehmden  et al., 1965).
4.4.   WEIGHT OF EVIDENCE
    Studies 1n rats  and mice Indicate  that  Inhalation  exposure  to coal  tars
results  1n  Increased   Incidence  of  lung  tumors   (Tye and  Stemmer,  1967;
Klnkead, 1973;  McConnell  and Specht,  1973;  MacEwen et al., 1976).   In  epi-
demic! ogle  studies  of   roofers exposed to coal  tars,  there was  an  elevated
risk  of  both  skin and  lung  cancer (Hammond  et  al.,  1976), while  coke  oven
workers exposed to coal tars  had  an  elevated risk  of  lung and  kidney cancers
(Redmond et al.,  1979).  The evidence for  carclnogenldty for coal  tars  In
animals  Is  "sufficient,"  and the  evidence  for  carclnogenldty 1n  humans  1s
"limited," bordering on "sufficient,"  using  the criteria for weight  of  evi-
dence proposed  by  the  Carcinogen  Assessment  Group  of  the  U.S.  EPA (Federal
Register,  1984).  Coal  tars  as  a chemical class are,  therefore,  most appro-
priately classified as a Group 81 chemical.
                                     -13-

-------
                    5.  REGULATORY STANDARDS AND CRITERIA







    NIOSH (1978) has  recommended  a 10-hour TWA  concentration  for coal  tars



(cyclohexane-extractable  fraction)  of  0.1  mg/m3.   The  ACGIH  (1980)  con-



siders coal  tar pitch volatHes to be a recognized  carcinogen  and  suggests a



TWA of 0.2 mg/m3.
                                     -14-

-------
                             6.  RISK ASSESSMENT
6.1.   ACCEPTABLE INTAKE SUBCHRONIC (AIS)
    Coal tars are a  class  of chemicals that are  known  to  be  animal  carcino-
gens and  for  which  a carcinogenic  potency  factor has been estimated  by  the
Carcinogen Assessment  Group from  human ep1dem1olog1c  data.   It  1s,  there-
fore, Inappropriate  to calculate an oral or  Inhalation AIS for coal tars.
6.2.   ACCEPTABLE INTAKE CHRONIC (AIC)
    Coal tars are a  class  of chemicals that are  known  to  be  animal  carcino-
gens and  for  which  a carcinogenic  potency  factor has been estimated  by  the
Carcinogen Assessment  Group from  human ep1dem1olog1c  data.   It  1s,  there-
fore, Inappropriate  to calculate an oral or  Inhalation AIC for coal tars.
6.3.   CARCINOGENIC  POTENCY (q^)
6.3.1.   Oral.   Pertinent  data  regarding  the  cardnogenldty  of coal  tars
following oral exposure were not available  for  calculating a  cardnogenldty
potency factor, q,*.
6.3.2.   Inhalation.    The   animal   studies  available  also  do  not   provide
sufficient  data  to  derive  a   q,*  using  the  linearized  multistage  model.
The  subchronlc   study  by  Klnkead  (1973)  reports  dose-related  Increases  1n
lung  tumors   In  mice exposed  to  coal  tar  aerosols  of between  0.2  and  10
mg/m3.   The  number   of  animals  per   group  and  number  of  tumor-bearing
animals were  not provided  In this  report, which  precludes  the derivation of
a  q,*.   The  chronic   study  of MacEwen  et  al.  (1976)  employed only  one
exposure  level and male rats at this  level had 100% tumor Incidence.   Since
male rats appear to  be  the most sensitive  spedes,  this group should be used
1n  risk  assessment;  however, a  q,*  cannot  be derived from data  when  only a
single exposure  1s  used and 100% tumor  Incidence 1s reported.
                                     -15-

-------
    The U.S.  EPA  (1982a) Cancer  Assessment  Group (CAG)  has  used  the eplde-
mlologic data  from  the  study of  Redmond  et  al.  (1979) along  with  the expo-
sure data  developed by  Mazumdar  et al.  (1975) to calculate  a  carcinogenic
potency factor  for  coke oven emissions.  In  the analysis  of the  study  of
Redmond et  al.  (1979),  the  CAG  grouped the  nonwhHe  coke  oven  workers  Into
four age and  exposure  groups as  summarized  in  Table  6-1.  Using these data,
CAG  calculated  a  unit risk   of   0.9xlO~3  for  lifetime  exposure  to  1
yg/m3  of  coal  tars.   This   incremental  risk  can also be  expressed  as  3.2
(mg/kg/day)"1  by  assuming  a 70  kg  man breathes  20  m3  of  air  per  day  and
that complete absorption occurs.
    Coal tar  is a by-product of  bituminous coal distillation in  coke produc-
tion.  Many components of coke  oven  emissions  are present in coal  tar, espe-
cially a wide  variety  of PAHs and their methylated derivatives.   However, it
might  be  suspected   that the exposure  mixture  would  be somewhat  different
during  exposure  to  oven emissions  as  compared  to exposure to  the  coal  tar
product after the coke oven distillation process 1s completed.
    Good  epidemiological data  for  exposure  to coal  tars  per ^e_  are  not
available  for risk  assessment   purposes.   Despite uncertainties  concerning
potential   differences   In  exposure  mixture  composition,  it 1s  felt  that
exposures  should be substantially similar and  that the coke oven data can be
used to estimate risk associated with coal tar exposure.
                                     -16-

-------
                           TABLE  6-1
     Average  Dose  Levels,  Lung  Cancer  Deaths,  Person-Years
Observation for Risk, and Rates Used to Estimate Dose-Response
    Relationships, by Model Used to Define Dose and by Age
                      at Entry to Study3
NonwhHe Workers Only
Dose Model Age at Dose
Entry Range'5
Zero lag 25-34 nonoven
0-99
100-199
200-299
300+
35-44 nonoven
0-149
150-299
300-499
450+
45.-S4 nonoven
0-249
250-449
450-699
700+
55-69 nonoven
0-249
250-449
450-749
750+
5-year lag 25-34 nonoven
0-49
50-149
150-199
200+
35-44 nonoven
0-99
100-199
200-349
350+
Average
Dose6
0
36.6
149.0
249.5
386.8
0
67.8
226.8
366.4
590.9
0
147.7
353.2
564.5
885.5
0
153.3
333.4
600.9
972.4
0
19.0
102.3
172.2
265.0
0
44.6
149.0
259.3
462.1
Lung Cancer
Deaths
3
1
0
3
4
4
0
2
3
5
17
1
4
4
8
4
1
1
4
10
3
1
0
4
3
4
0
2
4
4
Person-
Years
22,405
3,202
2,685
3,030
3,062
16,227
2,388
2,976
2,727
2,027
11,306
1,527
1,706
1,545
1,330
5,820
491
596
716
450
22,405
2,567
3,985
2,822
2,605
16,227
2,254
2,952
3,072
1,840
Yearly Rate
per 100,000
13.4
31.2
0
99.0
130.6
34.7
0
67.2
110.0
246.7
150.4
65.5
234.5
258.9
601.5
68.7
203.7
167.8
558.7
2222.2
13.4
39.0
0
141.7
115.2
24.7
0
67.8
130.2
217.4
                             -17-

-------
TABLE 6-1 (cont.)
NonwhHe Workers Only
Dose Model Age at
Entry
5-year lag 45-54
(cont.)



55-69




10-year lag 25-34




35-44




45-54




55-69




Dose
Rangeb
nonoven
0-199
200-349
350-599
600+
nonoven
0-199
200-399
400-649
650+
nonoven
0-49
50-99
100-149
150+
nonoven
0-99
100-149
150-249
250+
nonoven
0-149
150-249
250-499
500+
nonoven
0-149
150-299
300-549
550+
Average
Dose6
0
112.4
268.9
460.3
763.0
0
115.4'
293.0
535.5
851.7
0
18.8
76.8
120.6
193.1
0
46.7
123.5
191.5
353.0
0
76.4
193.0
362.4
641.8
0
95.3
299.8
439.4
729.7
Lung Cancer
Deaths
17
1
4
2
10
4
1
2
4
9
3
1
3
1
3
4
1
1
4
4
17
2
3
2
10
4
1
1
5
9
Person-
Years
11,306
1.828
1,397
1,573
1,310
5,820
516
665
567
503
22,405
3,964
3,371
3,226
1,418
16,227
3,956
2,283
2,360
1,519
11,306
2,308
1,308
1,607
1,162
5,820
660
576
505
512
Yearly Rate
per 100,000
150.4
54.7
286.3
127.2
763.4
68.7
193.8
300.8
705.5
1789.3
13.4
25.2
89.0
31.0
211.6
24.7
25.3
43.8
169.5
263.3
150.4
98.5
229.4
124.5
860.6
68.7
151.5
173.6
990.1
1757.8
       -18-

-------
                              TABLE 6-1  (cont.)
NonwhHe Workers Only
Dose Model Age at Dose
Entry Rangeb
15-year lag 25-34 nonoven
0-9
10-39
40-69
70+
35-44 nonoven
0-9
10-69
70-129
130+
45-54 nonoven
0-69
70-149
150-349
350+
55-69 nonoven
0-69
90-199
200-429
430+
Average
Dose6
0
1.5
27.1
55.3
100.3
0
1.6
43.3
97.1
197.7
0
24.4
104.7
222.7
486.6
0
48.7
141.3
331.4
604.9
Lung Cancer
Deaths
3
2
2
0
4
4
1
2
2
5
17
2
3
2
10
4
1
2
6
7
Person-
Years
22,405
4,457
2,303
3,098
2,121
16,227
2,374
3,014
2,601
2,129
11,306
1,623
1,612
1,512
1,361
5,820
602
609
579
461
Yearly Rate
per 100,000
13.4
44.9
86.8
0
188.6
24.7
42.1
66.4
76.9
234.9
150.4
123.2
186.1
132.3
734.8
68.7 .
166.1
328.4
1036.3
1518.4
aSource: U.S. EPA, 1982a



      -months exposure to CTPV
                                     -19-

-------
                                7.   REFERENCES



ACGIH  (American  Conference  of  Governmental  Industrial Hyglenlsts).   1980.

Documentation of the Threshold  Limit  Values,  4th  ed.   (Includes  Supplemental

Documentation, 1981, 1982, 1983).   Cincinnati, OH.  p.  102.



Brat,  S.V.,   C.  long  and  G.M. Williams.    1982.   Detection  of  genotoxlc

airborne chemicals  1n  rat liver culture  systems.  In: Genotoxlc  Effects  of

Airborne Agents, R.R.  T1ce,  D.L.  Costa and K.M.  Schalch,  Ed.   Plenum Press,

NY.  p. 619-632.



Doll,  R.,  M.P.  Vessey,   R.W.R.  Beasley,  et  al.    1972.   Mortality  of  gas-

workers — Final  report   of  a  prospective  study.   Br.  J.  Ind.  Med.   29:

394-406.  (Cited In NIOSH, 1978)



Federal  Register.   1984.-  Environmental  Protection  Agency Proposed  Guide-

lines for Carcinogenic Risk Assessment.  49 FR 46294-46299.
                  •


F1shbe1n, L.   1976.  Atmospheric  mutagens.   In:  Chemical  Mutagens,  Princi-

ples and Methods  for  Their Detection, A.  Hollaender,  Ed.   Plenum Press,  NY.

Vol. 4, p.  219-320.



G1bbs,  G.W.  and  I. Horowitz.   1979.   Lung  cancer  mortality 1n  aluminum  re-

duction  plant  workers.    J.  Occup.  Med.   21:  347-353.   (Cited  In  U.S.  EPA,

1982b)
                                     -20-

-------
Hammond, E.G.,  I.J.  Sellkoff,  P.L. Lawther  and  H.  Seldman.   1976.   Inhala-



tion of  benzpyrene and  cancer  1n man.   Ann.  NY Acad.  Sd.  271:  116-124.



(Cited  1n U.S. EPA, 1982b)







Hawley,  G.G.    1981.    The   Condensed  Chemical  Dictionary,  10th  ed.   Van



Nostrand Reinhold Company, New York.   p.  257-258.







Norton,  W.S.    1961.   An  investigation   of  the  carcinogenic  properties  of



various  coal  tars  or  commercial  fractions thereof.   Report  of  the Kettering



Laboratory, Department  of Preventive  Medicine  and  Industrial Health,  Univer-



sity of  Cincinnati.  32 p.  (Cited in NIOSH, 1978)







Horton,  A.M.,  R.  Tye  and K.L.  Stemmer.   1963.   Experimental  carcinogenesis



of  the lung.   Inhalation of  gaseous  formaldehyde or an aerosol  of  coal  tar



by  C3H mice.  J. Natl. Cancer Inst.  30: 31-43.  (Cited in NIOSH, 1978)







Kawai,  M.,  H.  Amamoto and K. Harada.   1967.   Epidemiologic study of occupa-



tional  lung cancer.   Arch.  Environ.  Health.  14:  859-864.   (Cited  in  U.S.



EPA, 1982b)







Kinkead,  E.R.   1973.   Toxicity  of coal  tar  aerosol.   .In.:  Proceedings of the



Fourth  Annual  Conference of  Environmental  Toxicology,  Fairborn, OH:  October



16-18,  p.  177-188.







Lloyd,  J.W.   1971.  Long term mortality  study of  steelworkers.   V.  Respira-



tory cancer  in  coke plant workers.  J.  Occup.  Med.   13(2):  53-68.  (Cited in



NIOSH,  1978)
                                     -21-

-------
MacEwen,  J.D.   and  E.H.  Vernot.   1976.   Carcinogenic   effects  of  chronic
Inhalation exposure of  animals  to coal  tar aerosol.   Toxic  Hazards Research
Unit  Annual  Technical  Report:  1976 Aerospace  Medical  Research  Laboratory.
Wright-Patterson A1r Force Base, OH: AMRL-TR-76-57.  (Cited in NIOSH, 1978)

MacEwen,  J.D.,  A.  Hall  and L.D. Scheel.   1976.   Experimental  oncogenesls In
rats  and  mice  exposed  to coal  tar  aerosols.   Presented  before  the Seventh
Annual  Conference  on  Environmental   Toxicology,   Dayton,  OH:  October  16,
p. 66-81.

Mazumdar, S.,  C.  Redmond, W.  Sollecito  and N.  Sussman.   1975.  An epidemlo-
loglcal   study  of  exposure  to  coal-tar-pitch   volatiles  among   coke  oven
workers.  APCA  J.  25(4): 382-389.  (Cited in NIOSH, 1978)

McConnell, E.E. and H.D.  Specht.   1973.   Lesions  found in animals exposed to
coal  tar aerosols,   in:  Proceedings   of  the  Fourth  Annual  Conference  on
Environmental Toxicology, Fairborn, OH:  October 16-18, p. 189-198.

McNeil,  D.   1983.   Tar  and pitch.  .In:  Kirk-Othmer  Encyclopedia  of Chemical
Toxicology,  3rd ed.,  Vol.  22, M.  Grayson,  Ed.   John Wiley and  Sons,  Inc.,
New York.  p. 564-600.

Mllham,  S.   1979.   Mortality  in aluminum reduction plant workers.  J. Occup.
Med.  21: 475-480.  (Cited  in U.S.  EPA,  1982b)
                                     -22-

-------
NIOSH  (National   Institute  for   Occupational   Safety  and  Health).    1978.



Criteria  for  a  Recommended  Standard...Occupational  Exposure  to  Coal  Tar



Products.  U.S.  DHEW,  PHS, CDC,  Rockvllle,  MO.   Publ. No.  78-107.







Redmond,  C.K.,   A.  Ciocco,  J.W.  Lloyd  and  H.W.  Rush.   1972.   Long  term



mortality study of steelworkers.  J. Occup. Med.   14(8):  621-629.   (CHed 1n



NIOSH, 1978)







Redmond,  C.K.,   B.R.  Stroblno  and  R.H.  Cypess.   1976.   Cancer  experience



among coke  by-product  workers.   Ann.   NY Acad.  Sc1.  p. 102-115.   (Cited 1n



NIOSH, 1978)







Redmond,  C.K., H.S.  Wleand,  H.E. Rockette,  R.  Sass and G.  Welnberg.   1979.



Long-term mortality experience of  steelworkers.   Prepared  under  Contract  No.



HSM-99-71-32.   NIOSH,  Cincinnati, OH:  June  1979.  (CHed 1n NIOSH,  1978)







Sawlckl,  E.,  O.E.  Meeker  and M.J. Morgan.   1965.   The  quantitative  composi-



tion  of  air  pollution source  effluents   1n  terms  of  aza  heterocycllc  and



polynuclear aromatic hydrocarbons.  Int.  J. A1r  Water Pollut.  9: 291-298.







Tye,  R.,  and  K.L.  Stemmer.  1967.  Experimental  cardnogenesis  of  the  lung.



II.  Influence  of phenols  1n the production  of carcinoma.  J.  Natl.  Cancer



Inst.  39: 175-186.  (CHed in NIOSH,  1978)







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.   45:79347-79357.
                                     -23-

-------
U.S. EPA.  1982a.   Carcinogen  Assessment  of Coke Oven  Emissions.   Office of



Health  and  Environmental  Assessment,  Office  of  Research and  Development,



Washington,  DC.  EPA 600/6-82-003.  NTIS PB 83-129551.







U.S.  EPA.   1982b.    Coal   Tars   Health  Effects  Assessment.   Environmental



Criteria and Assessment Office, Cincinnati, OH.  p. 10.  Internal draft.







U.S.  EPA.   1983.   Methodology and Guidelines  for  Reportable  Quantity Deter-



minations  Based on  Chronic Toxlclty  Data.   Prepared  by  the  Environmental



Criteria and Assessment Office,  Cincinnati,  OH,  OHEA  for  the Office of Solid



Waste and Emergency Response, Washington, DC.







von  Lehmden,   D.J.,  R.P.   Hangebrauck  and  J.E.  Meeker.   1965.   Polynuclear



hydrocarbon  emissions  from  selected  Industrial  processes.   J.  A1r  Pollut.



Control Assoc.  15: 306-315.
                                     -24-

-------
                                   APPENDIX

                         Summary Table for Coal Tars3
                  Species
Experimental
Dose/Exposure
Effect
Inhalation
AIS
AIC
Carcinogenic humans
potency

NO
NO
0-700* mg/m3- lung tumors 3.2b
month (mg/kg/day)"1
Oral

  AIS

  AIC
  Carcinogenic
  potency
                                  NO

                                  NO

                                  NO
aSource: U.S. EPA, 1982a

bTh1s value 1s not a q-|*, but Instead an Incremental risk value expressed
 1n equivalent units and  based  on  human  ep1dem1olog1cal  data from coke oven
 workers.

NO = Not derived
                                     -25-

-------