FINAL DRAFT
            United States                                     ECAO-CIN-P276
            Environmental Protection                               July, 1987
            Agency
EPA       Research and
            Development
            HEALTH AND ENVIRONMENTAL EFFECTS PROFILE
            FOR BENZO(6HI)PERYLENE
            Prepared for
            OFFICE OF SOLID WASTE AND
            EMERGENCY RESPONSE
           Prepared  by

           Environmental Criteria and  Assessment  Office
           Office of Health and  Environmental Assessment
           U.S. Environmental Protection  Agency
           Cincinnati, OH  45268

  Us. £OW
          m"~' ' Prof*,**-    DRAFT: D0 NOT CITE OR QUOTE
                 ecf'0n AO~-
             eoe^66*             N°TICE
        This document Is a preliminary  draft.  It has not been formally released
      by the U.S. Environmental Protection Agency and should  not at this stage be
      construed to represent Agency policy.  It Is  being circulated  for comments
      on Its technical accuracy and policy Implications.

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                                  DISCLAIMER







    This report  is  an external draft  for  review purposes only  and  does  not



constitute  Agency  policy.   Mention of  trade  names  or  commercial  products



does not constitute endorsement or recommendation for use.
                                      ii

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                                    PREFACE
    Health  and  Environmental  Effects  Profiles  (HEEPs)  are prepared  for  the
Office  of  Solid Waste  and Emergency  Response  by the  Office of  Health  and
Environmental  Assessment.   The  HEEPs are  Intended  to  support  listings  of
hazardous  constituents  of  a wide  range  of  waste  streams  under  Section 3001
of the  Resource  Conservation  and Recovery Act  (RCRA),  as  well  as to provide
health-related limits for  emergency actions under  Section  101  of the Compre-
hensive  Environmental   Response,  Compensation  and  Liability  Act  (CERCLA).
Both  published  literature  and   Information  obtained  from  Agency  program
office  files  are   evaluated  as  they  pertain   to  potential  human  health,
aquatic life and environmental effects  of hazardous  waste  constituents.  The
literature  searched and   the  dates  of  the  searches  are  Included  1n  the
section  titled  "Appendix:  Literature  Searched."   The  literature  search
material is current through November,  1985.

    Quantitative  estimates  are   presented   provided  sufficient  data  are
available.  For  systemic toxicants, these Include  Reference  doses (RfDs)  for
chronic exposures.   An  RfD is defined  as the amount of a chemical  to  which
humans  can be  exposed  on  a dally  basis over  an  extended  period  of  time
(usually a  lifetime) without suffering a  deleterious effect.   In the case of
suspected  carcinogens,  RfDs  are  not  estimated  In this  document  series.
Instead, a carcinogenic potency  factor  of  q-|*  1s  provided.   These  potency
estimates  are   derived  for   both  oral  and   Inhalation   exposures  where
possible.   In  addition,  unit  risk estimates  for air and  drinking  water  are
presented based on Inhalation and oral data,  respectively.

    Reportable quantities  (RQs)  based on both chronic  toxidty  and cardno-
genldty are derived.  The  RQ Is  used to  determine the  quantity of a hazard-
ous substance  for  which notification  1s  required  1n the event  of  a  release
as specified under  CERCLA.   These two RQs (chronic  toxidty  and cardnogen-
1c1ty)  represent  two of  six scores  developed   (the remaining  four  reflect
1gn1tab1l1ty, reactivity,  aquatic toxidty and acute mammalian toxidty).

    The  first  draft  of  this  document  was  prepared  by  Syracuse  Research
Corporation  under   EPA  Contract   No.   68-03-3228.   The  document was  subse-
quently  revised  after  reviews   by staff within  the Office  of Health  and
Environmental Assessment:  Carcinogen  Assessment Group,  Reproductive  Effects
Assessment Group,  Exposure Assessment Group,  and  the Environmental  Criteria
and Assessment Office 1n Cincinnati.

    The HEEPs will  become  part  of the  EPA RCRA and  CERCLA dockets.
                                      111

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                              EXECUTIVE SUMMARY

    Benzo(gh1)perylene 1s a pale yellow-green  solid  at  ambient  temperatures.
It  Is  soluble  In  1,4-d1oxane,  dlchloromethane,  benzene  and acetone  (IARC,
1983),  but  1s   practically   Insoluble  1n  water  (Pearlman  et  al.,   1984;
Yalkowsky and Valvanl, 1979).   It  reacts  with bromomalelc anhydride to  form
bromlnated compound  and  coronene  dicarboxyllc  anhydride derivatives  (IARC,
1983).   This compound  1s  neither  commercially  produced  nor  used  In  the
United States  (IARC,  1983).   It can  be  Isolated from coal  tar  (IARC,  1983)
or from products of hydrogenatlon of coal  (U.S.  EPA/NIH,  1986).
    If  released  to  the  aquatic   environment,   benzo(gh1Jperylene  1s   not
expected  to   hydrolyze,   oxidize   (by  R0»  radical  or  10p)  or   volatilize
significantly.
    A  static culture  flask-screening blodegradatlon  study  has  shown  that
benzo(gh1)perylene  can   be   significantly  blodegraded   (Fochtman,   1981);
however, mlcroblal oxidation  of  PAH requires  oxygen and will  not  proceed In
anoxlc sediments  or  water (U.S. EPA/NIH,  1986).   In the dissolved  state In
the  water column,  direct  photolysis  may be   an   Important  transformation
process  (U.S.  EPA/NIH,  1986); however, a  significant  portion  of  the  benzo-
(gh1Jperylene  present  In the aquatic environment  1s  expected  to  be  1n an
adsorbed   state,  which   may  not   be   susceptible   to  phototransformatlon.
Adsorption to  suspended  partlculate  matters  and  sediments  1n  water   Is an
Important  environmental  fate  process  for  this compound.  The  very  low water
solubility and   high  log  K     of  benzo(gh1)perylene  suggest  a  significant
potential  for  bloaccumulation;   however,  PAH  may  not   bioconcentrate  appre-
ciably  1n organisms  such as fish,  that  have  microsomal  oxldase, as   this
                                      1v

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enzyme metabolizes  PAH (Santodonato et  al.,  1981).   Therefore, bioaccumula-
tlon  potential may  be  dependent  on  the  organism  being  considered.   The
uniformity  In  the  concentration  of  benzo(gh1Jperylene In deep sediment cores
of  remote  lakes  (Tan  and  Heit,  1981)  Indicate  that  benzo(ghi)perylene  1s
very  persistent  under  anaerobic  and  dark  conditions.   If  released  to  the
atmosphere, benzo(ghiJperylene will  exist  almost  entirely In the particulate
(adsorbed)  phase.   The rate  of  photolysis has been  found  to  vary  with  the
adsorbing  substrate  (Behymer  and  Kites,  1985);  photolysis of  benzo(ghi)-
perylene  adsorbed  to  fly  ash may  have some  Importance, but  adsorption  to
carbon black  stabilizes the  compound toward  potential  phototransformatlon.
Benzo(ghi)perylene may  be  transported  over  long  distances 1n the atmospheric
aerosol.    Removal  from  the  air  may  occur by wet and  dry  deposition.   If
released  to soil,  benzo(gh1)perylene may be susceptible to  slow biodegrada-
tion under  aerobic conditions.  Under  most  conditions,  It 1s not expected to
leach or  volatilize from soils.
    Human  exposure  to  benzo(ghi)perylene occurs  primarily  through  the inha-
lation of  tobacco  smoke and  polluted  air,  and by the  Ingestion  of  contami-
nated food and water  (IARC,  1983).   It  occurs  ubiquitously In  products  of
Incomplete  combustion  and  in  coal  tar,  and is  a component  of  gasoline  and
diesel engine  exhaust;  it  also occurs naturally  1n crude oils  (IARC, 1983).
It has been widely detected  1n  drinking water,   surface water, groundwater,
rainwater  and  aquatic  sediments  (see  Tables  3-1  and  3-2),  In many  foods
(Santodonato et  al.,   1981;  Dennis  et al.,  1983) and  in the  ambient  atmo-
sphere (see Table 3-3).  The  average  dietary  intake of benzo(ghiJperylene in
England   has  been  estimated  to be  0.21  yg/day  (Dennis  et  al.,  1983);  the
average   adult  Intake  in  the United  States   from  drinking  water   has  been
estimated  to be  2.0 ng/day,  while  the inhalation Intake has  been  estimated

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to be  10  ng/day.   Its presence 1n  food  Is  a result of contamination  from  a
polluted environment  and  formation during cooking  by  pyrolysls  (Santodonato
et a!.,  1981;  Fazio  and Howard,  1983).  Its  concentration  1n the  ambient
atmosphere in the United States has apparently  been decreasing  over  the last
30 years.   The  ambient air  concentration  of benzo(gh1)perylene is  expected
to be higher  during winter than summer,  apparently  because  of  the  burning of
fossil fuel for  heating during winter  months  (Greenberg et  al.,  1985).
    Pertinent data  regarding the  toxlcity  of benzo(gh1)perylene  to  aquatic
organisms  could not  be located in  the  available literature as cited  In  the
Appendix.   Several   studies  reported  data  concerning residues  in  aquatic
organisms.  The following  data were  reported  for  species  that are  commonly
eaten by humans:  mussels  from Norway,  trace-87 ng/g  (Knutzen  and  Sortland,
1982); clams  from 3apan,  0.23-0.95 ng/g (Tsujl et  al., 1985);  lobsters from
eastern Canada, 0.19  ng/g before  Impoundment  and  51  ng/g  after  Impoundment
(Dunn and  Fee,  1979).   Obana et al.  (1983)  reported  BCF values  of 1000-1400
for  short-necked  clams,  T.   japonica,   exposed  to  0.06-0.13   pg/ft.  for  1-7
days.
    Pertinent data regarding  the  gastrointestinal  or  pulmonary  absorption of
benzo(gh1Jperylene could not be located  in  the  available  literature  as cited
1n the Appendix.  Data  from  other  structurally-related PAH  suggest,  however,
that benzo(ghi)perylene  Is  absorbed readily  from  the  gastrointestinal tract
(Rees et al., 1971) and  lungs  (Kotln  et  al., 1969; Vainio  et al.,  1976).   In
general,  PAH  are  highly lipld   soluble  and  can  pass  across  epithelial
membranes  (U.S.  EPA, 1980).
    Pertinent data  regarding  the  distribution, metabolism or excretion of
benzo(ghiJperylene could not be located  in  the  available  literature  as cited
In the Appendix.
                                      vi

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    Single  Intrapulmonary  Injections  of  0.16,  0.83  or 4.15  mg benzo(ghl)-
perylene  In  beeswax-trloctanoln  mixture  Into  groups of  34  or  35  rats
produced  a   low  Incidence  (4/34)  of  lung  squamous  cell  carcinomas  1n  the
high-dose group  after  lifetime  observation  (Deutsch-Wenzel  et a!.,  1983).
Lung tumors  did not  occur  1n  untreated or vehicle treated  controls, but IARC
(1983)  indicated that  the  tumors  in  the treated group may  be attributable to
Impurities In the test product, which was 98.5% pure.
    Tumorigenldty  of  benzo(gh1 )perylene was  not  demonstrated  1n mice  1n
skin  application  studies  involving  up  to  3  times/week   treatment  for  12
months  (Lijlnsky  and  Saff1ott1,  1965; Van Duuren  et a!., 1970;  Van  Duuren
and  Goldschmidt,  1976;  Muller,   1968;  Hoffmann  and  Wynder,  1966) in  skin
initiation-promotion  studies  using  croton oil  as a promoter  (Hoffman  and
Wynder,  1966)  and  PMA  as a  promoter   (Van   Duuren  et  al.,   1970)  and  by
bimonthly  subcutaneous  Injections   for   5   or   6   months  (Muller,  1968).
Enhancement   of the  dermal  carcinogeniclty of  benzo(a)pyrene  by simultaneous
application   of benzo(ghi)perylene has been reported  in  mice  (Goldschmidt  et
al.,  1973;   Van  Duuren  et al.,  1973;  Van  Duuren  and Goldschmidt,  1976),
indicating possible cocarcinogenicity of benzo(ghiJperylene.
    Benzo(gh1)perylene was mutagenlc  to j>. typhimurium strains  TA98,  TA100,
TA1537 and TA1538  (Andrews et  al., 1978; Hossanda  et al., 1979; Salamone  et
al., 1979)  and  TH677  (Kaden et  al.,   1979) when  assayed  In the presence  of
exogenous metabolic  activation preparations.   Intraperitoneal  injection  of
benzo(ghi Jperylene  into hamsters  on  day 10  of  gestation did not  Induce
transformations  In the embryo  cells (Quarles  et al., 1979).
    Pertinent  data  regarding  toxic,   teratogenic   or other  reproductive
effects of benzo(ghiJperylene could  not be located in  the available litera-
ture as cited in  the Appendix.

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    Data were  Insufficient  to derive an  RfD,  RQ,  q,* or  F  factor.   Benzo-
(ghl)perylene was placed In CAG Group D, wh}ch means that classification for
cardnogenlclty and  hazard  ranking  for cardnogenldty are not possible.

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                              TABLE OF  CONTENTS
                                                                       Page
1.  INTRODUCTION	   1

    1.1.   STRUCTURE AND CAS NUMBER	    1
    1.2.   PHYSICAL AND CHEMICAL PROPERTIES 	    1
    1.3.   PRODUCTION DATA	    2
    1.4.   USE DATA	    2
    1.5.   SUMMARY	-	    2

2.  ENVIRONMENTAL FATE AND TRANSPORT PROCESSES	    3

    2.1.   WATER	'	'	    3

           2.1.1.   Hydrolysis	    3
           2.1.2.   Oxidation 	    3
           2.1.3.   Photolysis	    3
           2.1.4.   Mlcroblal Degradation 	    4
           2.1.5.   Volatilization	    4
           2.1.6.   Adsorption	    5
           2.1.7.   Bloconcentratlon	    5
           2.1.8.   Persistence 	    6

    2.2.   AIR	    6
    2.3.   SOIL	    7

           2.3.1.   Mlcroblal Degradation	    7
           2.3.2.   Chemical Degradation	    7
           2.3.3.   Adsorption	    8
           2.3.4.   Volatilization	    8

    2.4.   SUMMARY	    8

3.  EXPOSURE	   10

    3.1.   WATER	   10
    3.2.   FOOD -.	   14
    3.3.   INHALATION	   15
    3.4.   DERMAL	   17
    3.5.   SUMMARY	   17

4.  PHARMACOKINETCS	   18

5.  EFFECTS .  .  -	   19

    5.1.   CARCINOGENICITY	   19
    5.2.   MUTAGENICITY	   20
    5.3.   TERATOGENICITY	   24
    5.4.   OTHER REPRODUCTIVE  EFFECTS 	   24
    5.5.   CHRONIC AND SUBCHRONIC TOXICITY	   24
    5.6.   OTHER RELEVANT INFORMATION 	   24
    5.7.   SUMMARY	   24
                                     1x

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                          TABLE OF CONTENTS  (cont.)

                                                                        Page
 6.  AQUATIC TOXICITY	   26

     6.1.   ACUTE	   26
     6.2.   CHRONIC	   26
     6.3.   PLANTS	   26
     6.4.   RESIDUES	   26
     6.5.   SUMMARY	   27

 7.  EXISTING GUIDELINES AND STANDARDS 	   28

     7.1.   HUMAN	   28
     7.2.   AQUATIC	   29

 8.  RISK ASSESSMENT	   30

 9.  REPORTABLE QUANTITIES 	   32

     9.1.   REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC
            TOXICITY	   32
     9.2.   WEIGHT OF EVIDENCE AND POTENCY FACTOR (F=1/ED10)
            FOR CARCINOGENICITY	   32

10.  REFERENCES	   36

APPENDIX: LITERATURE SEARCHED	   46

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LIST OF TABLES
No.
3-1
3-2
3-3
5-1
S-?
9-1
Title
Benzo(gh1 Jperylene Monitoring Data for Various Types
of Water 	
U.S. Sediment Monitoring Data for Benzo(ghi Jperylene. . .
U.S. A1r Monitoring Data for Benzo(gh1 Jperylene 	
Dermal and Injection Cardnogenlclty Studies of
Benzo(gh1 Jperylene 	
Mutagen1c1ty Testing of Benzo(gh1 Jperylene 	
Benzo(gh1)perylene: Minimum Effective Dose (MED) and
• Reoortable Quantity (RQ) 	
Paqe
. . 11
. . 13
. . 16
. . 21
23 "
. . 33

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                             LIST  OF ABBREVIATIONS
ADI                     Acceptable dally Intake
BCF                     Bioconcentratlon factor
Koc                     Soil sorptlon  coefficient
Kow                     Octanol/water  partition coefficient
MED                     Minimum effective dose
PAH                     Polycycllc aromatic hydrocarbons
PMA                     Phorbol myrlstate acetate
ppb                     Parts per billion
ppm                     Parts per million
ppt                     Parts per thousand
RfD                     Reference dose
RQ                      Reportable quantity
TLV                     Threshold-limit value
TWA                     Time-weighted  average
UV                      Ultraviolet
US                      Water solubility
                                      xll

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                               1.  INTRODUCTION

1.1.   STRUCTURE AND CAS NUMBER

    Benzo(gh1)perylene  Is  also  known as  1,12-benzoperylene  (U.S.  EPA/NIH,

1986).  The  structure,  empirical  formula, molecular weight  and  CAS  Registry

number for this chemical are as follows:
Empirical formula:  C__H.._

Molecular weight:  276.3

CAS Registry number:  191-24-2

1.2.   PHYSICAL AND CHEMICAL PROPERTIES

    Benzo(gh1)perylene  1s  a pale  yellow-green  crystalline solid at  ambient

temperature.   It  Is  soluble  1n  1,4-dloxane,  dlchloromethane,  benzene  and

acetone  (IARC,  1983), but  1s  practically Insoluble  1n  water.  Some of  the

relevant physical properties of this compound are listed  below:
Melting point:

Solubility 1n distilled
water at 25°C:
                            278.3

                            0.553

                            0.3

                            0.26


Kow:                        7.10 (estimated)



                            7.04 (estimated)


Vapor pressure at 25°C:      l.OlxlO'10 mm Hg
                      IARC, 1983

                      Pearlman et a!.,
                      1984
                      Yalkowsky and
                      Valvanl, 1979
                      Halters and Luthy,
                      1984

                      Yalkowsky and
                      Valvanl, 1979;
                      Walters and Luthy,
                      1984
                      Ruepert et a!.,
                      1985

                      Santodonato et  al.,
                      1981
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Henry's Law constant:       6.6xlO~8 atm-mVmol            Mabey  et  al.,  1981
                            (estimated from water
                            solubility of  0.553  yg/4)
                            1.44xlO~7 atm-mVmol
    Chemically, benzo(gh1)perylene reacts with bromomalelc anhydride  to  form
dlbromlnated  compound  and coronene  dlcarboxyllc  anhydride derivatives.   It
also reacts with NO and N0_ to form nltro derivatives  (IARC,  1983).
1.3.   PRODUCTION DATA
    The  compound   1s  neither  commercially  produced  nor  Imported  Into  the
United States  (IARC,  1983; USITC, 1984).   It  can be Isolated from coal  tar
(IARC, 1983) or from products of hydrogenatlon  of  coal  (U.S.  EPA/NIH,  1986).
1.4.   USE DATA
    There  Is  no  known commercial  use  of this  compound  (IARC, 1983).   Small
amounts of benzo(gh1)perylene are used for scientific  research.
1.5.   SUMMARY
    Benzo(gh1)perylene Is  a  pale  yellow-green  solid at  ambient  temperatures.
It  1s  soluble  In  l,4-d1oxane, dlchloromethane,  benzene and acetone  (IARC,
1983),  but  1s  practically   Insoluble   1n  water  (Pearlman  et  al.,  1984;
Yalkowsky  and  Valvanl, 1979).   It reacts with bromomalelc anhydride  to  form
bromlnated  compound  and coronene  dlcarboxyllc anhydride  derivatives  (IARC,
1983).   This   compound  1s  neither  commercially  produced  nor  used  In  the
United States  (IARC,  1983).    It  can  be Isolated  from coal tar  (IARC,  1983)
or from products of hydrogenatlon of coal (U.S. EPA/NIH, 1986).
0864p                               -2-                              10/31/86

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                2.  ENVIRONMENTAL FATE AND TRANSPORT PROCESSES
2.1.   WATER
2.1.1.   Hydrolysis.    Benzo(gh1Jperylene   contains   no  hydrolyzable  func-
tional groups;  therefore,  aquatic hydrolysis Is  not  expected  to be signifi-
cant  (Habey et a!., 1981).
2.1.2.   Oxidation.   The  rate  constants  for  the  oxidation  of benzo(ghl)-
perylene  with  photochemlcally  produced  R0_  radical  and  aO?  have  been
estimated  to be  <36  and  <360  M'1  hr'1,  respectively,  at  25°C  (Mabey  et
al.,  1981).   Assuming  that  concentrations  of  R0»  radical  and  10?  1n
natural  water  are  10~»  and  10"12  M  (Mabey  et  al.,   1981),   respectively,
the  respective half-lives are  estimated  to  be  >2000  and >20,000  years.
Therefore,   oxidation   by  RO   radical  and  *Q   1s   not  environmentally
relevant.
2.1.3.   Photolysis.   In  a cyclohexane  solvent,  benzo(gh1)perylene  exhibits
UV absorption  maxima  at 299,  311,  324,  328, 344,  362, 383,  392  and  396  nm
(IARC, 1983); therefore,  direct  photolysis 1n sunlight  1s  a definite possi-
bility.   In  the dissolved  state 1n the  water  column,  photolysis may  be  an
Important  transformation  process (U.S.  EPA/NIH,  1986);  however,  a  signifi-
cant  portion  of  the  benzo(gh1)perylene  1n  the  aquatic  environment  Is
expected to  be  present 1n the adsorbed  state  (Section  2.1.6.).   Behymer and
Hltes  (1985)  examined  the  atmospheric  photolysis  of  benzo(gh1Jperylene
adsorbed  to  various substrates  and  found relatively  significant  photolysis
when  adsorbed  to  silica  gel,  alumina  or  fly  ash,  but  only  slow  photolysis
when  adsorbed  to  carbon  black  adsorption  (Section  2.2.).   Therefore,  the
significance  of  potential  aquatic   photolysis  may depend  on the  adsorbing
substrate  as well  as  the  Intensity  of  the  sunlight  reaching  the  water
0864p                               -3-                              10/31/86

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column.  As the depth of water  Increases,  the  light  Intensity will  decrease;
as a  result,  photolysis will become  Increasingly  less significant  with  the
Increase 1n the depth of water.
2.1.4.   Hlcroblal  Degradation.    Fochtman  (1981)  examined  the  blodegrad-
abllHy of  benzo(gh1)perylene  1n a static  culture  flask-screening  procedure
1n which 1J4 of  the compound was dissolved  1n  an emulslfler  and  added  to  the
bacterial   suspension  (domestic   wastewater  seed)  at  a concentration  of  1-2
ppm.  The suspension was Incubated  for  7  days. A  fresh bacterial suspension
was prepared weekly using the seed  from the previous  week,  and the procedure
was continued for  28  days.   Approximately 60% of  the  benzo(gh1)perylene  was
usually degraded  during a  7-day  Incubation.   Thus,   benzo(gh1)perylene  was
found to be biodegradable;  Its  blodegradatlon rate was slightly higher  than
that of benzo(a)pyrene,  which underwent -41% blodegradatlon 1n 7 days.
    PAH with  at  least  four  aromatic  rings  are  degraded slowly  by microbes
and blodegradatlon  1s considered to be the ultimate  fate  process 1n natural
water  (U.S.  EPA/NIH, 1986);  however,  the  concentrations  of  microorganisms
capable of  oxidizing  the hydrocarbons  are  extremely   low In  all  but heavily
polluted fresh  and  marine  waters,  and most species of microorganisms  cannot
use PAH as a  sole carbon source.  Hlcroblal oxidation of  PAH requires  oxygen
and  will  not  proceed  1n  anoxlc  sediments  or water  (U.S.  EPA/NIH,  1986).
Thus,  1t   appears   that  the  significance  of  blodegradatlon  of  benzo(ghl)-
perylene  In  natural  waters  will depend  on the nature  of water.   In deep,
slow  moving,  turbid water,  blodegradatlon  may be  more significant than In
shallow, rapidly flowing, clear  streams.
2.1.5.   Volatilization.  Using  the vapor  pressure and  water  solubility at
25°C, Mabey et  al.  (1981)  estimated the Henry's  Law constant for benzo(ghl)-
perylene   to    be   1.44xlO~7   atm»m3/mol.    This  value   of   Henry's   Law


0864p                               -4-                              05/15/87

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  constant  Indicates that  the pollutant  Is  essentially  nonvolatile (Lyman  et
  al.,  1982);  therefore,  benzo(gh1)perylene  1s  not  expected  to  volatilize
  significantly  from the  aquatic  environment.
  2.1.6.    Adsorption.   Rump  (1984)  examined the partitioning  of  benzo(ghl)-
  perylene  between  water  and sediment  phase  with sediments  from two  rivers.
  The  amount  of benzo(gh1)perylene  that  partitioned  to the sediment was  found
  to be  2.5xl04-3.1xl05  times  greater  than  the amount   that  partitioned  to
  the  water column.
      The  estimated  K    values,  which  are  >1  million (Section  2.3.3.), and
  the  widespread  detection  of  benzo(gh1)perylene  1n  various  U.S. sediments
  (Section  3.1.) Indicate  that adsorption to suspended partlculate matter and
  sediments  1s  an  Important  environmental  process.   Movement  by sedlment-
  sorbed  benzo(gh1Jperylene  Is  probably  an  Important transport  process for
.  this compound  (U.S. EPA/NIH,  1986).
  2.1.7.    B1oconcentrat1on.   Estimation of  BCF can  be made  from the  follow-
  ing  equations  (Lyman et al.,  1982):
                           log BCF  = 0.76 log KQW 0.23                    (2-1)
                      log BCF = 2.791-0.564 log (WS  1n ppm)               (2-2)
  Based  on  a  water  solubility of  0.00026 ppm at 25°C and a  log K   of  7.10
  (Walters  and Luthy, 1984),  the BCF values estimated from Equations  2-1 and
  2-2  for  benzo(gh1Jperylene  are  146,500  and  65,000,   respectively,   which
  suggest   significant   bloaccumulatlon  potential.    PAH,  however,  may  not
  appreciably  bloconcentrate  1n organisms such  as  fish that contain mlcrosomal
  oxldase,  as  this   enzyme  may  metabolize  PAH   (Santodonato  et  al.,   1981).
  Therefore,   the  bloaccumulatlon  potential  may  be  very  dependent   on the
  organism  being considered.
 0864p                               -5-                              10/31/86

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2.1.8.   Persistence.  Tan  and HeH  (1981)  monitored  sediment  cores  taken

from Woods Lake and  Sagamore Lake  In  the  remote  Adirondack  Forest  of  upstate

New York  for  various.  PAH.   The following benzo(gh1)perylene  concentrations
     •
(ng/g dry sediment wt) were  found  at  various  depths  of  Woods  Lake:  1400 (0-4

cm), 500  (4-8  cm),  180 (8-11 cm), 110  (12-17  cm),  44 (24-26 cm),  46  (42-44

cm) and  59  (80-84 cm).   The constancy  1n  the concentration of  benzo(ghl)-

perylene  In  the  deeper sediment  cores  Indicates that  the  compound  1s  very

persistent  under  the  nonphotolytlc,  anoxlc  conditions   present  1n  deep

sediment cores.

2.2.   AIR

    Based on a  vapor pressure  of  10~10 mm Hg at 25°C (Mabey et a!.,  1981),

benzo(gh1)perylene Is  likely to exist almost  entirely  1n  the  partlcle-sorbed

state 1n  the atmosphere.   Yamasakl et al. (1982) monitored the  urban  air  of

a Japanese city for  an entire  year for  PAH  1n both  the vapor  and partlculate

phases;  the monitoring covered a  wide  temperature  range.   The  six-ring  PAH

(Including  benzo(gh1)perylene,   o-phenylenepyrene    and   anthracene)   were

detected  1n  the  partlculate phase but  not   In  the vapor  phase,   while  the

three- to five-ring  PAH were found 1n both phases with  the  partlonlng ratio

depending on temperature.

    Behymer and  HHes (1985)  examined  the  atmospheric photolysis  of  benzo-

(gh1Jperylene adsorbed onto  various  substrates.  With a  rotary  photoreactor

and a  medium-pressure mercury  lamp  as  the light source,  benzo(gh1Jperylene

exhibited the following photolytlc half-lives 1n the adsorbed state:


                     Substrate           Half-Life (hours)

                    SHIca gel                      7
                    Alumina                       22
                    Fly ash                       29
                    Carbon black               >1000
0864p                               -6-                              05/15/87

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Adsorption  to  carbon  black  clearly  stabilizes  the  phototransformatlon  of
benzo(gh1)perylene.  In  the  atmosphere,  adsorption to stabilizing substrates
will  allow  benzo(gh1)perylene to be  transported  over long  distances  1n the
atmospheric  aerosol.   Its  detection  In  the remote  rural  air  of  South
Carolina  (Keller  and  Bldleman, 1984)  and 1n  sediments  from remote  lakes  in
the  Adirondack  Forest,  NY (Tan and  Heit,  1981) may Indicate that long-range
transport occurs.
     Removal  of  adsorbed benzo(gh1Jperylene from  the  atmosphere  may  occur  by
wet  and  dry deposition.   Benzo(gh1)perylene  has  been detected  1n rainwater
(Lunde et a!.,  1976;  L1gock1 et  a!.,  1985).   Its presence In lake sediments
1n  the  Adirondack  Forest,  NY, has  been  attributed   to  physical  deposition
(Tan and Heit, 1981).
     Since  benzo(gh1)perylene  does   not   significantly  exist   1n  the  vapor
phase,  atmospheric  reaction  with   photochemlcally  produced  HO  radical  or
vapor phase photolysis Is not expected to be Important.
2.3.   SOIL
2.3.1.   Hlcroblal Degradation.   The soil bacterium Bacillus megaterlurn has
been  found   to  metabolize benzo(gh1Jperylene  and  other PAH  (U.S.  EPA/NIH,
1986); however,  sufficient data  are not  available  to  predict  the  signifi-
cance of  the  soil  blodegradatlon  for benzo(gh1)perylene.   Based  on  the .data
1n  Section   2.1.4.,  benzo(gh1Jperylene  may be   slowly  blodegraded   1n  soil
under aerobic conditions.
2.3.2.   Chemical  Degradation.   Pertinent   data  regarding   the  chemical
transformation of  benzo(gh1Jperylene 1n  natural  soils  could not  be  located
1n the available literature as cited 1n the Appendix.
0864p                               -7-                              10/31/86

-------
2.3.3.   Adsorption.   Estimation  of  KQC  can  be  made  from  the  following
regression equations (Lyman et a "I.,  1982):
                 log KQC = 0.44-0.54 log (HS 1n mol  fraction)         •  (2-3)
                          log  KQC =  1.00  log  K.QW 0.21                    (2-4)
Based  on  a water  solubility of  0.26 vg/8.  at 25°C  and a  log  K    of  7.10
(Walter and  Luthy, 1984),  the  K   values  estimated  from Equations  2-3  and
2-4  for  benzo(gh1)perylene  are  1.8  and  7.8 million,  respectively,  which
suggests so"1l  Immobility;  however,  the  detection  of benzo(gh1Jperylene  1n
several groundwaters  (Section 3.1.) Indicates  that leaching  can  occur  under
certain conditions.   Leaching may  occur  1n soils  that  contain  low  organic
matter (e.g.,  sand),  and  may also  occur  from sites  subjected to  spills  or
disposal  of appropriate  petroleum and coal materials that contain  high  con-
centrations of PAH  Including  benzo(gh1Jperylene;  however,  benzo(gh1)perylene
Is not expected to leach, 1n soil under most conditions.
2.3.4.   Volatilization.    Benzo(gh1)perylene   cannot   be   expected    to
volatilize significantly  from soil  surfaces  because of  Us very  low  vapor
pressure of 10~10 mm Hg at 25°C and  a  very high K   value of  -10*.
2.4.   SUMMARY
    If  released  to  the  aquatic  environment,   benzo(gh1)perylene  Is  not
expected  to  hydrolyze,  oxidize  (by R0?  radical   or  10?)  or  volatilize
significantly.   A static  culture  flask-screening  blodegradatlon  study  has
shown  that benzo(gh1)perylene  can  be  significantly blodegraded (Fochtman,
1981);  however,  mlcroblal  oxidation  of  PAH  requires  oxygen  and  will  not
proceed In anoxlc  sediments or  water  (U.S. EPA/NIH,  1986).   In the dissolved
state  In the water  column,  direct photolysis may  be an Important transforma-
tion  process  (U.S. EPA/NIH,  1986);  however,  a  significant portion of  the
benzo(gh1)perylene  present  1n the  aquatic  environment  1s  expected to  be 1n
an  adsorbed  state,  which  may  not  be  susceptible  to  phototransformatlon.

0864p                               -8-                               10/31/86

-------
Adsorption  to suspended  partlculate matters  and sediments  1n water  Is  an
Important environmental  fate  process for this compound.   The very low water
solubility  and  high  log  K    of   benzo(gh1)perylene  suggest  a   significant
potential for  bloaccumulatlon;  however,  PAH  may  not bloconcentrate appreci-
ably  1n  organisms  such  as  fish,  that have mlcrosomal oxldase, as  this enzyme
metabolizes  PAH  (Santodonato  et   al.,  1981).   Therefore,  bloaccumulatlon
potential may  be  dependent  on the  organism being considered.  The uniformity
In  the  concentration  of benzo(gh1Jperylene 1n deep  sediment  cores of remote
lakes (Tan  and He1t,  1981)  Indicates that benzo(gh1)perylene 1s very persis-
tent  under  anaerobic and  dark  conditions.   If  released  to  the   atmosphere,
benzo(gh1 )perylene will  exist almost entirely  In the partlculate (adsorbed)
phase.   The rate  of  photolysis has  been found  to  vary  with  the adsorbing
substrate   (Behymer   and   HHes,   1985);  photolysis  of  benzo(gh1 Jperylene
adsorbed to fly ash may have  some  Importance, but adsorption to carbon black
stabilizes  the compound  toward  potential  phototransformatlon.    Benzo(ghl)-
perylene may  be  transported over  long  distances  1n  the atmospheric aerosol.
Removal   from  the air may  occur-  by  wet  and  dry  deposition.   If  released  to
soil,  benzo(gh1)perylene may be  susceptible to slow  blodegradatlon  under
aerobic  conditions.   Under  most conditions,  It  Is  not  expected  to leach  or
volatilize from soils.
0864p                               -9-                              05/15/87

-------
                                 3.   EXPOSURE

    Human exposure  to  benzo(gh1)perylene occurs primarily through  the  Inha-
lation of  tobacco  smoke and polluted  air,  and by the  1ngest1on  of  contami-
nated  food  and  water  (IARC,  1983).    It  occurs  ubiquitously 1n  products  of
Incomplete combustion.  In  coal  tar  and  In  gasoline engine  exhaust;  It  also
occurs naturally In crude oils  (IARC,  1983).
3.1.   HATER
    Table 3-1 lists  various benzo(gh1Jperylene monitoring  data  for  drinking,
ground, surface and  rain  water;  Table 3-2  lists sediment  monitoring data  at
various U.S.  locations.   In  an analysis  of  the  U.S.  EPA  STORET  database,
benzo(gh1)perylene  was  positively  detected  1n  1.0%  of  914  surface  water
observation  stations  and  1.554 of 1211 effluent reporting stations  (Staples
et a!.,  1985).   Grlest (1980) detected  benzo(gh1Jperylene at  concentrations
of  7.3 yg/g  (dry  sediment)  In  the .sediment and  2.0  v9/&   In the  water
1n an  effluent  wastewater  channel  from a  coking  plant.  Walters  and  Luthy
(1984)  detected  levels  <90   ng/s.   1n  wastewaters  from  two  coal  coking
plants.
    In general,  PAH can be released  to water from  Industrial  and  municipal
effluents, atmospheric  fallout  and  precipitation,  road  runoff  (tire  wear,
bitumen and  asphalt surfaces,  cracked lubricating oils) and marine shipping
and harbor oil  (Santodonato et al., 1981).  Herrmann and Huebner (1982) have
suggested that  most PAH pollution of  rivers  In urban  areas originates  from
storm  water  overflows  containing  street  and  roof  dust  washed off  during
storms;  the  contribution  of  precipitation-borne  PAH  may  be  comparatively
small  1n such Instances.
0864p                               -10-                             10/31/86

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                                  TABLE  3-2

             U.S. Sediment Monitoring Data for Benzo(gh1)perylene
   Concentration
      (ng/g)
       Location
Sampling
  Date
Reference
32-120

14-130


12-32

7-150


70-600
1400  (0-4 cm depth)
500  (4-8 cm depth)
59  (80-84 cm depth)

620
Cayuga Lake, NY            1978
(deep water)
Cayuga Lake, NY
(IHtoral sediment)
Washington State
(bottom river sediment)
Columbia River
(suspended sediment)
Lake Erie                  NR
Woods Lake, NY             NR
Puget Sound, WA            NR
             Helt,  1985
1979-1980    Prahl et al..
             1984
             Eadle et al.,
             1982

             Tan and He1t,
             1981
             Varanasl
             et al.,  1985
NR = Not reported
0864p
            -13-
                  10/31/86

-------
    Based  on  the  monitoring  data  from  Table  3-1,  the  concentration  of
benzo(gh1)perylene 1n  drinking  water may  be -1.0  ppt  (ng/i).  Assuming  an
average  dally  water  Intake  of  2.0 8.  for  an adult,  the  Intake  of  benzo-
(gh1)perylene from drinking water 1s estimated to be 2.0  ng/day.
3.2.   FOOD
    In general,  PAH  found in food  are  present as a result  of contamination
from  a  polluted environment  or are  formed  during  the  cooking  (pyrolysis)
process  (Santodonato  et  a!.,  1981; Fazio  and Howard,  1983);  minute  amounts
of this chemical may also  originate from geochemlcal or  biosynthetlc  sources
(Fazio and Howard,  1983).
    The  following  benzo(gh1)perylene  concentrations   (In  ppb)   have  been
reported  for  various  foods  (Santodonato   et  a!.,  1981):  corn  oil  (0.6),
sunflower oil  (4.0),  soybean  oil  (1.0), olive oil (0.9), peanut  oil  (0.9),
smoked herring  (2.4),  smoked cod  (2.2),  smoked mackerel  (0.2-0.3),  charcoal-
broiled steaks  (6.7),  barbecued ribs  (4.7),  smoked  ham  (1.4),  barbecued beef
(4.3), smoked  bologna (0.04-0.20), smoked  mortadella  (0.4),  heavily  smoked
bacon  (3.0),  charcoal-broiled  hamburger  (trace-14.9),  broiled T-bone steak
(6.2-12.4) and heavily smoked ham (2.5-25.0).
    Dennis  et   al.  (1983)  examined  total-diet  samples  of  food  groups  in
England  and  found  the  following  mean  benzo(ghi)perylene  concentrations  (In
vg/kg)  in  the  various   food   groups:   cereal  (0.28),  meat  (0.05),  fish
(0.12),   oils   and   fats   (1.26),   fruit   and   sugar   (0.06),   vegetables
(0.06-0.08), beverages  (0.01)  and  milk (0.01).    Dennis  et  al.  (1983)  then
estimated  the  total  benzo(gh1Jperylene  dietary  load 1n  England  to  be 0.21
vg/person/day.   Based  on monitoring  of total-diet samples  collected  In the
Netherlands, Vaessen  et  al.  (1984) estimated the maximum food  intake to be
0.9 yg/person/day.


0864p                               -14-                             10/31/86

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3.3.   INHALATION
    Table  3-3  lists  recent (1979-1983) U.S. ambient  air  monitoring data for
benzo(gh1)perylene;  In  general,  the mean  concentrations  detected  are  <2.0
ng/m3.   The  average U.S.  urban  atmosphere  1n   the  early  1960s  has  been
reported  to  have had  a  concentration  of  ~8  ng/m3  (Santodonato et  al.,
1981).   In  1952-53,  the airborne concentration of benzo(gh1)perylene  1n Los
Angeles,  CA,  was reported  to  be 21 ng/m3,  which  was slightly  >3 times the
concentration  1n 1958-59  (Gordon  and  Bryan,  1973).   These  monitoring  data
suggest  that   the  ambient  atmospheric  load of  benzo(gh1Jperylene  has  been
generally  decreasing  over  the  past  30  years.  This  decrease  may be a result
of  decreases   1n coal  consumption  for  residential  heating   and  Industrial
uses,  restrictions  on open burning, and Improved  efficiency for  stationary
Incineration and combustion sources with  Improvements  of  pollution control.
The  higher  atmospheric  levels  of  benzo(gh1 )perylene  1n  wintertime  vs.
summertime  air  1n  New  Jersey  (see Table  3-3)  may  be a  reflection of  an
Increased use of fossil  fuel combustion for heating purposes.
    Assuming an  average ambient  air  benzo(gh1Jperylene  concentration of  -0.5
ng/m3  (from Table 3-3)  and a  human  air Intake  of  20 ma/day, the average
dally  Intake  can be  estimated  to  be 10  ng.   Matsumoto  and  Kashlmoto (1985)
used Japanese monitoring data  to estimate an average dally Intake of 27 ng.
    In  general,   PAH  are  emitted  to  the  atmosphere by  the  combustion  of
fossil fuels  (oil,  coal),  by vehicular  exhausts,  by open  burning  (agricul-
tural  burning,  forest fires,  structural  fires,  refuse  burning) and  by the
burning of wood,  especially for  residential heating (NRC, 1983).
    Benzo(gh1)perylene  has been  Identified  1n  mainstream   cigarette  smoke
1-39  ng/c1garette),   sldestream  cigarette  smoke   (98 ng/clgarette),  smoke-
filled rooms  (17 ng/m3)  and  mainstream  marijuana smoke  (0.7 ng/c1garette)
(IARC, 1983).

0864p                               -15-                             05/15/87

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                                  TABLE 3-3

          U.S.  A1r  Monitoring  Data for Benzo(gh1)perylene (1979-1983)
  Concentration
     (ng/m3)
      Location
 Sampling
   Date
  Reference
0.09-0.56 (mean)
0.09-3
0.02

0.11-1.0 (average)
2.0 (average)
0.59-2.74 (mean)
0.02-0.62 (mean)
0.20-1.31 (mean)

1.0 (mean)
four cities, New Jersey  summer  1981
Columbia, SC             1981-1982
rural South Carolina     1982

three sites,             1979
Washington State

Portland, OR             1984
four cities. New Jersey  winter 1982
                         summer 1982
                         winter 1983
Waterbury, VT
winter 1982
                Harkov et al.,
                1984

                Keller and
                Bldleman, 1984

                Prahl et al.,
                1984

                Llgockl
                et al., 1985

                Greenberg
                et al.. 1985
Sexton et al.,
1985
0864p
              -16-
                      10/31/86

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3.4.   DERMAL
    Pertinent data  regarding  dermal  exposure to benzo(gh1)perylene could not
be located In the available literature as cited 1n the Appendix.
3.5.   SUMMARY
    Human  exposure  to benzo(gh1)perylene occurs  primarily  through the Inha-
lation of  tobacco smoke and  polluted  air,  and by the  1ngest1on  of contami-
nated  food and water  (IARC,  1983).   It  occurs  ubiquitously  In  products of
Incomplete combustion  and  1n  coal  tar,  and  1s  a component of  gasoline and
dlesel engine exhaust;  1t  also occurs naturally  1n  crude  oils (IARC, 1983).
It has  been  widely detected  In drinking water,  surface water,  groundwater,
rainwater  and  aquatic  sediments   (see  Tables  3-1  and 3-2),  In  many  foods
(Santodonato et  a!.,  1981;  Dennis et al.,  1983) and  1n  the  ambient  atmo-
sphere (see Table 3-3).  The  average  dietary Intake  of benzo(gh1)perylene 1n
England  has  been estimated  to be  0.21  yg/day   (Dennis et  al.,   1983);  the
average  adult  Intake  1n  the  United  States  from drinking water has  been
estimated  to be  2.0 ng/day,  while  the Inhalation Intake  has  been estimated
to be  10 ng/day.   Its presence 1n  food  1s  a result of contamination from a
polluted environment  and  formation during cooking by  pyrolysls  (Santodonato
et al.,  1981;  Fazio  and  Howard,  1983).  Its  concentration  1n  the  ambient
atmosphere In the United States has apparently  been  decreasing over the last
30 years.   The  ambient air  concentration  of benzo(gh1)perylene  1s expected
to be higher during winter than summer,  apparently because of  the burning of
fossil fuel for  heating during winter  months  (Greenberg et  al., 1985).
0864p                               -17-                             10/31/86

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                             4.  PHARMACOKINETICS

    Pertinent data regarding the  gastrointestinal  or  pulmonary  absorption of
benzo(gh1)perylene could not be located  1n  the  available  literature  as  cited
in the Appendix.  Data  from  other  structurally-related  PAH  suggest,  however,
that benzo(gh1)perylene  1s  absorbed readily from  the  gastrointestinal  tract
(Rees et al., 1971) and  lungs  (Kotln  et  al.,  1969; Va1n1o et a!., 1976).  In
general,  PAH  are  highly   I1p1d   soluble   and  can  pass  across  epithelial
membranes (U.S. EPA, 1980).
    Pertinent  data  regarding  the  distribution, metabolism  or   excretion  of
benzo(gh1)perylene could not be located  1n  the  available  literature  as  cited
1n the Appendix.
0864p                               -18-                             10/31/86

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                                  5.   EFFECTS
5.1.   CARCINOGENICITY
    Pertinent  data  regarding  the tumorlgenlc  potential  of  orally-adminis-
tered benzo{gh1)perylene could not be  located  In  the available literature as
cited In the Appendix.
    Mixtures  of heated beeswax  and  tMoctanoln (1:1)  containing  0.16,  0.83
or  4.15  mg  benzo(gh1Jperylene  (98.554 pure) were  Injected  Into the left lung
of  groups of  34 or 35 female Osborne-Mendel  rats  after thoracotomy (Deutsch-
Wenzel  et  a!., 1983).   Additional  groups  of 35   rats  served as  vehicle,
untreated and positive [0.1,  0.3 or  1.0  mg benzo(a)pyrene]  controls.   All
rats  were necropsled  at  the  time  of  natural  death  or  when  sacrificed  at
morlbundHy,  but  hlstologlcal  examinations  were  limited  to  the  lungs  and
organs  showing gross  abnormalities.   Median survival  times  were  109,  114,
106,  104 and  118  weeks  In  the  low-,  middle- and high-dose  treated  groups,
the   vehicle   control  and  the  untreated  control  groups,   respectively.
Squamous cell  carcinomas of  the  lung  occurred  1n  0/35, 1/35 and 4/34 mice In
the low-, mid- and high-dose treated  groups, respectively.   Lung tumors were
not observed   1n either  the vehicle  or untreated  control groups, but  car-
cinomas  occurred at dose-related Incidences  1n the  positive  controls  (4/35,
21/35, 33/35).   The low Incidences of  lung  tumors  1n  the  treated mice were
considered  to  Indicate a  weak  effect  of  benzo(gh1)perylene  1n  this  assay,
but It was  noted  that the  response  might  have been caused by  Impurities  In
the 98.5% pure product that  was tested.  The  results of  this  study  should
therefore be regarded as Inconclusive.
    Benzo(gh1 Jperylene has  also  been  tested for  tumorlgenldty  In mice  In
skin  application  studies  Involving  up to  3  times/week  treatment  for  12
months (Lljlncky and Saff1ott1,  1965;  Van Duuren  et  al., 1970;  Van  Duuren
and Goldschmldt,  1976; Muller,  1968;   Hoffmann  and Wynder,  1966); 1n  skin

0864p                                -19-                             05/15/87

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Initiation-promotion  studies  using  croton  oil  as  a  promoter  (Hoffman  and
Wynder,  1966)  and  PMA as  a  promoter  (Van  Duuren et  a!., 1970);  and  by
bimonthly  subcutaneous  Injections for  5  or  6 months  (Muller,  1968).   The
results  of  these  studies   were  negative   (Table   5-1).    Although   1t  Is
difficult  to evaluate  carcinogenic potential  solely on the  basis  of  results
from these types  of  assays,  H should be noted  that positive responses  were
obtained  1n  many of  the  studies  with  PAH  of known  carclnogenldty  (e.g.,
benzo(a)pyrene).    Enhancement  of  the  dermal  carclnogenldty  of  benzo(a)-
pyrene  by  simultaneous application  of  benzo(gh1)perylene  has been  reported
In mice  (Goldschmldt  et al., 1973;  Van Duuren et al., 1973; Van  Duuren and
Goldschmldt,   1976),   Indicating   possible  cocarc1nogen1c1ty  of  benzo(ghl)-
perylene.
5.2.    HUTAGENICITY
    Benzo(gh1)perylene  has  been   reported  to  produce  mutation  to  hlstldlne
Independence  1n   Salmonella  typhlmurlum  strains  TA98,  TA100,  TA1537  and
TA1538  when  assayed  In  the presence,  but not  the  absence,  of  exogenous
metabolic  activation  preparations (Andrews  et al., 1978;  Mossanda  et  al.,
1979;  Salamone et al., 1979).   Benzo(gh1)perylene also produced  mutation to
8-azoguanlne  resistance  1n  S.   typhlmurlum  TM677  1n  the  presence  of
activation  preparations  (Kaden  et  al.,  1979).   These  studies  are  summa-
rized  1n Table 5-2.
    Intraperltoneal  Injection  of 30  mg/kg  benzo(gh1)perylene  Into  hamsters
(strain unspecified) on day  10 of  gestation  did  not Induce neoplastlc trans-
formation  In embryo  cells  that  were first  cultured  on  day 13  (Quarles et
al.,  1979)  (see  Table 5-2).   Additional Information regarding  the genotoxlc
potential  of  benzo(gh1)perylene  could  not   be  located  In  the  available
literature as cited In the Appendix.


0864p                               -20-                             07/21/87

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-------
5.3.   TERATOGENICITY
    Weaver  and  Gibson   (1979)   exposed  pregnant  rats  to  graded  airborne
concentrations of uncharacterlzed oil  shale  containing  PAH,  including benzo-
(ghi)perylene, on days  6-15 of  gestation.   No  treatment-related  teratogenic
effects were  observed  during  examination  of  fetuses  obtained by  Caesarean
section  on day  20  of  gestation.    Determination  of  a  benzo(ghi)perylene
specific effect  Is precluded,  however,  by  the uncharacterlzed nature  of  the
test material.
5.4.   OTHER REPRODUCTIVE EFFECTS
    Pertinent   data   regarding  other  reproductive   effects   of   benzo(ghl)-
perylene could  not  be  located  1n the available  literature  as cited  in  the
Appendix.
5.5.   CHRONIC AND SUBCHRONIC TOXICITY
    Pertinent  data regarding chronic and subchronlc toxiclty  of  benzo(ghl)-
perylene could  not  be  located  1n the available  literature  as cited  In  the
Appendix.
5.6.   OTHER RELEVANT INFORMATION
    Other  relevant information  regarding the  toxiclty  of  benzo(gh1 )perylene
could not be located  In the available literature as  cited 1n  the Appendix.
5.7.   SUMMARY
    Single  Intrapulmonary  Injections  of  0.16, 0.83  or 4.15  mg  benzo(ghi)-
perylene  1n  beeswax-trloctanoln mixture   Into   groups  of  34  or  35  rats
produced  a low  Incidence  (4/34)  of  lung  squamous cell  carcinomas  In  the
high-dose  group  after  lifetime  observation  (Deutsch-Wenzel  et al.,  1983).
Lung tumors did  not  occur  in untreated or  vehicle treated controls, but IARC
(1983) indicated that the  tumors in  the  treated  group  may be attributable to
Impurities in the test product, which was 98.5% pure.


0864p                               -24-                             10/31/86

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    Tumor 1 genIcHy  of  benzo(gh1 )perylene  was  not  demonstrated  1n  mice  In
skin  application  studies  Involving  up  to  3  times/week  treatment  for  12
months  (Lijlnsky  and Safflotti,  1965;  Van Duuren  et  al., 1970;  Van  Duuren
and  Goldschmidt,  1976;   Huller,  1968;  Hoffmann  and Wynder,  1966);  1n  skin
Initiation-promotion  studies  using  croton oil  as  a  promoter  (Hoffman  and
Wynder,  1966)  and  PMA  as  a  promoter   (Van  Duuren et  al.,  1970);  and  by
bimonthly  subcutaneous  Injections   for   5   or   6  months  (Muller,   1968).
Enhancement of  the dermal  cardnogenldty of  benzo(a)pyrene  by simultaneous
application of  benzo(gh1)perylene has been reported 1n mice  (Goldschmidt  et
al.,  1973;  Van  Duuren  et  al.,  1973;   Van  Duuren and  Goldschmidt,  1976),
Indicating possible cocarclnogenlc-lty of benzo(gh1 )perylene.
    Benzo(gh1)perylene was mutagenlc  to £. typhimurlum strains  TA98,  TA100,
TA1537 and TA1538  (Andrews  et al., 1978;  Mossanda  et  al., 1979;  Salamone  et
al.,  1979)  and  TM677 (Kaden  et  al.,  1979) when  assayed   1n the  presence  of
exogenous metabolic  activation  preparations.   Intraperltoneal  Injection  of
benzo(gh1Jperylene  Into hamsters  on day 10  of  gestation did  not  Induce
transformations  1n the embryo cells (Quarles  et al., 1979).
    Pertinent   data   regarding   toxic,   teratogenlc or   other  reproductive
effects  of  benzo(gh1)perylene   could   not   be   located   1n   the  available
literature as  dted 1n the Appendix.
0864p                               -25-                             05/15/87

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                             6.   AQUATIC TOXICITY
6.1.   ACUTE
    Pertinent  data  regarding  the acute  toxldty  of  benzo(ghi )perylene  to
aquatic organisms could  not  be  located in the available  literature  as  dted
1n the Appendix.
6.2.   CHRONIC
    Pertinent  data  regarding the  chronic  toxicity of benzo(gh1)perylene  to
aquatic organisms could  not  be  located in the available  literature  as  cited
in the Appendix.
6.3.   PLANTS
    Pertinent  data  regarding the  effects of  benzo{gh1Jperylene on  aquatic
plants  could  not be  located In  the  available  literature as  cited in  the
Appendix.
6.4.   RESIDUES
    The only  information regarding benzo(gh1Jperylene and  aquatic  organisms
consisted   of   bioconcentratlon  and residue  monitoring data.   Obana et  al.
(1983)  reported  BCF   values of   1000-1400  for  short-necked  clams.  Tapes
japonica.   exposed  to  0.06-0.13  yg/8.  for  1-7  days.   Tsuji  et  al.  (1985)
found  that clams  (unspecified  species)  collected in  Japanese waters  con-
tained  benzo(gh1)perylene residues  at  concentrations of  0.23-0.95  yg/kg.
Knutzen  and  Sortland   (1982)  reported  the  following   levels  (vg/kg  dry
weight) in  species  collected  from  polluted areas in Norway:  mussel, Hytelis
edulis.  trace-87;  periwinkle,   Littorina  littorea.   0.5;  limpet.   Patella
yulgata.  not  detected;   sponge,  Halichondria  panicea.   23;   toothed  wrack,
Fucus  serratus.  79; Ceramium rubrum.  4.  Maccubbin et al.  (1985)  found that
the  stomach contents  of  white  suckers, Catostomus commersoni.  from eastern
Lake  Erie  contained  2-14  ng/g  benzo(ghiJperylene.   Malins  et al.  (1985)


0864p                               -26-                             10/31/86

-------
reported  that  stomach  contents  of English sole, Parophrys vetulus. collected

In Puget  Sound  contained  75  ng/g dry weight.  Dunn and Fee (1979) found that


lobsters,  Homarus  amerlcanus.  caught 1n  waters  off  eastern Canada contained
       •
benzo(gh1Jperylene at  an  average concentration of 0.19 ng/g;  however,  It 1s


a  common  practice  for  lobsters to  be  kept  1n  Impoundments  for  weeks  or


months before being  sent  to  market.   Frequently,  these Impoundments  are made


of creosote-treated  wood,  which would be a  source  of benzo(gh1Jperylene and


other  PAH.  Dunn and  Fee (1979)  found  that  benzo(gh1 )perylene  residues  of


Impounded  lobsters averaged  51  ng/g,  a  250-fold Increase  over freshly caught


lobsters.  This may  constitute  a possible source of  human exposure to benzo-


(gh1Jperylene.


6.5.   SUMMARY

    Pertinent  data  regarding the  tox1c1ty  of  benzo(gh1)perylene  to aquatic


organisms  could  not  be located  In  the available literature as  cited In the


Appendix.   Several   studies  reported data  concerning residues   In  aquatic


organisms.  The  following data  were  reported  for species  that  are  commonly


eaten  by  humans:  mussels  from Norway, trace-87  ng/g (Knutzen  and Sortland,


1982); clams  from  Japan,  0.23-0.95 ng/g  (Tsujl  et al.,  1985);  lobsters from

eastern  Canada,  0.19 ng/g before  Impoundment  and 51  ng/g  after  Impoundment


(Dunn  and  Fee,  1979).   Obana et al.  (1983)  reported  BCF  values of 1000-1400


for  short-necked clams,  T.   japonlca.  exposed   to  0.06-0.13  vg/8.   for  1-7

days.
0864p                               -27-                             10/31/86

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                     7.  EXISTING GUIDELINES AND STANDARDS
7.1.   HUHAN
    Exposure criteria  and TLVs have  been developed for  PAH  as a  class,  as
well as  for  several Individual PAH.   OSHA has set an  8-hour  TWA  concentra-
tion limit  of  0.2 mg/m3  for  the  benzene-soluble  fraction of  coal  tar  pitch
volatiles  (anthracene,  benzo(a)pyrene,  phenanthrene,   acrldlne,   chrysene,
pyrene)  (OSHA,  1985).   NIOSH  (1977)  recommended  a  concentration  limit  for
coal tar,  coal  tar pitch, creosote and mixtures  of these substances  of  0.1
mg/m3  of  the cyclohexane-extractable fraction  of  the  sample,  determined  as
a  10-hour  TWA.   NIOSH  (1977)  concluded  that   these  specific   coal  tar
products, as well  as  coke oven emissions, are  carcinogenic and can Increase
the risk  of  lung  and skin cancer 1n  workers.   NIOSH  (1977) also recommended
a  celling limit  for  exposure  to  asphalt fumes  of 5  mg airborne  partlcu-
lates/m3 of air.
    Environmental   quality  criteria,   which   specify   concentration  limits
Intended  to  protect  humans  against  adverse health effects, have  been  recom-
mended  for  PAH  1n ambient water.   U.S. EPA  (1980) recommended a  concentra-
tion  limit  of  28  ng/l  for  the  sum  of  all  carcinogenic   PAH   1n  ambient
water.  This value 1s  based  on  a  mathematical extrapolation  of  the results
from  studies with mice treated  orally with  benzo(a)pyrene and acknowledges
the conservative  assumption  that  all carcinogenic  PAH  are equal  1n potency
to benzo(a)pyrene.  On  the basis of the animal  bloassay data, dally consump-
tion  of water   containing  28  ng/8. of carcinogenic  PAH  over  an entire life-
time  1s  estimated to keep the lifetime  risk  of cancer  development <1  chance
In 100,000.
0864p                               -28-                             10/31/86

-------
    U.S.  EPA has  not  recommended  an  ambient  water  quality criterion  for
noncardnogenlc  PAH as  a  class.   U.S.  EPA  (1980)  acknowledged that  data
suitable  for  quantitative risk assessment of noncardnogenlc  PAH are essen-
tially nonexistent.
7.2.   AQUATIC
    Guidelines  and  standards  for  the  protection of  aquatic  biota  from  the
effects  of  benzo(gh1)perylene, 1n  particular,  could not  be  located  In  the
available  literature  as  cited 1n  the  Appendix;  however, U.S.  EPA  (1980)
noted  that  acute toxldty  to  saltwater  aquatic life occurred at concentra-
tions  as  low as  300  yg/s, of  PAH 1n  general, and  would  occur  at  lower
concentrations In species more sensitive  than those  tested.   U.S. EPA (1980)
concluded that  the  database at that time was Inadequate  to generalize about
chronic or acute toxldty to freshwater organisms.
0864p                               -29-                             10/31/86

-------
                             8.   RISK ASSESSHENT

    Single  intrapulmonary  injections of  0.16,  0.83  or  4.15 mg  benzo(ghi)-
perylene  in  beeswax-trioctanoln   mixture   into  groups  of  34  or  35  rats
produced  a  low  incidence  (4/34)  of lung  squamous   cell  carcinomas   in  the
high-dose group  after lifetime  observation  (Deutsch-Wenzel  et a!.,  1983).
Lung tumors did not occur  in untreated  or  vehicle  treated  controls,  but IARC
(1983) indicated that the  tumors  in  the  treated  group may  be attributable to
impurities in the test product, which was 98.5% pure.
    Tumorigenicity  of benzo(ghi)perylene  was not  demonstrated  in  mice  in
skin  application  studies  involving  up to  3  times/week   treatment  for  12
months  (Lijinsky  and  Saffiotti,  1965;  Van Duuren et a!.,  1970;  Van  Duuren
and  Goldschmidt,  1976;  Muller,  1968;  Hoffmann  and   Wynder,  1966);  In  skin
initiation-promotion  studies  using  croton oil  as a  promoter   (Hoffman  and
Wynder,  1966)  and  PMA  as a  promoter  (Van  Duuren  et  al.,  1970);  or  by
bimonthly  subcutaneous  injections  for   5  or  6  months  (Muller,   1968)  (see
Table  5-1).   Enhancement  of  the dermal  carcinogenicity  of  benzo(a)pyrene by
simultaneous  application   of  benzo(ghi)perylene has  been  reported  in  mice
(Goldschmidt et  al.,  1973;  Van Duuren  et  al.,  1973;  Van Duuren and  Gold-
schmidt, 1976), indicating possible cocarcinogenicity  of benzo(ghi)perylene.
    Benzo(ghiJperylene was mutagenic to S. typhimurium  strains TA98,  TA100,
TA1537 and TA1538  (Andrews et  al.,  1978; Mossanda et al.,  1979;  Salamone et
al.,  1979)  and TM677 (Kaden et al., 1979) when  assayed in  the  presence of
exogenous metabolic  activation preparations.   Intraperitoneal   injection  of
benzo(gh1)perylene  into  hamsters  on  day   10  of  gestation  did   not  Induce
transformations 1n the embryo cells  (Quarles et al.,  1979)
0864p                               -30-                             05/15/87

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    Although  some  lung  tumors  occurred  In  the Intrapulmonary Injection study



with  rats  (Oeutsch-Wenzel  et  a!.,  1983),  possible cocarclnogenlcHy  with



benzo(a)pyrene on  mouse  skin  occurred,  and mutagenldty  1n different strains



of  S.  typhlmurlum was  demonstrated,  the  available  data are  Inadequate  for



evaluation  of  cardnogenlclty  of  benzo(gh1Jperylene.   The  Intrapulmonary



injection  study  1s limited  by the single  dose  treatment schedule,  unnatural



route  of  respiratory  exposure,  possibility  of  Impurities  1n  the  test



compound  and  lack  of  corroborating  data.  The mutagenldty  data  are limited



by  a  lack of  data In other test  systems.   A cocardnogen cannot  be regarded



as  a  complete  or procarclnogen  In  the   absence  of   supporting  evidence.



Evaluation of the carclnogenlclty of  benzo(gh1Jperylene  1s  further  limited



by  the lack of studies employing oral  or Inhalation routes of exposure.



    Pertinent  data   regarding   toxic,   teratogenlc   or   other  reproductive



effects of benzo(gh1)perylene  could  not be  located In the  available Utera-
                                                                           *


ture as  cited In  the Appendix.   This  lack  of data precludes  calculation  of



an  RfD (formerly called ADI) for benzo(gh1)perylene.
0864p                               -31-                             10/31/86

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                          9.  REPORTABLE QUANTITIES
9.1.   REPORTABLE QUANTITY (RQ)  RANKING BASED ON CHRONIC  TOXICITY
    Pertinent  data  regarding the  toxic  or reproductive  effects  of  benzo-
(gh1)perylene could not  be  located 1n  the  available literature as  cited  1n
the Appendix.  Weaver  and Gibson (1979) exposed  pregnant  rats  to  graded  air-
borne concentrations  of  uncharacteMzed oil shale containing  PAH,  Including
benzo(ghiJperylene,   on   days   6-15   of  gestation.   No  treatment-related
teratogenic effects were  observed  during  examination of  fetuses  obtained  by
Caesarean  section  on  day 20  of gestation.   Calculation  of  an RQ  from  this
study is  precluded (Table  9-1) by  the uncharacterlzed  nature  of  the  test
material (U.S. EPA,  1983).
9.2.   WEIGHT OF EVIDENCE AND POTENCY  FACTOR (F=1/ED1Q)  FOR CARCINOGENICITY
    Single  Intrapulmonary  injections   of  0.16,   0.83  or  4.15  mg  benzo(ghi)-
perylene  in  beeswax-trloctanoln  mixture   into  groups   of  34  or  35  rats
produced  a low  incidence'  14/34)  of   lung  squamous  cell  carcinomas  in  the
high-dose  group  after lifetime  observation  (Deutsch-Wenzel  et  a!.,  1983).
Lung tumors did  not occur in  untreated or vehicle  treated controls, but  IARC
(1983) indicated that the tumors in the treated  group  may be attributable to
Impurities in the test product,  which  was  98.5% pure.
    Tumorlgenicity  of benzo(ghiJperylene  was  not  demonstrated  in mice  in
skin  application studies  involving  treatment   up  to  3  times/week  for  12
months  (Lijinsky and  Saffiotti, 1965; Van   Duuren  et  a!.,  1970;  Van  Duuren
and  Goldschmidt, 1976;  Muller,  1968;  Hoffmann  and Wynder,  1966); in  skin
initiation-promotion  studies  using  croton   oil  as  a  promoter  (Hoffman  and
Wynder,   1966)  and  PMA  as  a  promoter  (Van Duuren  et  a!.,  1970);  or  by
bimonthly  subcutaneous   injections  for 5  or 6  months  (Muller,   1968)  (see
Table 5-1).   Enhancement of the dermal cardnogenicity  of benzo(a)pyrene by


0864p                               -32-                             05/15/87

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                                   TABLE  9-1



                              Benzo(gh1Jperylene



           Minimum Effective  Dose  (MED)  and  Reportable  Quantity  (RQ)





Route:



Dose:



Effect:



Reference:



RVd:



RVe:



Composite Score:



RQ:                     Data are not sufficient to derive an RQ.
0864p                               -33-                             10/31/86

-------
simultaneous  application  of  benzo(gh1Jperylene has  been reported  In  mice
(Goldschmldt  et  a!., 1973;  Van  Duuren et  al., 1973;  Van  Duuren and  Gold-
schmldt, 1976), Indicating possible cocarcinogenlcity  of benzo(ghiJperylene.
    Benzo(ghiJperylene was mutagenlc  to  S_. typhlmurium  strains TA98,  TA100,
TA1537 and  TA1538  (Andrews  et  al., 1978;  Hossanda et al., 1979;  Salamone  et
al.,  1979)  and TM677 (Kaden et  al.,  1979) when assayed in  the presence  of
exogenous metabolic  activation preparations.   Intraperitoneal  injection  of
benzo(ghi)perylene  Into  hamsters  on  day   10  of  gestation  did  not  Induce
transformations 1n the embryo cells (Quarles et  al.,  1979)
    Although some lung tumors  occurred In  the intrapulmonary  injection study
with  rats   (Deutsch-Henzel  et al.,  1983),  possible  cocarcinogenlcity  with
benzo(ghi)perylene  on mouse  skin  occurred,  and  mutagenlcity  1n  different
strains  of   S.   typhlmurium  was  demonstrated,  the   available   data  are
Inadequate  for evaluation of  the  carclnogenidty of  benzo(gh1Jperylene.  The
Intrapulmonary  Injection  study   is  limited  by the  single  dose  treatment
schedule, unnatural  route of  respiratory exposure, possibility  of  impurities
In  the  test  compound and  lack of  corroborating  data.   The mutagenlcity data
are limited  by a  lack of  data in  other test  systems.   A cocardnogen  cannot
be  regarded as  a  complete  or procarcinogen  in  the  absence  of  supporting
evidence.    Evaluation  of   the   cardnogenicHy  of   benzo{gh1 )perylene  1s
further  limited  by  the lack of  studies  employing  oral  or  inhalation  routes
of exposure.
    IARC (1983)  reported  that there was Insufficient evidence  regarding the
carcinogenic risk to  humans  and experimental  animals  associated with oral  or
Inhalation   exposure   to  benzo(gh1Jperylene.    Applying  the  criteria  for
evaluation  of  the  overall weight  of evidence for  the  carcinogenic  potential
for humans  proposed  by the  Carcinogen  Assessment Group  of the U.S.  EPA (U.S.


0864p                               -34-                             10/31/86

-------
EPA,  1984),  benzo(gh1Jperylene  1s  most  appropriately designated  a  Group 0,
Not  Classified  chemical.   Direct hazard  ranking  of  benzo(gh1Jperylene under
CERCLA Is therefore not possible.
0864p                               -35-                             10/31/86

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                               10.  REFERENCES







Andrews,  A.W.,  L.H.  Thibault  and  W.   Lijlnsky.   1978.   The  relationship



between  carclnogenlclty  and mutagenlclty  of  some polynuclear  hydrocarbons.



Mutat. Res.  51: 311-318.







Behymer,  T.D.  and  R.A.   H1tes.   1985.   Photolysis   of  polyaromatlc  hydro-



carbons adsorbed on simulated atmospheric  particles.   Environ.  Sc1.  Techno!.



19: 1004-1006.








Crane,  R.I.,  B. Crathorne  and  M.  Fielding.   1980.   The determination  and



levels  of  polycycllc  aromatic  hydrocarbons  In  source  and  treated  waters.



In:  Hydrocarbon  Halo.   Hydrocarbon  Aquatic  Environ,  B.K.  Afghan  and  D.



Mackay, Ed.  Plenum Press, New York.   p.  161-172.







Dennis, H.3., R.C. Massey,  D.3.  McWeeney and D. Watson.   1983.   Analysis of



polycycllc  aromatic  hydrocarbons  1n  UK  total  diets.   Food Chem.  Toxlcol.



21: 569-574.







Deutsch-Wenzel,  R.P.,  H.  Brune,  G.  Grimmer, G.  Dettbarn  and 3.  Mlsfeld.



1983.   Experimental  studies In rat  lungs on  the  carclnogenlclty and  dose-



response  relationships  of  eight  frequently  occurring  environmental  poly-



cycllc aromatic  hydrocarbons.   J.  Natl.  Cancer Inst.   71: 539-544.








Dunn,  B.P.  and  3. Fee.   1979.   Polycycllc aromatic  hydrocarbon carcinogens



1n commercial seafoods.  3. Fish.  Res.  Board Can.   36(12): 1469-1476.
0864p                               -36-                             10/31/86

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Eadle,  B.J.,  H.   Faust,  W.S.  Gardner  and  T.  Nalepa.   1982.   Polycycllc
aromatic  hydrocarbons  In  sediments  and  associated  benthos  In Lake  Erie.
Chemosphere.  11:  189-191.

Fazio,  T.   and  J.W.  Howard.   1983.   Polycycllc   aromatic  hydrocarbons  In
foods.   In:  Handbook of  Polycycllc  Aromatic  Hydrocarbons, A.  Bjorseth,  Ed.
Marcel Dekker Inc., New York.  p. 461-505.

Fochtman,  E.G.  1981.  Blodegradatlon and  Carbon  Adsorption  of Carcinogenic
and  Hazardous  Organic  Compounds.    U.S.  EPA, Cincinnati,  OH.  p. 38.   EPA
600/S2-81-032.

Goldschmldt, B.M.,  C. Katz  and  B.C.  Van Duuren.   1973.   The  cocarclnogenlc
activity of  non-carcinogenic  aromatic hydrocarbons (Abstr. No.  344).   Proc.
Am. Assoc:  Cancer  Res.  17:  84.                                 •          -

Gordon, B.3. and R.J. Bryan.   1973.   Patterns  In airborne polynuclear  hydro-
carbon concentrations at four  Los Angeles  sites.   Environ.  Sd.  Techno!.   7:
1050-1053.

Great Lakes Water  Quality Board.  1983.   An Inventory  of  Chemical  Substances
Identified  1n the Great Lakes  Ecosystem.   Volume 1  -  Summary.   Report  to the
Great Lakes Water  Quality Board,  Windsor, Ontario,  Can.   p. 195.

Greenberg,  A.,  F.  Darack, R.  Harkov, P.  L1oy and J.  Dalsey.   1985.   Poly-
cycllc  aromatic  hydrocarbons  In New Jersey:  A  comparison   of  winter  and
summer  concentrations  over   a   two-year  period.   Atmos.   Environ.    19:
1325-1339.

0864p                               -37-                             10/31/86

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Grlest, W.H.  1980.  Hultlcomponent polycycllc aromatic  hydrocarbon  analysis
of  Inland  water  and  sediment.   In:  Hydrocarbon  Halo.  Hydrocarbon  Aquatic
Environ, B.K. Afghan and D.  Mackay,  Ed.   Plenum Press,  New  York.   p.  173-183.

Harkov,  R.,  A.  Greenberg,   F.  Darack,  3.M.  Dalsey  and  P.3.  Lloy.   1984.
Summertime variations  in  polycyclic aromatic  hydrocarbons  at four  sites  1n
New Jersey.  Environ.  Sc1.  Technol.   18:  287-291.

Heit, H.   1985.   The  relationship  of  a coal fired power plant to  the levels
of polycycllc  aromatic  hydrocarbons (PAH)  1n  the sediment  of Cayuga  Lake.
Water A1r Soil  Pollut.   24:  41-61.

Herrmann, R. and  D.  Heubner.   1982.  Behavior  of  polycycllc  aromatic hydro-
carbons 1n the Exe estuary,  Devon UK.   Neth. J.  Sea.  Res.  15: 362.

Hoffmann,  D. and  E.L.  Wynder.   1966.    Contribution  to  the  carcinogenic
action of dlbenzopyrenes.   Z Krebsforsch.   68:  137-149.  (Ger.)

IARC  (International Agency  for  Research  on Cancer).   1983.   IARC  Monographs
on the  Evaluation of the Carcinogenic  Risk  of  Chemicals  to Man.   Benzo(ghl)-
perylene.   In:  Polynuclear   Aromatic  Compounds,  Part  1,  Chemical,  Environ-
mental and Experimental Data.  WHO,  IARC,  Lyon, France.  Vol. 32,  p.  195-204.

Kaden,  D.A.,  R.A.  HHes and  W.G.   Thllly.   1979.   Mutagenlclty  of  soot  and
associated   polycycllc  aromatic  hydrocarbons   to  Salmonella  typhlmurlum.
Cancer Res.  39: 4152-4159.
0864p                               -38-                             10/31/86

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Keller,  C.O.  and  T.F.  Bldleman.   1984.   Collection of  airborne  polycycllc
aromatic  hydrocarbons  and   other   organlcs   with   a   glass  fiber  fllter-
polyurethane foam system.  Atmos. Environ.  18: 837-845.

Knutzen,  J.  and B. Sortland.  1982.  Polycycllc  aromatic  hydrocarbons  (PAH)
1n  some  al.gae  and  Invertebrates  from moderately  polluted  parts  of  the  coast
of Norway.  Water Res.  16(4): 421-428.

Kotln,  P.,  H.L.  Falk  and  R.  Buser.   1969.    Distribution,  retention  and
elimination  of  C14-3,4-benzpyrene  after  administration  to  mice   and  rats.
J. Natl. Cancer Inst.  23: 541.

Llgockl,  M.P.,  C.  Leuenberger   and  J.F.  Pankow.   1985.   Trace  organic
compounds  1n  ra1n-III.    Particle  scavenging  of  neutral   organic  compounds.
Atmos. Environ.  19: 1619-1626.

L1J1nsky,.W.  and U.  Safflottl.   1965.   Relationships   between  structure  and
skin  tumorlgenlc  activity among  hydrogenated  derivatives  of several  poly-
cycllc aromatic  hydrocarbons.  Ann. Hal. Dermatol. CUn.  Sper.   19:  34-41.
(Cited In IARC, 1983)

Lunde, G., J.  Gether, N.  Gjos and  M.B.  Stobet Lande.   1976.   Organic micro-
pollutants 1n precipitation 1n Norway.  SNSF  Project, FR.9/76.  17  p.

Lyman, W.J.,  W.F.  Reehl  and  D.H.   Rosenblatt.    1982.   Handbook of  Chemical
Property  Estimation  Methods.  McGraw-Hill  Book  Co.,   New York.   p.  15-16,
4-9, 5-4, 5-10.


0864p                               -39-                             10/31/86

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Mabey, W.R.,  J.H.  Smith, R.T.  Podoll,  et al.   1981.   Aquatic Fate  Process


Data  for  Organic  Priority  Pollutants.   Monitoring  and  Data  Support  D1v.,


Office of  Water  Regulations and  Standards,  U.S.  EPAV  Washington;  DC.   EPA
                                      •

440/4-81-014.






Maccubbin, A.E., P.  Black,  L.  Trzedak and J.J. Black.   1985.  Evidence  for


polynuclear aromatic hydrocarbons 1n the  diet of bottom-feeding fish.   Bull.


Environ.  Contam.-Toxlcol.  34(6):  876-882.






Mallns,  D.C.,  M.M.  Krahn,  D.W.  Brown,   et  al.   1985.   Toxic chemicals  In


marine  sediment   and  biota  from  MukHeo,  Washington:  Relationships  with


hepatic  neoplasms   and  other  hepatic  lesions   1n  English  sole   (Parophyrs


vetulus).  J. Natl. Cancer Inst.  74(2):  487-494.



        »


Matsumoto, H. and  T.  Kashlmoto.   1985.   Average dally  respiratory  Intake  of


polycycllc aromatic  hydrocarbons  1n  ambient  air determined by capillary  gas


chromatography.   Bull. Environ. Contam.  Toxlcol.   34:  17-23.






Mossanda, K., F.  Poncelet,  A.  Fouassln and M. Herder.   1979.  Detection  of


mutagenlc  polycycllc aromatic  hydrocarbons   1n  African  smoked  fish.   Food


Cosmet. Toxlcol.   17: 141-143.






Muller, E.   1968.   Carcinogenic  substances 1n water and  soils.   XX.  Studies


on  the  carcinogenic properties  of  1,12-benzoperylene.   Arch.  Hyg.   152:


23-36.  (Cited In IARC, 1983)
0864p                               -40-                             10/31/86

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NIOSH  (National  Institute  for  Occupational  Safety  and  Health).   1977.
Criteria  for  a  Recommended  Standard...Occupational  Exposure  to  Coal  Tar
Products.  U.S. DHEW, PHS, CDC, Rockvllle, MD.  Publ. No. 78-107.

NRC  (National  Research Council).   1983.  Polycycllc  Aromatic  Hydrocarbons:
Evaluation   of  Sources   and   Effects.    National   Academy. Press,   National
Research Council,  Washington,  DC.

Obana, H., S.  Hor1,  A. Nakamura  and  T.  Kashlmoto.   1983.  Uptake and release
of polynuclear  aromatic hydrocarbons  by short-necked clams (Tapes japonlca).
Water Res.  17(9): 1183-1188.

OSHA  (Occupational  Safety and  Health  Administration).   1985.   OSHA  Safety
and Health Standards.  29  CFR  1910.1000.

Pearlman, R.S., S.H. Yalkowsky  and  S.  Banerjee.  1984.   Water  solubilities
of polynuclear  aromatic  and heteroaromatlc  compounds.   J. Phys. Chem.  Ref.
Data.  13: 555-562.

Prahl,  F.H.,  E.  Crecellus and  R.  Carpenter.   1984.   Polycycllc  aromatic
hydrocarbons In Washington coastal  sediments:  An evaluation  of atmospheric
and rlverene roots of Introduction.  Environ. Sc1.  Techno!.  18:  687-693.

Quarles, 3.M.,  M.W.  Sega,   C.K. Schenley  and  W.  Ujlnsky.  1979.   Transforma-
tion  of  hamster  fetal  cells  by  nltrosated   pesticides  1n a  transplacental
assay.  Cancer  Res.   39: 4525-4533.
0864p                               -41-                             10/31/86

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Rees, E.D.,  P.  Mandelstam, 3.Q.  Lowry  and H.  Llpscomb.   1971.   A study  of
the mechanism of  Intestinal absorption  of  benzo(a)pyrene.   Blochem.  Blophys.
Acta.  225: 96.

Ruepert,  C.,  A.  Grlnwls  and  H.  Govers.    1985.   Prediction  of  partition
coefficients  of  rensubstHuted  polycycllc  aromatic  hydrocarbons  from  C,0
                                                                           i o
chromatographlc  and structural  properties.   Chemosphere.   14:  279-291.

Rump,  H.H.   1984.   Behavior   of  some  organic  mlcropollutants  1n   river
sediments and groundwater.   Fresenlus Z. Anal.  Chem.   319:  165-171.

Salamone, M.F.,  J.A.  Heddle and M.  Katz.   1979.  The mutagenlc  activity  of
thirty  polycycllc  aromatic hydrocarbons (PAH)  and oxides  In urban  airborne
partlculates.  Environ. Int.  2:  37-43.                  ,

Santodonato,  J.,  P.   Howard  and  D. Basu.    1981.   Health  and  Ecological
Assessment  of Polynuclear  Aromatic Hydrocarbons.  Pathotox  Publishers  Inc.,
Park Forest South, IL.

Saxena,   J.,  O.K.  Basu and J.  Kozuchowskl.    1977.   Method  development  and
monitoring  of  polynuclear  aromatic  hydrocarbons  1n  selected  U.S.  waters.
U.S. EPA, Cincinnati, OH.  p.  84.  EPA 600/11-77-052.

Sexton,  K.,  K.S.  L1u,  S.B. Hayward and  J.D. Spengler.   1985.  Characteriza-
tion  and  source  apportionment   of   wintertime aerosol   1n  a  wood-burning
community.  Atmos. Environ.  19(8): 1225-1236.
0864p                               -42-                             10/31/86

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Sorrell,  R.K.,  H.J.  Brass  and R.  Reding.   1980.  A review of the occurrences
and  treatment  of polynuclear aromatic hydrocarbons  In  water.   Environ. Int.
4: 245-254.

Staples,  C.A.,  A.  Werner  and  T.  Hoogheem.   1985.   Assessment  of  priority
pollutant  concentrations   In  the  United  States  using  STORE!  database.
Environ.  Toxlcol. Chem.  4: 131-142.

Tan,  Y.L.  and H. He1t.   1981.   B1ogen1c  and  ablogenlc  polynuclear  aromatic
hydrocarbons  1n  sediments   from  two  remote  Adirondack  lakes.   Geochlm.
Cosmochlm. Acta.  45: 2267-2279.

Tsujl,  I.,  K.   Kolde,  H.  Morlyama,  K.  Tanabe  and  H.  Matsushita.   1985.
Detection  of  polynuclear  aromatic  hydrocarbons  In shellfishes,  seabottom
sediments  and  sea water  by high performance liquid chromatography.   Shokuhln
Elselgaku  Zasshl.  26(1): 50-55.   (Jap.)   [CA 104(10):81300p]

U.S.  EPA.  1980.   Ambient  Water  Quality  Criteria  for  Polynuclear  Aromatic
Hydrocarbons.   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-440/5-80-069.

U.S.  EPA.   1983.   Reportable  Quantity   Document  for  Benzo(gh1)perylene.
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.
0864p                               -43-                             07/27/87

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

U.S.  EPA/NIH  (National  Institute  of  Health).   1986.   OHM-TADS  (011  and
Hazardous Materials  Technical  Assistance  Data  System).   Online:  April  16,
1986.

USITC  (U.S.  International  Trade  Commission).   1984.  Imports  of  Benzenold
Chemicals and Products,  1983.   USITC  Publ.  1548, Washington,  DC.

Vaessen,  H.A.M.G.,  P.L.  Schuller,  A.A.  Jekel and  A.A.M.M.  Wllbers.  1984.
Polycycllc aromatic hydrocarbons 1n  selected foods;  analysis and  occurrence.
Toxlcol. Environ.  Chem.   7:  297-324.

Valnlo,  H.,  P. VolUa,  J.  Hartlola  and 0.  Pelkonen.   1976.' The fate  of
Intratracheally Installed benzo[a]pyrene In the  Isolated  perfused  rat  lung
of both  control and 20-methylcholanthrene pretreated rats.   Res.  Comm. Chem.
Pathol. Pharmacol.   13:  259-271.   (Cited In  U.S. EPA, 1980)

Van  Duuren,  B.L.  and B.M.  Goldschmldt.  1976.   Cocarclnogenlc  and  tumor-
promoting agents  1n tobacco cardnogenesls.  J.  Natl.  Cancer Inst.   56(6):
1237-1242.

Van  Duuren,  B.L.,   A.  SWak,  B.M.  Goldschmldt,  C.  Katz  and S.  Melchlonne.
1970.   Initiating  activity  of  aromatic hydrocarbons  1n  two-stage  cardno-
genesls.  J. Natl.  Cancer Inst.   44:  1167-1173.
0864p                               -44-                             07/27/87

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Van Duuren, B.L., C.  Katz  and  B.M.  Goldschmldt.   1973.   Brief communication:
Cocardnogenlc agents 1n tobacco  carclnogenesls.   J.  Natl.  Cancer  Inst.   51:
703-705.

Varanasl, U., W.L. Relchert, J.E. Stein,  D.W.  Brown  and  H.R.  Sanborn.   1985.
BloavaHablllty  and   blotransformatlon  of aromatic  hydrocarbons  In  benthlc
organisms exposed to  sediment  from  an  urban  estuary.   Environ.  Sc1.  Techno!.
19: 836-841.

Walters,  R.W.  and R.G.  Luthy.   1984.   Liquid/suspended solid  phase  parti-
tioning  of  polycycllc   aromatic  hydrocarbon  In  coal  coking  wastewaters.
Water Res.  18: 795-809.

Weaver, N.K. and  R.L. Gibson.   1979.  The U.S.  oil  shale  Industry:  A  health
perspective.  Am. Ind. Hyg. Assoc. 0.  40(6): 460-467.

Yalkowsky,  S.H.   and  S.C.   Valvanl.   1979.   Solubilities  and  partitioning.
2. Relationships  between  aqueous  solubilities,   partition  coefficients  and
molecular surface areas of  rigid  aromatic  hydrocarbons.  J.  Chem.  Eng.  Data.
24: 127-129.

Yamasakl, H., K.  Kuwata and H. Miyamoto.   1982.   Effects of ambient  tempera-
ture on aspects of airborne polycycllc  aromatic  hydrocarbons.   Environ.  Sc1.
Techno!.  16: 189-194.

Zoeteman,  B.C.J.,  E.  Degreef  and  F.J.3. Brlnkman.   1981.  Persistence  of
organic contaminants  1n ground water.   Lessons from  soil pollution Incidents
In the Netherlands.   Sc1. Total Environ.  21: 187-202.

0864p                               -45-                             05/15/87

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                                   APPENDIX

                              LITERATURE  SEARCHED



    This  profile  1s  based  on  data  Identified  by computerized  literature

searches of the following:


         GLOBAL
         TSCATS
         CASR online (U.S. EPA Chemical  Activities Status Report)
         CAS online STN International
         TOXLINE
         TOXBACK 76
         TOXBACK 65
         RTECS
         OHM TADS
         STORET
         SRC Environmental Fate Data Bases
         SANSS
         AQUIRE
         TSCAPP
         NTIS
         Federal Register


These  searches  were conducted  In  April, 1986.   In addition,  hand  searches

were  made  of   Chemical  Abstracts  (Collective  Indices  6  and  7),  and  the

following secondary sources were reviewed:


    ACGIH  (American  Conference of  Governmental  Industrial  Hyg1en1sts).
    1986.   Documentation  of the Threshold  Limit Values  and  Biological
    Exposure Indices, 5th ed.  Cincinnati, OH.

    ACGIH  (American  Conference of  Governmental  Industrial  Hyg1en1sts).
    1985-1986.    TLVs:  Threshold  Limit   Values  for   Chemical  Substances
    and  Physical  Agents  1n  the   Workroom   Environment  with  Intended
    Changes for 1985-1986.  Cincinnati,  OH.   114 p.

    Clayton,  G.D.   and   F.E.  Clayton,  Ed.    1981.   Patty's  Industrial
    Hygiene and Toxicology,  3rd rev.  ed..   Vol.  2A.    John  Wiley  and
    Sons, NY.   2878 p.

    Clayton,  G.D.   and   F.E.  Clayton,  Ed.    1981.   Patty's  Industrial
    Hygiene and Toxicology,  3rd rev.  ed.,   Vol.  2B.    John  WHey  and
    Sons, NY.   p. 2879-3816.
0864p                               -46-                             05/15/87

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    Clayton,   G.D.  and  F.E.  Clayton,  Ed.   1982.   Patty's   Industrial
    Hygiene and  Toxicology,  3rd  rev.  ed.,  Vol.  2C.   John  Wiley and
    Sons,  NY.   p.  3817-5112.

    Grayson,  H. and  D.  Eckroth,  Ed.   1978-1983.  K1rk-0thmer  Encyclo-
    pedia  of  Chemical Technology,  3rd ed.  John Wiley and Sons,  NY.   23
    Volumes.

    Hamilton,  A.  and H.L.  Hardy.  1974.  Industrial Toxicology,  3rd ed.
    Publishing Sciences  Group,  Inc.,  Littleton,  MA.   575 p.

    IARC  (International  Agency for  Research  on Cancer).   IARC  Mono-
    graphs on  the  Evaluation  of Carcinogenic  Risk  of  Chemicals   to
    Humans. WHO,  IARC,  Lyons,  France.

    Jaber, H.M.,  W.R.   Mabey,  S.T.  Liu,  T.W.  Chow and  H.L.  Johnson.
    1984.   Data aqulsHlon for environmental transport and fate  screen-
    Ing for compounds  of  Interest 1n  the Office  of  Solid Waste.  EPA
    600/6-84-010.   NTIS  PB84-243906.  SRI  International, Menlo Park, CA.

    NTP (National  Toxicology  Program).   1986.   Toxicology Research and
    Testing  Program.   Chemicals   on  Standard  Protocol.    Management
    Status.

    Ouellette,  R.P.  and  J.A.  King.  1977.    Chemical  Week  Pesticide
    Register.   McGraw-Hill  Book Co.,  NY.

    Sax, N.I.   1979.  Dangerous Properties of  Industrial  Materials, 5th
    ed.  Van Nostrand Relnhold Co., NY.

    SRI (Stanford  Research  Institute).   1984.   Directory  of  Chemical
    Producers.  Menlo Park,  CA.

    U.S.  EPA.   1985.   Status  Report on  Rebuttable Presumption  Against
    Registration  (RPAR) or  Special  Review Process.  Registration  Stan-
    dards  and  the Data Call  1n Programs.  Office  of  Pesticide Programs,
    Washington, DC.

    U.S. EPA.   1985.  CSB Existing Chemical  Assessment Tracking System.
    Name  and  CAS  Number Ordered  Indexes.   Office of Toxic  Substances,
    Washington, DC.

    USITC   (U.S.   International Trade   Commission).    1983.    Synthetic
    Organic Chemicals.  U.S.  Production  and Sales,  1982,  USITC  Publ.
    1422,  Washington, DC.

    Verschueren,  K.   1983.   Handbook of  Environmental  Data  on  Organic
    Chemicals, 2nd ed.   Van Nostrand  Relnhold Co., NY.

    Wlndholz,  M.,  Ed.  1983.   The Merck  Index,  10th  ed.   Merck and Co.,
    Inc.,  Rahway,  NJ.

    Worthing,   C.R   and  S.B. Walker, Ed.   1983.  The Pesticide  Manual.
    British Crop  Protection Council.   695 p.
0864p                               -47-                             05/15/87

          U.S. Environmental Protection Agency
          Region V, Library
          230 South Dearborn Street   '
          Chicago, Illinois   60604

-------
    In  addition,  approximately  30  compendia  of  aquatic toxlclty  data were

reviewed, Including the following:


    Battelle's  Columbus  Laboratories.   1971.   Water  Quality  Criteria
    Data  Book.   Volume  3.    Effects   of   Chemicals   on  Aquatic  Life.
    Selected  Data  from the  Literature  through 1968.   Prepared  for the
    U.S. EPA under Contract No. 68-01-0007.  Washington, DC.

    Johnson,  W.W.  and  M.T.  Flnley.   1980.  Handbook  of  Acute  Toxlclty
    of  Chemicals  to  Fish  and  Aquatic   Invertebrates.    Summaries  of
    Toxlclty  Tests  Conducted  at Columbia National  Fisheries  Research
    Laboratory.   1965-1978.    U.S.  Dept.  Interior,  F1sh  and  Wildlife
    Serv. Res. Publ. 137,  Washington, DC.

    McKee,  J.E. and  H.W.  Wolf.  1963.   Water  Quality  Criteria,  2nd ed.
    Prepared  for  the  Resources  Agency  of  California,  State  Water
    Quality Control Board.  Publ. No. 3-A.

    Plmental, D.  1971.   Ecological  Effects of Pesticides on Non-Target
    Species.  Prepared  for the U.S.  EPA, Washington, DC.  PB-269605.

    Schneider, B.A.   1979.   Toxicology  Handbook.   Mammalian and Aquatic
    Data.   Book 1: Toxicology  Data.  Office of Pesticide Programs,  U.S.
    EPA, Washington, DC.  EPA 540/9-79-003.  NTIS PB 80-196876.
0864p                               -48-                             05/15/87

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