~^1 r*
                                    TECHNICAL REPORT DATA
                            (fttae md Instructions on tht rtvent bffort eomplttinf)
 1. REPORT NO.
   EPA/600/8-88/010
                              2.
                                                           3. RECIPIENT'S ACCESSION NO.

                                                               PB88-182068/AS
 4. TITLE ANO SUBTITLE

   Health Effects Assessment for  Acenaphthene
                                                           6. REPORT DATE
                                                            . PERFORMING ORGANIZATION CODE
 '. AUTHOR(S)
                                                            •. PERFORMING ORGANIZATION REPORT NO.
 9. PERFORMING ORGANIZATION NAME ANO ADDRESS
                                                            10. PROGRAM ELEMENT NO.
                                                            11. CONTRACT/GRANT
 12. SPONSORING AGENCY NAME ANO ADDRESS
                                                            13. TYPE OF REPORT ANO PERIOD COVERED
  Environmental Criteria and Assessment Office
  Office of Research and Development
  U.S.  Environmental Protection  Agency
  Cincinnati. OH  45268
                                                           14. SPONSORING AGENCY CODE
                                                              EPA/600/22
 s. SUPPLEMENTARY NOTES
 6. ABSTRACT
   This  report summarizes and  evaluates information relevant  to a preliminary interim
 assessment of adverse health  effects associated with specific  chemicals or compounds.
 The  Office of Emergency and Remedial Response (Superfund)  uses these documents in
 preparing cost-benefit analyses  under Executive Order 12991  for decision-making under
 CERCLA.   All estimates of acceptable intakes and carcinogenic  potency presented in
 this document should be considered as preliminary and reflect  limited resources
 allocated to this project.  The  intent in these" assessments  is to suggest acceptable
 exposure levels whenever sufficient data are available.  The interim values presented
 reflect the relative degree of hazard associated with exposure or risk to the
 chemical(s) addressed.  Whenever possible, two categories  of values  have been
 estimated for systemic toxicants (toxicants for which cancer is not  the endpoint of
 concern).   The first, RfD£ or subchronic reference dose, is  an estimate of an exposure
 level that would not be expected to cause adverse effects  when exposure occurs during
 a limited time interval.  The RfD is an estimate of an exposure level that would not
 he expected to cause adverse  effects when exposure occurs  for  a significant portion
 of the  lifespan.  For compounds  for which there is sufficient  evidence of
 carcinogenicity, qi*s have been  computed, if appropriate,  based on oral and
 inhalation data if available.
                                KEY WORDS AND DOCUMENT ANALYSIS
                  DESCRIPTORS
                                              b.lOENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Croup
 *. DISTRIBUTION STATEMENT
  Public
                                              10. SECURITY CLASS (This Rtfort)

                                                Unclassified
21. NO. OF PAGES
                                              20. SECURITY CLASS (This page)
                                                Unclassified
                                                                        22. PRICE
EPA P«m 2220.1 (R«*. 4-77)   PREVIOUS EDITION is OMOLETE


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                                              EPA/600/8-88/010
                                              July, 1987
           HEALTH  EFFECTS  ASSESSMENT
               FOR ACENAPHTHENE
ENVIRONMENTAL  CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL  ASSESSMENT
      OFFICE  OF  RESEARCH AND DEVELOPMENT
    U.S.  ENVIRONMENTAL PROTECTION AGENCY
             CINCINNATI, OH 45268
                               «+*l Protection  Agency
                 0 S.  Environmental Pro
                 _,  .  T, 5  Library (5PL  iD)   ., ,.„«
                 g'S's! Dehorn Street,
                 tlj       TT   60604
                 Chicago, li'

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                                  DISCLAIMER
    This   document   has   been  reviewed   1n  accordance   with   the   U.S
Environmental  Protection  Agency's  peer  and  administrative  review policies
and approved for publication.  Mention of  trade names  or  commercial products
does not constitute endorsement or recommendation  for use.
                                     11

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                                    PREFACE


    This  report  summarizes  and evaluates Information relevant  to  a  prelimi-
nary  Interim assessment of  adverse health  effects associated  with  acenaph-
thene.   Pertinent  toxlcologlc  and  environmental  data  were  located  through
on-line  literature  searches of  the Chemical Abstracts,  TOXLINE,  CANCERLINE
and the  CHEMFATE/DATALOG data  bases.   The basic literature searched  support-
Ing this  document Is current  up to  Hay,  1986.   Secondary sources of  Informa-
tion have also been relied  upon In  the preparation of this report and repre-
sent  large-scale health assessment efforts that  entail extensive peer  and
Agency review.   The  following Office of  Health  and  Environmental  Assessment
(OHEA) sources have been extensively utilized:

    U.S.   EPA.   1980a.   Ambient  Water  Quality  Criteria  Document  for
    Acenaphthene.  Prepared  by the  Office  of   Health and  Environmental
    Assessment,  Environmental  Criteria  and  Assessment   Office,  Cincin-
    nati, OH  for the Office  of Water  Regulations and  Standards,  Wash-
    ington,  DC.  EPA 440/5-80-015.  NTIS PB  81-117269.

    U.S.   EPA.   1980b.   Hazard  Profile  for  Acenaphthene.   Prepared  by
    the  Office of  Health  and  Environmental Assessment,  Environmental
    Criteria  and  Assessment  Office,  Cincinnati,  OH  for the Office  of
    Solid Waste,  Washington, DC.

    U.S.   EPA.   1983.   Reportable  Quantity  Document  for  Acenaphthene.
    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.
                                     111

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                                   ABSTRACT


    Because  of  the  lack  of  data  for  the  carclnogenlclty  and  threshold
toxlclty  of acenaphthene  risk  assessment  values  cannot be  derived.   The
ambient water  quality  criterion of 0.2 mg/i  1s  based on organoleptlc data,
which has no known relationship  to potential human health effects.  Acenaph-
thene has been shown to produce  nuclear and cytologlcal changes  1n  mlcroblal
and plant  species (U.S. EPA,  1980a).   Results  of acenaphthene  mutagenlclty
studies  fn  microorganisms  (Guertn et  al.,  1978; Douglas et  al.,  1980} and
carclnogenlclty  study  (Neukom,  1974)  are  negative.   Despite  the negative
results  In  the  newt  (TrUurus  crlstatus)  the  fact  that acenaphthene  1s a
PAH,  a  class  of  chemicals  that  contain  carcinogens,  the   carcinogenic
potential of acenaphthene 1s of  great  concern.   Inadequate evidence to allow
any  conclusion  regarding  cardnogenldty  for   humans  appropriately  places
acenaphthene In Group 0 (U.S. EPA,  1986b).
                                      1v

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                               ACKNOWLEDGEMENTS
    The  Initial  draft  of  this  report  was  prepared  by Syracuse  Research
Corporation  under Contract No.  68-03-3112 for EPA's  Environmental  Criteria
and  Assessment Office,  Cincinnati,  OH.   Dr.  Christopher  DeRosa and  Karen
Blackburn  were the  Technical  Project  Monitors  and  John  Helms  (Office  of
Toxic  Substances) was  the Project Officer.   The final  documents  In  this
series  were prepared  for  the  Office of  Emergency  and Remedial  Response,
Washington, DC.

    Scientists  from  the following U.S. EPA offices provided  review  comments
for this document series:

         Environmental Criteria and Assessment Office, Cincinnati, OH
         Carcinogen Assessment Group
         Office of A1r Quality Planning and Standards
         Office of Solid Waste
         Office of Toxic Substances
         Office of Drinking Hater

Editorial review  for the document series  was provided  by the following:

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

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

    Bette Zwayer, Jacky Bohanon and Kim Davidson
    Environmental Criteria and Assessment Office
    Cincinnati, OH

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                              TABLE  OF  CONTENTS

                                                                       Page
1.  ENVIRONMENTAL CHEMISTRY AND FATE	    1

2.  ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS 	    3

3.  TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS ..... 	    4

    3.1.   SUBCHRONIC .	    4

           3.1.1.   Oral	    4
           3.1.2.   Inhalation	    4

    3.2.   CHRONIC	    4
    3.3.   TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS	    4
    3.4.   TOXICANT INTERACTIONS	    5

4.  CARCINOGENICITY 	    6

    4.1.   OTHER RELEVANT DATA	    6
    4.2.   WEIGHT OF EVIDENCE	    6

5.  REGULATORY STANDARDS AND CRITERIA 	 .  	    7

6.  RECOMMENDATIONS 	    8

7.  REFERENCES	    9
                                     vl

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                             LIST OF ABBREVIATIONS

CAS                     Chemical Abstract Service
DNA                     Deoxyrlbonuclelc acid
PAH                     Polynuclear aromatic hydrocarbon

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                      1.   ENVIRONMENTAL CHEMISTRY AND FATE

     Selected physical  and  chemical properties  and  environmental  fate  of
 acenaphthene are  presented  1n Table  1-1.
     The  half-life  of  acenaphthene   In  air,  water and  soil  could not  be
 located  In  the  available literature.  In  both air and  water, acenaphthene
 may  be partly  associated with participate  matter  (Callahan et  al., 1979).
 When adsorbed to  partlculate  matter In air,  acenaphthene  could potentially
 be  transported  long  distances  before  ultimately  being  removed  by  chemical
 reaction  or  by  rainfall  and  dry  deposition  (HSDB,  1986;  Llgockl  et  al.,
 1985).   The  part  of  acenaphthene  present  In the  atmosphere  In  the  vapor
 phase  Is expected  to  undergo direct  photolysis or  oxidation by reaction with
 photochemically  generated hydroxyl  radicals  (estimated  oxidation  half-life
 -19  hours)   (HSDB,  1986;  U.S.   EPA,  1986a).  In  water,  acenaphthene  Is
 expected to be  transported primarily as adsorbed matter  on  suspended solids
 and  may  persist  for  years adsorbed  to  sediments  (Bjoerseth et  al., 1979).
 Ultimate removal  by blodegradatlon may be possible  (Callahan et  al., 1979).
 Acenaphthene  Is  expected  to  strongly adsorb  to  soil.  Ultimate removal  by
 blodegradatlon 1s probably more rapid 1n soil  than In water (HSDB, 1986).
    According to  U.S. EPA  (1978), acenaphthene has been detected  In efflu-
 ents   from   petro-chemlcal,   pesticide  and   wood   preservative  Industries.
Acenaphthene  has  also been Identified In  gas  exhaust  (Grimmer  et al.,  1977)
and  cigarette smoke condensates (Harke et al., 1976;  Severson et al., 1976).
Quantitative  data  regarding oral  and Inhalation  exposure were  not located,
but  It appears that both routes of exposure may be  relevant.
0067h                               -1-                              12/03/86

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                                   TABLE  1-1

   Selected Physical  and Chemical  Properties  and  Half-Lives  for  Acenaphthene
           Property
        Value
  Reference
CAS number:

Chemical class:


Molecular weight:

Vapor pressure at 25°C:


Water solubility at 25°C:
Log octanol/water
partition coefficient:

Bloconcentratlon factor:
Log soil sorptlon coefficient:
Half-lives In
  A1r:

  Water:
 83-32-9

 polynuclear  aromatic
 hydrocarbon

 154.21

 4.47xlO~3 mm Hg


 3.88 mg/l


 3.92


 387 1n  blueglll
 sunflsh

 3.31 estimated

 4.27 estimated
 hours to days
 (vapor phase)
 years (adsorbed
 to sediments)
Mackay and
Shu1, 1981

Mackay and
Shul, 1981

Hansch and
Leo, 1985

Barrows
et al.. 1980

Lyman et al.,
1982
Sabljlc, 1984
U.S. EPA,
1986a
Bjoerseth
et al., 1979
0067h
-2-
     12/03/86

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           2.  ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS

     Pertinent  data regarding  the absorption of  acenaphthene following oral
or  Inhalation  exposure  could not  be  located  In the available  literature.
0067H                               -3-                              07/30/86

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                3.   TOXICITY IN HUMANS AND  EXPERIMENTAL ANIMALS
3.1.   SUBCHRONIC
3.1.1.   Oral.   Knobloch  et al. (1969) orally  administered 2  g/kg  acenaph-
thene  In olive  oil to  seven  young  rats  (sex not  specified)  dally  for  32
days.  The  effects  observed were loss of  body weight, changes  In peripheral
blood. Increased amlnotransferase  levels   1n blood serum,  mild  morphological
damage to the  liver  and  kidneys, and  mild  bronchitis  and localized Inflamma-
tion of  the  perlbronchlal  tissue.   No Information was  provided  regarding the
use of controls.
3.1.2.   Inhalation.   Reshetyuk  et  al. (1970) exposed  100 rats  to  acenaph-
thene  at a  concentration  of 12il.5 mg/m3 for  4  hours/day, 6  days/week for
5 months.  The authors reported  altered reflexes  1n  the  upper  airways  and an
Increase  1n  the concentration  of  nucleic adds  In  the liver.,   Hlstopatho-
loglcal  examination  of   the  lungs  revealed  aspedflc  pneumonia  with  the
bronchial  epithelium  showing  hyperplasla  and  metaplasia.    No  signs  of
malignancy were observed.  Further  details of this study  were  not provided.
3.2.   CHRONIC
    Pertinent data  regarding the effects of  chronic  exposure  to acenaphthene
following oral or  Inhalation routes of exposure could not  be  located  1n the
available literature.
3.3.   TERATOGENIC AND OTHER REPRODUCTIVE  EFFECTS
    Pertinent data  regarding teratogenlc or  reproductive effects of  acenaph-
thene  following  oral  or  Inhalation  exposure could  not be  located  1n  the
available literature.
0067h                               -4-                              07/30/81)

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 3.4.    TOXICANT INTERACTIONS
    Acenaphthene has been  shown to depress the  activity of dlmethylnltros-
 amlne demethylase  In  rats   (Argus et  al.,  1971;  Arcos et  al.,  1976).  This
 activity  Is   required   for   carclnogenesls  caused  by  d1methy1n1trosaro1ne;
 therefore,  acenaphthene  may  slightly  Inhibit dlmethylnltrosamlne  carclno-
 genesls.
    Buu-Hol  and Hlen-Do-Phouc  (1969)  Injected  male  Wlstar  rats IntrapeMto-
 neally  with  20  mg/kg  acenaphthene  1n  corn  oil.   The  rats  were  Injected
 IntraperHoneally   1  week   later  with  90  mg/kg  zoxazolamlne.   The  mean
 paralysis  time  of  acenaphthene-treated  rats was  found to  be  significantly
 greater  (p<0.01) than that  of vehicle Injected rats.  The  authors  believed
 that  these results  Indicated that  acenaphthene slows  the  detoxification  of
 zoxazolamlne, which usually  proceeds by hydroxylatlon.
0067h                               -5-                              10/29/86

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                              4.   CARCINOGENICITY
4.1.   OTHER RELEVANT DATA
    Neukomm  (1974)  reported  negative  results  In a  predictive carclnogenlclty
test   based  on   neoplastlc   Induction   In   the  newt,   TrUurus   crlstatus.
Acenaphthene was  Injected subcutaneously at unspecified  dose levels.
    MutagenlcHy  studies  of  acenaphthene   1n  Salmonella  typhlmurlum  gave
negative  results  In strain  TA98  with and  without  S-9  metabolic  activation
(Guerln  et  al.,   1978;  Douglas  et al..  1980) and  1n strains TA1535,  TA100,
TA1537  and  TA1538  with  S-9  metabolic  activation  (Douglas  et  al..  1980).
Acenaphthene also had no  effect on  the  recombination  rate  of two  auxotrophlc
strains  of  EscheMchla  coll.  as  Indicated  by  the  low  level of  prototroph
Induction  (Clark,  1953a).   Clark   (1953b)   also   tested   acenaphthene   for
mutagenlclty 1n Hlcrococcus pyrogens  var. aureus strain  FDA209 with  negative
results.
    Acenaphthene  has  been shown  to produce  nuclear and cytologlcal  changes
In microblal  and plant  species.  The changes observed, Including  Increased
cell  size and DNA  content,  are  associated with disruption of  the  spindle
mechanism during  mitosis.   Because  there  Is no  known  correlation  between
these  effects  and  the  biological  Impact of acenaphthone on  mammalian  cells,
studies  examining  these  changes  will  not  be  summarized  here.    Studies
concerning these mltotlc effects are reviewed 1n U.S.  EPA (1980a).
4.2.   WEIGHT OF  EVIDENCE
    Because of the  lack  of studies  concerning the carcinogenic potential of
acenaphthene,  the  compound can be  classified as  an IARC  Group  3  chemical
(Inadequate evidence  to allow any  conclusion regarding carclnogenlclty  for
humans).  According to  the  EPA  classification  scheme (U.S.  EPA,   19865),
acenaphthene 1s most appropriately Included  In Group D (not  classified).


0067h                               -6-                              02/12/87

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                     5.  REGULATORY STANDARDS AND CRITERIA

     The ambient water  quality criterion for acenaphthene,  based on organo-
 leptlc  data,  1s  0.02  mg/i  (U.S.  EPA.  1980a).   This  level  has  no  known
 relationship  to  potential  human  health effects.
0067h                               -7-                              07/30/86

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                              6.   RECOMMENDATIONS

    Because  of  the  lack  of  data  for   the  carclnogenlcUy  and  threshold
toxlclty  of acenaphthene,  risk   assessment  values cannot  be derived.   The
ambient water  quality criterion   of  0.2  mg/i  1s based on organoleptlc  data,
which has no known relationship to potential  human  health  effects.
    The  best  documented  effect  of acenaphthene  1s  Its  ability  to  cause
nuclear and  cytologlc changes 1n  plants  (U.S.  EPA,  1980a).  No  correlation
between these  effects and effects  on mammalian  cells  Is known.   Acenaphthene
has  tested   negative  In mutagenldty  studies   In  microorganisms  (Guerln  et
al.,  1978;   Douglas  et  al.,  1980; Clark,  1953a)  and  1n  a  carclnogenlcUy
study In  the newt,  Trlturus  crlstatus  (Neukom,  1974).  Despite the negative
results,  the fact  that  acenaphthene  1s  a  PAH, a class  of  chemicals  that
contain carcinogens.  Indicates  that the  primary  Issue requiring resolution
Is  the carclnogenlcUy  of  acenaphthene by  oral  or  Inhalation  exposure.
Acenaphthene has been found  In both air and water  (U.S. EPA,  1980a),  so that
both routes  of exposure may be Important.
    If  adequate  testing determines  that  acenaphthene  Is  not carcinogenic,
efforts should be  made  to  define  thresholds  for  noncarclnogenlc  toxlclty.
Data are needed to  determine  the  target organ(s) or  system(s) most  likely  to
be  Injured  by exposure to  acenaphth&ne.   Because  acenaphthene  has a  rela-
tively  low  vapor  pressure  (4.47xlO~3 mm  Hg  at  25°C), substantial  levels  1n
air are unlikely  and Initial  testing by oral  exposure  to  determine  sub-
chronic,  developmental  and  reproductive  toxlclty may be  more  Immediately
necessary.
0067h                               -8-                             10/29/86

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                                7.  REFERENCES

Arcos,   J.C.,   et  al.   1976.   Dlmethylnltrosamlne-demethylase:   Molecular
size-dependence  of repression  by polynuclear  hydrocarbons.   Nonhydrocarbon
repressers.   J.  Toxlcol.  Environ.  Health.   1:  395.   (Cited  1n  U.S.  EPA,
1980a)

Argus,  H.F.,  et al.   1971.   Molecular-slze-dependent  effects  of  polynuclear
hydrocarbons on  mixed function oxldases.   Possible action on cascade-coupled
operons.   Eur.  Blophys.  Congr.  Proc.  1st.  1:  187.   (CHed  1n  U.S.  EPA,
1980a)

Barrows, H.E.,  S.R. PetrocelH, K.J.  Hacek  and  J.J.  Carroll.   1980.   Blocon-
centratlon and  elimination  of selected  water  pollutants by blueglll  sunflsh,
Lepomls  macrochlrus.   In:  Dyn.,  Exposure Hazard  Assess. Toxic.  Chem.   Ann
Arbor Science, Ann Arbor, HI.  p.  379-392.

Bjoerseth, A.,  J.  Knutzen and  J.  Ske1.  1979.   Determination  of  polycycllc
aromatic  hydrocarbons- In sediments  and mussels from Saudafjord,  W.  Norway,
by glass capillary gas chromatography.  Sc1. Total  Environ.  13: 71-86.

Buu-Ho1, N.P.  and H1en-Do-Phouc.   1969.  Biological effect of  some  aromatic
polycycllc  hydrocarbons  and  their  heterocycllc   analogs.    Inhibition   of
zoxazolamlne hydroxylatlon  1n rats.   C.R. Hebd. Seances  Acad.  Scl. Ser.  D.
268: 423.  (Cited 1n U.S. EPA, 1980a)
0067h                               -9-                              07/30/86

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Callahan, M.A.,  H.W.  Sllmak,  N.W. Gabel, et al.  1979.  Water-related  envi-
ronmental  fate of  129 priority  pollutants.  Volume  II.  EPA  440/4-79-0298.
U.S. EPA. Washington, DC.

Clark,  J.   1953a.   The effects  of  chemicals on the  recombination rate  In
Bacterium coll.  J. Gen. M1crob1ol.  8:  45.   (Cited  In  U.S.  EPA,  1980a)

Clark,  J.   1953b.   The mutagenlc action of various  chemicals  on  Hlcrococcus
aureus.  Proc. Okla. Acad. Sc1.  34:  114.  (Cited 1n U.S. EPA,  1980a)

Douglas, G.R., E.R.  Nestmann,  J.L. Betts,  et al.  1980.  Mutagenlc activity
In pulp mill affluents.  Water  Chlorlnatlon:  Environ.  Impact Health Eff.   3:
865-880.

Grimmer, G., et  al.   1977.   Investigation  on the carcinogenic burden by air
pollution  In  man.   XV.  Polycycllc aromatic  hydrocarbons  1n automobile gas
exhaust —  An  Inventory.  Zentralbl. Bakterlol.  Parasltenkd., Infectlonskr.
Hyg. Abt.   1:  OMg. Relhe B.   164: 218.   (Cited  In U.S.  EPA,  1980a)

Guerln, M.R.,  et  al.   1978.    Polycycllc aromatic  hydrocarbons  from fossil
fuel conversion processes.  Cardnog. Compr. Surv.:  3.  Iss. Polynucl.  Arom.
Hydrocarbons:  21.  (Cited In U.S. EPA,  1980a)

Hansch, C.  end  A.J.  Leo.   1985.   Medchem  Project  Issue  No.  26.  Pomona
College, Claiemont, CA.
0067h                               -10-                             10/29/86

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Harke,  H.P.,  et  al.   1976.   Investigations of  polycycllc aromatic  hydro-
carbons  1n  cigarette  smoke.   Z.  Lebensm.  -  Unters.  Forsch.   162:  291.
(Cited In U.S. EPA.  1980a)

HSDB  (Hazardous Substance Data Bank).  1986.  Report No.  2659.   Online: 198&.

Knobloch, K.,  et  al.   1969.   Acute  and  subacute  toxlclty  of acenaphthene and
acenaphthylene.  Med. Pracy.  20: 210.  (CUed In  U.S.  EPA,  1980a)

Llgockl,  M.P.,  C.  Leuenberger  and  J.F.   Pankow.   1985.   Trace   organic
compounds 1n  rain.   II.  Gas  scavenging  of neutral  organic compounds.   Atmos.
Environ.  19:  1609-1617.

Lyman, W.J.,  W.F. Reehe  and D.H.  Rosenblatt.  1982.   Handbook of  Chemical
Property  Estimation  Methods.  Environmental  Behavior  of Organic  Compounds.
McGraw-Hill Book Co., New York.  p.  4-9.

Mackay, D. and W.Y.  Sh1u.   1981.  A critical  review of Henry's Law Constants
for  chemicals of  environmental  Interest.   3.  Phys.  Chem.   Ref.  Data.   19:
1175-1199.

Neukomm,   S.    1974.    The  Newt   test  for  studying  certain  categories of
carcinogenic  substances.    In:  Excerpta Medlca  Int.  Congr.  Sen.  No.  311.
Experimental   Model  Systems  In  Toxicology  and  Their  Significance  In  Man,
H.A.M. Duncan,  Ed.  Proc.  Evr.  Soc. Study Drug  Tox., Zurich, Switzerland.
June 1973.  Excerpta Medlca, Amsterdam.   (CUed  In  U.S. EPA, 1980a)
0067H                               -11-                            07/30/86

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Reshetyuk,  A.L.,  E.I.  Talaklna  and P.A.  En'yakova.   1970.   Toxlcologlcal
evaluation  of acenaphthene and  acenaphthylene.   Gtg.  Tr. Prof.  Zabol.   14:
46.

Sabljlc,  A.   1984.  Prediction  of  the  nature and strength  of  soil  sorptlon
of  organic  pollutants  by  molecular  topology.   J.  Agrlc.  Food  Chem.   32:
243-246.

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 U.S.  EPA.   1983.   Reportable  Quantity Document  for  Acenaphthene.   Prepared
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                                                r,+.T Protection
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                                     *i "
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