TECHNICAL REPORT DATA
                            (fuut rt»d Instntcttora on the rtvmt before completing)
   REPORT NO.
  EPA/600/8-88/011
              3. RECIPIENT'S ACCESSION HO.

                  PB88-17951Q
  . TITLE AND SUBTITLE

   Health Effects Assessment for Acenaphthylene
              B. REPORT DATE
                                                            B. PERFORMING ORGANIZATION CODE
  . AUTHOR(S)
                                                            B. PERFORMING ORGANIZATION REPORT NO
 ft. PERFORMING ORGANIZATION NAME AND ADDRESS
              10. PROGRAM ELEMENT NO.
                                                            11. CONTRACT/GRANT NO.
 TZ. SPONSORING AGENCY NAME AND ADDRESS
                                                            13. TYPE OF REPORT AND PERIOD COVERED
 'Environmental Criteria and Assessment Office
  Office of Research and Development
  li.S.  Environmental Protection Agency
  Cincinnati. OH  45268 __
              14. SPONSORING AGENCY CODE
                 EPA/600/22
   SUPPLEMENTARY NOTES
    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 32991  for decision-making under
  CERCLA.   All estimates of acceptable intakes and carcinogenic potency presented in
  this document should be considered  as preliminary and reflect limited resources
  allocated to this project.  The  intent in these assessments  is to suggest acceptable
  exposure levels whenever sufficient data are available.  The interim values presented
  reflect the relative degree of hazard associated with exposure or risk to the
  chemical(s) addressed.  Whenever possible, two categories  of values have been
  estimated for systemic toxicants (toxicants for which cancer is not the endpoint of
  concern).  The first, RfD$ or subchronic reference dose, is  an estimate of an exposure
  level  that would not be expected to cause adverse effects  when exposure occurs  during
  a  limited time interval.  The RfD is an estimate of an exposure level that would not
  be expected to cause adverse  effects when exposure occurs  for a significant portion
  of the lifespan.  For compounds  for which there is sufficient evidence of
  careinbgenicity, qi*s have been  computed, if appropriate,  based on oral and
  inhalation data if available.
17.
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        £vO S. Dearborn ?t:-oot,  lioois  1670
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1BL DISTRIBUTION STATEMENT
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                                             EPA/600/8-88/011
                                             May, 1987
          HEALTH EFFECTS ASSESSMENT
              FOR ACENAPHTHYLENE
ENVIRONMENTAL CRITERIA AND ASSESSMENT  OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
     OFFICE OF RESEARCH AND DEVELOPMENT
    U.S. ENVIRONMENTAL PROTECTION AGENCY
            CINCINNATI. OH 45268
                   U.S. Environmental Protection Ar
                   Region  5, Library        "'
                   2'30 S.  Dearborn

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                                  DISCLAIMER


    This   document   has   been   reviewed   In  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.
                                     1V

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                                    PREFACE

4
     This report  summarizes  and  evaluates  Information relevant  to  a  prelimi-
 nary  Interim  assessment  of adverse  health  effects associated  with  acenaph-
 thylene.   All  estimates   of  acceptable  Intakes  and  carcinogenic  potency
 presented  In  this  document should be  considered  as  preliminary and  reflect
 limited  resources   allocated  to  this  project.  Pertinent  toxlcologlc  and
 environmental  data  were  located through  on-line  literature searches of  the
 TOXLINE,   CANCERLINE  and   the   CHEMFATE/DATALOG  data  bases.    The   basic
 literature  searched  supporting  this  document  Is  current  up  to Hay,  1986.
 Secondary  sources of  Information have  also  been relied upon  In the  prepara-
 tion of this report and represent large-scale health assessment efforts  that
 entail extensive peer and Agency review.  The following Office  of  Health  and
 Environmental  Assessment  (OHEA)  sources have been  extensively  utilized:

     U.S.  EPA.    1980a.   Ambient  Water Quality  Criteria  Document  for
     Polynuclear   Aromatic   Hydrocarbons.   Prepared  by   the  Office   of
     Health  and   Environmental  Assessment,  Environmental  Criteria  and
     Assessment Office, Cincinnati,  OH for  the  Office  of Water  Regula-
     tions  and  Standards,  Washington,  DC.   EPA  440/5-80-069.   NTIS  PB
     81-117806.

     U.S. EPA.   1980b.  Hazard  Profile for Acenaphthylene.  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 Acenaphthylene.
     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.

     The Intent 1n these  assessments  1s to suggest acceptable exposure levels
 whenever sufficient data  were available.  Values  were  not  derived or larger
 uncertainty factors  were  employed when  the variable  data were  limited  1n
 scope  tending   to   generate  conservative   (I.e.,  protective)   estimates.
 Nevertheless,  the  Interim  values presented  reflect  the relative  degree  of
 hazard associated with exposure  or risk  to the chemlcal(s) addressed.

     Whenever possible,  two categories  of  values have  been  estimated  for
 systemic  toxicants  (toxicants  for   which  cancer  Is  not  the   endpolnt   of
 concern).   The first, RfD$  (formerly AIS) or subchronlc  reference dose.  Is
 an estimate of an exposure  level that would not be expected to  cause adverse
 effects when exposure occurs  during a  limited  time Interval  (I.e.,  for  an
 Interval that  does  not  constitute a  significant  portion  of  the  Hfespan).
 This type of exposure estimate  has  not  been extensively used,  or  rigorously
 defined, as previous  risk   assessment  efforts  have been  primarily directed
 towards exposures  from  toxicants  1n ambient  air or  water  where lifetime
 exposure  1s  assumed.   Animal   data  used   for  RFD§  estimates  generally
 Include exposures with durations of  30-90 days.   Subchronlc  human data  are
 rarely available.  Reported exposures  are usually from chronic occupational
 exposure situations  or  from  reports of  acute  accidental  exposure.   These
 values  are  developed   for  both   Inhalation  (RfD§j)  and   oral  (RfD$o)
 exposures.


                                      111

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 t  The  RfD  (formerly  AIC)   Is  similar  1n  concept  and  addresses  chronic
exposure.  It 1s an estimate of an exposure level that would not be expected
to cause  adverse  effects  when exposure occurs  for  a significant portion  of
the Ufespan  [see  U.S.  EPA (1980a) for a  discussion of  this concept].  The
RfD  1s  route-specific  and estimates  acceptable exposure for  either  oral
(RfOg)  or  Inhalation  (RfDj)   with the  Implicit  assumption  that  exposure
by other routes Is Insignificant.

    Composite  scores  (CSs)  for  noncardnogens have  also  been calculated
where  data  permitted.   These  values are  used   for  ranking reportable quan-
tities and  the methodology for their  development   Is explained  1n  U.S.  EPA
(1983).

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

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                                   ABSTRACT
    Data  sufficient  for  risk assessment  were  not  available  for acenaph-
thylene;  therefore,  no  risk  assessment   values  were  derived.   A Russian
Inhalation study where  rats  were exposed  to acenaphthylene  dust suggests a
carcinogenic  role  for  this  compound  (Rotenberg  and Mashblts,  1965).  The
lungs appear  to be a  target organ  for acenaphthylene  by either  Inhalation
(Rotenberg and  Mashblts,  1965; Reshetluk  et al., 1970)  or  oral  (Rotenberg
and Mashblts, 1965) exposure.  Continued mutagenlclty testing and  short-term
animal  cardnogenlclty  assays  to clarify  the  carcinogenic  role of acenaph-
thylene are recommended  as  a  first  step  In  the  testing of  acenaphthylene.

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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.   Or. 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 Water

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

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

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

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

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TABLE OF CONTENTS
                                          Page
1.
2.
3.






ENVIRONMENTAL CHEMISTRY AND FATE 	
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . . .
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 	
3.1. SUBCHRONIC 	
3.1.1. Oral 	
3.1.2. Inhalation 	
3.2. CHRONIC 	
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS 	
3.4. TOXICANT INTERACTIONS 	
. . 1
, , 4
. . 5
. . 5
. . 5
5
. . 6
. . 7
. . 7






5
ft
7.
4.1. HUMAN DATA 	 ,
4.2. BIOASSAYS 	 ,
4.2.1. Oral 	 ,
4.2.2. Inhalation 	 ,
4.3. OTHER RELEVANT DATA 	 	
4.4. WEIGHT OF EVIDENCE 	 	
REGULATORY STANDARDS AND CRITERIA 	
RECOMMENDATIONS 	
REFERENCES 	
	 8
	 8
	 8
	 8
	 8
	 8
	 10
	 11
	 12
      V11

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                             LIST  OF  ABBREVIATIONS
CAS                     Chemical Abstract Service
CS                      Composite score
Kow                     Octanol/water partition coefficient
LD5Q                    Dose lethal to 50X of recipients
MED                     Minimum effective dose
NOEL                    No-observed-effect level
PAH                     Polycycllc aromatic hydrocarbon
ppm                     Parts per  million
RV,j                     Dose-rating value
RVe                     Effect-rating value

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                     1.  ENVIRONMENTAL CHEMISTRY AND FATE

     Selected  physical  and  chemical  properties  and  environmental  fate  of
acenaphthylene are presented In Table 1-1.
     Acenaphthylene  Is  widely  distributed  1n  the  environment.   In  air.
acenaphthylene will  be present partly  In the vapor phase  and  partly In the
sorbed  state onto  aerosol particles.   Acenaphthylene  adsorbed  to partlcu-
lates  could  potentially  travel   great  distances   before  ultimately  being
removed  by  rainfall  or dry  deposition  (NRC,  1983;  Pankow  et  a"!.,  1984).
Acenaphthylene  In  the vapor phase  Is  expected to  undergo  direct photolysis
or  oxidation  by reaction  with  hydroxyl  radicals  or ozone  (estimated oxida-
tion half-life -1 hour)  (HSDB,  1986;  NRC, 1983;  U.S. EPA, 1986a).  In water,
acenaphthylene will be present  partly 1n solution  and  partly as sorbed onto
suspended  particles and sediments.   The  dissolved  portion  may  undergo rapid
hydrolysis  and  significant blodegradatlon  (Callahan  et  al.,   1979).   The
adsorbed  portion may  persist  for  years In  sediments  (Bjoerseth et  al.,
1979).   Based  on   the relatively  high  log  K     value,  acenaphthylene  1s
expected  to  strongly  adsorb  to  soil,  thus  persisting  In  the  upper  few
centimeters.  In soil. It may undergo blodegradatlon.
    Human  exposure data  specific  for  acenaphthylene could  not  be located  1n
the  available literature.   U.S.  EPA (1980a),  however,  reviewed monitoring
studies  In which total  PAH content  of  groundwater  varied  from 0.003-0.04
jig/l  and   total   PAH  content  of   surface  water  ranged  from  0.24-2.5
vg/i.   In  finished drinking  water  from  15  U.S. cities, total  PAH  content
ranged  from  0.3-138.5  ng/l. with  samples  from only  two cities >10  ng/t
(Basu and  Saxena, 1977;  1978).   The other major sources  of oral  exposure  of
humans to  PAH Is through  food.   Borneff  (1977)  estimated  this  contribution


0082H                               -1-                               12/03/86

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                                  TABLE  1-1

                   Selected  Physical and  Chemical  Properties
                   and Environmental  Fate of Acenaphthylene
CAS number:

Chemical class:


Molecular weight:

Vapor pressure:


Mater solubility:
Log octanol/water
partition coefficient:

Bloconcentratlon factor:
Half-lives In
  Air:
  Hater:
  Soil:
208-96-8

polycycllc aromatic
hydrocarbon

152.20

10~8 to 10~2 mm Hg
at 20°C (estimated)

3.93 mg/i at 25°C
(estimated)
4.07 (estimated)

18.0 green mussels
(Perna verldls)
NA
NA
NA
Callahan et al., 1979


Callahan et al., 1979



Callahan et al., 1979

Hungspreugs et al., 1984
NA = Not available
0082h
       -2-
                12/03/86

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at  ~3-4 mg  total  PAH/year.   These data  do  not Indicate what  proportion of
total  PAH  content  of water and  food 1s acenaphthylene, so 1t 1s not possible
to  estimate human  Intakes of acenaphthylene alone.   The data  reviewed and
presented  by U.S.  EPA (1980a) Imply that acenaphthylene  may be a small pro-
portion  of the total  PAH content  of  water  and food,  since  this compound 1s
not listed by name  In  tables  that present levels of the more abundant PAHs.
    Overall,  human exposure  to  acenaphthylene  may be expected to  occur  by
both  oral  and Inhalation routes and H  Is  Impossible to  predict which route
may be the more Important.
0082h                               -3-                              09/03/86

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           2.  ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
    Pertinent data regarding the absorption of acenaphthylene  following oral
or Inhalation exposure could not  be located  In  the  available literature.
0082h                               -4-                              09/03/86

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                3.  TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
 3.1.   SUBCHRONIC
 3.1.1.   Oral.   In  a  Polish study reported 1n  an  abstract, Knobloch  et  al.
 (1969) administered acenaphthylene  orally to  rats at  a  dose of 0.6 g/kg for
 40  days.   Treatment-related effects  observed  were considerable  body weight
 loss, changes  In  renal  function,  changes  In the peripheral  blood pattern and
 Increased serum amlnotransferase activities.
    In a Russian  study  (Rotenberg and  Mashblts,  1965), acenaphthylene In oil
 was  administered orally  to white  mice  at  a  dose  1/10  the  LD5Q  [LOrQ  =
 1760  (range  of 2800 to  1100)  mg/kg]  every other day  for 2  months.  Treated
 mice  showed  a  significant   lag   In weight  gain as  compared  with  controls.
 Hlstopathologlcal examination of  organs showed  signs  of  stasis 1n the paren-
 chymatous organs  and  albuminoid  degeneration  of the  liver.   The  most severe
 changes were observed In the lungs, which showed hemorrhage with destruction
 of  the  Interalveolar  septa and  focal bronchial  pneumonia.   Purulent  foci
 were  observed  In  Isolated cases,  and bronchogenlc lung  cancer was  diagnosed
 1n one mouse.  Further details  of this study were not  provided.
 3.1.2.   Inhalation.   In  a  Russian study  (Rotenberg  and  Hashblts,  1965),
 acenaphthylene was administered to  white  rats  Intratracheally In a  sunflower
 oil  solution or  by blowing acenaphthylene  powder  Into the  trachea.   The
 dosing  regimen used  was not  provided.   The  pulmonary tracts  of  animals
 sacrificed 1 month  after the experiment  began  showed signs  of tracheobron-
 chH1s and hyperemla,  edema and  necrosis of  the  epithelium  In  the  trachea
 and bronchi  with  the  formation  of ulcers.  No  further  details of this study
 were available.
0082h                               -5-                              09/03/86

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    In  an additional study reported by Rotenberg  and  Mashblts (1965). white
rats  were exposed to acenaphthylene  dust  at 0.5-1.25  mg/rn3  for  4 hours/day
for  4  months.   After 3  weeks  of  exposure,  a  delay   In  weight  gain and  a
tendency  toward decreased  blood  pressure were  observed.   Hlstopathologlcal
examination  revealed various degrees  of  malignancy In the lungs  of  almost
all treated  rats.   Focal  bronchitis and perlbronchUls with bronchlollzatlon
of the  alveolar and metaplasia of  the  bronchial  epithelium were  observed 1n
the mildest  cases.   Advanced cases showed desquamatlon  of  the bronchial  and
alveolar  epithelium,  paplllar  growths  In  the epithelium and.  In  three rats.
Isolated  regions  of  carcinoma  1n the  form  of  strands  of  epithelial  cells.
Further details of this study were not provided.
    In  a  Russian study by Reshetluk  et  al.  (1970), -100 white male rats  were
exposed  to  vapors of acenaphthylene  at a  concentration of 18±2.5  mg/m3,  4
hours/day, 6  exposures/week  for  5 months.   In exposed  rats,  reflexes  of  the
upper airways  were  altered and an  Increase  1n  the  concentration  of nucleic
acids In  the  liver was observed.   Hlstopathologlcal  examination of the lungs
revealed  aspeclflc  pneumonia as  the  major  pathology of  Inhalation exposure
to acenaphthylene.   Changes observed  In  the lungs  Included desquamatlon  of
the cells 1n  the  alveolar  epithelium  and  focal  bronchitis  accompanied  by
hyperplasla and metaplasia  of  the bronchial  epithelium.  No signs  of  malig-
nant  growth  were  observed In this  study.   No further   details  of  this study
were available.
3.2.    CHRONIC
    Pertinent  data  regarding the  toxic  effects  of  acenaphthylene following
chronic oral  or Inhalation  exposure  could not  be located In  the available
literature.
0082H                               -6-                              12/03/86

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" 313.   TERATOGEHICITY AND OTHER REPRODUCTIVE EFFECTS
      Pertinent  data  regarding  teratogenlc   and  other  reproductive  effects
  following oral or  Inhalation exposure could not be  located  In  the available
  literature.
  3.4.   TOXICANT INTERACTIONS
      Without providing  details, Reshetluk et  al.  (1970) stated  that  Inhala-
  tion  of  naphthalene  caused an  Increase In  the  sensitivity of  rats to  a
  single  Inhalation  exposure  of  acenaphthylene  at  7  mg/m3.   Observations
  recorded  Include  an   Increase  In   oxygen   "composition"   (as   written   by
  translator — probably  should  read "consumption")  (60%), an  Increase  In body
  (0.6*0.2°) and skin  temperature  (0.4+0.2°),  an Increase In  blood  peroxldase
  activity  (38%),   and  decreases   1n   blood   sugar   concentration  (10%)  and
  ascorbic acid In  the lungs (33%).
  0082H                                -7-                               12/03/86

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                              4.   CARCINOGENIC1TY
4.1.   HUMAN DATA
    Pertinent  data  regarding  the  carcinogenic  potential  of acenaphthylene In
humans  following oral  or Inhalation exposure  could not  be located  In  the
available literature.
4.2.   BIOASSAYS
4.2.1.   Oral.   Pertinent  data  regarding  the  oncogenlcHy of acenaphthylene
In orally exposed animals could not be located 1n  the available  literature.
4.2.2.   Inhalation.    Rotenberg   and   Mashblts  (1965)   reported   "various
degrees  of  malignancy11  In the  lungs  of almost all of an  unspecified number
of  rats  exposed  to acenaphthylene dust  at 0.5-1.25 mg/m3  for  4  hours/day
for 4 months.   Further  details  were not provided.  In  another  Russian study
with  male  white  rats,  hlstopathologlcal  lesions  Including hyperplasla  and
metaplasia  of  the  bronchial  epithelium,  but  no  signs  of malignancy,  were
reported  following  Inhalation  of acenaphthylene  vapors  at  18  mg/m3,  4
hours/day, 6 days/week for 5 months (Reshetluk et  a!., 1970).
4.3.   OTHER RELEVANT DATA
    Acenaphthylene  has  tested negative for  reverse mutations  In Salmonella
typhlmuMum  strains  TA1537   and  TA1538  with  S-9  metabolic   activation
(Gatehouse, 1980)  and 1n  strains  TA98  and TA100 with  and without  S-9  from
3-methylcholantrene Induced rats  (Florin  et al.,  1980).   Acenaphthylene  was
mutagenlc  In   S.  typhlmurlum  strain  TM677 with   S-9  metabolic  activation
(Kaden et al.. 1979).
4.4.   WEIGHT OF EVIDENCE
    Acenaphthylene  has  not  been  evaluated  for Mr>  carclnogenlclty  In humans
and  has   not   been  adequately  studied  for  Us   carcinogenic   activity  1n
0082H                               -8-                              01/20/87

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 animals;  therefore,  H  can be placed  In IARC Group 3 and In EPA Group 0, not
 classified,  according  to  the  CAG classification scheme (U.S.  EPA,  1986b).
 Given   Us  structural  realtlonshlp  to  known  carcinogenic  PAHs,  however,
 prudent public  health policy  would dictate  minimizing  exposure  until  more Is
 known about the health  hazards.
0082h                               -9-                               01/20/87

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                     5.   REGULATORY STANDARDS AND CRITERIA

    No  standards  or  criteria  are  available for acenaphthylene  alone.   The
U.S. EPA  (1980a)  derived ambient  water  quality criteria for  PAH based  upon
the  excess  cancer  risk  associated  with   benzo(a)pyrene,  a  known  animal
carcinogen.   For  excess  cancer   risks  of  10-s,   10-«   and  10-7,   these
criteria  are 28.0,  2.8  and  0.28 ng/i,  respectively,  for  consumption  of
6.5 g  of  aquatic  organism  and 2  I of water/day.   Based  on  consumption  of
aquatic  organisms alone,  these  criteria are  311.0,  31.1  and  3.11  ng/i,
respectively.
0082h                               -10-                             01/20/87

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                              6.   RECOMMENDATIONS

     Because  of  the  lack  of  data  for   the  carclnogenlcHy  and  threshold
 tox1c1ty  of acenaphthylene, risk assessment values  cannot  be derived.
     Acenaphthylene  Is  a  PAH,  a  class   of  chemicals  that  Includes  known
 carcinogens.   In a  Russian  study, malignancies  1n  the  lungs  of rats were
 associated  with  Inhalation exposure  to  acenaphthylene dusts  (Rotenberg  and
 MashbHs,  1965).   CarclnogenlcHy testing  of acenaphthylene should  be  a
 priority.   MutagenlcHy  studies  of acenaphthylene have  been negative  In  S.
 typhlmurlum strains  TA1537,  TA1538,  TA98 and TA100 (Gatehouse, 1980;  Florin
 et al., 1980), but positive In strain TM677 (Kaden  et al.,  1978).
     If  adequate  testing Indicates that  acenaphthylene Is not  carcinogenic,
 effort  should  be made to determine thresholds for noncardnogenlc  toxldty.
 Exposure  data specifically  for  acenaphthylene  could  not  be  located,  but
 assuming  exposure similar  to  other PAHs,  both oral and Inhalation  routes  of
 exposure  may  be of  concern.   From  the  Russian  studies  (Rohenberg  and
 MashbHs, 1965;  Reshetluk  et  al., 1970),  the  lungs  appear to be the  target
 organ;  additional  studies  may define  this further.   Continued mutagenldty
 testing,  particularly  In  eukaryotlc  systems,  and short-term animal   assays
may be useful  to qualitatively estimate the oncogenldty of this compound.
0082h                              -11-                             01/20/87

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HSOB (Hazardous Substance Data Bank).   1986.   No.  2661.  On-Llne.
Hungspreugs, M.,  S.  SUplpat, C.  Tonapong,  R.F. Lee,  H.L.  Wlndom and K.R.
Tenore.  1984.  Heavy metals and polycycllc hydrocarbon compounds  In benthlc
                                            • I*

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U.S.  EPA.   1980a.   Ambient Water  Quality  Criteria Document  for  Polynuclear
Aromatic Hydrocarbons.   Prepared  by the Office of Health  and  Environmental
Assessment, Environmental Criteria and Assessment  Office,  Cincinnati,  OH for
the  Office  of  Water   Regulations  and   Standards,   Washington,   DC.    EPA

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 HSDB  (Hazardous  Substance Data Bank).  1986.  No. 2661.  On-Une.

 Hungspreugs,  M., S.  Sllplpat,  C. Tonapong,  R.F.  Lee, H.L. Wlndom  and  K.R.
 Tenore.   1984.   Heavy metals  and polycycllc hydrocarbon compounds  In benthlc
 organisms of  the upper gulf of Thailand.  Marine Poll. Bull.  15(6):  213-218.

 Kaden,  O.A.,  R.A.  HHes  and  W.G.  ThUly.   1979.   HutagenlcHy of  soot  and
 associated  polycycllc   aromatic  hydrocarbons   to  Salmonella  typhlmurlum.
 Cancer Res.   39(10):  4152-1459.

 Knobloch, K., et al.   1969.   Acute and subacute toxldty of acenaphthene  and
 acenaphthylene.  Med. Pracy.  20: 210.  (Cited In U.S. EPA,  1983)

 NRC  (National Research  Council).   1983.   Polycycllc  aromatic  hydrocarbons.
 Evaluation  of  sources  and   effects.   Natl. Acad.   Press,  Washington,   DC.
 p. 3-7.

 Pankow,  J.F., L.H.  Isabella  and W.E. Asher.  1984.   Trace  organic compounds
 1n  rain.  I.  Sampler design and  analysis  by  adsorption/thermal  desorptlon
 (ATD).   Environ. Sc1. Techno!.  18: 310-318.

 Reshetluk,  A.L.,  E.I.  Talaklna  and  P.A.  En'lakova.   1970.  Toxlcologlc
 assessment of cenaphthene and acenaphthylene.   Gig. Tr.  Prof.  Zabol.   14(6):
 46-47.

 Rotenberg, lu.S. and  P.O.  MashbHs.  1965.   Toxlcologlc aspects of  acenaph-
 thylene.   G1g. Tr.  Prof.  Zabol.   9(9):  53-54.

0082h                               -13-                              01/20/87
                                         V  ?  feviromental

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U.S.  EPA.  1980a.   Ambient  Water  Quality Criteria  Document  for Polynuclear
Aromatic  Hydrocarbons.   Prepared by  the Office of  Health  and Environmental
Assessment,  Environmental  Criteria  and Assessment  Office,  Cincinnati,  OH for
the   Office   of   Water   Regulations  and  Standards,  Washington,  DC.   EPA
440/5-80-069.  NTIS  PB 81-117806.

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

U.S.  EPA.  1983.   Reportable Quantity Document  for  Acenaphthylene.   Prepared
by the  Office  of  Health  and  Environmental Assessment,  Environmental Criteria
and  Assessment  Office,  Cincinnati,  OH  for  the  Office  of  Emergency  and
Remedial Response, Washington, DC.

U.S.  EPA.   1986a.   Graphical  Estimations Modeling  System  (GEMS).   Fate  of
Atmospheric  Pollutants   (PAP)  Data  Base.   U.S. EPA,  Office  of Toxic  Sub-
stances. Washington,  DC.   On-Hne.

U.S.  EPA.   1986b.   Guidelines  for Carcinogenic  Risk Assessment.   Federal
Register.  51(185): 33992-34003.
0082h                               -14-                             02/09/87

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