FINAL DRAFT
              United States
              Environmenta, Protection                500ECAOCING01 2
>EPA       Research  and
              Development
             HEALTH AND ENVIRONMENTAL EFFECTS DOCUMENT
             FOR CYCLOPENTADIENE AND DICYCLOPENTADIENE
              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
                         DRAFT: DO NOT CITE OR QUOTE,

                                            •
                                NOTICE

          This document 1s 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.
                                       11

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                                    PREFACE
    Health and  Environmental  Effects  Documents (HEEDs) are  prepared  for  the
Office of  Solid  Waste  and Emergency Response  (OSWER).  This  document series
1s Intended to support  listings  under  the  Resource  Conservation and Recovery
Act (RCRA) as  well as  to provide health-related limits and  goals  for  emer-
gency and  remedial actions  under the Comprehensive  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 for  1n  this document
and  the  dates  searched  are  Included 1n  "Appendix:  Literature  Searched."
Literature search  material  Is  current up  to 8 months previous  to  the  final
draft date listed  on  the front  cover.   Final  draft document  dates  (front
cover) reflect the date the document Is sent to the Program Officer (OSWER).

    Several  quantitative  estimates  are  presented  provided  sufficient  data
are available.   For systemic toxicants,  these  Include Reference doses (RfOs)
for  chronic   and  subchronlc  exposures  for  both  the Inhalation  and  oral
exposures.   The  subchronlc  or  partial  lifetime  RfD, Is  an estimate of  an
exposure  level   that  would  not  be  expected  to  cause adverse  effects  when
exposure occurs  during  a  limited time  Interval,  for  example,  one  that  does
not constitute a significant portion of  the llfespan.   This type of exposure
estimate has  not been  extensively  used, or  rigorously  defined as previous
risk  assessment   efforts  have  focused   primarily   on   lifetime  exposure
scenarios.   Animal data  used  for  subchronlc  estimates  generally  reflect
exposure durations  of  30-90  days.   The  general  methodology  for  estimating
subchronlc RfDs  1s  the  same  as  traditionally  employed  for  chronic  estimates,
except that subchronlc data are utilized  when available.

    In  the  case  of   suspected   carcinogens,  RfDs  are  not  estimated.    A
carcinogenic potency  factor,  or  q-]*  (U.S.  EPA,  1980), 1s  provided Instead.
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 toxldty  and cardno-
genlclty are derived.   The RQ  1s used to determine  the quantity of a hazar-
dous substance for  which  notification  1s required  1n  the  event  of  a  release
as specified under  the  CERCLA.   These  two  RQs  (chronic toxldty and cardno-
genlclty)  represent two of six  scores developed  (the  remaining  four  reflect
1gn1tab1l1ty,  reactivity,  aquatic  toxldty,  and  acute mammalian  toxldty).
Chemical-specific RQs  reflect the lowest of  these  six  primary criteria.   The
methodology for  chronic  toxldty and  cancer-based RQs are defined  1n  U.S.
EPA, 1983 and 1986a, respectively.
                                      111

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                              EXECUTIVE SUMMARY

    Cyclopentadlene  1s  a  colorless   liquid  with  a  sweet  terpenlc  odor;
dlcyclopentadlene 1s  a colorless  crystalline solid with a  camphor-like odor
(Fefer and  Small,  1979).  Both compounds  are almost Insoluble  1n  water  but
are soluble  1n  a number  of  organic  solvents (Weast, 1985;  Wlndholz,  1983).
Cyclopentadlene  polymerizes  spontaneously at  ordinary  temperatures  to form
dlcyclopentadlene and reacts spontaneously  with oxygen.   Dlcyclopentadlene
Is the form  in  which Cyclopentadlene  1s sold commercially,  since it  1s more
stable (Fefer and  Small, 1979).   In  1985,  U.S.  production  of  dlcyclopenta-
dlene  (Including Cyclopentadlene) by  three  manufacturers  was   63.6  million
pounds (USITC, 1986).  These compounds are  recovered  as  by-products from the
thermal cracking of  hydrocarbons  and  from  the  carbonization of coal  (Fefer
and Small,  1979).    The  use pattern  for  dlcyclopentadlene  was reported  as
follows  (CMR,  1980): EPDM  (ethylene-propylene  dlene  monomer)  elastomers,
40%;  hydrocarbon resin systems, 30%;  unsaturated polyester  resins,  10%;  and
miscellaneous, Including  chemical  synthesis,  fire  retardants,  pesticides  and
agricultural chemicals, fuel and lube additives and adheslves,  20%.
    The  major  environmental  fate  and  transport  process  for  cyclo- and
dlcyclopentadlene  1n  water  appears  to  be   volatilization.   Volatilization
half-lives  of  dlcyclopentadlene from  typical  water bodies  (pond,  river  and
lake)  were  estimated  to  range  from 1.3-6.7  days.   Cyclopentadlene  1s even
more  volatile  than   dlcylopentadlene,  with  an  estimated  half-life of  2.4
hours from a  river 1  m deep  flowing  1  m/sec  with a wind velocity of 3 m/sec.
Photoox1dat1on may  also  contribute  to the removal  of  these compounds from
water.  Aquatic  hydrolysis,  microblal  degradation,  adsorption  and  bloconcen-
tratlon are  not  expected to be significant.  If released  to the atmosphere,
                                      1v

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cyclo- and dlcyclopentadlene  will  exist  almost  entirely 1n  the  vapor-phase
(Elsenrelch et al., 1981) and will  react  very rapidly with  hydroxyl radicals
and  ozone  (U.S.  EPA,  1987).   The half-life  for  the reaction  with hydroxyl
radicals or with ozone was  estimated  to  range from 45-103 minutes (U.S. EPA,
1987).  If released  to soil,  cyclopentadlene may be  susceptible  to signifi-
cant  leaching  (based on  estimated  K    values), and  significant  evaporation
1s  Hkely.   Dlcyclopentadlene  was  found  to  volatilize  more  slowly  from dry
soil  than  from moist  soil  (O'Donovan and  Woodward,  1977).  Based  on  esti-
mated K   values, dlcyclopentadlene will  have a low rate of  soil mobility.
    Cyclo- and dlcyclopentadlene  were detected  1n  drinking  water  (Keith et
al.,  1976; Shackelford and  Keith, 1976;  Kool et al.,  1982), In  groundwater
near  use  facilities  (O'Donovan  and  Woodward,  1977;  Burrows,  1978) and 1n
Industrial wastewater  effluents  (Perry et al., 1979; Shackelford  and Keith,
1976).  Cyclopentadlene can be  emitted to the atmosphere by  stack effluents
from  waste  Incineration  (Junk  and Ford,  1980),  by  emissions  from polymer
manufacture  (Graedel,  1978),  1n  exhausts from  hydrocarbon  fuel  combustion
(Se1z1nger and  D1m1tr1ades, 1972) and  1n emissions  from coal  carbonization
or  hydrocarbon cracking  processes.   No ambient air or food  monitoring data
for either compound were  available.   Cyclopentadlene  was  detected  1n tobacco
smoke at levels of 0.06-7 yg/clgarette (Hlgglns et  al.,  1983).
    There were no  data  regarding  the  toxldty of cyclopentadlene  to aquatic
biota,  and  very little  regarding dlcyclopentadlene.   Reported LC-n  values
for  dlcyclopentadlene  were  6.9  mg/S.   for   Daphnla  sp.,   42.3   mg/S.  for
rainbow  trout  and  75.2  for  bluegllls  (Velslcol   Chem.  Corp.,  1980).   An
ECcQ  of 5.3 mg/l  for  Tetrahymena pyrlformls  was also  reported  (Yoshloka
et al.,  1985).

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    Pertinent data  regarding the  pharmacoklnetlcs  of cyclopentadlene  could
not be located 1n the available  literature as  cited  1n Appendix  A.
    LHton  B1onet1cs  (1976)  reported  that  nearly  all  of  an  oral  dose  of
14C-dUyclopentad1ene was  absorbed by  the gastrointestinal  tract  of  mice,
rats  and  dogs.   Peak  plasma levels were  reached more  rapidly In mice  and
dogs  than  In rats.   Clearance from  the  plasma occurred In two  phases,  with
half-lives for the  first  phase  of 4 and 10 hours for mice  and  dogs,  respec-
tively, and  for  the second phase, of 18, 18 and  27 hours for mice,  rats  and
dogs,  respectively.   The  half-life.for  the first  phase of elimination  for
rats  was   not calculated.   The  radioactivity  was   distributed  to  a  wide
variety of  organs  and  tissues  1n mice,  rats  and  dogs within  4  hours  of
dosing and  disappeared  rapidly  from these  tissues.   Disappearance of  radio-
activity from the tissues  was much more  rapid  1n mice than  1n dogs and rats.
Only  small  amounts  of  radioactivity  were detected at  72  hours In mice  and
rats  and  at 7 days  In  dogs.  All three  species had common urinary  metabo-
lites  (not Identified), and  very  little  of  the radioactivity  measured  In the
urine  was  attributable   to   nonmetabollzed   l4C-d1cyclopentad1ene.    The
presence  of  conjugates  In  the  urine was  Indicated  as  well.   Dlcyclopenta-
dlene was excreted primarily 1n  the urine among all  three species.
    Dow  (1987)  reported  several  subchronlc  Inhalation  toxldty studies  of
cyclopentadlene  1n  rats,   guinea  pigs,  rabbits  and  dogs.   The  only  effects
reported were a  necrotlc  left ventricle  In one dog exposed to  250  ppm (676
mg/ma)  for  135,  7-hour  exposures  1n  194  days  and  cloudy  swelling  of  the
liver  and kidney 1n  rats  exposed  to 500  ppm  (1352  mg/m3)  for 35,  7-hour
exposures  1n 54  days.   Shashklna  (1965)  reported  leukopenla,  anemia  and
lesions of the trachea, bronchi,  lungs,  liver,  kidneys,  spleen, thyroid,  CNS
and  lymphatic elements  1n  rats exposed to  cyclopentadlene at  a  concentration
                                      v1

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of  0.35  mg/a,  4  hours/day,  6  days/week for  6 months.   Little  Information
regarding  the acute  toxldty of  cyclopentadlene  was  available.   Shashklna
(1965)  reported  2-hour  Inhalation  LC  s   of  39  mg/st  for  rats  and  14
mg/8.  for  mice.   Cyclopentadlene  has  an Irritating  terpene-llke  odor,  and
although systemic  Injury  was considered  unlikely  at  a  concentration  of  250
ppm  (676  mg/m3),   a  much  lower  TLV-TWA  of  75 ppm  (200 mg/m3)  was  adopted
from  the  standpoint  of  comfort  (ACGIH, 1986).   The  ACGIH committee  also
recommended  deletion  of   the  STEL  until  additional   quantifying  data  1s
acquired.
    Dodd et al. (1982)  observed  structural  and functional  kidney  alterations
In  male  rats  exposed  by Inhalation  to  >1 ppm  (>5.4  mg/m3)  dlcyclopenta-
dlene  for  6  hours/day, 5 days/week  for  up to 90  days, and an  Increase  1n
relative liver  weight  1n  male rats exposed by  the  same exposure  regimen but
at  a  concentration of  51  ppm (276 mg/m3).   Dodd  et  al.  (1982)  reported  an
Increased body  weight gain  1n  female mice  and Increased  mortality (attrib-
uted  to  pulmonary congestion)  1n both  sexes  at  a  concentration of  51  ppm
(276  mg/m3)  for  6 hours/day,  5  days/week  for  up to  64  and  60 exposures,
respectively.    Liver  dysfunction, manifested  by  a  slight Increase  In serum
albumin In  the  5.1 and 51  ppm  (27.6  and 276 mg/m3) mice  (64 exposures)  and
Increased relative  liver  weight  (5.1  ppm females  only; 64  exposures),  was
also observed.
    Klnkead et  al. (1971)  reported  subchronlc  Inhalation toxldty studies  1n
rats  and  dogs.   Rats  exposed to >35.2  ppm  (>190.3 mg/m3)  for 7 hours/day,
5 days/week for 89 exposures exhibited  kidney lesions.  These effects  were
not  noted  at  19.7   (106.5  mg/m3)   ppm.   Minimal  changes  1n  biochemical
parameters  were  observed  1n  dogs  exposed  to  23.5  ppm   (127.1  mg/m3),  7
hours/day, 5 days/week  for  89 exposures.  These effects were not  observed  at

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8.9  ppm  (45.1  mg/m3).   Shashklna   (1965)  reported  protelnurla  and  hlsto-
pathologlcal lesions  of  the trachea, bronchi, lungs,  liver,  kidney,  spleen,
thyroid,  CNS and  lymphatic elements  In  rats  exposed to 0.02 mg/i,  4 hours/
day, 6 days/week for  6 months.   No  effects  were  reported 1n a 12-month study
using mink  that  were exposed to <800 ppm  (170  mg/kg/day)  dlcyclopentadlene
In the diet for 12 months  (Aulerlch et  a!., 1979).   Rats and mice exposed to
<750 and  273  ppm dlcyclopentadlene  1n  the  diet, respectively, for  13 weeks
exhibited no effects  (Litton  B1onet1cs,  1976).   No  treatment-related effects
occurred  in dogs given  dlcyclopentadlene in the diet  at  concentrations >100
ppm  for  13 weeks  (Litton  Blonetlcs,  1980).   Oral  LD5Qs  for  dlcyclopenta-
diene 1n  rats and mice were similar and  ranged  from ~200-500 mg/kg (Hart and
Dacre,   1977;   Klnkead  et   a!.,   1971).   Inhalation  LC5 s  In  mice,  rats,
guinea  pigs  and  rabbits  ranged  from -150-800  ppm  (811-4326 mg/m3)/4 hours
(Klnkead et al.,  1971; Gage, 1970).
    When  exposed  by  Inhalation  to  dlcyclopentadlene,  7 hours/day,  5 days/
week  for  2  weeks,   rats  had convulsions  and  hemorrhage  of  the lungs  and
thymus and  died  at  332  ppm (1795 mg/m3);  mice  died  at 72 and 146  ppm (389
and  789  mg/m3),  and  dogs  had  diarrhea at 20  ppm (108  mg/m3)  and  lack  of
control of  hindquarters  at  47  ppm  (254 mg/m3)  (Klnkead et al.,  1971).   No
effects were observed 1n beagles fed  dlcyclopentadlene In the diet  at <375
ppm  for  14 days  (Litton  Blonetlcs,  1976).  Decreased  body weight  gain  or
weight  loss  and  hematologlcal  effects  occurred  at  all  dietary  levels
(10-10,000  ppm)  of  dlcyclopentadlene 1n mink  treated for  21  days  (Aulerlch
et al., 1979).
    Like  cyclopentadiene,  dlcyclopentadlene has a  disagreeable odor.   It 1s
noticeably  Irritating  when  a   concentration  of  10  ppm  1s  exceeded.   In
humans, dlcyclopentadlene  at  a  concentration  of 1  ppm  caused  eye and throat

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Irritation and olfactory fatigue, but  no  fatigue  was  reported  at 5.5 ppm for
30  minutes.   Headaches were  reported  by  exposed workers,  but  the  workers
became Inured to this effect.
    Cardnogenlclty data were  not available for  cyclopentadlene or  dlcyclo-
pentadlene.   Therefore,  these   compounds  have   an   EPA   Group  D   welght-
of-ev1dence  classification   (U.S.   EPA,   1986b).    Negative   results   were
obtained  1n  mutagenldty  experiments of d1cyclopentad1ene  1n  £._ typh1mur1um
and £.. cerevlslae.
    D1cyclopentad1ene was not maternally  toxic,  fetotoxlc  or  teratogenlc and
did not  affect  reproductive  performance 1n rats,  at  concentrations  <750 ppm
1n  the  diet  (Litton Blonetlcs,  1980).  No malformations,  deleterious  effect
on  reproductive  Indices or  toxic  effects  on the  parents were  observed  1n an
oral  3-generat1on  reproductive  toxlclty study using  rats  (LHton Blonetlcs,
1980).   In a  12-month study  using  mink,  significant  decreases 1n  testls
weight and  In  kit body weight  were observed at  dietary concentrations  >800
ppm (170 mg/kg/day) and >200 ppm (42 mg/kg/day),  respectively.
    A  subchronlc  Inhalation RfD  of  3  mg/m3 or  61   mg/day  was  derived  for
cyclopentadlene  by dividing  the  NOEL of  87.3  mg/kg/day [137 mg/m3  (676
mg/m3  for  135  7-hour exposures  1n  194 days)] for rats  1n the  study  summa-
rized by  Dow (1987) by an  uncertainty factor of  100.   At the  LOAEL of 260
mg/m3  (1352  mg/m3  for 35  7-hour  exposures  1n  53   days),  rats had  hlsto-
pathologlcal  lesions  In the  Hver  and  kidney.    Data  were Insufficient  to
derive a  chronic  Inhalation  RfD and  subchronlc  and  chronic  oral  RfDs  for
cyclopentadlene.  An RQ of 1000 was  derived  for  cyclopentadlene based  on the
LOAEL.
    A  subchronlc  Inhalation  RfD  of  0.002 mg/m3  or  0.04 mg/day  was  derived
for dlcyclopentadlene  by  dividing  the  LOAEL of  0.61 mg/kg/day  [0.96  mg/m3
(5.4 mg/m3,  6  hours/day,  5 days/week)],  which  was associated  with  Impaired
                                      1x

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kidney  function  1n rats  1n  the  study  by Dodd  et  al.  (1982), by  an uncer-
tainty  factor  of  1000.   A  chronic Inhalation  RfD  of 0.0002 mg/m3  or  0.004
mg/day  was  also  derived by  dividing  this LOAEL by an  uncertainty  factor of
10,000, but very little confidence was placed 1n the chronic Inhalation RfD.
    A  subchronlc oral  RfD  of  0.3 mg/kg/day or 22  mg/day was  derived  for
dlcylopentadlene by dividing  the  NOEL of 32 mg/kg/day  [calculated  from body
weight  and  food  consumption data  for "the 690 ppm  group  1n the 3-generat1on
dietary  study using  rats  by  Litton  Blonetlcs  (1980)]  by an  uncertainty
factor  of  100.   At the LOAEL  of  42 mg/kg/day 1n the diet,  the offspring of
mink  had  reduced  body  weight  after  4  weeks  of .nursing  (Aulerlch  et  al.,
1979).  A chronic  oral  RfD  of  0.03 mg/kg/day or 2 mg/day was also derived by
dividing the  NOEL  by an  uncertainty  factor of  1000.   Medium  confidence was
placed  1n  the chronic  oral  RfD  because 1t was  based  on  an  extensive sub-
chronic data  base.  An RQ  of  100  was  derived  based on  the Impaired kidney
function of rats In the Inhalation  study by Dodd et al.  (1982).

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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	     3
    1.4.   USE DATA	     5
    1.5.   SUMMARY	     5

2.  ENVIRONMENTAL FATE AND TRANSPORT	     6

    2.1.   AIR	     6

           2.1.1.   Reaction with Hydroxyl Radicals 	     6
           2.1.2.   Reaction with Ozone 	     6
           2.1.3.   Reaction with Atomic Oxygen 	     6

    2.2.   WATER	     6

           2.2.1.   Hydrolysis	     6
           2.2.2.   Photooxldatlon	     7
           2.2.3.   M1crob1al Degradation 	     7
           2.2.4.   Volatilization	     7
           2.2.5.   Adsorption	     8
           2.2.6.   B1oconcentrat1on	     8

    2.3.   SOIL	     9

           2.3.1.   M1crob1al Degradation 	     9
           2.3.2.   Adsorption	     9
           2.3.3.   Volatilization. .  .-	     9

    2.4.   SUMMARY	    10

3.  EXPOSURE	    11

    3.1.   WATER	    11
    3.2.   FOOD	    11
    3.3.   INHALATION	    11
    3.4.   DERMAL EXPOSURE	    12
    3.5.   SUMMARY	    12

4.  AQUATIC TOXICITY	    13

    4.1.   ACUTE TOXICITY	    13
    4.2.   CHRONIC EFFECTS	    13
    4.3.   PLANT EFFECTS	    13
    4.4.   SUMMARY	    13
                                     x1

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                          TABLE OF CONTENTS  (cont.)

                                                                        Page
 5.   PHARMACOKINETCS	    14

     5.1.    ABSORPTION	    14
     5.2.    DISTRIBUTION	    15
     5.3.    METABOLISM	    16
     5.4.    EXCRETION	    17
     5.5.    SUMMARY	    17

 6.   EFFECTS	    19

     6.1.    SYSTEMIC TOXICITY	    19

            6.1.1.    Inhalation Exposures	    19
            6.1.2.    Oral Exposures	    23
            6.1.3.    Other Relevant Information	    25

     6.2.    CARCINOGENICITY	    28
     6.3.    MUTAGENICITY	    29
     6.4.    TERATOGENICITY	    29
     6.5.    OTHER REPRODUCTIVE  EFFECTS 	    29
     6.6.    SUMMARY	    30

 7.   EXISTING GUIDELINES AND STANDARDS 	    34

     7.1.    HUMAN.  . .	    34
     7.2.    AQUATIC	.34

 8.   RISK ASSESSMENT	    35

     8.1.    CARCINOGENICITY. .  .,	    35
     8.2.    SYSTEMIC TOXICITY	    35

            8.2.1.    Inhalation Exposure 	    35
            8.2.2.    Oral Exposure	  .    38

 9.   REPORTABLE QUANTITIES 	    40

     9.1.    BASED ON SYSTEMIC TOXICITY 	    40
     9.2.    BASED ON CARCINOGENICITY	    46

10.   REFERENCES	    49

APPENDIX A: LITERATURE SEARCHED	    58
APPENDIX B: SUMMARY TABLE FOR CYCLOPENTADIENE	    61
APPENDIX C: SUMMARY TABLE FOR OICYCLOPENTADIENE	    62

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                               LIST OF TABLES

No.                               Title                                Page

1-1     1977 Production Data for Cyclopentadlene and
        D1cyclopentad1ene 	    4

6-1     LDso and LCjo Values of D1cyclopentad1ene	   26

9-1     Inhalation Toxldty Summary for Cyclopentadlene Using
        the Rat	   41

9-2    -Toxicity Summary for Dlcyclopentadiene	   42

9-3     Inhalation Composite Score for Cyclopentadlene
        Using the Rat	   44

9-4     Cyclopentadlene: Minimum Effective Dose (MED) and
        Reportable Quantity (RQ)	   45

9-5     Inhalation Composite Scores for D1cyclopentad1ene 	   47

9-6     Dlcyclopentadiene: Minimum Effective Dose (MED) and
        Reportable Quantity (RQ)	   48
                                    X111

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                             LIST  OF  ABBREVIATIONS

BCF                     Bloconcentratlon factor
BUN                     Blood urea nitrogen
bw                      Body weight
CNS                     Central nervous system
CS                      Composite score
EC5Q                    Concentration effective to 50% of recipients
                        (and all other subscripted concentration levels;
l.p.                    Intraperltoneal
K                       Octano")/water partition coefficient
                        Concentration lethal to 50% of recipients
                        (and all other subscripted dose levels)
LD5Q      -              Dose lethal to 5054 of recipients
LOAEL                   Lowest-observed-adverse-effect level
MED                     Minimum effective dose
NOEL                    No-observed-effect level
ppb                     Parts per billion
ppm                     Parts per million
RfD                     Reference dose
RQ                      Reportable quantity
RV.                     Dose-rating value
RV                      Effect-rating value
SGOT                    Serum glutamlc oxaloacetlc transamlnase
SGPT                    Serum gluatamlc pyruvlc transamlnase
STEL                    Short-term exposure limit
TLC                     Thin-layer chromatography
TLV                     Threshold limit value
TWA                     Time-weighted average
v/v                     Volume per volume
                                      x1v

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                               1.  INTRODUCTION

1.1.   STRUCTURE AND CAS NUMBER

    Cyclopentadlene  Is  also  known  by  the  synonyms  1,3-cyclopentadlene,

pentole,  pyropentylene and  r-pent1ne  (SANSS.  1987).   Dlcyclopentadlene  Is

also   known   by  the   synonyms   3a,4,7,7a-tetrahydro-4,7-methano-!H-1ndene,

3a,4,7,7a-tetrahydro-4,7-methano1ndene,  bieye 1 opentad1ene,   b1s(cyclopenta-

dlene),  tr1cyclo[5.2.1,0(sup2,6)]deca-3,8-d1ene  and  cyclopentadiene  dlmer

(SANSS,  1987).   The  structures,  molecular weights,  empirical  formulas  and

CAS  Registry  numbers  for  cyclopentadlene  and  dicyclopentadlene  are  as

follows:
                                      H
                                 CH2     CH



                                HC =CH


                              Cyclopentadlene            Dlcyclopentadlene

Molecular weight:                66.10                        132.21
Empirical formula:               ^-S^b                         t-10^12
CAS number:                      542-92-7                     77-73-6
1.2.   PHYSICAL AND CHEMICAL PROPERTIES

    Cyclopentadlene 1s a  colorless  liquid  with a sweet  terpenlc  odor  (Fefer

and Small,  1979).   It  Is  mlsclble with alcohol,  ether, benzene and  carbon

tetrachlorlde and  Is  soluble In carbon  dlsulflde,  aniline, acetic add  and

liquid petroleum  (Wlndholz,  1983).  Selected  physical  properties of  cyclo-

pentadlene are as follows:


Melting point:              -85°C                    Fefer  and  Small,  1979

Boiling point:              41.5°C                    Fefer  and  Small,  1979

Density (20/4°C):           0.8024  g/ms.              Fefer  and  Small,  1979




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Water solubility:
  at 25°C                   1800 ppm                 Amoore and Hautala,  1983
Vapor pressure:
  at 20°C                   364 mm Hg                BoubHk et al.f  1984
  at 25°C                   439 mm Hg                Boubllk et al..  1984
Log Kow:                    1.887 (calculated)        U.S.  EPA,  1987
Air conversion factor:      1  mg/m3 = 0.37 ppm
  at 20°C
A1r odor threshold:         1.9 ppm (v/v)             Amoore and Hautala,  1983

    Dlcyclopentadlene forms colorless  crystals  and has a  camphor-Uke odor.
It  exists  1n  two  stereolsomerlc  forms,  the endo  and exo  Isomers;  however,
the  commercial  product  Is  predominantly  the endo  Isomer  (Fefer and  Small,
1979).   Dlcyclopentadlene  1s   soluble  1n  alcohol,  ether  and  acetic  add
(Weast,  1985).  Selected  physical  properties  of  dlcyclopentadlene  are  as
follows:

Melting point:              33.6°C                   Fefer  and  Small,  1979
Boiling point:              170°C (decomposes)        Fefer  and  Small,  1979
Density (35/4°C):           0.9970 g/ml              Fefer  and  Small,  1979
Water solubility:           40 ppm (estimated)        Smith  et al.,  1980
Vapor pressure:
  at 20°C                   1.4 mm Hg                Rosenblatt et  al., 1975
  at 34.1°C                 5 mm Hg                  Perry  and  Green,  1984
  at 47.6°C                 10 mm Hg                 Perry  and  Green,  1984
Log Kow:                    2.894 (calculated)        U.S.  EPA,  1987
A1r conversion factor:      1  mg/m3 = 0.185 ppm
  at 20°C
A1r odor threshold:         0.0057 ppm (v/v)         Amoore and Hautala,  1983

    Cyclopentadlene  polymerizes  spontaneously  at  ordinary temperatures  to
form  dlcyclopentadlene  and reacts  spontaneously  with oxygen  to form brown.
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gummy products that  usually  contain  substantial  amounts  of peroxides.   Since
cyclopentadlene contains two conjugated  double bonds  and an active methylene
group, 1t can undergo a  dlene  addition  with  almost any unsaturated compound.
It  1s  readily  halogenated  and  can  undergo  condensation  reactions  at  the
methylene group (Fefer and Small, 1979).
1.3.   PRODUCTION DATA
    Production and Import data are  listed  1n  Table 1-1.   Three U.S. manufac-
turers  reported  a combined  production  of  63.6 million pounds  of  dlcyclo-
pentadlene  (Including cyclopentadlene)  1n 1.985  (USITC,  1986).   Current U.S.
manufacturers of dlcyclopentadlene are as follows (SRI, 1986):
                                                      Annual Capacity
                                                     (millions of Ibs.)
    Chemical Exchange Ind.
      Advanced Aromatic  Chem. (Galena Park, TX)              60
    Dow Chemical (Freeport, TX)                              25
    Exxon Corp. (Baton Rouge, LA)                            45

    Dlcyclopentadlene 1s  the form  1n  which  cyclopentadlene  1s  sold  commer-
cially, since H 1s  more  stable  chemically.   Dlcyclopentadlene can easily be
cracked  to  cyclopentadlene  by  distillation  for   consumer  use   (Fefer  and
Small, 1979).
    Cyclo- and  dlcyclopentadlene are commercially  recovered  as  by-products
from the  thermal  cracking  of hydrocarbons (such as naphtha and gas oil)  and
from the  carbonization of coal.  Cyclopentadlene 1s recovered from the  other
hydrocarbons by the  distillation of the total cracked product  and 1s  heated
to ~100°C  to convert the monomer  to dlcyclopentadlene.   Much  of  the  cyclo-
and  dlcyclopentadlene  available  from  these  processes  1s  not  recovered
commercially (Fefer and  Small,  1979).
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                                  TABLE 1-1
       1977 Production Data for CyclopentacHene and D1cyclopentad1ene*
Producer, Location
Type of
Production
Production Range
(pounds)
Cyclopentadlene
Velslcol Chem., Memphis, TN
Arapahoe Chem., Boulder, CO
Boulder Sci., Bouider, CO
Gulf 011, Belle Chasse, LA
Hydron Lab., New Brunswick, NJ
Eastman Kodak, Rochester, NY
Amer. Cyanamld, Bound Brook, NJ
Confidential
manufacturer
manufacturer
manufacturer
manufacturer
manufacturer
manufacturer
Importer
manufacturer
confidential
1-10
<1000
1-10
<1000
none
<1000
thousand

million



confidential
                              D1cyclopentad1ene
                 •
Carbide Isoprene Corp., Ponce, PR
Dow Chem., Freeport, TX
Exxon, Baton Rouge, LA
Monsanto, Alvln, TX
U.S. Indus. Chem., Tuscola, IL
Velslcol. Marshall, IL
Gulf Oil, Belle Chasse, LA
Gulf 011, Port Arthur, TX
Chem. Exchange, Galena Park, TX
Hydron Lab., N. Brunswick, NJ
Ashland Chem., Dublin, OH
Mitsubishi, New York, NY
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      manufacturer
      Importer
      Importer
Neville Chem., Santa Fe Springs, CA
      importer
10-50 million
1-10 million
10-50 million
10-50 million
1-10 million
confidential
0.1-1.0 million
10-50 million
0.1-1.0 million
<1000
none
10-50 million  *
1-10 million
*Source: U.S. EPA (1977)
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1.4.   USE DATA
    The  use  pattern  for  dlcyclopentadlene  was  reported  as  follows  (CMR,
1980): EPDH  (ethylene-propylene  dlene monomer) elastomers,  40%;  hydrocarbon
resin  systems,  3054;  unsaturated  polyester resins,  10%;  and  miscellaneous,
Including  chemical  synthesis, fire  retardants,  pesticides  and  agricultural
chemicals, fuel and lube additives and adheslves,  20%.
1.5.   SUMMARY
    Cyclopentadlene  1s  a  colorless   liquid   with  a  sweet  terpenlc  odor;
dlcyclopentadlene  1s  a  colorless  crystalline  solid with  a  camphor-Uke odor
(Fefer and Small,  1979).  Both compounds  are  almost Insoluble  In  water  but
are soluble  1n  a number  of  organic  solvents  (Weast, 1985;  Wlndholz,  1983).
Cyclopentadlene  polymerizes  spontaneously at  ordinary  temperatures  to  form
dlcyclopentadlene  and reacts  spontaneously  with  oxygen.   Dlcyclopentadlene
1s  the form  1n  which Cyclopentadlene 1s sold  commercially,  since  It  1s more
stable (Fefer  and  Small, 1979).   In  1985, U.S.  production  of  dlcyclopenta-
dlene  (Including Cyclopentadlene) by  three manufacturers  was 63.6  million
pounds (USITC, 1986).  These  compounds are recovered as  by-products from the
thermal  cracking of hydrocarbons  and from the carbonization of coal  {Fefer
and Small,  1979).    The  use  pattern  for  dlcyclopentadlene  was  reported  as
follows  (CMR,   1980):  EPDM  (ethylene-propylene  dlene  monomer)  elastomers,
40%;  hydrocarbon resin  systems,  30%;  unsaturated polyester  resins,  10%;  and
miscellaneous,  Including  chemical  synthesis, fire  retardants,  pesticides  and
agricultural  chemicals, fuel and lube additives and adheslves,  20%.
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                     2.  ENVIRONMENTAL FATE AND TRANSPORT
2.1.   AIR
    The vapor  pressures of  cyclo- and  dlcyclopentadlene Indicate  that  they
will  exist  almost  entirely 1n  the  vapor-phase  In  the ambient  atmosphere
(Elsenrelch et a!., 1981).
2.1.1.   Reaction with  Hydroxyl  Radicals.   The estimated rate constants  for
the  vapor-phase  reaction  of cyclo-  and  dlcyclopentadlene  with  photocheml-
cally  produced  hydroxyl   radicals   1n   the   atmosphere are  1.6xlO~*   and
1.4xlO~10   cm3/molecule-sec,   respectively,   at   25°C   (U.S.  EPA,   1987).
Assuming  a  typical  atmospheric hydroxyl  radical  concentration  of  8xl05
molecules/cm3  (U.S.   EPA,   1987),  half-lives  are   -90 and  103  minutes,
respectively.
2.1.2.   Reaction with Ozone.   The estimated  rate constant  for   the  vapor-
phase  reaction  of  either  cyclo- or  dlcyclopentadlene  with ozone  1n  the
atmosphere  1s  4.0xlO~16  cm3/molecule-sec (U.S.  EPA,  1987).   Assuming  a
typical  atmospheric   ozone concentration of 6x10"   molecules/cm3   (U.S.
EPA, 1987), the half-life Is -48 minutes.
2.1.3.   Reaction  with Atomic  Oxygen.   The  rate  constant   for  the  vapor-
phase  reaction  of   cyclopentadlene with  atomic oxygen  (03P)  1s  reported  to
be  5.4X10"11  cmVmolecule-sec  (Graedel,  1978).   Assuming a typical  atmo-
spheric  atomic  oxygen  concentration  of  2.5x10*  molecules/cm3  (Graedel,
1978), the  half-life  1s -5.9 days.   Although  this reaction  1s  environment-
ally  significant,  It  may not be competitive with  other  reactions, specific-
ally reaction with  hydroxyl radicals or ozone.
2.2.   WATER
2.2.1.   Hydrolysis.   Since  cyclo- and  dlcyclopentadlene do  not  contain  any
hydrolyzable groups, environmental hydrolysis  1s unlikely.


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2.2.2.   Photooxldatlon.  As a  general  chemical  class, both  cyclopentadlene
and  Us  dlmer,  being  oleflns,  may react  at  an  environmentally  significant
rate 1n natural waters  with  photochemlcally produced  oxldant  species  such as
hydroxyl radicals and  singlet  oxygen  (Mill and Mabey,  1985).   The half-life
of oleflns with hydroxyl radicals  1s  -13-14 days  and  the half-life of cyclic
oleflns with  singlet  oxygen  Is  -40 days 1n typical natural  water.  Dlcyclo-
pentadlene  was  observed  to  undergo  Indirect  photolysis  In natural  water
under experimental conditions.
2.2.3.   Hlcroblal  Degradation.   The limited  biodegradatlon data  available
Indicate  that  cyclo- and  dlcyclopentadlene  resist  mlcroblal   degradation.
Kawasaki (1980) used  the Japanese  MITI  test  to  demonstrate  this,  and Spain
and  SomervUle  (1985)  Incubated  dlcyclopentadlene 1n  natural  water and sedi-
ment samples  and  found no difference between  sterile  and  nonsteMle tests.
Spanggord  et  al.   (1979)  observed  very slow  blotransformatlon of  dlcyclo-
pentadlene  1n  the soils and waters of  the  Rocky Mountain  Arsenal.   Cyclo-
pentadlene did  not  degrade  under anaerobic conditions  with  sewage  sludge or
natural sediments  as mlcroblal  Inocula (Schlnk,  1985).
2.2.4.   Volatilization.  Smith  et al.  (1980)  reported  that  the ratio  of
the  reaeratlon  of dlcyclopentadlene  to  oxygen  from  water  at 25°C Is  0.54.
According to these Investigators, the average rate constants  for  the  reaera-
tlon of  oxygen  from  a  typical   pond  (2  m  deep),   river (3  m deep) and  lake
(5 m deep)  are  0.008, 0.04  and  0.01  hours'1,  respectively.  Based on  these
data, the  volatilization  half-lives of  dlcyclopentadlene from  typical  water
bodies are estimated as follows:
                        pond              6.7  days
                        river            1.3  days
                        lake              5.3  days
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    Based  on  experimentally measured  equilibria data  (Hine and  Mookerjee,
1975), the Henry's Law constants for cyclopentene and  pentadlene  at  25°C  are
-0.06 and  0.12 atm-mVmol, respectively.   If  cyclopentadlene Is assumed  to
have  a   similar  Henry's  Law  constant,  then  volatilization from  water   Is
expected  to  be rapid  {Lyman  et. al.,  1982).  Using  the  method  outlined  1n
Lyman et  al.   (1982), and  a Henry's Law  constant  value of  0.09  atm-mVmol,
the volatilization half-life of  cyclopentadlene  from a river 1 m deep  flow-
Ing 1 m/sec with  a wind velocity of 3  m/sec 1s  estimated to be  -2.4  hours.
The estimated  Henry's  Law  constant  of 0.02  atm-mVmol  calculated  from  the
vapor pressure and water solubility of  this  compound  (see  Section 1.2.) will
result 1n  a similar  half-life  (2.4 hours) for evaporation.   The  volatiliza-
tion rate  from deeper bodies of water  or  less  rapidly moving bodies  of water
will be slower.
2.2.5.   Adsorption.  The   log  K    values   of  cyclo- and  dlcyclopentadlene
(1.887 and 2.894) suggest  that  adsorption  to sediment  In water  may  not  be
significant.
2.2.6.   B1oconcentrat1on.   The BCF of  an organic  chemical  can be  estimated
using the  following regression equation (Lyman et al., 1982):
                         log BCF  =  0.76  log  KQW - 0.23                   (2-1)
For  cyclo- and dlcyclopentadlene,   the  BCF   values  calculated from  Equation
2-1 are  ~16 and  99, based  on  their respective  log  K   values of  1.887  and
2.894.   These  BCF  values  Indicate that  the  compounds  are  not  expected  to
bloconcentrate significantly 1n aquatic organisms.
    Dlcyclopentadlene did  not bloconcentrate  In plants  grown  under  hydro-
ponlc conditions  (O'Donovan and Woodward,  1977).
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2.3.   SOIL
2.3.1.   M1crob1al  Degradation.   Slow  b1otransfbrmat1on  of  dlcyclopenta-
dlene was  observed 1n  soils  from the  Rocky Mountain Arsenal  (Spanggord  et
al.,  1979).   Additional data  (see  Section 2.2.3.) Indicate  that  cyclo- and
dlcyclopentadlene are not readily blodegraded.
2.3.2.   Adsorption.   The   K    of  an  organic  chemical   can  be   estimated
from the following regression equations (Lyman et al., 1982):
                     log KQC =  3.64 -  0.55  log WS  (In  ppm)               (2-2)
                        log  KQC  =  0.544 log KQW +  1.377                  (2-3)
For  dlcyclopentadlene,   the  K    values calculated  from  Equations 2-2  and
2-3  are  ~570 and  890,  respectively,  based on  a  water  solubility  of  40  ppm
and  a log K    of 2.894 (see  Section  1.2.).   For cyclopentadlene, the  K
values calculated  from  Equations  2-2  and 2-3  are  -70 and 250,  respectively,
based  on  a  water  solubility  of 1800  ppm  and   a  log  K   of  1.887  (see
Section  1.2.).    KQC   values   of  70-250   Indicate  high  to  medium  soil
mobility, while  K   values  between 500 and 2000  Indicate  low  soil mobility
(Swann et  al., 1983).   Therefore,  dlcyclopentadlene  1s  expected   to  have  a
low degree of mobility In most soils.
2.3.3.   Volatilization.    0'Donovan   and   Woodward   (1977)    examined   the
volatilization  of dlcyclopentadlene  (14C)  from  soil  columns  subjected  to
air  flow  across  their surface.   In dry soil, the soil  retained >959i  of  the
Initial radioactivity after 250 hours  of treatment.   Only  62% of  the Initial
radioactivity was retained  over the same time period using moist soil.
    Evaporation from  soil may  be  a significant fate  process  for  cyclopenta-
dlene given  Us  relatively high  vapor pressure,  low soil K   (see  Section
2.3.2.) and tendency to volatilize rapidly  from water.
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2.4.   SUMMARY
    The  major  environmental  fate  and  transport  process   for   cyclo- and
dlcyclopentadlene  1n water  appears  to be  volatilization.    Volatilization
half-lives of  dlcyclopentadlene from typical  water  bodies (pond,  river  and
lake) were  estimated to  range  from 1.3-6.7  days.   Cyclopentadlene Is  even
more  volatile than  dlcylopentadlene,  wHh  an  estimated half-life  of  2.4
hours from a  river 1 m deep  flowing  1 m/sec  with  a wind velocity  of 3  m/sec.
Photooxldatlon may  also  contribute  to  the  removal  of  these compounds  from
water.  Aquatic  hydrolysis,  mlcroblal degradation,  adsorption  and bloconcen-
tratlon are not  expected  to  be significant.    If  released  to  the  atmosphere,
                                                             •
cyclo- and dlcyclopentadlene  will  exist almost  entirely  1n the  vapor-phase
(E1senre1ch et a!.,  1981) and will  react very  rapidly with hydroxyl radicals
and  ozone  (U.S.  EPA, 1987).   The half-life  for  the reaction with hydroxyl
radicals or wHh ozone was estimated  to range  from 45-103 minutes (U.S.  EPA,
1987).  If released  to  soil, cyclopentadlene may be susceptible  to signifi-
cant  leaching (based on  estimated  K   values),  and significant  evaporation
1s  Hkely.   Dlcyclopentadlene was found to  volatilize  more slowly  from dry
soil  than  from moist soil  (O'Donovan  and Woodward,  1977).   Based  on  esti-
mated K   values, dlcyclopentadlene will have a low rate of soil mobility.
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                                 3.   EXPOSURE

    In  an occupational  exposure  survey conducted  between  1972  and  1974,
NIOSH (1984)  estimated  that 41,366 U.S.  workers  are potentially  exposed  to
dlcyclopentadlene.
3.1.   WATER
    Dlcyclopentadlene was qualitatively  detected  In  drinking water collected
1n New Orleans, LA,  In  1974 (Keith  et  a!.,  1976).  Cyclopentadlene was Iden-
tified 1n polluted drinking water from  Czechoslovakia,  at  a concentration  of
3.6 ppb  (Novack et  al., 1973).  Qualitative detection  of  cyclopentadlene  1n
drinking  waters  (location  not  specified)  has  been reported  (Kool  et  al.,
1982; Shackelford  and Keith, 1976).
    Groundwater and  soil  samples near  a  commercial  production facility using
dlcyclopentadlene   (O'Donovan  and   Woodward,  1977)  and  near  a  U.S.  Army
Installation  (Burrows,  1978)  were  found to contain dlcyclopentadlene,  pre-
sumably  because of  waste disposal  practices.   Perry et al.  (1979)  examined
63  U.S.   Industrial  wastewater effluents  and  found  cyclopentadlene  In  one
sample at  a concentration  between  10 and  100  ppb and dlcyclopentadlene  1n
two samples at levels <10 ppb.  Dlcyclopentadlene was  Identified  1n  chemical
plant effluents on  the Mississippi River,  LA,  and  1n  Memphis, TN (Shackel-
ford and  Keith, 1976).   The U.S.  EPA STORET  Data Base  contained  no  monitor-
Ing data for cyclopentadlene.
3.2.   FOOD
    Pertinent  food  monitoring  data for  cyclo- and dlcyclopentadlene  could
not be located 1n  the available literature as cited  In  Appendix A.
3.3.   INHALATION
    Pertinent  ambient  atmospheric   monitoring  data  could  not  be   located  1n
the  available literature   as  cited  1n  Appendix A.    Jarke  et  al.  (1981)

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detected  cyclopentadlene   In  Indoor  air  1n  homes  1n  Washington,  DC,  and
Chicago, IL, although the source of the compound was not Identified.
    Cyclopentadlene can be emitted  to  the atmosphere  by stack  effluents from
waste Incineration (Junk and Ford,  1980), by  emissions  from polymer  manufac-
ture  (Graedel,   1978),  and  In  exhausts   from  hydrocarbon  fuel  combustion
(Selzlnger and D1m1tr1ades, 1972).   In  addition,  emissions  from coal  carbon-
ization  processes  or  hydrocarbon  cracking processes  may contain  cyclo- or
dlcyclopentadlene.   H1gg1ns  et   al.   (1983)  detected  cyclopentadlene  1n
tobacco  smoke   at   levels ranging  from   0.06-7  v9/Cigarette;  therefore,
exposure  to  the compound  from  cigarette  smoke  may be significant.   As tar
delivery per cigarette Increased, so did the-amount of cyclopentadlene.
3.4.   DERMAL EXPOSURE
    Pertinent dermal  monitoring data could not  be located  In  the  available
literature as cited 1n Appendix A.
3.5.   SUMMARY
    Cyclo- and dlcyclopentadlene  were detected  In drinking water  (Keith et
al.,  1978;  Shackelford and Keith,  1976;  Kool et  al.,  1982),  In groundwater
near  user  facilities (O'Donovan and  Woodward,  1977;  Burrows,  1978),  and 1n
Industrial wastewater  effluents (Perry et al.,  1979; Shackelford  and Keith,
1976).   Cyclopentadlene can be  emitted to the  atmosphere  by stack  effluents
from  waste Incineration  (Junk  and  Ford,  1980),  by  emissions  from  polymer
manufacture  (Graedel,  1978),   1n exhausts  from hydrocarbon  fuel  combustion
(Selzlnger  and  D1m1tr1ades,  1972), and 1n  emissions  from coal carbonization
or  hydrocarbon  cracking processes.   No ambient air or  food monitoring data
for either  compound  were  available.  Cyclopentadlene  was  detected  In tobacco
smoke at levels  of 0.06-7  yg/dgarette (Hlgglns et al., 1983).
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                             4.  AQUATIC TOXICITY
4.1.   ACUTE TOXICITY
    Data  regarding  the  toxlclty  of  dlcyclopentadlene to  aquatic  organisms
were limited.   Velslcol  Chem. Corp.  (1980)  reported 96-hour  LC5Q  values of
42.3  mg/8.  for   rainbow  trout,  Sal mo  galrdnerl.  and  75.2  mg/8.  for  blue-
gills,  Lepomls   macrochlrus.   These  Investigators  also  reported  a  48-hour
LC5Q of  6.9 mg/8.  for  the  water  flea, Daphnla  sp.   Yoshloka  et al. (1985)
determined  a  24-hour  EC5Q  of  5.3  mg/8.  for  Inhibition of  cell  multiplica-
tion  of  the  dilate  protozoan,  Tetrahymena  pyrlformls.    Aquatic  toxlclty
data  regarding  cyclopentadlene  could  not  be  located  1n   the  available
                               •
literature as cited 1n Appendix A.
4.2.   CHRONIC EFFECTS
    Pertinent  data   regarding the  chronic toxlclty  of cyclopentadlene  and
dlcyclopentadlene to aquatic  organisms  could  not  be  located 1n the available
literature as cited 1n Appendix A.
4.3.   PLANT EFFECTS
    Pertinent  data   regarding the  effects of  cyclopentadlene and  dlcyclo-
pentadlene  on  aquatic  plants  could  not be located  1n the available litera-
ture as cited 1n Appendix A.
4.4.   SUMMARY
    There were  no data regarding the toxlclty of  cyclopentadlene to aquatic
biota,  and  very Uttle  regarding  dlcyclopentadlene.   Reported  LC5Q values
for  dlcyclopentadlene  were   6.9   mg/l  for   Daphnla   sp.,   42.3  mg/2.  for
rainbow  trout   and  75.2  for  bluegllls  (Velslcol  Chem.  Corp.,  1980).   An
EC,-n  of  5.3  mg/l   for  Tetrahymena  pyrlformls  was  also  reported  (Yoshloka
et al., 1985).
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                             5.   PHARMACOKINETICS
5.1.   ABSORPTION
    Pertinent data  regarding  the absorption of cyclopentadlene could  not  be
located 1n the available literature as cited 1n Appendix A.
    LUton B1onet1cs  (1976)  performed a  pharmacoklnetlcs study of  dlcyclo-
pentadlene using  three mammalian  species.   Young  adult male  groups  of  24
Swiss Webster mice,  12  Sprague-Dawley rats, and 5 purebred  beagle  dogs  were
given  single oral  doses  of  40,  110 and   100  mg/kg  bw uniformly  labeled
l4C-d1cyclopentad1ene  (97% pure)  1n  corn  oil,  respectively.   The  average
peak  plasma  levels  2  hours  after  dosing  were  11.36  and  39.9  vg  l4C-d1-
                      t
cyclopentadlene/ma  1n  mice   and  dogs,   respectively.    In  rats,   the  peak
plasma level  of 23.28 yg/mi was  measured  6 hours after dosing.
    Urine,  feces  and  expired  air  were  collected  at   various  times  after-
dosing,  and  the  animals  were   sacrificed  at   these  times  for  analysis  of
radioactivity  1n  organs and  tissues, the  carcass (mice  and  rats) and  the
gastrointestinal tract.  At some of the  sacrifice times, recovery  of  radio-
activity was  low  because of  volatilization; therefore,  1t was not  possible
to estimate  the extent  of  absorption.  In mice,  recovery of  radioactivity at
24  hours  was >95%.   Of  the administered  radioactivity,  75% was detected  1n
the  urine,  17%  In  the  feces and 6%  1n  the  expired air collected over  24
hours.  The  amount  of  radioactivity  remaining 1n  the carcass was  1.4%,  and
2% was  found In the gastrointestinal tract.   Thus, at  least 82% of  the  dose
was absorbed 1n 24 hours.
    In  rats, recovery  of  radioactivity was  >94% at 72  hours.   Of  the  admin-
istered radioactivity,  75% was  recovered  1n the urine,  15%  1n  the  feces and
2.5%  1n the expired  air  collected  over  72 hours.   At  72 hours,  1.78% was
present  1n  the carcass  and  0.35%  was  found  1n the  gastrointestinal  tract.
Thus, at least 79% of the dose was absorbed  1n  72 hours.

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    In dogs,  recovery  of  radioactivity was -86% at  72  hours.   Of  the admin-
istered  dose,  81% was  recovered  1n the  urine and  4%  1n the  feces  (radio-
activity  In  the expired  air  was  not  measured);  therefore,  at least  81% of
the  dose was  absorbed  by the  gastrointestinal  tract  1n  72 hours,  which
Indicates  that  almost  all of  an  administered  dose was  absorbed from  the
gastrointestinal  tract  and that  the  rate  of absorption  was  more rapid 1n
mice and dogs than 1n rats.
5.2.   DISTRIBUTION
    Pertinent data  regarding  the  distribution of cyclopentadlene  could  not
be located 1n the available literature as cited 1n Appendix A.
    Litton Blonetlcs  (1976)  measured the radioactivity present  1n  a variety
of  tissues after  a  single  oral  dose  (see  Section  5.1.)  of  l4C-d1cyclo-
pentadlene was  given  to mice,  rats  and dogs.  The  radioactivity  was  widely
distributed to the organs and  tissues  1n  mice.   High levels  of radioactivity
were  detected 1n  all  tissues,  1 and  2  hours after  dosing.  The highest
levels  occurred  1n  the  urinary  bladder  (without  contents),  gall  bladder
(without  contents)  and  fat.    (Hereafter,   reference  to  urinary  or  gall
bladder  Indicates  that the  measurement  was  made without  contents.)  Liver,
kidneys  and   adrenals  also  contained   relatively  high  levels.   The  radio-
activity declined rapidly 1n all  tissues  except the  urinary  bladder and fat,
6 hours  after  dosing.   At 72 hours, measurable quantUHes  of radioactivity
were still detected 1n  all  tissues,  with  the  highest levels  In the liver and
kidney.   In  rats, the  radioactivity was also  distributed widely.  As  with
the mice,  high  levels  of  radioactivity were  detected 1n all tissues 1  and 2
hours  after   dosing,   and  the  highest  levels   were measured  1n   the  fat,
adrenals  and  urinary  bladder.   At   24  hours,   the  highest  levels  of
radioactivity  were  found  1n  the  urinary   bladder,   liver  and   kidneys.


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Radioactivity declined  1n  all  tissues  except the  urinary  bladder after  24
hours, but at a  slower  rate than 1n mice.   Radioactivity was  still  detected
In all  tissues   at  72  hours,  and  the  highest levels  were  measured  1n  the
skin,  liver  and  kidneys.   In  dogs, radioactivity  was distributed  widely.
The  highest  levels  were measured  1n   the  bile,  gall  bladder,  stomach  and
urinary bladder  at  4 hours.   At 24 hours,  the radioactivity had  declined In
all  tissues, and   the  highest  amounts occurred  1n  the  bile  and  urinary
bladder.
    Radioactivity was stm  detected 7 days  after  dosing,  with  the  highest
levels occurring  1n the fat and  liver.  Radioactivity was also  detected In
the  eyes  at 4  hours,  then  declined  rapidly.  Within  72 hours,  the  radio-
activity  1n  the eyes had  declined  steadily,  but was still  detected  after  7
days.
5.3.   METABOLISM
    Pertinent data  regarding the metabolism of cyclopentadlene  could  not  be
located 1n the available literature as cited 1n Appendix A.
    In the  LHton  B1onet1cs  (1976)  study (see Section  5.1.)  urinary  metabo-
lites of  dlcyclopentadlene were  not  Identified specifically,  but analysis  by
TLC  Indicated  that  the  urine of mice  and rats  each had  seven components.
Six  components  were found 1n the  urine of  dogs.   The  Rf values of  these
components were similar; therefore, common  metabolites  were Indicated 1n all
three species.  Only 1-3%  of the radioactivity was  attributed  to nonmetabo-
Hzed l4C-d1cyclopentad1ene  In  all  three species.   When the urine from all
species was  subjected  to  enzymatic hydrolysis  by glusulase (beta-glucuronl-
dase  and  sulfatase)  and   extracted,   radioactivity was   recovered  1n  the
extract,  Indicating  the presence of urine conjugates.
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5.4.   EXCRETION
    Pertinent data  regarding the  excretion  of  cyclopentadlene could  not  be
located 1n the available literature as cited 1n  Appendix A.
    In  the  LHton  B1onet1cs  (1976)  study,  elimination  curves  for  the
disappearance of  radioactivity  from  plasma  of  mice,  rats and dogs  treated
orally  with   l4C-d1cyclopentad1ene  were  blphaslc.   In  mice,  the  half-life
was 4  hours   for  the first  phase and  18 hours for  the second  phase.   For
rats.   Insufficient data  were obtained for the  first  phase of  elimination  to
accurately calculate  the half-life  of  this  phase,  while the half-life  for
the second phase  was  18 hours.   The  elimination half-lives  for dogs  were  10
hours  for the first phase and 27 hours for the second phase.
    Most  of  the  radioactivity  was  eliminated  1n   the  urine  of  mice  by  24
hours   and In the urine of  rats  and dogs  by  72  hours  (see  Section  5.1.).
Radioactivity was also  excreted  1n the feces and  expired  air.   Amounts
excreted  at  other  times  were difficult  to estimate  because  of low recovery.
Dogs also excreted small amounts of radioactivity 1n the bile.
5.5.   SUMMARY
    Pertinent data  regarding the  pharmacoklnetlcs of  cyclopentadlene  could
not be located 1n the available  literature as cited 1n Appendix A.
    LHton Blonetlcs  (1976)  reported  that  nearly  all  of an  oral dose  of
a*C-d1cyclopentad1ene was  absorbed  by  the  gastrointestinal  tract of  mice,
rats and  dogs.    Peak plasma levels  were reached  more  rapidly  In mice and
dogs than  1n rats.   Clearance  from  the plasma  occurred  1n two phases,  with
half-lives for the  first  phase  of 4 and  10  hours  for  mice and dogs,  respec-
tively, and  for  the  second  phase, of 18, 18  and 27  hours for  mice, rats and
dogs,   respectively.   The half-life  for  the  first  phase of elimination  for
rats was  not calculated because of  Insufficient data.   The radioactivity was


0013d                                -17-                             05/26/87

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distributed to  a  wide variety of  organs  and  tissues 1n mice,  rats  and  dogs
within  4  hours  of   dosing  and   disappeared  rapidly  from  these  tissues.
Disappearance of  radioactivity from the tissues was much more  rapid In  mice
than In dogs and  rats.   Only small amounts  of radioactivity were detected at
72  hours  1n mice  and rats and  at 7  days  1n dogs.   All  three  species  had
common urinary  metabolites  (not  Identified), and  very little  of  the  radio-
activity  measured 1n  the  urine  was  attributable  to  nonmetabollzed l*C-d1-
cyclopentadlene.  The  presence  of  conjugates 1n  the urine was  Indicated as
well.  D1cyclopentad1ene was excreted  primarily  1n  the urine  among all  three
species.
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                                  6.   EFFECTS
6.1.   SYSTEMIC TOXICITY
6.1.1.   Inhalation Exposures.
    6.1.1.1.   SUBCHRONIC — The   following   multi-species   studies   were
reviewed  by Dow  Chemical  (1987).   However,  Dow  stated  that  these  studies
were  not  published and only  a  summary was available.  Besides  lacking some
experimental details,  such as the  type of  animals  used,  the summary data did
not provide any  Information  regarding the purity  of the  tested  compounds.
Until better study data can be acquired,  the  Dow  (1987)  Information  will  be
used  1n  some of the RfD and  RQ  determinations.  Dow (1987) exposed 24 rats,
9  guinea  pigs,  3  rabbits  and 1  dog  (beagle)  to 250 ppm  (676  mg/m3) cyclo-
pentadlene  for  135  seven-hour   periods  1n 194  days.  None  of the  animals
exhibited any toxic effects.  The  dog had  a necrotlc left ventricle that was
considered  noncompound related.
    In  this study  (Dow,  1987),  four  mongrel  dogs  were  exposed to  400  ppm
(1081  mg/m3)  cyclopentadlene  for  28  six-hour  periods,  followed  by  16
six-hour  periods  over  60  days   at 800  ppm (2163  mg/m3).   No  effects  were
noted.
    These  Investigators  exposed  five  male and  five female rats to  500  ppm
(1352 mg/m3) cyclopentadlene  for  35  seven-hour  periods  1n 53  days.   Cloudy
swelling  1n the  liver and  kidney  and  vacuollzatlon of  the  renal  tubular
epithelium  were   observed.    The  lung,   heart,   spleen,   testes,  growth,
behavior,  gross appearance,  mortality,  body  and   organ  weights,   blood  and
bone marrow were unaffected.
    In the  same study,  five male  and  five  female rats,  four male guinea pigs
and one  female rabbit  were exposed  to  35 seven-hour exposures at  250  ppm
(676 mg/m3) 1n  53 days.  No effects were observed.


0013d                               -19-                             05/26/87

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    Dow (1987) reported  a  study conducted by Exxon  1n which  2  dogs,  10 rats
and 10  guinea  pigs were exposed  to  a  concentration of 993 ppm (2685  mg/m3)
cyclopentadlene  for  20  six-hour  periods In  4 weeks.   The  rats  had  mild
pneumonia, causing four  deaths 1n the   experimental animals  and two  deaths
1n the  controls.   The Investigators commented  that the effects of  toxlclty
were "not obvious."
    Shashklna  (1965)  exposed  rats to cyclopentadlene at concentrations  of  0
or  0.35  mg/i,  4  hours/day,  6 days/week   for   6  months.   Experimental
details,  such  as  numoers of rats, strain and  sex,  were  not  reported.   After
6 months, leukopenla was observed 1n some of  the rats,  and the number  of red
blood  cells   and  the hemoglobin decreased  1n  comparison  with  controls.
Increases In  the threshold of neuromuscular excitability  and blood  pressure
were  also observed.   H1stopatholog1cal  examination  of  the  rats  revealed
proHferatlve  and  sclerotic lesions  of  the  trachea, bronchi  and lungs,  and
albuminoid degeneration  of  cells  1n  the  liver  and  kidneys.  Shrivelled cells
observed  1n  the CNS  were  located primarily In  the brain stem.  Lesions  1n
the  spleen  were  described as  an "Impoverishment  of the pulp 1n  lymphold
cells."   FolUcular epithelial  changes  were observed In the  thyroid.   These
changes Increased after  the recovery period.
    Dodd  et  al.  (1982)  exposed groups  of 51  male and 51  female  Fischer  334
rats  and  45 male  and 45  female  B6C3F1  mice  to 9554 pure dlcyclopentadlene
vapor for 6  hours/day, 5 days/week at concentrations of 0, 1,  5.1  or  51  ppm
(0, 5.4,  27.6  or  276 mg/m3)  for 90 days.  Groups  of nine  animals/sex were
sacrificed  after  10,  30   and 64  Inhalation   exposures,  and  postexposure
sacrifices were  made  at 29  and  92 days.   Parameters  of  toxlclty  examined
Included  clinical  observations,  body weight, organ  weights  (kidneys,  liver,
lung  and  testes),  food  and water consumption  (rats  only),  urlnalysls (rats

0013d                               -20-                             05/26/87

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only), serum  chemistry  and hematologlcal, ophthalmologlcal  and  gross patho-
logical evaluations.  Hlstologlcal  evaluation of all  rat  kidney and urinary
bladders  was  performed,  and  other  selected  tissues  were examined  for  the
high dose and  control  rats after 64  Inhalation  exposures.  Several of these
parameters were  affected.   Functional and structural  changes  In the kidneys
of  male   rats  were  observed.    Exposure-related Increases  1n  relative  and
absolute  kidney  weight  were observed 1n  the  51 ppm  males.   Renal dysfunc-
tion,  determined  by urlnalysls  and urinary chemistry,  occurred 1n  the  5.1
and  51 ppm male  rats.   Additional  dlcyclopentadlene-related effects observed
at >1  ppm were tubular  protein  accumulation  and  epithelial cell  casts.  Host
of  these  effects  subsided  or   decreased  1n  severity  upon  termination  of
exposure.   Urine  concentrating  ability declined  In  the 51  ppm  males during
the  postexposure period.   The   5.1  ppm males  were  affected similarly  but
these  effects were reversible.   Kidney  lesions such  as severe tubular hyper-
plasla,  tubular   protelnosls  and  Interstitial   nephritis  at  >5.1   ppm  were
revealed  by  hlstologlcal  examination.   Some of  these were  attributable  to
the  nephrotoxlc  effect  of dlcyclopentadlene and others to  the  normal  aging
process 1n these  rats.  The authors concluded  that  exposure to dlcyclopenta-
dlene  at  concentrations >1 ppm  led to nephrotoxlclty, which  was  manifested
by   structural   and  functional  alterations.    These  effects  subsided   or
decreased In severity upon  termination  of  exposure.   Kidney lesions resembl-
ing  chronic glomerulonephrltis were  observed  1n  all  male rats, Including  the
controls,  at  the end of  the study.   An  Increase 1n  relative liver weight,
which  was reversible,  was also  noted  1n  the 51  ppm  male  rats.   An Increase
In body weight gain  1n  female  mice at 51 ppm was noted.   In the 51 ppm mice
of  both   sexes,  -20% mortality attributable  to pulmonary congestion  (not
confirmed by hlstologlcal  examination)  with  some cases of  renal  failure  was


0013d                              , -21-                             05/26/87

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observed.  Liver  dysfunction was manifested  by a  slight  Increase  1n  serum
albumin  1n  5.1  and 51  ppm  female  mice.  Increased  relative and  absolute
liver weight was  observed  In the 5.1 ppm female mice;  no  other  effects were
observed 1n rats or mice.
    Klnkead et  al.  (1971)  exposed  groups  of  12 male  and 12 female  Harlan
Wlstar  rats  to dlcyclopentadlene (98%  pure)  at concentrations  of  0,  19.7,
35.2 or  73.8  (0, 106.5, 190.3  or 399.1  mg/ma)  for 7 hours/day,  5 days/week
for 89  exposure  days or 18 calendar weeks.  Parameters  of toxlclty examined
Included clinical  signs, body weight,  liver and kidney  weight and gross and
hlstopathologlcal  examination  of a  variety of  tissues  1n the  thoracic and
abdominal cavities.   The only  tox1colog1cally  significant effects  observed
were convulsions  1n 3.8 and 19.7 ppm  females  at  exposure  days  19 and 45,
respectively,  and dose-related  kidney  lesions  1n  both sexes at  concentra-
tions >35.2 ppm.   The  kidney lesions were  described as  round cell accumula-
tions,  dilated  tubules, casts and tubular  degeneration.   The kidney lesions
were more severe and frequent 1n treated males  as compared with females.
    These Investigators  exposed  groups  of three male beagle  dogs  to 0, 8.9,
23.5  or  32.4   ppm  (0,  48.1,  127.1  or  175.2  mg/m3)   dlcyclopentadlene,  7
hours/day,  5  days/week  for  89  days.   Parameters  of  toxlclty  examined
Included  body   weight,  clinical  signs,   hematocrlt,  total and  differential
white blood  cell counts, BUN,  S60T,  SGPT, serum add  phosphatase and  serum
alkaline  phosphatase values, urlnalysls,  liver  and kidney weight,  electro-
cardiograms, gross  pathological  examination and  microscopic  examination of a
variety  of  tissues  from   the   cranial,   thoracic  and  abdominal  cavities.
Minimal  changes  In the  biochemical  parameters  were measured.   BUN  and add
phosphatase values  Increased 1n the 32.4  ppm group after  20  days.  Alkaline
phosphatase values  Increased at the same  concentration  after  85  days.   SGOT

0013d                    .           -22-                             05/26/87

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and  add  phosphatase values  Increased  at  23.5  ppm 1n  20  days.  A  minimal
decrease  1n  neutrophlls was  observed  after 85  days.   Although  the  authors
did  not  consider any of  these effects to  be  of any  physiological  signifi-
cance, they determined the NOEL to be between 8.9 and 23.5 ppm for dogs.
    Shashklna  (1965)  exposed  rats  to 0  or 0.02  mg/s.  dicyclopentadlene,  4
hours/day, 6  days/week  for  6 months.   The number,  strain or  sex  was  not
reported.   In  contrast with  cyclopentadlene,  no  effect  on  hematologlcal
Indices was  observed,  but Increased urinary  protein was observed.   As  with
cyclopentadlene,  Increased   neuromuscular  excitability  and  blood  pressure
were  observed.   The  same lesions  In the  trachea,  bronchi,  lungs,  liver,
kidneys,  spleen  and  thyroid  observed after exposure  to  cyclopentadlene  were
observed  for  the dlmer.  Shrivelled cells  of  the CNS,  located  primarily  In
the brain stem and cortex, were observed.
    6.1.1.2.    CHRONIC -- Pertinent  data  regarding  the  chronic  Inhalation
toxldty  of cyclopentadlene could not be  located  1n  the  available literature
as cited  In Appendix A.
6.1.2.    Oral Exposures.
    6.1.2.1.    SUBCHRONIC — Pertinent data regarding  the  subchronlc  oral
toxldty  of cyclopentadlene could not be  located  1n  the  available literature
as cited  In Appendix A.
    Aulerlch  et  al.  (1979)  gave  groups  of  30  (6  males and  24  females/group)
3-month-old,  dark variety  mink 0,  100,  200, 400 and 800  ppm  (0,  24,  42,  85,
170  mg/kg/day  by authors'  estimate) dicyclopentadlene  1n  the  diet   for  12
months  (through one  reproductive  cycle).   Endpolnts of toxldty  examined
Included  mortality,  body  weight,   food  consumption,  hematocrU,  hemoglobin
values,  differential  leukocyte  count,  organ  weights and  gross and  micro-
scopic evaluation of organs and  tissues.  The  only  effect was  reduced testes
weight In 800 ppm males.

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    Litton  Blonetlcs  (1976)  reported  oral  studies  using  rats  and  mice.
Groups  of  30  male  and 30  female  Sprague-Dawley  rats  were  given  dietary
dlcyclopentadlene  (purity  98-99%)  1n  the  diet at  concentrations  of 0,  80,
250 and  750 ppm for  13 weeks,  followed by  a  4-week recovery period.   End-
points of  toxldty examined  Included body weight,  food  consumption,  mortal-
ity,  appearance,   behavior,  ophthalmoscoplc  examination,  hematology,  blood
chemistry,  uMnalysIs,  organ weight,  gross  examination  and hlstopathologlcal
examination  of  a  variety of  organs  and  tissues   1n  five males  and  five
females 1n the control and high-dose group.   No effects were observed.
    Groups  of  32  male and  32  female ICR  Swiss  Albino mice  were  given
dlcyclopentadlene  1n the diet at concentrations of  0,  28,  91,  273  ppm for 13
weeks  (LHton  B1onet1cs, 1976).   The  4-week  recovery period  was  eliminated
In  this  experiment.   The  same  endpolnts of  toxlclty that were examined 1n
the  rat  experiment  were also  examined In  the mouse  experiment,  with  the
exception  of  ophthalmoscoplc  examination 1n  mice.  - No evidence of  toxlclty
was observed.
    LHton  B1onet1cs  (1980) gave  groups of four male and  four female beagle
dogs  dlcyclopentadlene   (98-99% pure)  1n the  diet  at  concentrations  of  0,
100,  300  and  1000  ppm  for 13 weeks.  Seventeen of  the  dogs were found  to be
Infected  with  parasites (G1ard1a  canls  cysts, Isospora oocysts and  Trlcho-
monas). but the parasites were considered  to be nonpathogenlc, so  the dogs
were  Included  1n  the   study without  treatment to  eliminate  the  parasites.
Evaluated  parameters of  toxlclty  Included general  condition, body  weight,
behavior,  food  consumption, fecal  consistency, clinical  pathological  evalua-
tion  Including  clinical  chemistry,  limited  hlstopathologlcal (control  and
high  dose)  of  a  variety of  organs  and   tissues,  hematology,  urlnalysls,
ophthalmologlcal  examination  and   necropsy.   No  evidence of toxlclty  was


0013d                               -24-                             05/26/87

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observed  with  the  exception   of   Intestinal  distress  (vomiting  and  soft
stools)  1n  the treated  dogs  and especially  1n  the high-dose  group.   These
signs were also observed  1n the controls.   It  1s unlikely  that these effects
were due  to treatment  because  of  the  presence  of parasites  (Glardla  canls
and Isospora). which often affect the gastrointestinal  organs.
    6.1.2.2.   CHRONIC — Pertinent   data   regarding    the   chronic   oral
toxldty  of  cyclopentadlene  or  dlcyclopentadlene could  not be  located  1n
the available literature as cited In Appendix A.
6.1.3.   Other Relevant  Information.   Little  Information was found  concern-
Ing  the  acute  toxldty  of cyclopentadlene  In  animals.    Shashklna  (1965)
reported  Inhalation  LC5Qs  of  39  mg/ft.  for 2  hours  for  rats  and  14  mg/s.
for  2  hours  for   mice.   Rabbits  given  subcutaneous  Injections   of  3  ml
cyclopentadlene exhibited narcosis,  had  convulsions  and  died (Von Oettlngen,
1940).  No effects were noted when doses of 0.5-1 ml were used.
    ACGIH (1986)  provided Information concerning  the  organoleptlc  effect  of
cyclopentadlene.   This  chemical  has  an Irritating  terpene-Uke  odor.   At
levels  >250  ppm (676 mg/m3), human  sensory response  was  unfavorable.   Even
though  systemic  Injury  was unlikely  at concentrations  averaging  250  ppm,
ACGIH   (1986)  judged  that  a   concentration  much  lower  than  250  ppm  was
necessary from  the  standpoint  of  comfort,  and  recommended a TLV-TWA  of  75
ppm (-200 mg/ma).  They did not recommend the use of a  STEL.
    The  acute  toxlclty  of dlcyclopentadlene  has  been  studied  extensively
(Table  6-1).   Oral exposure to  dlcyclopentadlene  Is  -2 times  more toxic  to
mice than to  rats.  By Inhalation, dlcyclopentadlene  1s -2 times more toxic
to mice than  to  rats and 5 times  more toxic  to  mice  than  to guinea pigs  or
rabbits.  Signs  of  toxldty 1n these species Included  convulsions, Irrita-
tion  of extremities  and loss   of  coordination.    Similar  effects  In  beagle


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                                  TABLE 6-1



                  1050 and 1050 Values of  Dlcyclopentadlene
Species/Sex
Rat/NS
Rat/M
Rat/F
Rat/F
House/M
Mouse/F
Mouse/M
Rats/H
Rats/F
Rats/NS
Guinea
p1gs/M
RabbHs/M
Rat/NS
Rabbi t/NS
Rabbi t/NS
Route
oral
oral
oral
oral
oral
oral
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Intraperltoneal
dermal
dermal
LD50 or LC50
820 mg/kg
520 mg/kg
378 mg/kg
0.353 mi/kg
190 mg/kg
250 mg/kg
145 ppm (784
mg/m3}/4 hours
360 ppm (1947
mg/m3)/4 hours
385 ppm (2082
mg/m3)/4 hours
660 ppm (3569
mg/m3)/4 hours
771 ppm (4169
mg/m3)/ 4 hours
771 ppm (4169
mg/m3)/4 hours
0.31 mi/kg
5.08 ml/kg
6.72 mi/kg
Reference
Smyth et al., 1954
Hart and Dacre, 1977;
LUton Blonetlcs, 1976
Hart and Dacre, 1977;
Litton Blonetlcs, 1976
Klnkead et al., 1971
Hart and Dacre, 1977;
Litton Blonetlcs, 1976
Hart and Dacre, 1977;
Litton Blonetlcs, 1976
Klnkead et al., 1971
Klnkead et al., 1971;
Klnkead et al., 1971
Gage, 1970
Klnkead et al., 1971
Klnkead et al., 1971
Klnkead et al., 1971
Klnkead et al., 1971
Smyth et al., 1954
NS = Not specified
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dogs were  noted  at 272-773  ppm  (1471-4180 mg/m3) by  Inhalation,  along with
eye and  nose  Irritation and  tremors  (Klnkead et al.,  1971).   In  short-term
experiments,  3  of  4  rats  survived  ten 6-hour  dally  exposures  at 250  ppm
(1352  mg/m3)  and  all  rats  survived  fifteen  6-hour  exposures at 100  ppm
(541 mg/m3)  (Gage, 1970).   When  rats  were  given  fourteen 1.0 mi/kg  doses
subcutaneously,  leukocytosls was  observed 96 hours after exposure.
    Klnkead et  al.  (1971)   studied  the effects  of  Inhalation exposure  of
rats,  mice and  dogs  to  dicyclopentadlene,  7  hours/day,  5 days/week  for  2
weeks.   Groups of  six male  and six female  Harlan Hlstar rats were  exposed to
concentrations  of   0,  72,  146   or 332  ppm  (0,  389,  789  or  1795  mg/m3).
Death,  convulsions  and  hemorrhage  of  the   lungs  and thymus occurred at  332
ppm.   No  clinical  signs,  effects  on  weight  gain  or  gross  lesions  were
observed at 72  or  146  ppm.   Groups  of  six  male and six  female albino mice
were exposed  to concentrations of 0, 47,  72  or  146  ppm  (0, 254,  389 or  789
mg/m3),  which resulted  1n  deaths,  unaccompanied  by  convulsions or  gross
lesions,  In the  72 and 146  ppm  groups.   One male beagle  dog  per  concentra-
tion was  exposed  to  0,  20,  47  or  72  ppm  (0, 108,  254  or 389  mg/m3).
Effects  Included diarrhea at  20  ppm, and  diarrhea,  excessive  salivation  and
lack of control  of  hindquarters  at 47  ppm.  The 72 ppm dog was Inactive,  but
showed  no other  effects.
    Litton B1onet1cs (1976) fed  groups of  one male and  one female  beagle  dog
dicyclopentadlene   1n  the diet at 0,  40,  125  or  375 ppm  for  14  days.   No
effects were observed 1n  mortality,  appearance,  behavior, hematology, clini-
cal chemistry,  urlnalysls,  organ  weights  or  gross or  hlstologlcal  examina-
tions.
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    AuleMch  et  al.  (1979)  treated  groups  of  five  male  and  five  female
juvenile pastel mink with dlcyclopentadlene 1n  the  diet  at  concentrations  of
0, 10,  100, 1000  or  10,000 ppm  for  21 days,  followed  by a 7-day  recovery
period.  Evaluated  parameters of  toxldty Included  body  weight,  food  con-
sumption, mortality,  signs  of Intoxication, behavioral  changes,  hematocrlt,
differential  leukocyte  counts  and gross  and  hlstologlcal  examinations  of
major  organs.   Four males  and two  females at  10,000  ppm  died  during  the
study.  Effects Included either decreased  body  weight  gain  or weight loss  or
both  at all   doses,  decreased  food  consumption  at  1000   and  10,000  ppm,
significantly  decreased  hematocrlt at  10,000  ppm and  percentage   of  band-
neutrophlls at  all doses.   No  treatment-related gross  or  hlstopathologlcal
lesions  were  observed,  but  absolute  heart,  liver  and  spleen  weights  were
significantly reduced 1n 10,000 ppm males compared with controls.
    Like cyclopentadlene, dlcyclopentadlene  has a  disagreeable odor  that  1s
detectable  at <0.2 ppm  (1.08  mg/m3),  but   1s  not  noticeably  Irritating
until  a concentration of 10 ppm  (54 mg/ma)  1s exceeded (ACGIH, 1986).   In
humans,  1  ppm (5.4 mg/ma)  dlcyclopentadlene   caused  eye and throat Irrita-
tion  and olfactory  fatigue  after  24 minutes, but no  fatigue was  reported  In
subjects exposed  to  5.5  ppm (29.7 mg/m3) for 30  minutes  (Klnkead  et  al.,
1971).  Workers exposed to  dlcyclopentadlene  for  2  months  reported  headaches
that  disappeared  after  another  3 months of  exposure.   Thus,  Inurement  to
some  of the effects of dlcyclopentadlene may have resulted.
6.2.    CARCINOGENICITY
    Pertinent  data  regarding  the  carc1nogen1c1ty  of  cyclopentadlene  or
dlcyclopentadlene  could not  be  located  In the  available literature  as  cited
1n Appendix A.  These chemicals are not scheduled for testing by NTP (1987).
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6.3.   MUTAGENICITY
    Pertinent data  regarding  the mutagenlclty  of cyclopentadlene could  not
be located 1n the available literature as cited 1n Appendix A.
    LHton  Blonetlcs   (1980)  conducted  mutagenlclty  assays  using  dlcyclo-
pentadlene.  Two  lots of  dlcyclopentadlene were  tested by  plate assay  1n
Salmonella  typhlmuMum strains  TA1535,  TA1537,  TA1538,  TA98,  TA100 and  In
Saccharomyces cerevlslae  strain D4  with and  without  S-9 metabolic  activa-
tion.  Doses  of dlcyclopentadlene used  1n  the activation and  nonactlvatlon
experiments  ranged   from   0.001-5   and  0.001-10  pi/plate,   respectively.
Negative results were obtained In all strains with and  without  activation.
6.4.   TERATOGENICITY
    Pertinent data  regarding  the teratogenldty of  cyclopentadlene could  not
be located 1n the available literature as dted In Appendix A.
    Litton Blonetlcs  (1980) gave groups  of  -20 pregnant  CRL:COBS  CD  (SO)  BR
rats  0,  80, 250  and  750  ppm  dlcyclopentadlene  (98-99% pure)  In the  diet
during days  6-15 of  gestation.   No  significant  dose-related  effect on  the
dams,  fetuses  or  reproductive  performance  was observed and no  teratogenlc
effects were observed.
6.5.   OTHER REPRODUCTIVE EFFECTS
    Pertinent  data  regarding  the   other  reproductive  effects   of  cyclo-
pentadlene  could  not  be  located  1n  the available literature  as cited  1n
Appendix A.
    LHton  Blonetlcs  (1980)  conducted a 3-generatlon  reproduction  study  of
dlcyclopentadlene In  rats.  Groups of  10 male and  20 female CRL:COB  (SD)  BR
rats  (the  Fn parents)  were  given  nominal  dietary concentrations of 0,  80
and 750 ppm  (87 and 9254  of the  desired concentration,  or 70  and 690  ppm,  was
achieved,  respectively)  dlcyclopentadlene and  were mated twice to yield  two


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groups of  offspring (F,  generation).   The second  group was mated  twice to
give  rise  to  the second  generation,  and the subsequent  generation  was  pro-
duced 1n a  similar  manner.   No deleterious effects  of  treatment  on  male and
female fertility,  gestation,  newborn viability,  pup  viability,  lactation,
pup weight, sex  ratio,  live pups/Utter or general  condition  were observed.
Necropsy results  of parents  from any generation  were  not  exceptional.   No
malformations  were observed 1n any generation.
    The only  additional  Information regarding other  reproductive  effects of
dlcyclopentadlene was an  oral  study  using  mink.   Aulerlch et al.  (1979)  gave
groups of  30  (6 males and  24 females/group) 3-month-old,  dark  variety  mink
0, 100, 200,  400 and 800 ppm  (0, 24, 42,  85  and  170 mg/kg/day,  estimated by
the  authors)  dlcyclopentadlene  1n  the  diet  for  12  months  (animals  were
treated during  one  reproductive  season).   Treatment with  dlcyclopentadlene
had  no  effect  on  length of  gestation,  litter  size,  sex  ratio,  kit  (off-
spring) mortality,  kit  blomass during lactation, lactatlng  female weight or
male  fertility.  The  only  effects  observed  were  a  significant  decrease
(p<0.05) 1n  testls  weight  In the 800 ppm males  and a  significant  decrease
(p<0.05) 1n  kit  body  weight  at  the three  highest  doses  after  4  weeks of
nursing.  The authors  suggested  that this  result was attributable either to
a direct toxlcologlcal  effect on the kits by Ingesting the chemical In  milk
or to an upset In maternal metabolism, which affected lactation.
6.6.   SUMMARY
    Dow  (1987)  reported  several  subchronlc  Inhalation toxlclty  studies of
cyclopentadlene  In  rats, guinea  pigs,  rabbits  and  dogs.  The only effects
reported were  a necrotlc left ventricle 1n  one dog  exposed to 250  ppm   (676
mg/m3) for  135  seven-hour exposures  1n  194 days and cloudy  swelling  of the
liver and  kidney In rats exposed  to 500 ppm (1352  mg/m3)  for  35  seven-hour


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exposures  1n 54  days.   Shashklna  (1965)  reported  leukopenla,  anemia  and
lesions of the trachea, bronchi,  lungs,  liver,  kidneys,  spleen,  thyroid,  CNS
and lymphatic elements In  rats  exposed  to  cyclopentadlene at a concentration
of  0.35  mg/a, 4  hours/day,  6  days/week  for  6 months.   Little  Information
regarding  the acute  tox1c1ty of  cyclopentadlene  was available.   Shashklna
(1965)  reported  2-hour  Inhalation  LC5Qs  of  39  mg/8,  for  rats  and  14
mg/s,  for  mice.   Cyclopentadlene  has  an  Irritating  terpene-llke  odor,  and
although systemic  Injury  was considered unlikely  at  a concentration  of  250
ppm  (676  mg/m3),   a  much  lower  TLV-TWA of  75  ppm  (200 mg/m3)  was  adopted
from the standpoint of comfort (AC6IH, 1986).
    Dodd et  al. (1982)  observed  structural  and functional kidney alterations
1n  male  rats  exposed by  Inhalation to  >1  ppm (>5.4 mg/m3)  dlcyclopenta-
dlene  for  6  hours/day,  5  days/week  for  up to  90  days,  and an  Increase In
relative liver weight  1n  male rats exposed  by  the  same  exposure regimen but
at  a  concentration of 51  ppm (276 mg/m3).   Dodd  et  al.  (1982)  reported an
Increased body weight  gain  In  female mice and  Increased  mortality (attrib-
uted  to  pulmonary congestion)  1n both  sexes  at a  concentration of  51  ppm
                                                             »
(276  mg/m3)  for  6  hours/day,  5  days/week  for  up to  64 and 60 exposures,
respectively.  Liver  dysfunction, manifested  by a  slight Increase  In serum
albumin 1n  the  5.1  and 51  ppm  (27.6  and 276 mg/m3) mice  (64 exposures)  and
Increased relative  liver  weight  (5.1  ppm females  only;  64  exposures),  was
also observed.
    Klnkead  et al. (1971)  reported subchronlc  Inhalation  toxlclty studies 1n
rats  and  dogs.   Rats  exposed to >35.2 ppm  (>190.3  mg/m3)  for  7 hours/day,
5 days/week  for  89 exposures exhibited  kidney lesions.   These  effects  were
not  noted  at  19.7   (106.5   mg/m3)   ppm.   Minimal  changes  1n  biochemical
parameters  were   observed   1n  dogs  exposed   to  23.5  ppm (127.1  mg/m3),  7


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hours/day, 5 days/week for 89 exposures.  These  effects  were  not  observed at
8.9  ppm  (45.1  mg/m3).   Shashklna   (1965)  reported  protelnuMa  and  hlsto-
pathologlcal lesions  of  the  trachea, bronchi, lungs, liver,  kidney,  spleen,
thyroid,  CNS and  lymphatic elements 1n  rats  exposed to 0.02 mg/t, 4 hours/
day, 6 days/week for  6 months.  No  effects  were  reported 1n a 12-month study
using mink  that  were exposed to  <800  ppm  (170  mg/kg/day)  dlcyclopentadlene
1n the diet for 12 months  (Aulerlch  et  al., 1979).   Rats and mice exposed to
<750 and  273  ppm dlcyclopentadlene  1n  the  diet, respectively, for 13 weeks
exhibited no effects  (Litton  81onet1cs,  1976).   No  treatment-related  effects
occurred  In dogs given  dlcyclopentadlene In the diet at  concentrations  >100
ppm  for  13  weeks  (LHton  B1onet1cs, 1980).  Oral  LD5Qs  for  dlcyclopendlene
In  rats   and  mice  were  similar  and ranged  from  ~200-500  mg/kg (Hart  and
Dacre,   1977;   Klnkead  et  al.,   1971).   Inhalation  LC5Qs  1n  mice,  rats,
guinea  pigs  and rabbits  ranged  from -150-800  ppm  (811-4326 mg/m3)/4 hours
(Klnkead  et al.. 1971; Gage,  1970).
    When  exposed  by  Inhalation  to  dlcyclopentadlene,  7 hours/day,   5 days/
week  for 2  weeks,   rats  had convulsions   and  hemorrhage of  the lungs  and
                                                  »
thymus  and  died at  332  ppm  (1795 mg/m3),  mice  died  at 72 and 146 ppm (389
and  789  mg/m3) and  dogs  had diarrhea  at  20 ppm  (108 mg/m3)  and   lack  of
control  of  hindquarters at  47  ppm  (254 mg/m3)  (Klnkead et al.,  1971).   No
effects  were  observed 1n beagles fed  dlcyclopentadlene 1n the diet  at <375
ppm  for  14  days  (Litton  B1onet1cs, 1976).  Decreased  body weight   gain  or
weight   loss  and  hematologlcal  effects  occurred   at   all  dietary   levels
(10-10,000  ppm)  of  dlcyclopentadlene In mink  treated for  21  days  (Aulerlch
et al.,  1979).
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    Like cyclopentadlene,  dlcyclopentadlene  has  a disagreeable odor.   It  Is
noticeably  Irritating when  a  concentration  of  10  ppm  Is  exceeded.   In
humans,  dlcyclopentadlene  at a  concentration of  1  ppm  (5.4 mg/m3)  caused
eye  and  throat  Irritation  and  olfactory  fatigue,  but  no  fatigue   was
reported at  5.5 ppm  (29.7  mg/m3) for  30  minutes.  Headaches were  reported
by exposed workers, but the workers  became  Inured to  this  effect.
    Carc1nogen1c1ty data were  not available for  cyclopentadlene  or  dlcyclo-
pentadlene.  Negative  results  were obtained  In  mutagenlclty experiments  of
dlcyclopentadlene 1n S^ typh1mur1um and S^ cerevlslae.
    Dlcyclopentadlene was not maternally toxic,  fetotoxlc  or  teratogenlc  and
did not  affect  reproductive  performance In rats, at concentrations  <750  ppm
1n the  diet  (LHton B1onet1cs,  1980).  No malformations,  deleterious  effect
on reproductive  Indices  or  toxic  effects  on the  parents were observed 1n  an
oral  3-generat1on  reproductive  toxldty study using rats  (LHton B1onet1cs,
1980).    In a  12-month  study  using  mink,  significant decreases In  testls
weight  and  1n  kit body  weight  were  observed at  dietary concentrations >800
ppm (170 mg/kg/day) and >200 ppm (42 mg/kg/day),  respectively.
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                     7.   EXISTING GUIDELINES AND STANDARDS
7.1.   HUMAN
    ACGIH  (1986-1987)  adopted  a  TLV-TWA  of  75  ppm   (-200   mg/m3)   for
cyclopentadlene; however,  no  STEL  was recommended.  The TLV  was  recommended
by  ACGIH (1986)  because  distinct  discomfort  was  noted  at  higher  levels.
OSHA   (1985)   promulgated   a  standard   of   75   ppm   (-200   mg/m3)   for
cyclopentadlene.
    A  TLV-TWA  of  5  ppm  (-30  mg/ma)  was   recommended  and   adopted   for
dlcyclopentadlene because  olfactory fatigue was not  noted  during  a 30-m1nute
exposure of humans to 5.5 ppm (ACGIH,  1986, 1986-1987).
7.2.   AQUATIC
    Guidelines  and  standards  for  the  protection  of aquatic organisms  from
the effects of  cyclopentadlene  and  dlcyclopentadlene could not  be located 1n
the available literature as cited 1n Appendix A.
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                              8.   RISK  ASSESSMENT
8.1.   CARCINOGENICITY
    Pertinent  data  regarding  the  carc1nogen1c1ty  of  cyclopentadlene  and
dlcyclopentadlene could not  be  located 1n the available  literature  as cited
In  Appendix A.   Thus,  these  chemicals  cannot  be  evaluated  as  to  their
potential  carc1nogen1c1ty  for   humans.    Therefore,  according   to  the  EPA
Guidelines  for  Carcinogen Risk  Assessment (U.S.  EPA, 1986b),  both  chemicals
are 1n Group D, not classifiable as to human carclnogenlcHy.
8.2.   SYSTEMIC TOXICITY
8.2.1.   Inhalation Exposure.
    8.2.1.1.   LESS   THAN  LIFETIME  EXPOSURES   (SUBCHRONIC)  --  Dow   (1987)
summarized  several  subchronlc Inhalation  studies  of  cyclopentadlene  1n rats,
dogs, guinea  pigs and rabbits.   In these studies, the animals  were  exposed
to  concentrations  of  250-993 ppm  (676-2685  mg/m3) for  6 or 7  hours/day for
<194 days.  The  only  observed toxic effects occurred In  rats  exposed  to 500
ppm  (1352  mg/m3)  for  35  seven-hour exposures  1n  53 days.   Multiplying 1352
mg/m3  by  7  hours/24  hours  and   by  35  days/53 days  yields  an  expanded
exposure  of  260  mg/m3.   No effects  were  observed  1n  rats,  guinea  pigs,
rabbits  or  a  dog  exposed  to  250  ppm  (676   mg/m3)  for  135  seven-hour
exposures  1n  194  days  (expanded  to 137  mg/m3), In 4 dogs exposed  to 400
ppm  (1081  mg/m3)  for  16  six-hour  exposures  followed  by 800  ppm  (2163
mg/m3) for  28 six-hour exposures  In 60  days  (TWA expanded exposure  of 270
mg/m3),  or  1n  rats,  guinea  pigs or   rabbits   exposed  to  250  ppm  (676
mg/m3) for 35 seven-hour exposures  1n 53 days (expanded  to 130  mg/m3).
    Shashklna  (1965)  described  a  variety  of  effects  1n   rats  exposed  to
cyclopentadlene  at  359  mg/m3,   4  hours/day,  6 days/week  for  6  months;
however,   this  study  did  not  provide sufficient detail  regarding  numbers,

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sex,  strain  or  experimental  protocol,  to  assess  the  reliability  of  the
results.  Thus,  the  expanded exposure of  260  mg/m3, which  produced  effects
1n rats  (Dow,  1987),  1s the LOAEL; the highest NOEL  below  this  LOAEL  1s 137
mg/m3,  which  had no effect  on  rats,  guinea pigs, rabbits  and  dogs.   Multi-
plying  137   mg/m3  by  the  reference  rat  Inhalation  rate   of  0.223  mVday
and dividing by  the reference  rat  body weight  of  0.35 kg gives  a transformed
NOEL  of 87.3 mg/kg/day.   Dividing by an  uncertainty  factor of 100  (10 for
Interspecles extrapolation and  10  to  protect  the  most sensitive Individuals)
yields  a  subchronlc  Inhalation  RfD for  cyclopentadlene of  0.9  mg/kg/day,  or
61  mg/day  for  a  70  kg  man.   Dividing  61  mg/day  by 20  mVday yields  a
concentration  In air  of  3  mg/m3.   Very  low  confidence 1s  placed 1n  this
RfD,  because the  summary by  Dow  (1987)  was brief  and the  data were not
available for evaluation.
    Several   subchronlc Inhalation  studies using  rats,  mice  and  dogs  were
available for dlcyclopentadlene.   Shashklna  (1965) described several  effects
1n  rats exposed to dlcyclopentadlene at  20 mg/ma,  4  hours/day,  6 days/week
for  6  months;  however,  this  study  provided  Insufficient   detail  regarding
            •>
number,  sex,  strain   or  experimental  protocol,   to  adequately  assess  the
reliability  of  the  results.   Klnkead  et al.  (1971)  found Increases In serum
levels  of  liver  enzymes  In  dogs  exposed to  dlcyclopentadlene at 23.5 and
32.4  ppm   (127.1  and  175.3   mg/m3),   7   hours/day,   5  days/week  for  89
exposures.   The expanded  exposures  are 26.5  and 36.5  mg/m3,  respectively.
No  effects  were  found at  8.9  ppm  (48.1  mg/m3),  7 hours/day,  5  days/week
(expanded   exposure  of   10.0   mg/m3).    Kidney   lesions  occurred  1n  rats
exposed to  35.2 and 73.8  ppm (190.3  and  399.1 mg/m3),  7 hours/day,  5 days/
week  for 89  exposures (Klnkead et al.,  1971).    The  expanded  exposures are
39.6  and 83.1   mg/m3,  respectively.   No  kidney  lesions  were observed  at
19.7  ppm  (106.5 mg/m3),  7  hours/day,   5 days/week,  but   female rats  had

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convulsions  at  this  level.   Dodd  et  al.  (1982)  exposed mice  and rats  to
dlcyclopentadlene  at  1,  5.1 or  51  ppm  {5.4, 27.6  or  276 mg/m3),  6  hours/
day, 5 days/week for 90 days.   The  expanded exposures  are 0.96,  A.9 and 49.3
mg/m3,  respectively.   Mice  had   evidence  of   liver   dysfunction  at  4.9
mg/ma  and renal  failure  and  death  at  49.3 mg/m3.   Rats  had  liver  dys-
function  at  all  exposures.   Transformed  animal doses  In mg/kg/day  corre-
sponding  to  these  Inhalation exposure  levels are calculated  1n  Section 9.1.
The lowest dose tested, 0.61  mg/kg/day  for  the  rats  at  the expanded exposure
level  of  0.96  mg/m3 (Dodd et al.,  1982),  1s  the LOAEL  In  these  subchronlc
Inhalation studies.   The  dose  1s  calculated  by multiplying  0.-96  mg/m3  by
the  reference   rat   Inhalation  rate of  0.223  m3/day  and dividing by  the
reference  rat  body  weight  of  0.35  kg.  Dividing  0.61   mg/m3  by   an  uncer-
tainty factor of  1000  (10 for  Interspedes  extrapolation, 10  to protect the
most  sensitive  Individuals  and  10  for  the use of  a  LOAEL)  results  1n  a
subchronlc Inhalation  RfD for  dlcyclopentadlene  of  0.006 mg/kg/day or 0.04
mg/day.   Dividing  by  a  ventilation rate of 20  mVday  yields  a  concentra-
tion 1n air of  0.002 mg/m3.
    8.2.1.2.    CHRONIC EXPOSURES  -- Data  regarding  the   effects of chronic
Inhalation exposure  to cyclopentadlene  and  dlcyclopentadlene  could not  be
located 1n the  available  literature as cited In  Appendix A.   The  subchronlc
Inhalation studies  of cyclopentadlene,  while of  sufficient  duration  for  a
subchronlc RfD,  were not  of sufficient  duration  for  a chronic  RfD.
    The subchronlc  Inhalation LOAEL for  dlcyclopentadlene of  0.61 mg/kg/day
could  be  used  to derive  a chronic  Inhalation RfD for dlcyclopoentadlene  by
applying  an  uncertainty  factor of  10,000   (an  additional factor  of   10  Is
needed  because  the  study was  subchronlc).   An RfD  of  0.06 yg/kg/day  or
0.004  mg/day (0.0002  mg/m3),  results  from these  calculations.   Very  low
confidence 1s placed 1n this  RfD because 1t  1s based  on  a  subchronlc LOAEL.

0013d                               -37-                       '      05/26/87

-------
8.2.2.   Oral Exposure.
    8.2.2.1.   LESS  THAN  LIFETIME  EXPOSURES  (SUBCHRONIC) — Pertinent  data
regarding  the  effects of  subchronlc  oral  exposure to  cyclopentadlene could
not be  located  1n the available  literature as cited 1n  Appendix  A.   An RfD
for subchronlc  Inhalation  exposure  to  cyclopentadlene  was  calculated  from
data  summarized  by Dow (1987)  (see  Section 8.2.1.1.).    Very  low  confidence
was placed  1n  the  subchronlc Inhalation  RfD.   It  1s  not appropriate  to
derive  a  subchronlc  oral  RfD from  these  data  because  of the  additional
uncertainty associated with route-to-route extrapolation.
    Several  subchronlc dietary studies of  dlcyclopentadlene were  available.
No effects were observed  1n  rats  treated at dietary concentrations <750 ppm,
In mice  treated  at concentrations <273 ppm  or  In  dogs  treated  at  concentra-
tions   <1000  ppm  for  13  weeks (Litton  B1onet1cs,  1976, 1980).   No  effects
were  observed 1n  a 3-generatlon study using rats  treated at dietary concen-
trations  <690  ppm (Litton  B1onet1cs,  1980).   Based  on  the body  weight and
food  consumption   data  provided  1n  these  studies,  equivalent  dosages  were
calculated.   For  rats In the  13-week  study,  750  ppm  was   equivalent  to  56
mg/kg/day  for  males  and  66 mg/kg/day  for  females.  For mice, 273  ppm was
equivalent  to 48  mg/kg/day  for  males  and 65 mg/kg/day for   females.   For
dogs,   1000 ppm was  equivalent to 29  mg/kg/day for both males  and females.
In the  3-generat1on  study,  690 ppm was equivalent  to -32 mg/kg/day for males
and 50 mg/kg/day for  females.
    Aulerlch et al.  (1979) maintained groups  of mink on diets  that provided
dlcyclopentadlene  doses  of 24, 42,  85 or 170 mg/kg/day  for 12 months.   The
treatment  period   Included  one breeding season.    The   only effects   were  a
significantly  reduced  testlcular weight   1n  the  170   mg/kg/day   males  and
significantly  decreased  body  weight  of  the  offspring after 4 weeks  of
nursing  at >42 mg/kg/day.
0013d                               -38-              '               05/26/87

-------
    Thus, 42  mg/kg/day  1s the LOAEL,  and  the highest NOEL below  this  LOAEL
1s 32 mg/kg/day  1n  male rats 1n the  3-generat1on  study.   Dividing this  NOEL
by an uncertainty factor  of  100  (10  for  Interspedes  extrapolation and  10 to
protect the most sensitive Individuals)  results  In  a  subchronlc  oral  RfD for
dlcyclopentadlene of 0.3 mg/kg/day, or 22 mg/day for a 70 kg human.
    8.2.2.2.   CHRONIC  EXPOSURES —  Data regarding  the  effects  of  chronic
oral exposure  to cyclopentadlene  or  dlcyclopentadlene could not  be  located
1n  the  available literature as  cited  1n Appendix A.   The subchronlc  oral
NOEL of  32 mg/kg/day  for dlcyclopentadlene  (see  Section  8.2.2.1.)  can  be
used to  derive a chronic oral RfD.   Dividing  32  mg/kg/day  by  an uncertainty
factor  of  1000  (an  additional factor  of 10 1s needed because  the 3-genera-
tlon study  1s considered  to be  subchronlc)  results  1n  an RfD  for  dlcyclo-
pentadlene of 0.03  mg/kg/day,  or 2 mg/day for a  70  kg human.   Medium confi-
dence 1s  placed  1n  this  RfD because  H  1s based on  an  extensive  subchronlc
data base.
0013d                               -39-                             05/26/87

-------
                           9.   REPORTABLE  QUANTITIES
9.1.   BASED ON SYSTEMIC TOXICITY
    Studies regarding  the  toxldty of cyclopentadlene  and  dlcyclopentadlene
were  discussed  1n  Chapter  6,  and  those  of  sufficient  duration  showing
effects are summarized 1n Tables 9-1 and  9-2.
    Shashklna  (1965)   described  a  variety  of  effects  In   rats  exposed  by
Inhalation  to  cyclopentadlene,  but  the  researchers  provided  Insufficient
detail regarding numbers,  sex,  strain of  rats  used  or  experimental  protocol,
to  adequately assess  the  reliability of  the  results.   For  these  reasons,
this  study  will not be  considered for  the  RQ.   In the study  summarized  by
Dow  (1987),  10  rats  exposed by  Inhalation  to an  equivalent  human  dose  of
28.4  mg/kg/day  for  53 days  had  cloudy  swelling of the Hver  and  kidney and
vacuollzatlon  of the  renal  tubule  epithelium.   These  effects  warrant  an
RV   of  5.   Multiplying 28.4 mg/kg/day by  70 kg and dividing  by a  factor  of
10  to approximate chronic  exposure yields  an MED  of 199 mg/day, which corre-
sponds  to  an  RVd  of  2.1.   Multiplying  the  RVd by  the  RVg results  1n  a
CS  of  11,  which corresponds to an  RQ of  1000  (Tables  9-3 and  9-4).   The Dow
Chemical  study  has  not  been  published  at  this time  and,  therefore,  the
confidence  1n  this  study 1s low.   The presented  data  have  been taken from a
summary  of  the  multi-species  study provided to  the  EPA by Dow  (1987).  In
addition,  the purity  of  the compound was not specified.   However,  because
this  study  represents  the best  available data,  1t has been used  for deter-
mining the RQ.
     For  dlcyclopentadlene, the  study by  Sashklna  (1965)  will  not  be  con-
sidered  for RQ  derivation  for reasons stated previously.
0013d                               -40-                             05/26/87

-------




























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-------
                                  TABLE 9-3

         Inhalation  Composite  Score  for Cyclopentadlene Using the Rata
                Chronic
Animal Dose    Human HED—RVd           Effect            RVe    CS     RQ
(mg/kg/day)     (mg/day)


   162.8         199b       2.1    Cloudy swelling of        5     11    1000
                                   liver and kidney;
                                   vacuollzatlon of renal
                                   tubule epithelium


aSource: Dow, 1987

bThe dose was divided by a factor of 10 to approximate chronic exposure.
0013d                               -44-                             05/26/87

-------
                                   TABLE  9-4
                                Cyclopentadlene
           Minimum Effective  Dose  (MED) and Reportable  Quantity  (RQ)
Route:
Dose*:
Effect:
Reference:
RVd:
RVe
Composite Score:
RQ:
Inhalation
199 mg/day
cloudy swelling of liver and kidney; vacuollzatlon
of renal tubule epithelium
Dow, 1987
2.1
5
11
1000
*Equ1valent human dose
0013d                               -45-                             05/26/87

-------
    As seen  from Table 9-2,  the  most  severe effect of exposure  to  dUyclo-
pentadlene was  death  and renal  failure  1n  mice  treated  at an  equivalent
human dose of  5 mg/kg/day In the  study  by Dodd et al. (1982).   The effects
warrant an RVg  of 10.  Multiplying  5  mg/kg/day by 70  kg and dividing  by  a
factor of 10 to  approximate  chronic  exposure  results  In an MED of 35 mg/day,
which  corresponds  to  an  RVrf  of  3.2.   Multiplying  the  RV.  by  the  RVg
yields-the CS of 32, which corresponds  to an RQ of 100 (Tables 9-5 and 9-6).
    The next most  severe  effects  were  the  liver  dysfunction In  mice and the
kidney  dysfunction and  hlstopathologlcal  lesions 1n  the  kidneys  of  rats
(RV =8) treated  at an equivalent  human  dose of 0.5  mg/kg/day.   Multiplying
by 70 kg  and dividing by 10  yields  the  MED of  3.5 mg/day,  which corresponds
to an RV. of 4.6.  The CS 1s 37, which  corresponds to  an RQ of 100.
    Protein  accumulation  In  the renal  tubules, which was  Indicative but not
definitive evidence of renal  damage, occurred  In  rats  at  an equivalent human
dose  of  0.1  mg/kg/day,   which  warrants  an   RV   of  7.   Multiplying  0.1
mg/kg/day by 70  kg and  dividing by 10  results In  an MED of 0.7 mg/day,, which
corresponds  to  an RV.  of  5.6.    Multiplying the RV.  by  the  RV   yields
the CS of 40, which corresponds to an RQ of 100.
    Other  less   severe  effects  occurred  at  higher doses  (see  Table  9-2);
therefore, CSs  need  not  be derived for  these  effects.  Table 9-5 shows  that
the  highest  CS, 40,  was  obtained from  data  on protein  accumulation  In the
renal  tubules  1n  the study  by Dodd  et  al.  (1982);  therefore,  the  RQ for
dlcyclopentadlene  1s 100.
9.2.   BASED ON CARCINOGENICITY
    Data  regarding the cardnogenlclty of  cyclopentadlene  and dlcyclopenta-
dlene  could  not  be located  1n the available  literature putting both  com-
pounds  1n the  EPA we1ght-of-ev1dence  Category  D.  Therefore, F  factors and
RQs based on cardngenlclty cannot be derived.

0013d                               -46-                             09/02/87

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-47-
05/26/87

-------
                                  TABLE 9-6
                              D1cyclopentad1ene
          Minimum  Effective Dose  (MED) and Reportable Quantity  (RQ)


Route:                  Inhalation
Dose*:                  0.7 mg/day
Effect:                 protein  accumulation  1n renal  tubules
Reference:              Dodd et  al.t 1982
RVd:                    5.6
RVe                     7
Composite Scoore:       40
RQ:                     100
^Equivalent human dose
0013d                               -48-                             05/26/87

-------
                                10.   REFERENCES

ACGIH  (American  Conference  of  Governmental  Industrial Hyg1en1sts).   1986.
Documentation of the Threshold  Limit  Values  and  Biological  Exposure Indices,
5th ed.  Cincinnati, OH.  p. 163-164.

ACGIH   (American   Conference  of    Governmental   Industrial   Hyg1en1sts).
1986-1987.   Threshold  Limit Values  and  Biological   Exposure  Indices  for
1986-1987.  Cincinnati, OH.  p.  14-17.

Amoore, 3.E. and E. Hautala.  1983.   Odor  as  an  aid to chemical  safety: Odor
thresholds  compared with  threshold  limit  values  and  volatilities for  214
Industrial  chemicals  1n air  and  water dilution.   J.  Appl.  Toxlcol.   3(6):
272-290.

AuleMch, R.J.,  T.H.  Coleman,  D.  Polln,  R.K. Ringer  and K.  Howell.   1979.
Toxicology  study  of dllsopropyl  methylphosphonate and dlcyclopentadlene  1n
mallard  ducks,  bobwhlte quail  and  mink.   Final  Report.   Dept. of  Poultry
Science, Michigan State University.  NTIS  AD-A087257/2.

BoubHk,  T.,  V.  Fried and  E.  Hala.   1984.  The vapor  pressures of  pure
substances:   Selected  values  of  the  temperature  dependence  of the  vapour
pressures of  some  pure substances  1n  the normal  and low  pressure  region.
Vol 17.  Elsevler Science Pub!., Amsterdam, Netherlands.

Burrows,  W.D.   1978.    Development  of guidelines  for  contaminated soil  and
groundwater  at  U.S. Army  Installations.   Jt. Conf.  Sens.  Environ.  Pollut.
U.S. Army Med. Bloeng.  Res. Dev. Lab., Frederick, MD.   (CA 89:017917q)

0013d                               -49-                             05/04/87

-------
CMR (Chemical  Marketing  Reporter).   1980.  Chemical  Profile.   Dlcyclopenta-
dlene.  Chemical Marketing Reporter,  July 21,  1980.

Dodd,   D.E.,  L.C.  Longo  and  D.L.  Elsler.   1982.   D1cyclopentad1ene  vapor
ninety-day Inhalation  study on  rats and  mice.   Bushy  Run Research  Center
Export, PA.  TSCA  8e submission by  Exxon Chem.  Amer. Doc.  I.D.  88-8300464,
Odd Doc. I.D. 8EHQ-0283-0364.   Microfiche No.  OTS 204864.

Dow, 1987.  Unpublished data.   Dow Chemical U.S.A.,  Midland, MI.

Elsenrelch,  S.3.,  B.B.  Looney  and D.J.  Thornton.   1981.   Airborne  organic
contaminants   1n the  Great Lakes  ecosystem.   Environ.   Sc1.  Techno!.   15:
30-38.

Fefer,  M.  and  A.B. Small.   1979.   Cyclopentadlene  and  dlcyclopentadlene.
In: K1rk-0thmer Encyclopedia ,of  Chemical Technology,  3rd ed, M.  Grayson  and
D. Eckroth, Ed.  Oohn Wiley and Sons, Inc., NY.  p.  417-429.

Gage,   J.C.   1970.   The  subacute toxldty  of  109 Industrial chemicals.   Br.
3. Ind. Med.   27: 1-18.

Graedel, T.E.   1978.   Chemical  Compounds  In  the Atmosphere.  Academic Press
New York.  p. 99, 7.

Hart,   E.R. and  J.C.  Dacre.   1977.   No title  provided.   Proc.  First  Int.
Congr.  Toxlcol. Toronto,  G.L.  Place  and  W.A.M.  Duncan,  Ed.   (Cited  In
Sandmeyer, 1981}


0013d                               -50-                             05/04/87

-------
Higglns,  C.E.,  W.H.  Grlest and  G.  Olerlch.   1983.   Application  of  Tenax
trapping  to  analysis  of   gas  phase  organic  compounds  1n  ultra-low  tar
cigarette smoke.  J. Assoc. Off. Anal. Chem.  66(5): 1074-1083.

H1ne, J.  and  P.M.  Mookerjee.   1975.  The Intrinsic  hydrophlllc  character  of
organic  compounds.   Correlations  In  terms  of structural  contributions.   J.
Org. Chem.  40: 292-297.

Jarke,  F.H.,  A.  Dravnleks  and  S.H.  Gordon.  1981.  Organic  contaminants  In
Indoor  air  and  their   relation  to  outdoor  contaminants.   Ashrae  Trans.
87(1): 153-166.

Junk,  G.A.  and  C.S.   Ford.   1980.   A  review   of organic  emissions  from
selected combustion processes.   Chemosphere.  9(4): 187-230.

Kawasaki,  M.   1980.  Experiences  with  the test  scheme  under   the  chemical
control  law  of  Japan:  An  approach  to  structure-activity  correlations.
Ecotoxlc. Environ. Saf.   4: 444-454.

Keith,  L.H.,  A.W.  Garrison,  F.R.   Allen,  et al.   1976.   Identification, of
organic  compounds  In  drinking  water from thirteen  U.S. cities.   In:  Identi-
fication and  Analysis  of Organic Pollutants  1n  Water, L.H.  Keith,  Ed.   Ann
Arbor Press, Ann Arbor,  MI.  p. 329-373.

Klnkead,  E.R.,  U.C.  Pozzanl,  O.L.  Geary  and  C.P. Carpenter.   1971.   The
mammalian  toxldty of  dlcyclopentadlene.   Toxlcol.  Appl.  Pharmacol.  . 20:
552-561.


0013d                               -51-                              05/04/87

-------
Kool, H.O.,  C.F.  Van  Kreljl  and B.C.J. Zoeteman.   1982.   Toxicology assess-
ment of  organic  compounds  1n drinking water.  Crlt.  Rev.  Env.  Control.   12:
307-357.

Litton  Blonetlcs.  1976.   Mammalian  lexicological  Evaluation  of  DIHP  and
DCPD.   (Final  Report).   Litton Blonetlcs Inc., Kensington,  HD.   NTIS ADA058
323/7.

Litton  Blonetlcs, Inc.  1980.   Mammalian  lexicological  Evaluation  of  DIMP
and  DCPD (Phase  2).   Litton  Blonetlcs,  Inc., Kensington,  MD.   Contract  #
DAMD.  17-77-C-7003.  NTIS AD-A082685.

Lyman,  W.J.,  W.F. Reehl and D.H.  Rosenblatt.   1982.  Handbook  of Chemical
Property  Estimation  Methods. McGraw-Hill Book  Co., New York.   p. 4-9;  5-4;
15-29.

M1H, T.  and W.  Mabey.  1985.   Photochemical  transformations.   In.: Environ-
mental  Exposure  from  Chemicals,  Volume I, W.B.  Neely and G.E. Blau, Ed.   CRC
Press,  Inc., Boca Raton, FL.  p. 208-210.

NIOSH   (National  Institute  for  Occupational  Safety  and  Health).   1984.
Current  Awareness File.   Registry  of  Toxic  Effects of  Chemical Substances
(RTECS).  Cincinnati, OH.

Novack,  J.,  J.  Zlutlcky,  V.  Kubelka and  G.  Mostecky.   1973.   Analysis  of
organic  constituents  present 1n drinking water.  J. Chromatogr..  76: 45-50.
0013d                               -52-                             05/04/87

-------
NTP  (National  Toxicology   Program).    1987.   Management   Status   Report.
1/13/87.

O'Donovan, P.A. and  J.E.  Woodward.   1977.   Investigation of  the  soil  trans-
location  and  phytoxldty  of   DIMP  and  DCPD.   In:  1953-01(01 )FP.   (NTIS
ADA058790).  Aerojet. Ordnance Manf.  Co.,  Downey, CA.  p. 51.

OSHA  (Occupational  Safety  and Health  Administration).   1985.   Permissible
Exposure Levels.  29 CFR 1910-1000.

Perry,   R.H.  and  D.W.  Green.   1984.   Perry's Chemical  Engineer's  Handbook,
6th ed.  McGraw-Hill Book Co.,  New York.  p.  3-54.

Perry,  D.L., C.C. Chuang,  G.A. Jungclaus  and J.S. Warner.   1979.   Identifi-
cation  of  organic  compounds  1n  Industrial  effluent discharges.   U.S.  EPA,
Office Res. Devel.,  Athens, GA.  p.  41.  EPA 600/4-79-016.  NTIS PB-294894.

Rosenblatt, D.H., T.A.  Miller, J.C.  Dacre,  I.  Muul  and  D.R.  Cogley.   1975.
Problem definition  studies  of  potential environmental  pollutants  II.  Physi-
cal,  Chemical,  Tox1colog1cal  and Biological  Properties of  16  Substances.
TR-7509.  Army  Med.  Bloeng.  Res.  Develop.  Lab., Fort  Detrlck,  MD.   Appendix
J, p. 01-J8.

Sandmeyer,  E.E.  1981.    All cyclic  hydrocarbons.   Iri:  Patty's   Industrial
Hygiene and Toxicology,  G.D. Clayton  and  F.E.  Clayton,   Ed.  John Wiley  and
Sons Inc., New York.  23(3): 3232-3251.
0013d                               -53-                             05/26/87

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SANSS  (Structure and  Nomenclature Search System).  1987.   Chemical  Informa-
tion System (CIS),  Baltimore,  MD.

Schlnk, B.   1985.   Degradation of  unsaturated hydrocarbons by  methanogenlc
enrichment cultures.  FEMS Microbiology Ecology.   31:  69-77.

Selzlnger,  D.E.  and  B.  D1m1tr1ades.   1972.    Oxygenates   1n  exhaust  from
simple hydrocarbon  fuels.  3.  A1r  Pollut. Control Assoc.   22: 47-51.

Shackelford,  W.M.  and  L.H.  Keith.   1976.   Frequency  of  Organic  Compounds
Identified  1n  Hater.    EPA-600/4-76-062.   U.S.   Environmental   Protection
Agency, Athens, GA.  p.  105,  111.

Shashklna, L.F.  1965.   The maximum permissible  concentration  of cyclopenta-
dlene  and  dlcyclopentadlene  1n the atmosphere of  Industrial  premises.   G1g.
Tr. Prof. Zabol.  9(12): 13-19.  (In Russian with English translation).

Smith, J.H.,  D.C.  Bomberger,  Jr.  and O.L.  Haynes.  1980.   Prediction  of the
volatilization rates  of  high-volatility  chemicals  from  natural  water bodies.
Environ. Scl. Technol.  14: 1332-1337.

Smyth,  H.F.,  C.P.   Carpenter  and C.S.  Well.   1954.  Range-finding  toxldty
data 11st V.  Arch. Ind. Hyg.  Occup. Med.  10:  61-68.

Spain,  G.C.  and C.C. Somervllle.   1985.   Fate and toxlclty  of  high density
missile  fuels RJ-5  and  JP-9  1n aquatic   test  systems.   Chemosphere.   14:
239-248.


0013d                               -54-                             05/26/87

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Spanggord, R.J., T.W.  Chou  and W.R. Mabey.  1979.   Studies  of  Environmental
Fates of  DIMP and  DCPD.   SRI  International,  Menlo Park, CA.   p.  54.   NTIS
AD-A078 263/7.

SRI  (Stanford  Research  Institute).   1986.   1986  Directory   of  Chemical
Producers: United  States  of  America.   SRI International,  Henlo  Park,  CA.
p. 589.

Swann, R.L.,  D.A.  Laskowskl,  P.O.  McCall, K.  Vanderkuy  and  H.J. Dlshburger.
1983.  A  rapid method for  the estimation  of the  environmental  parameters
octanol/water  partition  coefficient,  soil  sorptlon constant,  water to  air
ratio and water solubility.  Res. Rev.  85: 17-28.

U.S. EPA.  1977.   Computer  print-out  of  nonconfldentlal  production data from
TSCA Inventory. 'OPTS, CID, U.S. EPA, Washington, DC.

U.S.  EPA.   1980.   Guidelines  and  Methodology  Used 1n  the Preparation  of
Health  Effect  Assessment   Chapters  of  the  Consent Decree Water  Criteria
Documents.  Federal Register.  45(231): 49347-49357.

U.S. EPA.  1983.   Methodology and Guidelines  for  Reportable Quantity Deter-
minations  Based  on  Chronic  Toxldty  Data.   Prepared  by the  Environmental
Criteria and Assessment Office,  Cincinnati,  OH,  OHEA for the Office of  Solid
Waste and Emergency Response, Washington, DC.
0013d                               -55-                             05/26/87

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U.S. EPA.   1986a.   Methodology  for  Evaluating Potential  Carclnogenldty  1n
Support of  Reportable Quantity  Adjustments  Pursuant  to CERCLA  Section  102.
Prepared by  the Office  of Health  and Environmental Assessment,  Carcinogen
Assessment Group, Washington, DC for the Office of  Solid Waste and Emergency
Response,  Washington, DC.

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

U.S. EPA.   1987.   Graphical Exposure  Modeling System  (GEMS).   Octanol-Water
Partition  Coefficient (CLOGP)  and/or  Fate  of  Atmospheric Pollutants  (FAP)
Computer Data Systems.  Research Triangle Park, NC.

USITC  (U.S.  International  Trade  Commission).    1986.   Synthetic  Organic
Chemicals.   United  States  Production  and  Sales,  1985.   USITC Publ.  1892,
Washington, DC.  p.  29, 38.

Velslcol   Chem.  Corp.    1980.    D1cyclopentad1ene   Information  with  cover
letter.  FYI Submission.  U.S.  EPA, Washington, DC.   FYI-OTS-1080-0089.

von  Oettlngen,  W.F.   1940.   Toxlclty and Potential Dangers of Aliphatic and
Aromatic  Hydrocarbons.   A  Critical  Review  of  the  Literature.   U.S.  Public
Health Bulletin No.  255.  p. 37-40.

Weast,  R.C.,  Ed.   1985.   CRC  Handbook  of  Chemistry  and Physics,  66th ed.
CRC  Press, Inc., Boca Raton, FL.  p. C-244.
0013d                               -56-                             05/26/87

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Wlndholz, H.,  Ed.  1983.   The Merck  Index,  10th  ed.   Merck and Co., Rahway,
NO.  p. 393.

Yoshloka, Y., Y. Ose and T. Sato.  1985.  Testing for  the  toxldty of chemi-
cals with tetrahymena pyrlformls.   Sd.  Total  Environ.  43(1-2): 149-158.
0013d                               -57-                             05/26/87

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                                  APPENDIX A

                              LITERATURE  SEARCHED



    This  HEED  1s  based  on  data  Identified  by  computerized  literature

searches of the following:


         TSCATS
         CASR online (U.S. EPA Chemical Activities Status Report)
         TOXLINE
         TOXBACK 76
         TOXBACK 55
         RTECS
         OHM TADS
         STORET
         SRC Environmental Fate Data Bases
         SANSS
         AQUIRE
         TSCAPP
         NTIS
         Federal Register


These searches  were  conducted in January, 1987.   In  addition,  hand  searches

were made  of  Chemical  Abstracts (Collective Indices  5-9),  and  the.following

secondary sources should be 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  Hyglenlsts).
    1986-1987.  TLVs: Threshold  Limit  Values for  Chemical Substances 1n
    the  Work   Environment  adopted  by  ACGIH with  Intended Changes  for
    1986-1987.  Cincinnati, OH.  Ill 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  Wiley  and
    Sons, NY.   p. 2879-3816.

    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.
0013d                               -58-                             05/26/87

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    Grayson, M.  and D.  Eckroth,  Ed.  1978-1984.   Kirk-Othmer  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,  A.T.   L1eu,  T.W.  Chou  and  H.L.  3ohnson.
    1984.   Data  acquisition   for   environmental   transport   and  fate
    screening for compounds  of Interest  to  the Office of  Solid  Waste.
    SRI   International,  Menlo  Park,   CA.    EPA   600/6-84-010.    NTIS
    PB84-243906.

    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,  I.N.   1984.   Dangerous Properties  of  Industrial  Materials,  6th
    ed.  Van Nostrand Reinhold Co.,  NY.

    SRI  (Stanford   Research  Institute).   1986.   Directory of  Chemical
    Producers.   Menlo Park,  CA.

    U.S.  EPA.   1986.   Report  on  Status  Report  in  the  Special  Review
    Program,  Registration   Standards  Program  and  the  Data  Call   in
    Programs.   Registration  Standards  and  the  Data  Call  in  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).    1985.   Synthetic
    Organic  Chemicals.   U.S.   Production  and   Sales,  1984, USITC  Publ.
    1422, Washington,  DC.

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

    Windholz, 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.
0013d                               -59-                             05/26/87

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

    McKee, O.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.
                          60604-3590
0013d                               -60-                             05/26/87

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