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DRAFT: DO NOT CITE OR QUOTE,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
0013d -1- 05/04/87
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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.
0013d -2- 05/26/87
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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).
0013d -3- 05/26/87
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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)
0013d
-4-
05/04/87
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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%.
0013d -5- . 05/26/87
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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.
0013d . -6- 05/26/87
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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
0013d -7- 05/26/87
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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).
0013d -8- 05/04/87
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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.
0013d -9- 05/26/87
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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.
0013d -10- 05/26/87
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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)
0013d -11- 09/02/87
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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).
0013d -12- 05/26/87
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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).
0013d -13- 05/04/87
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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.
0013d -14- 05/26/87
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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.
0013d -15- 05/26/87
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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.
0013d -16- 05/26/87
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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.
0013d -18- 05/26/87
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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.
0013d -23- 05/26/87
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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
0013d -25- 05/26/87
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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
0013d
-26-
05/04/87
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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.
0013d -27- 05/26/87
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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).
0013d -28- 05/26/87
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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
0013d -29- 09/02/87
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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
0013d -30- 05/26/87
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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
0013d -31- 05/26/87
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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).
0013d -32- 05/26/87
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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.
0013d -33- 05/26/87
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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.
0013d -34- 05/26/87
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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,
0013d -35- 09/02/87
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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
0013d -36- 05/26/87
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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 HEDRVd 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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0013d
-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
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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
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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
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Arbor Press, Ann Arbor, MI. p. 329-373.
Klnkead, E.R., U.C. Pozzanl, O.L. Geary and C.P. Carpenter. 1971. The
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552-561.
0013d -51- 05/04/87
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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
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0013d -52- 05/04/87
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NTP (National Toxicology Program). 1987. Management Status Report.
1/13/87.
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ADA058790). Aerojet. Ordnance Manf. Co., Downey, CA. p. 51.
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Exposure Levels. 29 CFR 1910-1000.
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6th ed. McGraw-Hill Book Co., New York. p. 3-54.
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Problem definition studies of potential environmental pollutants II. Physi-
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0013d -53- 05/26/87
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0013d -54- 05/26/87
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Spanggord, R.J., T.W. Chou and W.R. Mabey. 1979. Studies of Environmental
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U.S. EPA. 1983. Methodology and Guidelines for Reportable Quantity Deter-
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0013d -55- 05/26/87
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U.S. EPA. 1986a. Methodology for Evaluating Potential Carclnogenldty 1n
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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,
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Velslcol Chem. Corp. 1980. D1cyclopentad1ene Information with cover
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von Oettlngen, W.F. 1940. Toxlclty and Potential Dangers of Aliphatic and
Aromatic Hydrocarbons. A Critical Review of the Literature. U.S. Public
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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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