FINAL DRAFT
United States ECAO-CIN-P276
Environmental Protection July, 1987
Agency
EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS PROFILE
FOR BENZO(6HI)PERYLENE
Prepared for
OFFICE OF SOLID WASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
Us. £OW
m"~' ' Prof*,**- DRAFT: D0 NOT CITE OR QUOTE
ecf'0n AO~-
eoe^66* N°TICE
This document Is a preliminary draft. It has not been formally released
by the U.S. Environmental Protection Agency and should not at this stage be
construed to represent Agency policy. It Is being circulated for comments
on Its technical accuracy and policy Implications.
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DISCLAIMER
This report is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
ii
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PREFACE
Health and Environmental Effects Profiles (HEEPs) are prepared for the
Office of Solid Waste and Emergency Response by the Office of Health and
Environmental Assessment. The HEEPs are Intended to support listings of
hazardous constituents of a wide range of waste streams under Section 3001
of the Resource Conservation and Recovery Act (RCRA), as well as to provide
health-related limits for emergency actions under Section 101 of the Compre-
hensive Environmental Response, Compensation and Liability Act (CERCLA).
Both published literature and Information obtained from Agency program
office files are evaluated as they pertain to potential human health,
aquatic life and environmental effects of hazardous waste constituents. The
literature searched and the dates of the searches are Included 1n the
section titled "Appendix: Literature Searched." The literature search
material is current through November, 1985.
Quantitative estimates are presented provided sufficient data are
available. For systemic toxicants, these Include Reference doses (RfDs) for
chronic exposures. An RfD is defined as the amount of a chemical to which
humans can be exposed on a dally basis over an extended period of time
(usually a lifetime) without suffering a deleterious effect. In the case of
suspected carcinogens, RfDs are not estimated In this document series.
Instead, a carcinogenic potency factor of q-|* 1s provided. These potency
estimates are derived for both oral and Inhalation exposures where
possible. In addition, unit risk estimates for air and drinking water are
presented based on Inhalation and oral data, respectively.
Reportable quantities (RQs) based on both chronic toxidty and cardno-
genldty are derived. The RQ Is used to determine the quantity of a hazard-
ous substance for which notification 1s required 1n the event of a release
as specified under CERCLA. These two RQs (chronic toxidty and cardnogen-
1c1ty) represent two of six scores developed (the remaining four reflect
1gn1tab1l1ty, reactivity, aquatic toxidty and acute mammalian toxidty).
The first draft of this document was prepared by Syracuse Research
Corporation under EPA Contract No. 68-03-3228. The document was subse-
quently revised after reviews by staff within the Office of Health and
Environmental Assessment: Carcinogen Assessment Group, Reproductive Effects
Assessment Group, Exposure Assessment Group, and the Environmental Criteria
and Assessment Office 1n Cincinnati.
The HEEPs will become part of the EPA RCRA and CERCLA dockets.
111
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EXECUTIVE SUMMARY
Benzo(gh1)perylene 1s a pale yellow-green solid at ambient temperatures.
It Is soluble In 1,4-d1oxane, dlchloromethane, benzene and acetone (IARC,
1983), but 1s practically Insoluble 1n water (Pearlman et al., 1984;
Yalkowsky and Valvanl, 1979). It reacts with bromomalelc anhydride to form
bromlnated compound and coronene dicarboxyllc anhydride derivatives (IARC,
1983). This compound 1s neither commercially produced nor used In the
United States (IARC, 1983). It can be Isolated from coal tar (IARC, 1983)
or from products of hydrogenatlon of coal (U.S. EPA/NIH, 1986).
If released to the aquatic environment, benzo(gh1Jperylene 1s not
expected to hydrolyze, oxidize (by R0» radical or 10p) or volatilize
significantly.
A static culture flask-screening blodegradatlon study has shown that
benzo(gh1)perylene can be significantly blodegraded (Fochtman, 1981);
however, mlcroblal oxidation of PAH requires oxygen and will not proceed In
anoxlc sediments or water (U.S. EPA/NIH, 1986). In the dissolved state In
the water column, direct photolysis may be an Important transformation
process (U.S. EPA/NIH, 1986); however, a significant portion of the benzo-
(gh1Jperylene present In the aquatic environment 1s expected to be 1n an
adsorbed state, which may not be susceptible to phototransformatlon.
Adsorption to suspended partlculate matters and sediments 1n water Is an
Important environmental fate process for this compound. The very low water
solubility and high log K of benzo(gh1)perylene suggest a significant
potential for bloaccumulation; however, PAH may not bioconcentrate appre-
ciably 1n organisms such as fish, that have microsomal oxldase, as this
1v
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enzyme metabolizes PAH (Santodonato et al., 1981). Therefore, bioaccumula-
tlon potential may be dependent on the organism being considered. The
uniformity In the concentration of benzo(gh1Jperylene In deep sediment cores
of remote lakes (Tan and Heit, 1981) Indicate that benzo(ghi)perylene 1s
very persistent under anaerobic and dark conditions. If released to the
atmosphere, benzo(ghiJperylene will exist almost entirely In the particulate
(adsorbed) phase. The rate of photolysis has been found to vary with the
adsorbing substrate (Behymer and Kites, 1985); photolysis of benzo(ghi)-
perylene adsorbed to fly ash may have some Importance, but adsorption to
carbon black stabilizes the compound toward potential phototransformatlon.
Benzo(ghi)perylene may be transported over long distances 1n the atmospheric
aerosol. Removal from the air may occur by wet and dry deposition. If
released to soil, benzo(gh1)perylene may be susceptible to slow biodegrada-
tion under aerobic conditions. Under most conditions, It 1s not expected to
leach or volatilize from soils.
Human exposure to benzo(ghi)perylene occurs primarily through the inha-
lation of tobacco smoke and polluted air, and by the Ingestion of contami-
nated food and water (IARC, 1983). It occurs ubiquitously In products of
Incomplete combustion and in coal tar, and is a component of gasoline and
diesel engine exhaust; it also occurs naturally 1n crude oils (IARC, 1983).
It has been widely detected 1n drinking water, surface water, groundwater,
rainwater and aquatic sediments (see Tables 3-1 and 3-2), In many foods
(Santodonato et al., 1981; Dennis et al., 1983) and in the ambient atmo-
sphere (see Table 3-3). The average dietary intake of benzo(ghiJperylene in
England has been estimated to be 0.21 yg/day (Dennis et al., 1983); the
average adult Intake in the United States from drinking water has been
estimated to be 2.0 ng/day, while the inhalation Intake has been estimated
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to be 10 ng/day. Its presence 1n food Is a result of contamination from a
polluted environment and formation during cooking by pyrolysls (Santodonato
et a!., 1981; Fazio and Howard, 1983). Its concentration 1n the ambient
atmosphere in the United States has apparently been decreasing over the last
30 years. The ambient air concentration of benzo(gh1)perylene is expected
to be higher during winter than summer, apparently because of the burning of
fossil fuel for heating during winter months (Greenberg et al., 1985).
Pertinent data regarding the toxlcity of benzo(gh1)perylene to aquatic
organisms could not be located in the available literature as cited In the
Appendix. Several studies reported data concerning residues in aquatic
organisms. The following data were reported for species that are commonly
eaten by humans: mussels from Norway, trace-87 ng/g (Knutzen and Sortland,
1982); clams from 3apan, 0.23-0.95 ng/g (Tsujl et al., 1985); lobsters from
eastern Canada, 0.19 ng/g before Impoundment and 51 ng/g after Impoundment
(Dunn and Fee, 1979). Obana et al. (1983) reported BCF values of 1000-1400
for short-necked clams, T. japonica, exposed to 0.06-0.13 pg/ft. for 1-7
days.
Pertinent data regarding the gastrointestinal or pulmonary absorption of
benzo(gh1Jperylene could not be located in the available literature as cited
1n the Appendix. Data from other structurally-related PAH suggest, however,
that benzo(ghi)perylene Is absorbed readily from the gastrointestinal tract
(Rees et al., 1971) and lungs (Kotln et al., 1969; Vainio et al., 1976). In
general, PAH are highly lipld soluble and can pass across epithelial
membranes (U.S. EPA, 1980).
Pertinent data regarding the distribution, metabolism or excretion of
benzo(ghiJperylene could not be located in the available literature as cited
In the Appendix.
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Single Intrapulmonary Injections of 0.16, 0.83 or 4.15 mg benzo(ghl)-
perylene In beeswax-trloctanoln mixture Into groups of 34 or 35 rats
produced a low Incidence (4/34) of lung squamous cell carcinomas 1n the
high-dose group after lifetime observation (Deutsch-Wenzel et a!., 1983).
Lung tumors did not occur 1n untreated or vehicle treated controls, but IARC
(1983) indicated that the tumors in the treated group may be attributable to
Impurities In the test product, which was 98.5% pure.
Tumorigenldty of benzo(gh1 )perylene was not demonstrated 1n mice 1n
skin application studies involving up to 3 times/week treatment for 12
months (Lijlnsky and Saff1ott1, 1965; Van Duuren et a!., 1970; Van Duuren
and Goldschmidt, 1976; Muller, 1968; Hoffmann and Wynder, 1966) in skin
initiation-promotion studies using croton oil as a promoter (Hoffman and
Wynder, 1966) and PMA as a promoter (Van Duuren et al., 1970) and by
bimonthly subcutaneous Injections for 5 or 6 months (Muller, 1968).
Enhancement of the dermal carcinogeniclty of benzo(a)pyrene by simultaneous
application of benzo(ghi)perylene has been reported in mice (Goldschmidt et
al., 1973; Van Duuren et al., 1973; Van Duuren and Goldschmidt, 1976),
indicating possible cocarcinogenicity of benzo(ghiJperylene.
Benzo(gh1)perylene was mutagenlc to j>. typhimurium strains TA98, TA100,
TA1537 and TA1538 (Andrews et al., 1978; Hossanda et al., 1979; Salamone et
al., 1979) and TH677 (Kaden et al., 1979) when assayed In the presence of
exogenous metabolic activation preparations. Intraperitoneal injection of
benzo(ghi Jperylene into hamsters on day 10 of gestation did not Induce
transformations In the embryo cells (Quarles et al., 1979).
Pertinent data regarding toxic, teratogenic or other reproductive
effects of benzo(ghiJperylene could not be located in the available litera-
ture as cited in the Appendix.
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Data were Insufficient to derive an RfD, RQ, q,* or F factor. Benzo-
(ghl)perylene was placed In CAG Group D, wh}ch means that classification for
cardnogenlclty and hazard ranking for cardnogenldty are not possible.
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 2
1.4. USE DATA 2
1.5. SUMMARY - 2
2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES 3
2.1. WATER ' ' 3
2.1.1. Hydrolysis 3
2.1.2. Oxidation 3
2.1.3. Photolysis 3
2.1.4. Mlcroblal Degradation 4
2.1.5. Volatilization 4
2.1.6. Adsorption 5
2.1.7. Bloconcentratlon 5
2.1.8. Persistence 6
2.2. AIR 6
2.3. SOIL 7
2.3.1. Mlcroblal Degradation 7
2.3.2. Chemical Degradation 7
2.3.3. Adsorption 8
2.3.4. Volatilization 8
2.4. SUMMARY 8
3. EXPOSURE 10
3.1. WATER 10
3.2. FOOD -. 14
3.3. INHALATION 15
3.4. DERMAL 17
3.5. SUMMARY 17
4. PHARMACOKINETCS 18
5. EFFECTS . . - 19
5.1. CARCINOGENICITY 19
5.2. MUTAGENICITY 20
5.3. TERATOGENICITY 24
5.4. OTHER REPRODUCTIVE EFFECTS 24
5.5. CHRONIC AND SUBCHRONIC TOXICITY 24
5.6. OTHER RELEVANT INFORMATION 24
5.7. SUMMARY 24
1x
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TABLE OF CONTENTS (cont.)
Page
6. AQUATIC TOXICITY 26
6.1. ACUTE 26
6.2. CHRONIC 26
6.3. PLANTS 26
6.4. RESIDUES 26
6.5. SUMMARY 27
7. EXISTING GUIDELINES AND STANDARDS 28
7.1. HUMAN 28
7.2. AQUATIC 29
8. RISK ASSESSMENT 30
9. REPORTABLE QUANTITIES 32
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC
TOXICITY 32
9.2. WEIGHT OF EVIDENCE AND POTENCY FACTOR (F=1/ED10)
FOR CARCINOGENICITY 32
10. REFERENCES 36
APPENDIX: LITERATURE SEARCHED 46
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LIST OF TABLES
No.
3-1
3-2
3-3
5-1
S-?
9-1
Title
Benzo(gh1 Jperylene Monitoring Data for Various Types
of Water
U.S. Sediment Monitoring Data for Benzo(ghi Jperylene. . .
U.S. A1r Monitoring Data for Benzo(gh1 Jperylene
Dermal and Injection Cardnogenlclty Studies of
Benzo(gh1 Jperylene
Mutagen1c1ty Testing of Benzo(gh1 Jperylene
Benzo(gh1)perylene: Minimum Effective Dose (MED) and
Reoortable Quantity (RQ)
Paqe
. . 11
. . 13
. . 16
. . 21
23 "
. . 33
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
BCF Bioconcentratlon factor
Koc Soil sorptlon coefficient
Kow Octanol/water partition coefficient
MED Minimum effective dose
PAH Polycycllc aromatic hydrocarbons
PMA Phorbol myrlstate acetate
ppb Parts per billion
ppm Parts per million
ppt Parts per thousand
RfD Reference dose
RQ Reportable quantity
TLV Threshold-limit value
TWA Time-weighted average
UV Ultraviolet
US Water solubility
xll
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
Benzo(gh1)perylene Is also known as 1,12-benzoperylene (U.S. EPA/NIH,
1986). The structure, empirical formula, molecular weight and CAS Registry
number for this chemical are as follows:
Empirical formula: C__H.._
Molecular weight: 276.3
CAS Registry number: 191-24-2
1.2. PHYSICAL AND CHEMICAL PROPERTIES
Benzo(gh1)perylene 1s a pale yellow-green crystalline solid at ambient
temperature. It Is soluble 1n 1,4-dloxane, dlchloromethane, benzene and
acetone (IARC, 1983), but 1s practically Insoluble 1n water. Some of the
relevant physical properties of this compound are listed below:
Melting point:
Solubility 1n distilled
water at 25°C:
278.3
0.553
0.3
0.26
Kow: 7.10 (estimated)
7.04 (estimated)
Vapor pressure at 25°C: l.OlxlO'10 mm Hg
IARC, 1983
Pearlman et a!.,
1984
Yalkowsky and
Valvanl, 1979
Halters and Luthy,
1984
Yalkowsky and
Valvanl, 1979;
Walters and Luthy,
1984
Ruepert et a!.,
1985
Santodonato et al.,
1981
0864p
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10/31/86
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Henry's Law constant: 6.6xlO~8 atm-mVmol Mabey et al., 1981
(estimated from water
solubility of 0.553 yg/4)
1.44xlO~7 atm-mVmol
Chemically, benzo(gh1)perylene reacts with bromomalelc anhydride to form
dlbromlnated compound and coronene dlcarboxyllc anhydride derivatives. It
also reacts with NO and N0_ to form nltro derivatives (IARC, 1983).
1.3. PRODUCTION DATA
The compound 1s neither commercially produced nor Imported Into the
United States (IARC, 1983; USITC, 1984). It can be Isolated from coal tar
(IARC, 1983) or from products of hydrogenatlon of coal (U.S. EPA/NIH, 1986).
1.4. USE DATA
There Is no known commercial use of this compound (IARC, 1983). Small
amounts of benzo(gh1)perylene are used for scientific research.
1.5. SUMMARY
Benzo(gh1)perylene Is a pale yellow-green solid at ambient temperatures.
It 1s soluble In l,4-d1oxane, dlchloromethane, benzene and acetone (IARC,
1983), but 1s practically Insoluble 1n water (Pearlman et al., 1984;
Yalkowsky and Valvanl, 1979). It reacts with bromomalelc anhydride to form
bromlnated compound and coronene dlcarboxyllc anhydride derivatives (IARC,
1983). This compound 1s neither commercially produced nor used In the
United States (IARC, 1983). It can be Isolated from coal tar (IARC, 1983)
or from products of hydrogenatlon of coal (U.S. EPA/NIH, 1986).
0864p -2- 10/31/86
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2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES
2.1. WATER
2.1.1. Hydrolysis. Benzo(gh1Jperylene contains no hydrolyzable func-
tional groups; therefore, aquatic hydrolysis Is not expected to be signifi-
cant (Habey et a!., 1981).
2.1.2. Oxidation. The rate constants for the oxidation of benzo(ghl)-
perylene with photochemlcally produced R0_ radical and aO? have been
estimated to be <36 and <360 M'1 hr'1, respectively, at 25°C (Mabey et
al., 1981). Assuming that concentrations of R0» radical and 10? 1n
natural water are 10~» and 10"12 M (Mabey et al., 1981), respectively,
the respective half-lives are estimated to be >2000 and >20,000 years.
Therefore, oxidation by RO radical and *Q 1s not environmentally
relevant.
2.1.3. Photolysis. In a cyclohexane solvent, benzo(gh1)perylene exhibits
UV absorption maxima at 299, 311, 324, 328, 344, 362, 383, 392 and 396 nm
(IARC, 1983); therefore, direct photolysis 1n sunlight 1s a definite possi-
bility. In the dissolved state 1n the water column, photolysis may be an
Important transformation process (U.S. EPA/NIH, 1986); however, a signifi-
cant portion of the benzo(gh1)perylene 1n the aquatic environment Is
expected to be present 1n the adsorbed state (Section 2.1.6.). Behymer and
Hltes (1985) examined the atmospheric photolysis of benzo(gh1Jperylene
adsorbed to various substrates and found relatively significant photolysis
when adsorbed to silica gel, alumina or fly ash, but only slow photolysis
when adsorbed to carbon black adsorption (Section 2.2.). Therefore, the
significance of potential aquatic photolysis may depend on the adsorbing
substrate as well as the Intensity of the sunlight reaching the water
0864p -3- 10/31/86
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column. As the depth of water Increases, the light Intensity will decrease;
as a result, photolysis will become Increasingly less significant with the
Increase 1n the depth of water.
2.1.4. Hlcroblal Degradation. Fochtman (1981) examined the blodegrad-
abllHy of benzo(gh1)perylene 1n a static culture flask-screening procedure
1n which 1J4 of the compound was dissolved 1n an emulslfler and added to the
bacterial suspension (domestic wastewater seed) at a concentration of 1-2
ppm. The suspension was Incubated for 7 days. A fresh bacterial suspension
was prepared weekly using the seed from the previous week, and the procedure
was continued for 28 days. Approximately 60% of the benzo(gh1)perylene was
usually degraded during a 7-day Incubation. Thus, benzo(gh1)perylene was
found to be biodegradable; Its blodegradatlon rate was slightly higher than
that of benzo(a)pyrene, which underwent -41% blodegradatlon 1n 7 days.
PAH with at least four aromatic rings are degraded slowly by microbes
and blodegradatlon 1s considered to be the ultimate fate process 1n natural
water (U.S. EPA/NIH, 1986); however, the concentrations of microorganisms
capable of oxidizing the hydrocarbons are extremely low In all but heavily
polluted fresh and marine waters, and most species of microorganisms cannot
use PAH as a sole carbon source. Hlcroblal oxidation of PAH requires oxygen
and will not proceed 1n anoxlc sediments or water (U.S. EPA/NIH, 1986).
Thus, 1t appears that the significance of blodegradatlon of benzo(ghl)-
perylene In natural waters will depend on the nature of water. In deep,
slow moving, turbid water, blodegradatlon may be more significant than In
shallow, rapidly flowing, clear streams.
2.1.5. Volatilization. Using the vapor pressure and water solubility at
25°C, Mabey et al. (1981) estimated the Henry's Law constant for benzo(ghl)-
perylene to be 1.44xlO~7 atm»m3/mol. This value of Henry's Law
0864p -4- 05/15/87
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constant Indicates that the pollutant Is essentially nonvolatile (Lyman et
al., 1982); therefore, benzo(gh1)perylene 1s not expected to volatilize
significantly from the aquatic environment.
2.1.6. Adsorption. Rump (1984) examined the partitioning of benzo(ghl)-
perylene between water and sediment phase with sediments from two rivers.
The amount of benzo(gh1)perylene that partitioned to the sediment was found
to be 2.5xl04-3.1xl05 times greater than the amount that partitioned to
the water column.
The estimated K values, which are >1 million (Section 2.3.3.), and
the widespread detection of benzo(gh1)perylene 1n various U.S. sediments
(Section 3.1.) Indicate that adsorption to suspended partlculate matter and
sediments 1s an Important environmental process. Movement by sedlment-
sorbed benzo(gh1Jperylene Is probably an Important transport process for
. this compound (U.S. EPA/NIH, 1986).
2.1.7. B1oconcentrat1on. Estimation of BCF can be made from the follow-
ing equations (Lyman et al., 1982):
log BCF = 0.76 log KQW 0.23 (2-1)
log BCF = 2.791-0.564 log (WS 1n ppm) (2-2)
Based on a water solubility of 0.00026 ppm at 25°C and a log K of 7.10
(Walters and Luthy, 1984), the BCF values estimated from Equations 2-1 and
2-2 for benzo(gh1Jperylene are 146,500 and 65,000, respectively, which
suggest significant bloaccumulatlon potential. PAH, however, may not
appreciably bloconcentrate 1n organisms such as fish that contain mlcrosomal
oxldase, as this enzyme may metabolize PAH (Santodonato et al., 1981).
Therefore, the bloaccumulatlon potential may be very dependent on the
organism being considered.
0864p -5- 10/31/86
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2.1.8. Persistence. Tan and HeH (1981) monitored sediment cores taken
from Woods Lake and Sagamore Lake In the remote Adirondack Forest of upstate
New York for various. PAH. The following benzo(gh1)perylene concentrations
(ng/g dry sediment wt) were found at various depths of Woods Lake: 1400 (0-4
cm), 500 (4-8 cm), 180 (8-11 cm), 110 (12-17 cm), 44 (24-26 cm), 46 (42-44
cm) and 59 (80-84 cm). The constancy 1n the concentration of benzo(ghl)-
perylene In the deeper sediment cores Indicates that the compound 1s very
persistent under the nonphotolytlc, anoxlc conditions present 1n deep
sediment cores.
2.2. AIR
Based on a vapor pressure of 10~10 mm Hg at 25°C (Mabey et a!., 1981),
benzo(gh1)perylene Is likely to exist almost entirely 1n the partlcle-sorbed
state 1n the atmosphere. Yamasakl et al. (1982) monitored the urban air of
a Japanese city for an entire year for PAH 1n both the vapor and partlculate
phases; the monitoring covered a wide temperature range. The six-ring PAH
(Including benzo(gh1)perylene, o-phenylenepyrene and anthracene) were
detected 1n the partlculate phase but not In the vapor phase, while the
three- to five-ring PAH were found 1n both phases with the partlonlng ratio
depending on temperature.
Behymer and HHes (1985) examined the atmospheric photolysis of benzo-
(gh1Jperylene adsorbed onto various substrates. With a rotary photoreactor
and a medium-pressure mercury lamp as the light source, benzo(gh1Jperylene
exhibited the following photolytlc half-lives 1n the adsorbed state:
Substrate Half-Life (hours)
SHIca gel 7
Alumina 22
Fly ash 29
Carbon black >1000
0864p -6- 05/15/87
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Adsorption to carbon black clearly stabilizes the phototransformatlon of
benzo(gh1)perylene. In the atmosphere, adsorption to stabilizing substrates
will allow benzo(gh1)perylene to be transported over long distances 1n the
atmospheric aerosol. Its detection In the remote rural air of South
Carolina (Keller and Bldleman, 1984) and 1n sediments from remote lakes in
the Adirondack Forest, NY (Tan and Heit, 1981) may Indicate that long-range
transport occurs.
Removal of adsorbed benzo(gh1Jperylene from the atmosphere may occur by
wet and dry deposition. Benzo(gh1)perylene has been detected 1n rainwater
(Lunde et a!., 1976; L1gock1 et a!., 1985). Its presence In lake sediments
1n the Adirondack Forest, NY, has been attributed to physical deposition
(Tan and Heit, 1981).
Since benzo(gh1)perylene does not significantly exist 1n the vapor
phase, atmospheric reaction with photochemlcally produced HO radical or
vapor phase photolysis Is not expected to be Important.
2.3. SOIL
2.3.1. Hlcroblal Degradation. The soil bacterium Bacillus megaterlurn has
been found to metabolize benzo(gh1Jperylene and other PAH (U.S. EPA/NIH,
1986); however, sufficient data are not available to predict the signifi-
cance of the soil blodegradatlon for benzo(gh1)perylene. Based on the .data
1n Section 2.1.4., benzo(gh1Jperylene may be slowly blodegraded 1n soil
under aerobic conditions.
2.3.2. Chemical Degradation. Pertinent data regarding the chemical
transformation of benzo(gh1Jperylene 1n natural soils could not be located
1n the available literature as cited 1n the Appendix.
0864p -7- 10/31/86
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2.3.3. Adsorption. Estimation of KQC can be made from the following
regression equations (Lyman et a "I., 1982):
log KQC = 0.44-0.54 log (HS 1n mol fraction) (2-3)
log KQC = 1.00 log K.QW 0.21 (2-4)
Based on a water solubility of 0.26 vg/8. at 25°C and a log K of 7.10
(Walter and Luthy, 1984), the K values estimated from Equations 2-3 and
2-4 for benzo(gh1)perylene are 1.8 and 7.8 million, respectively, which
suggests so"1l Immobility; however, the detection of benzo(gh1Jperylene 1n
several groundwaters (Section 3.1.) Indicates that leaching can occur under
certain conditions. Leaching may occur 1n soils that contain low organic
matter (e.g., sand), and may also occur from sites subjected to spills or
disposal of appropriate petroleum and coal materials that contain high con-
centrations of PAH Including benzo(gh1Jperylene; however, benzo(gh1)perylene
Is not expected to leach, 1n soil under most conditions.
2.3.4. Volatilization. Benzo(gh1)perylene cannot be expected to
volatilize significantly from soil surfaces because of Us very low vapor
pressure of 10~10 mm Hg at 25°C and a very high K value of -10*.
2.4. SUMMARY
If released to the aquatic environment, benzo(gh1)perylene Is not
expected to hydrolyze, oxidize (by R0? radical or 10?) or volatilize
significantly. A static culture flask-screening blodegradatlon study has
shown that benzo(gh1)perylene can be significantly blodegraded (Fochtman,
1981); however, mlcroblal oxidation of PAH requires oxygen and will not
proceed In anoxlc sediments or water (U.S. EPA/NIH, 1986). In the dissolved
state In the water column, direct photolysis may be an Important transforma-
tion process (U.S. EPA/NIH, 1986); however, a significant portion of the
benzo(gh1)perylene present 1n the aquatic environment 1s expected to be 1n
an adsorbed state, which may not be susceptible to phototransformatlon.
0864p -8- 10/31/86
-------
Adsorption to suspended partlculate matters and sediments 1n water Is an
Important environmental fate process for this compound. The very low water
solubility and high log K of benzo(gh1)perylene suggest a significant
potential for bloaccumulatlon; however, PAH may not bloconcentrate appreci-
ably 1n organisms such as fish, that have mlcrosomal oxldase, as this enzyme
metabolizes PAH (Santodonato et al., 1981). Therefore, bloaccumulatlon
potential may be dependent on the organism being considered. The uniformity
In the concentration of benzo(gh1Jperylene 1n deep sediment cores of remote
lakes (Tan and He1t, 1981) Indicates that benzo(gh1)perylene 1s very persis-
tent under anaerobic and dark conditions. If released to the atmosphere,
benzo(gh1 )perylene will exist almost entirely In the partlculate (adsorbed)
phase. The rate of photolysis has been found to vary with the adsorbing
substrate (Behymer and HHes, 1985); photolysis of benzo(gh1 Jperylene
adsorbed to fly ash may have some Importance, but adsorption to carbon black
stabilizes the compound toward potential phototransformatlon. Benzo(ghl)-
perylene may be transported over long distances 1n the atmospheric aerosol.
Removal from the air may occur- by wet and dry deposition. If released to
soil, benzo(gh1)perylene may be susceptible to slow blodegradatlon under
aerobic conditions. Under most conditions, It Is not expected to leach or
volatilize from soils.
0864p -9- 05/15/87
-------
3. EXPOSURE
Human exposure to benzo(gh1)perylene occurs primarily through the Inha-
lation of tobacco smoke and polluted air, and by the 1ngest1on of contami-
nated food and water (IARC, 1983). It occurs ubiquitously 1n products of
Incomplete combustion. In coal tar and In gasoline engine exhaust; It also
occurs naturally In crude oils (IARC, 1983).
3.1. HATER
Table 3-1 lists various benzo(gh1Jperylene monitoring data for drinking,
ground, surface and rain water; Table 3-2 lists sediment monitoring data at
various U.S. locations. In an analysis of the U.S. EPA STORET database,
benzo(gh1)perylene was positively detected 1n 1.0% of 914 surface water
observation stations and 1.554 of 1211 effluent reporting stations (Staples
et a!., 1985). Grlest (1980) detected benzo(gh1Jperylene at concentrations
of 7.3 yg/g (dry sediment) In the .sediment and 2.0 v9/& In the water
1n an effluent wastewater channel from a coking plant. Walters and Luthy
(1984) detected levels <90 ng/s. 1n wastewaters from two coal coking
plants.
In general, PAH can be released to water from Industrial and municipal
effluents, atmospheric fallout and precipitation, road runoff (tire wear,
bitumen and asphalt surfaces, cracked lubricating oils) and marine shipping
and harbor oil (Santodonato et al., 1981). Herrmann and Huebner (1982) have
suggested that most PAH pollution of rivers In urban areas originates from
storm water overflows containing street and roof dust washed off during
storms; the contribution of precipitation-borne PAH may be comparatively
small 1n such Instances.
0864p -10- 10/31/86
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10/31/86
-------
TABLE 3-2
U.S. Sediment Monitoring Data for Benzo(gh1)perylene
Concentration
(ng/g)
Location
Sampling
Date
Reference
32-120
14-130
12-32
7-150
70-600
1400 (0-4 cm depth)
500 (4-8 cm depth)
59 (80-84 cm depth)
620
Cayuga Lake, NY 1978
(deep water)
Cayuga Lake, NY
(IHtoral sediment)
Washington State
(bottom river sediment)
Columbia River
(suspended sediment)
Lake Erie NR
Woods Lake, NY NR
Puget Sound, WA NR
Helt, 1985
1979-1980 Prahl et al..
1984
Eadle et al.,
1982
Tan and He1t,
1981
Varanasl
et al., 1985
NR = Not reported
0864p
-13-
10/31/86
-------
Based on the monitoring data from Table 3-1, the concentration of
benzo(gh1)perylene 1n drinking water may be -1.0 ppt (ng/i). Assuming an
average dally water Intake of 2.0 8. for an adult, the Intake of benzo-
(gh1)perylene from drinking water 1s estimated to be 2.0 ng/day.
3.2. FOOD
In general, PAH found in food are present as a result of contamination
from a polluted environment or are formed during the cooking (pyrolysis)
process (Santodonato et a!., 1981; Fazio and Howard, 1983); minute amounts
of this chemical may also originate from geochemlcal or biosynthetlc sources
(Fazio and Howard, 1983).
The following benzo(gh1)perylene concentrations (In ppb) have been
reported for various foods (Santodonato et a!., 1981): corn oil (0.6),
sunflower oil (4.0), soybean oil (1.0), olive oil (0.9), peanut oil (0.9),
smoked herring (2.4), smoked cod (2.2), smoked mackerel (0.2-0.3), charcoal-
broiled steaks (6.7), barbecued ribs (4.7), smoked ham (1.4), barbecued beef
(4.3), smoked bologna (0.04-0.20), smoked mortadella (0.4), heavily smoked
bacon (3.0), charcoal-broiled hamburger (trace-14.9), broiled T-bone steak
(6.2-12.4) and heavily smoked ham (2.5-25.0).
Dennis et al. (1983) examined total-diet samples of food groups in
England and found the following mean benzo(ghi)perylene concentrations (In
vg/kg) in the various food groups: cereal (0.28), meat (0.05), fish
(0.12), oils and fats (1.26), fruit and sugar (0.06), vegetables
(0.06-0.08), beverages (0.01) and milk (0.01). Dennis et al. (1983) then
estimated the total benzo(gh1Jperylene dietary load 1n England to be 0.21
vg/person/day. Based on monitoring of total-diet samples collected In the
Netherlands, Vaessen et al. (1984) estimated the maximum food intake to be
0.9 yg/person/day.
0864p -14- 10/31/86
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3.3. INHALATION
Table 3-3 lists recent (1979-1983) U.S. ambient air monitoring data for
benzo(gh1)perylene; In general, the mean concentrations detected are <2.0
ng/m3. The average U.S. urban atmosphere 1n the early 1960s has been
reported to have had a concentration of ~8 ng/m3 (Santodonato et al.,
1981). In 1952-53, the airborne concentration of benzo(gh1)perylene 1n Los
Angeles, CA, was reported to be 21 ng/m3, which was slightly >3 times the
concentration 1n 1958-59 (Gordon and Bryan, 1973). These monitoring data
suggest that the ambient atmospheric load of benzo(gh1Jperylene has been
generally decreasing over the past 30 years. This decrease may be a result
of decreases 1n coal consumption for residential heating and Industrial
uses, restrictions on open burning, and Improved efficiency for stationary
Incineration and combustion sources with Improvements of pollution control.
The higher atmospheric levels of benzo(gh1 )perylene 1n wintertime vs.
summertime air 1n New Jersey (see Table 3-3) may be a reflection of an
Increased use of fossil fuel combustion for heating purposes.
Assuming an average ambient air benzo(gh1Jperylene concentration of -0.5
ng/m3 (from Table 3-3) and a human air Intake of 20 ma/day, the average
dally Intake can be estimated to be 10 ng. Matsumoto and Kashlmoto (1985)
used Japanese monitoring data to estimate an average dally Intake of 27 ng.
In general, PAH are emitted to the atmosphere by the combustion of
fossil fuels (oil, coal), by vehicular exhausts, by open burning (agricul-
tural burning, forest fires, structural fires, refuse burning) and by the
burning of wood, especially for residential heating (NRC, 1983).
Benzo(gh1)perylene has been Identified 1n mainstream cigarette smoke
1-39 ng/c1garette), sldestream cigarette smoke (98 ng/clgarette), smoke-
filled rooms (17 ng/m3) and mainstream marijuana smoke (0.7 ng/c1garette)
(IARC, 1983).
0864p -15- 05/15/87
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TABLE 3-3
U.S. A1r Monitoring Data for Benzo(gh1)perylene (1979-1983)
Concentration
(ng/m3)
Location
Sampling
Date
Reference
0.09-0.56 (mean)
0.09-3
0.02
0.11-1.0 (average)
2.0 (average)
0.59-2.74 (mean)
0.02-0.62 (mean)
0.20-1.31 (mean)
1.0 (mean)
four cities, New Jersey summer 1981
Columbia, SC 1981-1982
rural South Carolina 1982
three sites, 1979
Washington State
Portland, OR 1984
four cities. New Jersey winter 1982
summer 1982
winter 1983
Waterbury, VT
winter 1982
Harkov et al.,
1984
Keller and
Bldleman, 1984
Prahl et al.,
1984
Llgockl
et al., 1985
Greenberg
et al.. 1985
Sexton et al.,
1985
0864p
-16-
10/31/86
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3.4. DERMAL
Pertinent data regarding dermal exposure to benzo(gh1)perylene could not
be located In the available literature as cited 1n the Appendix.
3.5. SUMMARY
Human exposure to benzo(gh1)perylene occurs primarily through the Inha-
lation of tobacco smoke and polluted air, and by the 1ngest1on of contami-
nated food and water (IARC, 1983). It occurs ubiquitously In products of
Incomplete combustion and 1n coal tar, and 1s a component of gasoline and
dlesel engine exhaust; 1t also occurs naturally 1n crude oils (IARC, 1983).
It has been widely detected In drinking water, surface water, groundwater,
rainwater and aquatic sediments (see Tables 3-1 and 3-2), In many foods
(Santodonato et a!., 1981; Dennis et al., 1983) and 1n the ambient atmo-
sphere (see Table 3-3). The average dietary Intake of benzo(gh1)perylene 1n
England has been estimated to be 0.21 yg/day (Dennis et al., 1983); the
average adult Intake 1n the United States from drinking water has been
estimated to be 2.0 ng/day, while the Inhalation Intake has been estimated
to be 10 ng/day. Its presence 1n food 1s a result of contamination from a
polluted environment and formation during cooking by pyrolysls (Santodonato
et al., 1981; Fazio and Howard, 1983). Its concentration 1n the ambient
atmosphere In the United States has apparently been decreasing over the last
30 years. The ambient air concentration of benzo(gh1)perylene 1s expected
to be higher during winter than summer, apparently because of the burning of
fossil fuel for heating during winter months (Greenberg et al., 1985).
0864p -17- 10/31/86
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4. PHARMACOKINETICS
Pertinent data regarding the gastrointestinal or pulmonary absorption of
benzo(gh1)perylene could not be located 1n the available literature as cited
in the Appendix. Data from other structurally-related PAH suggest, however,
that benzo(gh1)perylene 1s absorbed readily from the gastrointestinal tract
(Rees et al., 1971) and lungs (Kotln et al., 1969; Va1n1o et a!., 1976). In
general, PAH are highly I1p1d soluble and can pass across epithelial
membranes (U.S. EPA, 1980).
Pertinent data regarding the distribution, metabolism or excretion of
benzo(gh1)perylene could not be located 1n the available literature as cited
1n the Appendix.
0864p -18- 10/31/86
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5. EFFECTS
5.1. CARCINOGENICITY
Pertinent data regarding the tumorlgenlc potential of orally-adminis-
tered benzo{gh1)perylene could not be located In the available literature as
cited In the Appendix.
Mixtures of heated beeswax and tMoctanoln (1:1) containing 0.16, 0.83
or 4.15 mg benzo(gh1Jperylene (98.554 pure) were Injected Into the left lung
of groups of 34 or 35 female Osborne-Mendel rats after thoracotomy (Deutsch-
Wenzel et a!., 1983). Additional groups of 35 rats served as vehicle,
untreated and positive [0.1, 0.3 or 1.0 mg benzo(a)pyrene] controls. All
rats were necropsled at the time of natural death or when sacrificed at
morlbundHy, but hlstologlcal examinations were limited to the lungs and
organs showing gross abnormalities. Median survival times were 109, 114,
106, 104 and 118 weeks In the low-, middle- and high-dose treated groups,
the vehicle control and the untreated control groups, respectively.
Squamous cell carcinomas of the lung occurred 1n 0/35, 1/35 and 4/34 mice In
the low-, mid- and high-dose treated groups, respectively. Lung tumors were
not observed 1n either the vehicle or untreated control groups, but car-
cinomas occurred at dose-related Incidences 1n the positive controls (4/35,
21/35, 33/35). The low Incidences of lung tumors 1n the treated mice were
considered to Indicate a weak effect of benzo(gh1)perylene 1n this assay,
but It was noted that the response might have been caused by Impurities In
the 98.5% pure product that was tested. The results of this study should
therefore be regarded as Inconclusive.
Benzo(gh1 Jperylene has also been tested for tumorlgenldty In mice In
skin application studies Involving up to 3 times/week treatment for 12
months (Lljlncky and Saff1ott1, 1965; Van Duuren et al., 1970; Van Duuren
and Goldschmldt, 1976; Muller, 1968; Hoffmann and Wynder, 1966); 1n skin
0864p -19- 05/15/87
-------
Initiation-promotion studies using croton oil as a promoter (Hoffman and
Wynder, 1966) and PMA as a promoter (Van Duuren et a!., 1970); and by
bimonthly subcutaneous Injections for 5 or 6 months (Muller, 1968). The
results of these studies were negative (Table 5-1). Although 1t Is
difficult to evaluate carcinogenic potential solely on the basis of results
from these types of assays, H should be noted that positive responses were
obtained 1n many of the studies with PAH of known carclnogenldty (e.g.,
benzo(a)pyrene). Enhancement of the dermal carclnogenldty of benzo(a)-
pyrene by simultaneous application of benzo(gh1)perylene has been reported
In mice (Goldschmldt et al., 1973; Van Duuren et al., 1973; Van Duuren and
Goldschmldt, 1976), Indicating possible cocarc1nogen1c1ty of benzo(ghl)-
perylene.
5.2. HUTAGENICITY
Benzo(gh1)perylene has been reported to produce mutation to hlstldlne
Independence 1n Salmonella typhlmurlum strains TA98, TA100, TA1537 and
TA1538 when assayed In the presence, but not the absence, of exogenous
metabolic activation preparations (Andrews et al., 1978; Mossanda et al.,
1979; Salamone et al., 1979). Benzo(gh1)perylene also produced mutation to
8-azoguanlne resistance 1n S. typhlmurlum TM677 1n the presence of
activation preparations (Kaden et al., 1979). These studies are summa-
rized 1n Table 5-2.
Intraperltoneal Injection of 30 mg/kg benzo(gh1)perylene Into hamsters
(strain unspecified) on day 10 of gestation did not Induce neoplastlc trans-
formation In embryo cells that were first cultured on day 13 (Quarles et
al., 1979) (see Table 5-2). Additional Information regarding the genotoxlc
potential of benzo(gh1)perylene could not be located In the available
literature as cited In the Appendix.
0864p -20- 07/21/87
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5.3. TERATOGENICITY
Weaver and Gibson (1979) exposed pregnant rats to graded airborne
concentrations of uncharacterlzed oil shale containing PAH, including benzo-
(ghi)perylene, on days 6-15 of gestation. No treatment-related teratogenic
effects were observed during examination of fetuses obtained by Caesarean
section on day 20 of gestation. Determination of a benzo(ghi)perylene
specific effect Is precluded, however, by the uncharacterlzed nature of the
test material.
5.4. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of benzo(ghl)-
perylene could not be located 1n the available literature as cited in the
Appendix.
5.5. CHRONIC AND SUBCHRONIC TOXICITY
Pertinent data regarding chronic and subchronlc toxiclty of benzo(ghl)-
perylene could not be located 1n the available literature as cited In the
Appendix.
5.6. OTHER RELEVANT INFORMATION
Other relevant information regarding the toxiclty of benzo(gh1 )perylene
could not be located In the available literature as cited 1n the Appendix.
5.7. SUMMARY
Single Intrapulmonary Injections of 0.16, 0.83 or 4.15 mg benzo(ghi)-
perylene 1n beeswax-trloctanoln mixture Into groups of 34 or 35 rats
produced a low Incidence (4/34) of lung squamous cell carcinomas In the
high-dose group after lifetime observation (Deutsch-Wenzel et al., 1983).
Lung tumors did not occur in untreated or vehicle treated controls, but IARC
(1983) indicated that the tumors in the treated group may be attributable to
Impurities in the test product, which was 98.5% pure.
0864p -24- 10/31/86
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Tumor 1 genIcHy of benzo(gh1 )perylene was not demonstrated 1n mice In
skin application studies Involving up to 3 times/week treatment for 12
months (Lijlnsky and Safflotti, 1965; Van Duuren et al., 1970; Van Duuren
and Goldschmidt, 1976; Huller, 1968; Hoffmann and Wynder, 1966); 1n skin
Initiation-promotion studies using croton oil as a promoter (Hoffman and
Wynder, 1966) and PMA as a promoter (Van Duuren et al., 1970); and by
bimonthly subcutaneous Injections for 5 or 6 months (Muller, 1968).
Enhancement of the dermal cardnogenldty of benzo(a)pyrene by simultaneous
application of benzo(gh1)perylene has been reported 1n mice (Goldschmidt et
al., 1973; Van Duuren et al., 1973; Van Duuren and Goldschmidt, 1976),
Indicating possible cocarclnogenlc-lty of benzo(gh1 )perylene.
Benzo(gh1)perylene was mutagenlc to £. typhimurlum strains TA98, TA100,
TA1537 and TA1538 (Andrews et al., 1978; Mossanda et al., 1979; Salamone et
al., 1979) and TM677 (Kaden et al., 1979) when assayed 1n the presence of
exogenous metabolic activation preparations. Intraperltoneal Injection of
benzo(gh1Jperylene Into hamsters on day 10 of gestation did not Induce
transformations 1n the embryo cells (Quarles et al., 1979).
Pertinent data regarding toxic, teratogenlc or other reproductive
effects of benzo(gh1)perylene could not be located 1n the available
literature as dted 1n the Appendix.
0864p -25- 05/15/87
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6. AQUATIC TOXICITY
6.1. ACUTE
Pertinent data regarding the acute toxldty of benzo(ghi )perylene to
aquatic organisms could not be located in the available literature as dted
1n the Appendix.
6.2. CHRONIC
Pertinent data regarding the chronic toxicity of benzo(gh1)perylene to
aquatic organisms could not be located in the available literature as cited
in the Appendix.
6.3. PLANTS
Pertinent data regarding the effects of benzo{gh1Jperylene on aquatic
plants could not be located In the available literature as cited in the
Appendix.
6.4. RESIDUES
The only information regarding benzo(gh1Jperylene and aquatic organisms
consisted of bioconcentratlon and residue monitoring data. Obana et al.
(1983) reported BCF values of 1000-1400 for short-necked clams. Tapes
japonica. exposed to 0.06-0.13 yg/8. for 1-7 days. Tsuji et al. (1985)
found that clams (unspecified species) collected in Japanese waters con-
tained benzo(gh1)perylene residues at concentrations of 0.23-0.95 yg/kg.
Knutzen and Sortland (1982) reported the following levels (vg/kg dry
weight) in species collected from polluted areas in Norway: mussel, Hytelis
edulis. trace-87; periwinkle, Littorina littorea. 0.5; limpet. Patella
yulgata. not detected; sponge, Halichondria panicea. 23; toothed wrack,
Fucus serratus. 79; Ceramium rubrum. 4. Maccubbin et al. (1985) found that
the stomach contents of white suckers, Catostomus commersoni. from eastern
Lake Erie contained 2-14 ng/g benzo(ghiJperylene. Malins et al. (1985)
0864p -26- 10/31/86
-------
reported that stomach contents of English sole, Parophrys vetulus. collected
In Puget Sound contained 75 ng/g dry weight. Dunn and Fee (1979) found that
lobsters, Homarus amerlcanus. caught 1n waters off eastern Canada contained
benzo(gh1Jperylene at an average concentration of 0.19 ng/g; however, It 1s
a common practice for lobsters to be kept 1n Impoundments for weeks or
months before being sent to market. Frequently, these Impoundments are made
of creosote-treated wood, which would be a source of benzo(gh1Jperylene and
other PAH. Dunn and Fee (1979) found that benzo(gh1 )perylene residues of
Impounded lobsters averaged 51 ng/g, a 250-fold Increase over freshly caught
lobsters. This may constitute a possible source of human exposure to benzo-
(gh1Jperylene.
6.5. SUMMARY
Pertinent data regarding the tox1c1ty of benzo(gh1)perylene to aquatic
organisms could not be located In the available literature as cited In the
Appendix. Several studies reported data concerning residues In aquatic
organisms. The following data were reported for species that are commonly
eaten by humans: mussels from Norway, trace-87 ng/g (Knutzen and Sortland,
1982); clams from Japan, 0.23-0.95 ng/g (Tsujl et al., 1985); lobsters from
eastern Canada, 0.19 ng/g before Impoundment and 51 ng/g after Impoundment
(Dunn and Fee, 1979). Obana et al. (1983) reported BCF values of 1000-1400
for short-necked clams, T. japonlca. exposed to 0.06-0.13 vg/8. for 1-7
days.
0864p -27- 10/31/86
-------
7. EXISTING GUIDELINES AND STANDARDS
7.1. HUHAN
Exposure criteria and TLVs have been developed for PAH as a class, as
well as for several Individual PAH. OSHA has set an 8-hour TWA concentra-
tion limit of 0.2 mg/m3 for the benzene-soluble fraction of coal tar pitch
volatiles (anthracene, benzo(a)pyrene, phenanthrene, acrldlne, chrysene,
pyrene) (OSHA, 1985). NIOSH (1977) recommended a concentration limit for
coal tar, coal tar pitch, creosote and mixtures of these substances of 0.1
mg/m3 of the cyclohexane-extractable fraction of the sample, determined as
a 10-hour TWA. NIOSH (1977) concluded that these specific coal tar
products, as well as coke oven emissions, are carcinogenic and can Increase
the risk of lung and skin cancer 1n workers. NIOSH (1977) also recommended
a celling limit for exposure to asphalt fumes of 5 mg airborne partlcu-
lates/m3 of air.
Environmental quality criteria, which specify concentration limits
Intended to protect humans against adverse health effects, have been recom-
mended for PAH 1n ambient water. U.S. EPA (1980) recommended a concentra-
tion limit of 28 ng/l for the sum of all carcinogenic PAH 1n ambient
water. This value 1s based on a mathematical extrapolation of the results
from studies with mice treated orally with benzo(a)pyrene and acknowledges
the conservative assumption that all carcinogenic PAH are equal 1n potency
to benzo(a)pyrene. On the basis of the animal bloassay data, dally consump-
tion of water containing 28 ng/8. of carcinogenic PAH over an entire life-
time 1s estimated to keep the lifetime risk of cancer development <1 chance
In 100,000.
0864p -28- 10/31/86
-------
U.S. EPA has not recommended an ambient water quality criterion for
noncardnogenlc PAH as a class. U.S. EPA (1980) acknowledged that data
suitable for quantitative risk assessment of noncardnogenlc PAH are essen-
tially nonexistent.
7.2. AQUATIC
Guidelines and standards for the protection of aquatic biota from the
effects of benzo(gh1)perylene, 1n particular, could not be located In the
available literature as cited 1n the Appendix; however, U.S. EPA (1980)
noted that acute toxldty to saltwater aquatic life occurred at concentra-
tions as low as 300 yg/s, of PAH 1n general, and would occur at lower
concentrations In species more sensitive than those tested. U.S. EPA (1980)
concluded that the database at that time was Inadequate to generalize about
chronic or acute toxldty to freshwater organisms.
0864p -29- 10/31/86
-------
8. RISK ASSESSHENT
Single intrapulmonary injections of 0.16, 0.83 or 4.15 mg benzo(ghi)-
perylene in beeswax-trioctanoln mixture into groups of 34 or 35 rats
produced a low incidence (4/34) of lung squamous cell carcinomas in the
high-dose group after lifetime observation (Deutsch-Wenzel et a!., 1983).
Lung tumors did not occur in untreated or vehicle treated controls, but IARC
(1983) indicated that the tumors in the treated group may be attributable to
impurities in the test product, which was 98.5% pure.
Tumorigenicity of benzo(ghi)perylene was not demonstrated in mice in
skin application studies involving up to 3 times/week treatment for 12
months (Lijinsky and Saffiotti, 1965; Van Duuren et a!., 1970; Van Duuren
and Goldschmidt, 1976; Muller, 1968; Hoffmann and Wynder, 1966); In skin
initiation-promotion studies using croton oil as a promoter (Hoffman and
Wynder, 1966) and PMA as a promoter (Van Duuren et al., 1970); or by
bimonthly subcutaneous injections for 5 or 6 months (Muller, 1968) (see
Table 5-1). Enhancement of the dermal carcinogenicity of benzo(a)pyrene by
simultaneous application of benzo(ghi)perylene has been reported in mice
(Goldschmidt et al., 1973; Van Duuren et al., 1973; Van Duuren and Gold-
schmidt, 1976), indicating possible cocarcinogenicity of benzo(ghi)perylene.
Benzo(ghiJperylene was mutagenic to S. typhimurium strains TA98, TA100,
TA1537 and TA1538 (Andrews et al., 1978; Mossanda et al., 1979; Salamone et
al., 1979) and TM677 (Kaden et al., 1979) when assayed in the presence of
exogenous metabolic activation preparations. Intraperitoneal injection of
benzo(gh1)perylene into hamsters on day 10 of gestation did not Induce
transformations 1n the embryo cells (Quarles et al., 1979)
0864p -30- 05/15/87
-------
Although some lung tumors occurred In the Intrapulmonary Injection study
with rats (Oeutsch-Wenzel et a!., 1983), possible cocarclnogenlcHy with
benzo(a)pyrene on mouse skin occurred, and mutagenldty 1n different strains
of S. typhlmurlum was demonstrated, the available data are Inadequate for
evaluation of cardnogenlclty of benzo(gh1Jperylene. The Intrapulmonary
injection study 1s limited by the single dose treatment schedule, unnatural
route of respiratory exposure, possibility of Impurities 1n the test
compound and lack of corroborating data. The mutagenldty data are limited
by a lack of data In other test systems. A cocardnogen cannot be regarded
as a complete or procarclnogen In the absence of supporting evidence.
Evaluation of the carclnogenlclty of benzo(gh1Jperylene 1s further limited
by the lack of studies employing oral or Inhalation routes of exposure.
Pertinent data regarding toxic, teratogenlc or other reproductive
effects of benzo(gh1)perylene could not be located In the available Utera-
*
ture as cited In the Appendix. This lack of data precludes calculation of
an RfD (formerly called ADI) for benzo(gh1)perylene.
0864p -31- 10/31/86
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9. REPORTABLE QUANTITIES
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC TOXICITY
Pertinent data regarding the toxic or reproductive effects of benzo-
(gh1)perylene could not be located 1n the available literature as cited 1n
the Appendix. Weaver and Gibson (1979) exposed pregnant rats to graded air-
borne concentrations of uncharacteMzed oil shale containing PAH, Including
benzo(ghiJperylene, on days 6-15 of gestation. No treatment-related
teratogenic effects were observed during examination of fetuses obtained by
Caesarean section on day 20 of gestation. Calculation of an RQ from this
study is precluded (Table 9-1) by the uncharacterlzed nature of the test
material (U.S. EPA, 1983).
9.2. WEIGHT OF EVIDENCE AND POTENCY FACTOR (F=1/ED1Q) FOR CARCINOGENICITY
Single Intrapulmonary injections of 0.16, 0.83 or 4.15 mg benzo(ghi)-
perylene in beeswax-trloctanoln mixture into groups of 34 or 35 rats
produced a low incidence' 14/34) of lung squamous cell carcinomas in the
high-dose group after lifetime observation (Deutsch-Wenzel et a!., 1983).
Lung tumors did not occur in untreated or vehicle treated controls, but IARC
(1983) indicated that the tumors in the treated group may be attributable to
Impurities in the test product, which was 98.5% pure.
Tumorlgenicity of benzo(ghiJperylene was not demonstrated in mice in
skin application studies involving treatment up to 3 times/week for 12
months (Lijinsky and Saffiotti, 1965; Van Duuren et a!., 1970; Van Duuren
and Goldschmidt, 1976; Muller, 1968; Hoffmann and Wynder, 1966); in skin
initiation-promotion studies using croton oil as a promoter (Hoffman and
Wynder, 1966) and PMA as a promoter (Van Duuren et a!., 1970); or by
bimonthly subcutaneous injections for 5 or 6 months (Muller, 1968) (see
Table 5-1). Enhancement of the dermal cardnogenicity of benzo(a)pyrene by
0864p -32- 05/15/87
-------
TABLE 9-1
Benzo(gh1Jperylene
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route:
Dose:
Effect:
Reference:
RVd:
RVe:
Composite Score:
RQ: Data are not sufficient to derive an RQ.
0864p -33- 10/31/86
-------
simultaneous application of benzo(gh1Jperylene has been reported In mice
(Goldschmldt et a!., 1973; Van Duuren et al., 1973; Van Duuren and Gold-
schmldt, 1976), Indicating possible cocarcinogenlcity of benzo(ghiJperylene.
Benzo(ghiJperylene was mutagenlc to S_. typhlmurium strains TA98, TA100,
TA1537 and TA1538 (Andrews et al., 1978; Hossanda et al., 1979; Salamone et
al., 1979) and TM677 (Kaden et al., 1979) when assayed in the presence of
exogenous metabolic activation preparations. Intraperitoneal injection of
benzo(ghi)perylene Into hamsters on day 10 of gestation did not Induce
transformations 1n the embryo cells (Quarles et al., 1979)
Although some lung tumors occurred In the intrapulmonary injection study
with rats (Deutsch-Henzel et al., 1983), possible cocarcinogenlcity with
benzo(ghi)perylene on mouse skin occurred, and mutagenlcity 1n different
strains of S. typhlmurium was demonstrated, the available data are
Inadequate for evaluation of the carclnogenidty of benzo(gh1Jperylene. The
Intrapulmonary Injection study is limited by the single dose treatment
schedule, unnatural route of respiratory exposure, possibility of impurities
In the test compound and lack of corroborating data. The mutagenlcity data
are limited by a lack of data in other test systems. A cocardnogen cannot
be regarded as a complete or procarcinogen in the absence of supporting
evidence. Evaluation of the cardnogenicHy of benzo{gh1 )perylene 1s
further limited by the lack of studies employing oral or inhalation routes
of exposure.
IARC (1983) reported that there was Insufficient evidence regarding the
carcinogenic risk to humans and experimental animals associated with oral or
Inhalation exposure to benzo(gh1Jperylene. Applying the criteria for
evaluation of the overall weight of evidence for the carcinogenic potential
for humans proposed by the Carcinogen Assessment Group of the U.S. EPA (U.S.
0864p -34- 10/31/86
-------
EPA, 1984), benzo(gh1Jperylene 1s most appropriately designated a Group 0,
Not Classified chemical. Direct hazard ranking of benzo(gh1Jperylene under
CERCLA Is therefore not possible.
0864p -35- 10/31/86
-------
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Mabey, W.R., J.H. Smith, R.T. Podoll, et al. 1981. Aquatic Fate Process
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Maccubbin, A.E., P. Black, L. Trzedak and J.J. Black. 1985. Evidence for
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Environ. Contam.-Toxlcol. 34(6): 876-882.
Mallns, D.C., M.M. Krahn, D.W. Brown, et al. 1985. Toxic chemicals In
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»
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Van Duuren, B.L., C. Katz and B.M. Goldschmldt. 1973. Brief communication:
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tioning of polycycllc aromatic hydrocarbon In coal coking wastewaters.
Water Res. 18: 795-809.
Weaver, N.K. and R.L. Gibson. 1979. The U.S. oil shale Industry: A health
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Yalkowsky, S.H. and S.C. Valvanl. 1979. Solubilities and partitioning.
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24: 127-129.
Yamasakl, H., K. Kuwata and H. Miyamoto. 1982. Effects of ambient tempera-
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Techno!. 16: 189-194.
Zoeteman, B.C.J., E. Degreef and F.J.3. Brlnkman. 1981. Persistence of
organic contaminants 1n ground water. Lessons from soil pollution Incidents
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0864p -45- 05/15/87
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APPENDIX
LITERATURE SEARCHED
This profile 1s based on data Identified by computerized literature
searches of the following:
GLOBAL
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
CAS online STN International
TOXLINE
TOXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted In April, 1986. In addition, hand searches
were made of Chemical Abstracts (Collective Indices 6 and 7), and the
following secondary sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyg1en1sts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyg1en1sts).
1985-1986. TLVs: Threshold Limit Values for Chemical Substances
and Physical Agents 1n the Workroom Environment with Intended
Changes for 1985-1986. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2B. John WHey and
Sons, NY. p. 2879-3816.
0864p -46- 05/15/87
-------
Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
Grayson, H. and D. Eckroth, Ed. 1978-1983. K1rk-0thmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. WHO, IARC, Lyons, France.
Jaber, H.M., W.R. Mabey, S.T. Liu, T.W. Chow and H.L. Johnson.
1984. Data aqulsHlon for environmental transport and fate screen-
Ing for compounds of Interest 1n the Office of Solid Waste. EPA
600/6-84-010. NTIS PB84-243906. SRI International, Menlo Park, CA.
NTP (National Toxicology Program). 1986. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, N.I. 1979. Dangerous Properties of Industrial Materials, 5th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1984. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1985. Status Report on Rebuttable Presumption Against
Registration (RPAR) or Special Review Process. Registration Stan-
dards and the Data Call 1n Programs. Office of Pesticide Programs,
Washington, DC.
U.S. EPA. 1985. CSB Existing Chemical Assessment Tracking System.
Name and CAS Number Ordered Indexes. Office of Toxic Substances,
Washington, DC.
USITC (U.S. International Trade Commission). 1983. Synthetic
Organic Chemicals. U.S. Production and Sales, 1982, USITC Publ.
1422, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0864p -47- 05/15/87
U.S. Environmental Protection Agency
Region V, Library
230 South Dearborn Street '
Chicago, Illinois 60604
-------
In addition, approximately 30 compendia of aquatic toxlclty data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxlclty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxlclty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, F1sh and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, D. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0864p -48- 05/15/87
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