United States
Environmental Protection
1=1 m m Agency
EPA/690/R-02/009F
Final
1-31-2002
Provisional Peer Reviewed Toxicity Values for
Indeno[l ,2,3-cd)pyrene
(CASRN 193-39-5)
Derivation of an Oral RfD
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

-------
Acronyms and Abbreviations
bw	body weight
cc	cubic centimeters
CD	Caesarean Delivered
CERCLA	Comprehensive Environmental Response, Compensation and Liability Act
of 1980
CNS	central nervous system
cu.m	cubic meter
DWEL	Drinking Water Equivalent Level
FEL	frank-effect level
FIFRA	Federal Insecticide, Fungicide, and Rodenticide Act
g	grams
GI	gastrointestinal
HEC	human equivalent concentration
Hgb	hemoglobin
i.m.	intramuscular
i.p.	intraperitoneal
IRIS	Integrated Risk Information System
IUR	inhalation unit risk
i.v.	intravenous
kg	kilogram
L	liter
LEL	lowest-effect level
LOAEL	lowest-observed-adverse-effect level
LOAEL(ADJ)	LOAEL adjusted to continuous exposure duration
LOAEL(HEC)	LOAEL adjusted for dosimetric differences across species to a human
m	meter
MCL	maximum contaminant level
MCLG	maximum contaminant level goal
MF	modifying factor
mg	milligram
mg/kg	milligrams per kilogram
mg/L	milligrams per liter
MRL	minimal risk level
MTD	maximum tolerated dose
MTL	median threshold limit
1

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NAAQS
National Ambient Air Quality Standards
NOAEL
no-observed-adverse-effect level
NOAEL(ADJ)
NOAEL adjusted to continuous exposure duration
NOAEL(HEC)
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-observed-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional inhalation reference concentration
p-RfD
provisional oral reference dose
PBPK
physiologically based pharmacokinetic
PPb
parts per billion
ppm
parts per million
PPRTV
Provisional Peer Reviewed Toxicity Value
RBC
red blood cell(s)
RCRA
Resource Conservation and Recovery Act
RDDR
Regional deposited dose ratio (for the indicated lung region)
REL
relative exposure level
RfC
inhalation reference concentration
RfD
oral reference dose
RGDR
Regional gas dose ratio (for the indicated lung region)
s.c.
subcutaneous
SCE
sister chromatid exchange
SDWA
Safe Drinking Water Act
sq.cm.
square centimeters
TSCA
Toxic Substances Control Act
UF
uncertainty factor

microgram
(.imol
micromoles
voc
volatile organic compound
11

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1-31-2002
PROVISIONAL PEER REVIEWED TOXICITY VALUES FOR
INDENO(l,2,3-cd)PYRENE (CASRN 193-39-5)
Derivation of an Oral RfD
Background
On December 5, 2003, the U.S. Environmental Protection Agency's (EPA's) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1.	EPA's Integrated Risk Information System (IRIS).
2.	Provisional Peer-Reviewed Toxicity Values (PPRTV) used in EPA's Superfund
Program.
3.	Other (peer-reviewed) toxicity values, including:
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in EPA's Integrated Risk Information System (IRIS). PPRTVs are
developed according to a Standard Operating Procedure (SOP) and are derived after a review of
the relevant scientific literature using the same methods, sources of data, and Agency guidance
for value derivation generally used by the EPA IRIS Program. All provisional toxicity values
receive internal review by two EPA scientists and external peer review by three independently
selected scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multi-program consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all EPA programs, while PPRTVs are developed specifically for
the Superfund Program.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a five-year basis and updated into the active database. Once an IRIS
value for a specific chemical becomes available for Agency review, the analogous PPRTV for
that same chemical is retired. It should also be noted that some PPRTV manuscripts conclude
that a PPRTV cannot be derived based on inadequate data.
1

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1-31-2002
Disclaimers
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and RCRA program offices are advised to carefully review the information provided
in this document to ensure that the PPRTVs used are appropriate for the types of exposures and
circumstances at the Superfund site or RCRA facility in question. PPRTVs are periodically
updated; therefore, users should ensure that the values contained in the PPRTV are current at the
time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV manuscript and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center for OSRTI. Other EPA programs or external parties who may
choose of their own initiative to use these PPRTVs are advised that Superfund resources will not
generally be used to respond to challenges of PPRTVs used in a context outside of the Superfund
Program.
Questions Regarding PPRTVs
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
INTRODUCTION
An RfD for indeno(l,2,3-cd)pyrene (IP) is not available on IRIS (U.S. EPA, 2001), in the
HE AST (U.S. EPA, 1997), or in the Drinking Water Regulations and Health Advisory list (U.S.
EPA, 2000), and the chemical was never reviewed by the RfD/RfC Work Group (U.S. EPA,
1995). A 1984 HEA for Polycyclic Aromatic Hydrocarbons (PAHs) did not derive an RfD for IP
because the chemical was designated a probable human carcinogen, and noncancer toxicity
values were not derived for carcinogens at that time (U.S. EPA, 1984). A Drinking Water
Criteria Document for Polycyclic Aromatic Hydrocarbons (PAHs) (U.S. EPA, 1990) declined to
derive an RfD for IP due to lack of suitable data. No other pertinent EPA documents were
located in the CARA list (U.S. EPA, 1991, 1994). The ATSDR Toxicological Profile for PAHs
(ATSDR, 1995) declined to derive oral MRLs for IP due to lack of suitable data. Other review
documents used were IARC (1973, 1983, 1987) and WHO (1997). The NTP (2001)
management status report was checked for relevant studies. Literature searches of the following
databases were conducted from 1989 to December 2000 for relevant studies: TOXLINE,
2

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1-31-2002
MEDLINE, TSCATS, GENETOX, HSDB, CANCERLIT, CCRIS, EMIC/EMICBACK,
DART/ETICBACK, and RTECS.
REVIEW OF THE PERTINENT LITERATURE
Human Studies
The available reviews (ATSDR, 1995; IARC, 1983, 1987; U.S. EPA, 1984, 1990)
reported no data regarding the toxicity of IP to humans following oral exposure. No relevant
data were found in the literature search.
Animal Studies
No oral animal studies of IP suitable for derivation of an RfD were located in either the
literature search or available reviews (ATSDR, 1995; IARC, 1983, 1987; U.S. EPA, 1984, 1990).
FEASIBILITY OF DERIVING A PROVISIONAL RfD FOR
INDENO(l,2,3-cd)PYRENE
A provisional RfD for IP cannot be derived because of the lack of human and animal oral
data.
REFERENCES
ATSDR (Agency for Toxic Substances and Disease Registry). 1995. Toxicological Profile for
Polycyclic Aromatic Hydrocarbons (PAHs). U.S. Department of Health and Human Services,
Public Health Service, Atlanta, GA.
IARC (International Agency for Research on Cancer). 1973. IARC Monographs on the
Evaluation of Carcinogenic Risk of the Chemical to Man. Certain Polycyclic Aromatic
Hydrocarbons and Heterocyclic Compounds. Vol. 3, p. 45-68.
IARC (International Agency for Research on Cancer). 1983. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans. Polynuclear Aromatic
Compounds. Part 1. Chemical, Environmental and Experimental Data, Vol. 32,
p. 135.
IARC (International Agency for Research on Cancer). 1987. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans. Suppl. 7, p. 58.
3

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1-31-2002
NTP (National Toxicology Program). 2001. Management Status Report. Examined April 4,
2001. Online, http://ntp-server.niehs.nili.gov/main pages/NTP ALL STDY PG.html
U.S. EPA. 1984. Health Effects Assessment for Polycyclic Aromatic Hydrocarbons (PAH).
Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial Response,
Washington, DC.
U.S. EPA. 1990. Drinking Water Criteria Document for Polycyclic Aromatic Hydrocarbons
(PAHs). Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking Water, Washington,
DC.
U.S. EPA. 1991. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. April.
U.S. EPA. 1994. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. December.
U.S. EPA. 1995. Monthly status report of RfD/RfC and CRAVE Work Groups (As of
09/01/95). Office of Research and Development, National Center for Environmental
Assessment, Cincinnati, OH.
U.S. EPA. 1997. Health Effects Assessment Summary Tables (HEAST). FY-1997 Update.
Prepared by the Office of Research and Development, National Center for Environmental
Assessment, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington,
DC. July. EPA/540/R-97/036. NTIS PB 97-921199.
U.S. EPA. 2000. Drinking Water Regulations and Health Advisories. Office of Water,
Washington, DC. Examined April 4, 2001. Online.
http://www.epa. gov/ ost/drinking/ standards/
U.S. EPA. 2001. Integrated Risk Information System (IRIS). Office of Research and
Development, National Center for Environmental Assessment, Washington, DC. Examined
April 4, 2001. Online, http://www.epa.gov/iris/
WHO (World Health Organization). 1997. Environmental Health Criteria. 202: WHO (1997)
Non-heterocyclic polycyclic aromatic hydrocarbons. International Programme on Chemical
Safety, Geneva, Switzerland.
4

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1-31-2002
Provisional Peer Reviewed Toxicity Values for
Indeno[l,2,3-cd]pyrene
(CASRN 193-39-5)
Derivation of an Oral Slope Factor
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

-------
Acronyms and Abbreviations
bw	body weight
cc	cubic centimeters
CD	Caesarean Delivered
CERCLA	Comprehensive Environmental Response, Compensation and Liability Act
of 1980
CNS	central nervous system
cu.m	cubic meter
DWEL	Drinking Water Equivalent Level
FEL	frank-effect level
FIFRA	Federal Insecticide, Fungicide, and Rodenticide Act
g	grams
GI	gastrointestinal
HEC	human equivalent concentration
Hgb	hemoglobin
i.m.	intramuscular
i.p.	intraperitoneal
IRIS	Integrated Risk Information System
IUR	inhalation unit risk
i.v.	intravenous
kg	kilogram
L	liter
LEL	lowest-effect level
LOAEL	lowest-observed-adverse-effect level
LOAEL(ADJ)	LOAEL adjusted to continuous exposure duration
LOAEL(HEC)	LOAEL adjusted for dosimetric differences across species to a human
m	meter
MCL	maximum contaminant level
MCLG	maximum contaminant level goal
MF	modifying factor
mg	milligram
mg/kg	milligrams per kilogram
mg/L	milligrams per liter
MRL	minimal risk level
MTD	maximum tolerated dose
MTL	median threshold limit
1

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NAAQS
National Ambient Air Quality Standards
NOAEL
no-observed-adverse-effect level
NOAEL(ADJ)
NOAEL adjusted to continuous exposure duration
NOAEL(HEC)
NOAEL adjusted for dosimetric differences across species to a human
NOEL
no-observed-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional inhalation reference concentration
p-RfD
provisional oral reference dose
PBPK
physiologically based pharmacokinetic
PPb
parts per billion
ppm
parts per million
PPRTV
Provisional Peer Reviewed Toxicity Value
RBC
red blood cell(s)
RCRA
Resource Conservation and Recovery Act
RDDR
Regional deposited dose ratio (for the indicated lung region)
REL
relative exposure level
RfC
inhalation reference concentration
RfD
oral reference dose
RGDR
Regional gas dose ratio (for the indicated lung region)
s.c.
subcutaneous
SCE
sister chromatid exchange
SDWA
Safe Drinking Water Act
sq.cm.
square centimeters
TSCA
Toxic Substances Control Act
UF
uncertainty factor

microgram
(.imol
micromoles
voc
volatile organic compound
11

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1-31-2002
PROVISIONAL PEER REVIEWED TOXICITY VALUES FOR
INDENO(l,2,3-cd)PYRENE (CASRN193-39-5)
Derivation of an Oral Slope Factor
Background
On December 5, 2003, the U.S. Environmental Protection Agency's (EPA's) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1.	EPA's Integrated Risk Information System (IRIS).
2.	Provisional Peer-Reviewed Toxicity Values (PPRTV) used in EPA's Superfund
Program.
3.	Other (peer-reviewed) toxicity values, including:
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in EPA's Integrated Risk Information System (IRIS). PPRTVs are
developed according to a Standard Operating Procedure (SOP) and are derived after a review of
the relevant scientific literature using the same methods, sources of data, and Agency guidance
for value derivation generally used by the EPA IRIS Program. All provisional toxicity values
receive internal review by two EPA scientists and external peer review by three independently
selected scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multi-program consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all EPA programs, while PPRTVs are developed specifically for
the Superfund Program.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a five-year basis and updated into the active database. Once an IRIS
value for a specific chemical becomes available for Agency review, the analogous PPRTV for
that same chemical is retired. It should also be noted that some PPRTV manuscripts conclude
that a PPRTV cannot be derived based on inadequate data.
1

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1-31-2002
Disclaimers
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and RCRA program offices are advised to carefully review the information provided
in this document to ensure that the PPRTVs used are appropriate for the types of exposures and
circumstances at the Superfund site or RCRA facility in question. PPRTVs are periodically
updated; therefore, users should ensure that the values contained in the PPRTV are current at the
time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV manuscript and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center for OSRTI. Other EPA programs or external parties who may
choose of their own initiative to use these PPRTVs are advised that Superfund resources will not
generally be used to respond to challenges of PPRTVs used in a context outside of the Superfund
Program.
Questions Regarding PPRTVs
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
INTRODUCTION
A carcinogenicity assessment for indeno(l,2,3-cd)pyrene (IP) is available on IRIS (U.S.
EPA, 2001). This assessment, verified 02/07/1990, was based on a Carcinogen Assessment of
Coke Oven Emissions (U.S. EPA, 1984a) and a Drinking Water Criteria Document for
Polycyclic Aromatic Hydrocarbons (PAHs) (U.S. EPA, 1990). IP was assigned to weight-of-
evidence Group B2, probable human carcinogen, based on increased incidences of epidermoid
carcinomas in a lung implantation study in rats (Deutsch-Wenzel et al., 1983), injection site
sarcomas in a subcutaneous injection assay in mice (Lacassagne et al., 1963) and skin tumors in
dermal application studies in mice (Hoffman and Wynder, 1966; Rice et al., 1985a, 1986).
Supporting data from genotoxicity tests included positive results for mutations in bacteria
(LaVoie et al., 1979; Hermann et al., 1980; Rice et al., 1985b) and human lymphocytes (Durant
et al., 1996). It was noted that IP is a component of mixtures that are known to produce cancer in
humans, although there are no human data that specifically link IP with human cancers.
2

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1-31-2002
However, due to the lack of adequate oral data for IP, an oral slope factor was not included on
IRIS (U.S. EPA, 2001).
U.S. EPA (1990) explored the use of a relative potency factor approach to derive slope
factors for IP and other PAHs from the existing slope factor for benzo[a]pyrene. However, the
CRAVE Work Group decided not to include relative potency information for PAHs on IRIS
because the methodology was not sufficiently developed, the underlying database had not been
sufficiently reviewed, and surrounding issues (e.g., route-to-route extrapolation) had not received
sufficient peer review (U.S. EPA, 1994a). The HEAST (U.S. EPA, 1997) reports the availability
of the weight-of-evidence assessment on IRIS, but contains no additional information. The
Drinking Water Standards and Health Advisories list (U.S. EPA, 2000) includes the cancer group
B2 designation for IP, but does not include additional cancer risk information. A Health Effects
Assessment for Polycyclic Aromatic Hydrocarbons (PAHs) (U.S. EPA, 1984b) was located, but
no relevant documents specific to IP were found in the CARA database (U.S. EPA, 1991,
1994b).
The International Agency for Research on Cancer (IARC, 1973, 1983, 1987) evaluated IP
for carcinogenicity and placed the chemical in Group 2B (possible human carcinogen), finding
that there is sufficient evidence that IP is carcinogenic to experimental animals and that the
chemical was mutagenic to Salmonella typhimurium in the presence of an exogenous metabolic
system. CalEPA derived an oral slope factor for IP, but it is based on a relative potency factor
approach (CalEPA, 1999). ACGIH (2000) has not assessed the carcinogenicity of IP. WHO
(1997), the ATSDR (1995) Toxicological Profile for Polycyclic Aromatic Hydrocarbons (PAHs)
and the NTP (2001) management status report were searched for relevant information. Literature
searches of the following databases were conducted from 1989 to December 2000 for relevant
studies: TOXLINE, MEDLINE, TSCATS, GENETOX, HSDB, CANCERLIT, CCRIS,
EMIC/EMICBACK, DART/ETICBACK, and RTECS.
REVIEW OF THE PERTINENT LITERATURE
Human Studies
Available reviews reported no human data regarding the carcinogenic potential of IP by
oral exposure (ATSDR, 1995; IARC, 1983, 1987; U.S. EPA, 1984b, 1990). No relevant data
were located in the literature search.
Animal Studies
No oral animal studies of IP suitable for derivation of an oral slope factor were located in
either the literature search or available reviews (ATSDR, 1995; IARC, 1983, 1987; U.S. EPA,
1984b, 1990).
3

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1-31-2002
Other Studies
A dose-related statistically significant increase in incidence of epidermoid carcinomas in
the lung and thorax occurred in rats receiving lifetime lung implants of IP (Deutsch-Wenzel et
al., 1983). Mice receiving intraperitoneal injections (580 (.ig/mouse) of IP did not exhibit a
significant tumor incidence (LaVoie et al., 1987). Lacassagne et al. (1963) reported 10 of 14
(71%) male mice and 1 of 14 (7%) female mice developed sarcomas following subcutaneous
injection of 0.6 mg of IP. Hoffman and Wynder (1966) reported that skin painting of mice with
IP at concentrations of 0.5 and 0.1% resulted in skin carcinomas in 5 of 20 (25%), and 3 of 20
(15%) animals, respectively, after 12 months of exposure. Similar treatment with IP at
concentrations of 0.05% and 0.01% produced no skin tumors in mice. Chronic topical
application of up to 9.2 (j,g of IP in acetone to the backs of mice for a lifetime resulted in no
tumor induction (Habs et al., 1980). Positive results for DNA adduct formation (Rice et al.,
1990) and tumor initiation with TPA promotion (Rice et al., 1985a, 1986, 1990) were obtained
with IP. Genotoxicity studies indicate positive results for mutations in bacteria (only in the
presence of metabolic activation) (LaVoie et al., 1979; Hermann et al., 1980; Rice et al., 1985b)
and human B-lymphoblastoid cells (Durant et al., 1996).
FEASIBILITY OF DERIVING A PROVISIONAL ORAL SLOPE FACTOR FOR
INDENO(l,2,3-cd)PYRENE
A provisional oral slope factor for IP cannot be derived because human and animal oral
cancer data are lacking.
REFERENCES
ACGIH (American Conference of Governmental Industrial Hygienists). 2000. TLVs® and
BEIs®: Threshold Limit Values for Chemical Substances and Physical Agents, Biological
Exposure Indices. Cincinnati, OH.
ATSDR (Agency for Toxic Substances and Disease Registry). 1995. Toxicological Profile for
Polycyclic Aromatic Hydrocarbons (PAHs). U.S. Department of Health and Human Services,
Public Health Service, Atlanta, GA.
CalEPA (California Environmental Protection Agency). 1999. Air Toxics Hot Spots Program
Risk Assessment Guidelines. Part II: Technical Support Document for Describing Available
Cancer Potency Factors. April. Office of Environmental Health Hazard Assessment. Online.
http ://www. oehha. ca. gov/air/cancer guide/hsca2 .html
4

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1-31-2002
Deutsch-Wenzel, R., H. Brune, G. Grimmer et al. 1983. Experimental studies in rat lungs on the
carcinogenicity and dose-response relationships of eight frequently occurring environmental
polycyclic aromatic hydrocarbons. J. Natl. Cancer Inst.
71: 539-544. (Cited in ATSDR, 1995)
Durant J.L., W.F. Busby Jr., A.L. Lafleur et al. 1996. Human cell mutagenicity of oxygenated,
nitrated and unsubstituted polycyclic aromatic hydrocarbons associated with urban aerosols.
Mutat. Res. 371: 123-157.
Habs, M., D. Schmahi and J. Misfeld. 1980. Local carciongenicity of some environmentally
relevant polycyclic aromatic hydrocarbons after lifelong topical application to mouse skin. Arch.
Geschwulstforsch. 50:266-274. (Cited in ATSDR, 1995)
Hermann, M., J.P. Durand, J.M. Charpentier et al. 1980. Correlations of mutagenic activity with
polynuclear aromatic hydrocarbon content of various mineral oils. In: Polynuclear Aromatic
Hydrocarbons: Chemisty and Biological Effects, 4th Int. Symp., A. Bjorseth and A.J. Dennis, Ed.
Battelle Press, Columbus, OH. p. 899-916. (Cited in WHO, 1997)
Hoffmann, D. and E.L. Wynder. 1966. On the carcinogenic effect of dibenzopyrenes. Z.
Krebsforsch. 68: 137-149. (German) (Cited in ATSDR, 1995)
IARC (International Agency for Research on Cancer). 1973. IARC Monographs on the
Evaluation of Carcinogenic Risk of the Chemical to Man. Certain Polycyclic Aromatic
Hydrocarbons and Heterocyclic Compounds. Vol. 3, p. 45-68.
IARC (International Agency for Research on Cancer). 1983. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans. Polynuclear Aromatic
Compounds. Part 1. Chemical, Environmental and Experimental Data, Vol. 32,
p. 135.
IARC (International Agency for Research on Cancer). 1987. IARC Monographs on the
Evaluation of the Carcinogenic Risk of Chemicals to Humans. Suppl. 7, p. 58.
Lacassagne, A., N.P. Buu-Hoi, F. Zajdela et al. 1963. [Carcinogenic activity of
fluoranthene-based polycyclic aromatic hydrocarbons.] Acta. Unio. Int. Contra. Cancrum. 19:
490-496. (French) (Cited in WHO, 1997)
LaVoie, E.J., E.V. Bedenko, N. Hirota et al. 1979. A comparison of the mutagenicity,
tumor-initiating activity and complete carcinogenicity of polynuclear aromatic hydrocarbons. In:
Polynuclear Aromatic Hydrocarbons, P.W. Jones and P. Leber, Ed. Ann Arbor Science
Publishers, Ann Arbor, MI. p. 705-721. (Cited in ATSDR, 1995)
5

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1-31-2002
LaVoie, E.J., J. Braley, J.E. Rice and A. Rivenson. 1987. Tumorigenic activity for non-alternant
polynuclear aromatic hydrocarbons in newborn mice. Cancer Lett. 34:15-20. (Cited in
ATSDR, 1995)
NTP (National Toxicology Program). 2001. Management Status Report. Examined April 4,
2001. Online, http://ntp-server.niehs.nili.gov/main pages/NTP ALL STDY PG.html
Rice, J.E., D.T. Coleman, T.J. Hosted et al. 1985a. On the metabolism, mutagenicity, and
tumor-initiating activity of indeno[l,2,3-cd]pyrene. In: Polynuclear Aromatic Hydrocarbons:
Mechanism, Methods and Metabolism, M. Cooke and A.J. Dennis, Ed. Batelle Press, Columbus,
OH. p. 1097-1109. (Cited in ATSDR, 1995)
Rice, J.E., D.T. Coleman, T.J. Hosted et al. 1985b. Identification of mutagenic metabolites in
indeno[l,2,3-cd]pyrene formed in vitro with rat liver enzymes. Cancer Res. 45: 5421-5425.
(Cited in ATSDR, 1995)
Rice, J.E., T.J. Hosted Jr., M.C. DeFloria et al. 1986. Tumor-initiating activity of major in vivo
metabolites of indeno[ 1,2,3-cd]pyrene on mouse skin. Carcinogenesis. 7: 1761-1764. (Cited in
ATSDR, 1995)
Rice, J.E., E.H. Weyand, C. Burrill and E.J. Lavoie. 1990. Fluorine probes for investigating the
mechanism of activation of indeno[l,2,3-cd]pyrene to a tumorigenic agent. Carcinogenesis. 11:
1971-1974.
U.S. EPA. 1984a. Carcinogen Assessment of Coke Oven Emissions. Office of Health and
Environmental Assessment, Environmental Criteria and Assessment Office, Washington, DC.
U.S. EPA. 1984b. Health Effects Assessment for Polycyclic Aromatic Hydrocarbons (PAH).
Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial Response,
Washington, DC.
U.S. EPA. 1986. Guidelines for Carcinogen Risk Assessment. Federal Register.
51(185): 33992-34003.
U.S. EPA. 1990. Drinking Water Criteria Document for Polycyclic Aromatic Hydrocarbons
(PAHs). Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Water, Washington, DC.
U.S. EPA. 1991. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. April.
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1-31-2002
U.S. EPA. 1994a. CRAVE meeting notes (February 1994) on polycyclic aromatic
hydrocarbons. Reported May 11, 1994.
U.S. EPA. 1994b. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC. December.
U.S. EPA. 1995. Monthly status report of RfD/RfC and CRAVE Work Groups (As of
09/01/95). Office of Research and Development, National Center for Environmental
Assessment, Cincinnati, OH.
U.S. EPA. 1997. Health Effects Assessment Summary Tables (HEAST). FY-1997 Update.
Prepared by the Office of Research and Development, National Center for Environmental
Assessment, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington,
DC. July. EPA/540/R-97/036. NTIS PB 97-921199.
U.S. EPA. 2000. Drinking Water Regulations and Health Advisories. Summer 2000. Office of
Water, Washington, DC. Examined April 4, 2001. Online.
http://www.epa. gov/ ost/drinking/ standards/
U.S. EPA. 2001. Integrated Risk Information System (IRIS). Office of Research and
Development, National Center for Environmental Assessment, Washington, DC. Examined
April 4, 2001. Online, http://www.epa.gov/iris/
WHO (World Health Organization). 1997. Environmental Health Criteria. 202: WHO (1997)
Non-heterocyclic polycyclic aromatic hydrocarbons. International Programme on Chemical
Safety, Geneva, Switzerland.
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