United States
Environmental Protection
Agency
Office of Research and
Development
Washington, DC 20460
EPA/600/R-93/089
July 1993
Provisional Guidance for
Quantitative Risk
Assessment of Polycyclic
Aromatic Hydrocarbons

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EPA/600/R-93/089
July 1993
PROVISIONAL GUIDANCE FOR QUANTITATIVE RISK ASSESSMENT OF
POLYCYCLIC AROMATIC HYDROCARBONS
f
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
Printed on Recycled Paper

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DISCLAIMER
This document has been reviewed in accordance with U.S. Environmental
Protection Agency policy and approved for publication. Mention of trade names or
commercial products does not constitute endorsement or recommendation for use.

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PREFACE
The Office of Health and Environmental Assessment (OHEA) has prepared this
Interim Guidance Document at the request of the Office of Emergency and Remedial
Response. The purpose of this publication is to provide interim guidance for the
quantitative risk assessment of polycyclic aromatic hydrocarbons (PAH).
For a more complete discussion of potential hazards from PAH exposure, the
reader is referred to the 1992 Drinking Water Criteria Document for Polycyclic
Aromatic Hydrocarbons (PAH). A literature search was not done in support of this
short guidance document. A comprehensive, multimedia document for polycyclic
aromatic hydrocarbons is in preparation by OHEA.
This document was prepared by Drs. Rita Schoeny and Ken Poirier,
Environmental Criteria and Assessment Office, Cincinnati, OH and reviewed by
Jeanette Wiltse, Office of Health and Environmental Assessment, and Drs. V. James
Cogliano and Robert McGaughy, Human Health Assessment Group, OHEA,
Washington, DC.
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TABLE OF CONTENTS
Page
INTRODUCTION 				 						 1
ESTIMATED ORDERING OF POTENTIAL POTENCIES OF PAHS		 		 4
CONCLUSIONS 					 6
REFERENCES 								,16
LIST OF TABLES
No.	Title	Page
1	Incidence of Lung Adenomas Observed in Newborn Mice
for Various PAHs 			 8
2	Tumor Incidence in Female Osbome-Mendel Rats Administered
PAHs by Intrapulmonary Injection	 9
3	Tumor Initiating Activity of PAHs in Female CD-1 Mouse
Skin 				 10
4	Relative Potency Estimates for PAH Based on Skin Tumor
Data 			 11
5	Summary of Relative Potency Estimates for Indicator PAHs	 12
6	Comparative Potency Estimates Based on Single Data Sets as
Calculated by Clement Associates, 1988 			 13
7	Ranges and Combined Potencies for Seven PAHs		 14
8	Estimated Order of Potential Potencies of Selected PAH Based on
Mouse Skin Carcinogenesis			15
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INTRODUCTION
The Office of Health and Environmental Assessment (OHEA) recently completed
an extensive document entitled "Drinking Water Criteria Document (DWCD) for
Polycyclic Aromatic Hydrocarbons (PAHs)." In this document, weight-of-evidence
judgments of Group B2, probable human carcinogen, are presented for seven PAHs;
namely, benz[a]anthracene (BM), benzo[b]fluoranthene (BBF), benzo[k]-fluoranthene
(BKF), benzo[a]pyrene (BAP), chrysene (CHY), dibenz[a,h]anthracene (DBA), and
indeno[1,2,3-cd]pyrene (IDP). All of these categorizations were found appropriate by
the Carcinogen Risk Assessment Verification Endeavor (CRAVE), and files are
available on the Agency's Integrated Risk Information System (IRIS) data base (U.S.
EPA, 1993).
The 1986 Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1986) support
the calculation of quantitative risk estimates for those materials for which there is a
reasonable concern for potential human health risk; for example, PAHs categorized as
B2, probable human carcinogen. In the 1992 DWCD for PAHs, a quantitative risk
estimate for oral exposure to BAP was given as a range of values from 4.5-9.0 per
(mg/kg)/day with a geometric mean of 5.8 per (mg/kg)/day; the"drinking water unit risk
calculated from the mean was 1.7E-4 per (|ig/L) (U.S. EPA, 1992).
NOTE: At the June 1992 meeting of the CRAVE a revised risk estimate was
verified. It was noted that an error had been made in the 1991 document "Dose-
Response Analysis of Ingested Benzo[a]pyrene" which is cited in the DWCD for PAHs.
In the calculation of the doses in the Brune et al. (1981) study it was erroneously
concluded that doses were given in units of mg/year, whereas it was in fact
mg/kg/year. When the doses are corrected the slope factor is correctly calculated as
11.7 per (mg/kg)/day as opposed to 4.7 per (mg/kg)/day as reported in the DWCD.
The correct range of slope factors is 4.5-11.7 per (mg/kg)/day with a geometric mean
of 7.3 per (mg/kg)/day. A drinking water unit risk based on the revised slope factor is
2.1 E-4 per (jxg/L). These values are being changed on IRIS and an Erratum to the
DWCD is being prepared.
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Data were insufficient for the calculation of slope factors for any other PAHs
discussed in the DWCD. While PAHs in general, and BAP in particular, are
well-studied as carcinogens, data are by and large unsuitable for the calculation of
quantitative risk estimates by conventional methods for one or more of the following
reasons.
•	Data were from exposures not typically used in deriving quantitative
estimates for oral or inhalation exposure (e.g., skinpainting or
subcutaneous exposure).
•	Study populations were too small.
•	Studies were done at only one exposure level.
•	Dose-response data were not reported.
EPA quantitative risk estimates for mixtures of PAHs have often assumed that all
carcinogenic PAHs are equipotent to BAP, and that the carcinogenic effect of the
mixture can be estimated by the sum of the effects of each individual PAH (U.S. EPA,
1980). It has been recognized that some PAHs are less carcinogenic in animal
studies than is BAP, so that application of this policy could result in an overestimation
of the effect of those PAHs. On the other hand, PAH mixtures are likely to contain
carcinogenic PAHs that are not considered indicator compounds and thus would not
be measured. Some PAHs, moreover, have been shown to be more potent animal
carcinogens than BAP.
This practice has been inconsistent; some risk assessments applied the BAP
slope factor to all measured PAHs, rather than only those categorized as probable or
possible human carcinogens. This would be expected to result in an overestimation of
the mixture risk. Other risk assessments have used comparative potencies for PAHs
published in the open literature, those cited in a contractor report to EPA (Clement
Associates, 1988), or those based on ranking of PAHs presented in an Erratum to the
Ambient Water Quality Criteria for PAHs (U.S. EPA, 1983).
This paper presents some comparative risk estimates for assessment of
potentially carcinogenic PAHs. These are not proposed as toxicity equivalency factors
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(TEF). A series of guiding criteria have been discussed for the application of a TEF to
mixtures (U.S. EPA, 1991). They include the following:
1.	A demonstrated need for the TEF. The PAHs meet this criterion. PAHs are found
in all media; as a group they are among the most common contaminants at waste
sites. PAHs are the subject of constant inquiry at the Superfund Technical
Support Center. The lack of numerical estimates of risk for any PAH except BAP
has had the potential for negative impacts on many risk-based regulatory
decisions.
2.	A well-defined group of chemicals. This criterion is also met. Any compound
consisting of three or more fused aromatic rings qualifies as a PAH. At this time
OHEA is limiting the definition to exclude all compounds with substituents on the
ring or compounds with anything other than carbon and hydrogen in their
composition. For purposes of this paper (and the Multimedia Document in
preparation), only those PAHs classified as B2, probable human carcinogen, are
being considered.
3.	A broad base of toxicologic data. The data for PAHs are limited. Studies have,
for the most part, been confined to carcinogenicity, genotoxicity and metabolism
studies (generally concerned with the identification of metabolites that are
genotoxic or carcinogenic). For this reason and others below, a weighting of
- potential potency is recommended only for carcinogenicity.
4.	Consistency in the relative toxicity of congeners across toxicological endpoints,
both in vivo and in vitro. As noted above there is not a broad toxicological data
base. Consistency is observed among cancer bioassays in various animal
models and by different routes. The point of congruency is in the generation of
biologically active metabolites; if the PAH is administered to a system capable of
"activating" metabolism, then tumors will be observed. If the site of administration
is capable of metabolism (e.g., skin), contact point tumors will be observed. If the
PAH can be absorbed and metabolized, then distant site tumors will also be
observed. There are data which show that genotoxicity for individual PAHs and
mixtures of PAHs are generally proportional to tumorigenicity. There are also
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some limited data to indicate that immunotoxicity is roughly correlated with
carcinogenic potency. Data for other noncancer effects are generally lacking but
indicate that carcinogenicity is the most sensitive endpoint for PAH toxicity. The
ranking of potential potency in this document is recommended only for PAH
carcinogenicity.
5. Demonstrated additivity between the toxicity of individual congeners. Few studies
have been reported which are an adequate test of an additivity assumption. In
this regard the data bases for PAH, PCB congeners and dibenzo-p-dioxins and
dibenzofurans are about of equal quality. Both additive and nonadditive effects
have been observed for the carcinogenicity or genotoxicity of PAHs by various
routes. Both inhibition and cocarcinogenicity have been observed for mixtures of
PAHs; effects are dependent on route and proportion of materials and solvents
(see U.S. EPA, 1992 for a review). It is logical to assume that in skin PAHs act
as their own promoters; most B2, probable human carcinogens, in this group
have been shown to be complete carcinogens in mouse skin. There have been
few demonstrations that one PAH can serve as a promoter for a different PAH.
According to the Guidelines for the Health Risk of Chemical Mixtures (U.S. EPA,
1986),.. none of the models for toxicant interactions can predict the magnitude
of toxicant interactions in the absence of extensive data." The Guidelines make
no recommendation as to the use of any risk model for promotion.
The guidelines further state the following:
Based on current information, additivity assumptions are expected to yield
generally neutral risk estimates (i.e., neither conservative nor lenient) and
are plausible for component compounds that induce similar types of effects
at the same sites of action (U.S. EPA, 1986).
A National Research Council Report (NRC, 1988) notes that a consideration of
the mathematical considerations of low-dose extrapolation shows that interactions
which are demonstrable at high doses will not be detectable at low doses. All of
the above indicates that the use of an additivity assumption for PAHs is not
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contraindicated and is consistent with the practice of the Risk Assessment
Guidelines.
6.	Some mechanistic rationale as to why TEFs would be applicable to a particular
group of chemicals. This criterion is met for PAHs assuming that one accepts the
hypothesis that mutation or some DNA change is a necessary step in
carcinogenesis. All the PAHs for which ranking of potential potency is proposed
can be shown both to induce tumors in animals and genetic changes (generally
mutations) in some systems.
7.	Some method of gaining consensus as to what TEFs ought to be. This process
has not yet been undertaken for PAHs. The proposed ranking of potential
potency was developed by a small group of OHEA scientists and has received
only OHEA review.
In summary, not all of the guiding criteria are met for TEF. For this reason OHEA
has chosen not to label the risk assessment numbers in this document a "toxicity
equivalency factor" but rather an "estimated order of potential potency." It should be
recognized in the application of these risk estimates that there are many limitations.
First, these risk estimates are applicable only to cancer evaluation. Second, additivity
of PAH response has not been proved (or refuted). Last, the estimated order of
potential potency described herein is an OHEA interim recommendation and does not
constitute an Agency consensus.
ESTIMATED ORDERING OF POTENTIAL POTENCIES OF PAHS
In studies of rodents, wherein BAP was assayed for carcinogenicity in conjunction
with other PAHs, a range of carcinogenic potencies were observed. For example, as
seen in Table 1, several PAHs were less effective in tumor induction in a mouse lung
adenoma assay than was BAP at smaller or equivalent doses (LaVoie et al., 1987).
Likewise, ranges of potency have been observed in many species and by different
routes; for example, intrapulmonary injection in rat lungs (Table 2) and skin painting in
mice (Table 3).
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Inspection of these data suggest that one should be able to estimate orders of
potential carcinogenic potencies for various PAHs by comparison with the activity of a
standard compound. If BAP is used as the standard, then estimates of individual slope
factors could be done as a percentage of the calculated slope factor for BAP. This
approach could be applied to estimating the amounts of group B2 (probable human
carcinogen) PAHs in a particular exposure situation and calculating their weighted
contribution (by comparison to BAP) to total carcinogenic activity of the mixture.
The choice of the data set or sets to be used for estimating the potency is
important, as is the modeling procedure used to provide estimates of carcinogenic
activity. A discussion of various approaches is given in the DWCD (U.S. EPA, 1992).
Previous work attempted to derive relative potencies for PAHs. One derivation
was done by T. Thorslund of ICF-Clement Associates on contract to U.S. EPA. An
interim report (Clement Associates, 1988) is described in some detail in U.S. EPA
(1992). In this report data were used from studies wherein BAP and several other
PAHs were administered in the same time frame by routes including skin painting,
intraperitoneal or subcutaneous injection, and lung implantation. For each study
considered, a comparison was made between BAP carcinogenic activity and the
activity of a particular PAH in that same report.
Two forms of dose-response models were used: either P(d) = 1-exp[-a(1+bd)]; or
P(d) = 1-exp[-a(1+bd)2], where a and b are background and exposure-related
parameters, respectively (Clement Associates, 1988). The first equation is simply a
one-hit model, which is a special case (one-stage) of the multistage model. The
second equation is a special case of the multistage model with two stages and an
additional assumption that the first and second transition rates are identical relative to
their respective background rates. In the application of these models it was assumed
that carcinomas can develop from papillomas. For studies which reported only
combined tumors or did not classify tumors, the simple form, or one-stage model was
used. The two-stage model was used for data in which malignant tumors were
reported separately.
In deriving the potency for each PAH relative to BAP, it was assumed that the
PAHs and BAP have similar dose-response curves, but that it takes a proportionally
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larger concentration of non-BAP material to induce an equivalent tumor response.
The relative potency of each PAH was calculated as the ratio of the estimated
transition rates with the potency of BAP indexed as 1. Point estimates (maximum
likelihood estimates) were compared rather than upper bounds. An example of
relative potencies from one data set is given in Table 4. In this and all subsequent
tables, transition rates and relative potencies for PAHs are given as reported in
Clement Associates (1988). This is to allow the reader to follow derivation of the
numbers; it is acknowledged that the number of significant figures is a reflection only
of the precision of numerical calculations and does not accurately transmit the degree
of experimental uncertainty.
The result of all calculations based on 11 separate studies is a range of
comparative potencies; the ranges reported in Clement Associates (1988) for PAHs
classified as B2, probable human carcinogen, are given in Table 5.
Clement Associates (1988) selected what they considered to be the most
appropriate relative potency for each PAH based on a consideration of qualitative
differences in studies. Their selections are presented in Table 6. It should be noted
that the application of study selection criteria other than those described in the
Clement Associates (1988) report could result in the selection of different "most
appropriate" relative potencies. In this context, a peer review panel convened in 1988
to review the DWCD on PAHs and felt that potencies based on the Deutsch-Wenzel et
al. (1983) study would be less reliable than those based on other bioassays because
of the unusual route of exposure (surgical implantation of wax pellets in the lung).
Arguments for the validity of this exposure method have also been presented,
however.
Other approaches for obtaining a single estimate of relative potency are feasible;
for example, taking a mean, a weighted mean, or some other measure of central
tendency of the individual estimates comprising the range. Calculated means are
given in Table 7 as well as order of magnitude potencies based on the following
rounding scheme: 0.51-5.0 = 1.0; 0.051-0.50 = 0.1; 0.0051-0.050 = 0.01.
The approach chosen here was to select a test system that provides a complete -
set of comparisons. Of the data sets modeled in Clement 1988, mouse skin painting
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bioassays wherein PAHs were tested as complete carcinogens rather than as initiators
only, meets this criterion. This data set is compiled from four reports with standard
study protocols, using adequate numbers of test animals (20-36). These studies are
not without deficiencies. For example, neither the Bingham and Falk (1969) paper nor
Wynder and Hoffmann (1959) reported solvent control tumor incidences. Estimated
orders of potential potencies based on skin painting tests as reported by Clement
(1988) are given in Table 8. These are rounded to orders of magnitude using the rule
presented above.
The values in Table 8 are recommended for interim use. They are based on well
conducted studies using a standard, easily comparable endpoint well-known to be
associated with exposure to PAHs; namely, complete carcinogenesis after repeated
exposure to mouse skin. The potencies of PAH for comparison were calculated by
Clement Associates (1988) using both forms of the model (one and two stages as
indicated in Table 8). For this exercise no claim as to biological relevance is made for
the modeling procedure; rather, it represents a convenient curve-fitting procedure,
based on plausible assumptions. It is recommended that only the order of magnitude
ranking be used. The quality of the data and the analysis thereof do not support any
greater precision.
CONCLUSIONS
- The values in Table 8 are provided for interim use. Research on relative
potencies for PAHs and on the development of a TEF methodology is being
undertaken by OHEA and other parts of the Agency. Areas of research include: the
assumption of additivity of carcinogenic activity of PAHs; the basis for choice of
studies and data sets; and the choice of modeling procedures.
In summary, a series of relative potency values (orders of magnitude) is provided
as temporary guidance for the risk evaluation of PAHs. It is recognized that the list of
PAHs in Table 8 is not sufficiently extensive to meet the needs of Programs and
Regions; part of the continuing work on PAHs will be the consideration of the expert
panel approach of ranking PAH hazards undertaken by OERR. Also in progress is
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work to expand the series to include PAH for which there are animal carcinogenicity
studies that did not include BAP as a positive control.
The guidance in this paper should be applied only to assessment of carcinogenic
hazard from oral exposure to PAHs. There is currently no inhalation unit risk for BAP
that has been found acceptable by the CRAVE. At this time, there is no basis for
judgment that BAP or other PAHs will be equipotent by oral and inhalation routes.
The documented effects of particulate matter and other cocarcinogens on BAP
carcinogenic effects in animal lungs are confounding issues for the derivation of an
inhalation unit risk for BAP and the establishment of potencies for inhalation vs. oral
exposure to other PAHs.
In order to apply this guidance of relative potencies to mixtures, empirical data
are needed on the additivity (or lack thereof) of carcinogenic effects of PAHs.
Results of testing simple mixtures of PAHs and mixture components must be
compared to assessments made from bioassays of complex environmental mixtures.
Research of this nature is being undertaken by the U.S. EPA Health Effects Research
Laboratory and by several research groups under contract to the Electrical Power
Research Institute.
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TABLE 1
Incidence of Lung Adenomas Observed in Newborn Mice
for Various PAHsa
Treatment
Total Dose
(umol)
Lung Adenomas
Incidence
% Response
Control13
0
0/35
0 -
Benzo[a]pyrene
1.1
23/31
74.2
Benzo[b]fluoranthene
0.5
5/32
15.6
Benzo[j]fluoranthene
1.1
15/39
38.5
Benzo[k]fluoranthene
2.1
4/34
11.8
lndeno[1,2,3-cd]pyrene
2.1
1/20
5.0
aSource: Adapted from LaVoie et al., 1987
bDimethylsulfoxide was used as the vehicle control.
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TABLE 2


Tumor Incidence in Female Osborne-Mendei Rats Administered
PAHs by Intrapulmonary Injection3
T reatment
Total Dose
(mg)
Epidermoid Carcinomas
Incidence
% Response
CONTROLb
0
0/35
0
Benzo[a]pyrene
1.0
33/35
94.3
Benzo[b]fluoranthene
1.0
9/35
25.7
Benzo[e]pyrene
5.0
1/35 "
2.9
Benzo[k]fluoranthene
4.15
12/27
44.4
lndeno[1,2,3-cd]pyrene
4.15
21/35
60.0
Benzo[g, h, ijperylene
4.15
4/34
11.8
aSource: adapted from Deutsch-Wenzel et al., 1983
bNeither untreated nor vehicle (beeswax and trioctanoin pellets) controls were
observed to develop epidermoid carcinomas.
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TABLE 3
Tumor Initiating Activity of PAHs in Female CD-1 Mouse Skina
Treatment
Total
Initiating
Dose (|ig)
Incidence
Tumor Response13
% Response
# Tumors/
Animal
Control0
0
0/20
0
0
Benzo[a]pyrene
30
17/20
85.0
4.9
Benzo[b]fluoranthene
30
12/20
60.0
2.3
Benzo[j]fluoranthene
30
6/20
30.0
0.6
Benzo[k]fluoranthene
30
1/20
5.0
0.1
aData from LaVoie et al., 1982. Initiating doses were applied in 10 doses, one every other day followed by
applications of TPA 3 times/week for 20 weeks.
bTumors were largely papillomas.
cAcetone was used as the vehicle control.

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TABLE 4


Relative Potency Estimates for PAH Based on Skin Tumor Dataa
Treatment
Total Dose
Tumor
Estimated
Relative

(mg/animal)
Incidence
Transition
Potency13



Rate

DMSO
0
0/35
—
—
Acetone
0
0/36
—
—
BAP
1.7
8/43
3.92
1.0

2.8
24/35



4.6
22/36


BBF
3.4
2/38
0.656
0.167

5.6
5/34



9.2
20/37


BJF
3.4
1/38
0.241
0.241

5.6
1/35



9.2
2/38


BKF
3.4
1/39
0.078
0.020

5.6
0/38



9.2
0/38


'IDP
3.4
1/35
0.081
0.021

5.6
0/37



9.2
0/37


aSource: Data from Habs et al. (1980); transition rates and relative potencies from
Clement Assoc. (1988).
bModel: P(d)=1-exp[-a(1+bd2)]
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TABLE 5
Summary of Relative Potency Estimates for Indicator PAHsa
Compound
Test System
Mouse Skin
Carcinogenesis
Subcutaneous
Injection into
Mice
Intrapulmonary
Administration to
Rats
Initiation-
Promotion on
Mouse Skin
Intraperitoneal
Injection in Newborn
Mice
Benzo[a]pyrene
1.0
1.0
1.0
1.0
1.0
Benz[a]anthracene
0.145°



0.057, 0.524,
0.496d
Benzo[b]fluoranthene
0.167®

0.140
0.258f, 0.1259
0.232, 1.067,
0.874h
Benzo[k]fluoranthene
0.020s

0.066
0.022f
0.040, 0.097,
0.044*1
Chrysene
0.0044'


0.0409
0.125, 0.33d
Dibenz[ah]anthracene
1.11'
2.82j, 4.50k



lndeno[1,2,3-cd]pyrene
0.021®, 0.089*

0.232
0.074*
0.013h
aWhere more than one potency estimate is shown, they were derived from the same study using different tumor types as endpoints. Both
forms of the dose-response model in the text were used.
bDeutsch-Wenzel et al., 1983
cBingham and Falk, 1969
dWislocki et al., 1986
eHabs et a!., 1980
fLaVoie et al., 1982
gVan Duuren et al., 1966
^LaVoie et al., 1987
'Wynder and Hoffmann, 1959
Ipfeiffer, 1977
kBryan and Shimkin, 1943
'Hoffmann and Wynder, 1966

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TABLE 6
Comparative Potency Estimates Based on Single Data Sets as Calculated by
Clement Associates, 1988
Compound
Relative
Potency
Reference
Benzo[a]pyrene
1.0

Benzo[a]anth racene
0.145a
Bingham and Falk, 1969
Benzo[b]fluoranthene
0.140a
, Deutsch-Wenzel et al., 1983
Benzo[k]fluoranthene
0.066a
Deutsch-Wenzel et al., 1983
Chrysene
0.0044a
Wynder and Hoffmann, 1959
Dibenzo[a, h]anth racene
1.11a
Wynder and Hoffmann, 1959
lndeno[1,2,3-cdJpyrene
0.232b
Deutsch-Wenzel et al., 1983
aModel: P(d)=1-exp[-a(1+bd)2]
bModel: P(d)=1-exp[-a(1+bd)]
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TABLE 7
Ranges and Combined Potencies for Seven PAHs*
Compound
Range
Potency Relative to BAP
Simple Mean
Geometric
Mean
Order of
Magnitude
Benzo[a]pyrene
—
—
—
1.0
Benzo[a]anthracene
0.057-0.524
0.31
0.22
0.1
Benzo[b]fluoranthene
0.125-1.067
0.41
0.29
0.1
Benzo[k]fluoranthene
0.020-0.097
0.05
0.04
0.01
Chrysene
0.0044-0.33
0.12
0.05
0.01
Dibenz[a,h]anthracene
1.11-4.5
2.81
2.42
1.0
lndeno[1,2,3-cd]pyrene
0.013-0.232
0.08
0.08
0.1
*Relative potencies given in the range are from Clement Associates, 1988. Both forms of the dose-response model
the text were used.

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TABLE 8
Estimated Order of Potential Potencies of Selected PAH Based
on Mouse Skin Carcinogenesis
Compound
Relative Potency3
Reference
Benzo[a]pyrene
1.0
1.0

Benz[a]anthracene
0.145
0.1
Bingham and Falk,
1969
Benzo[b]fluoranthene
0.167
' 0.1
Habs et al., 1980
Benzo[k]fluoranthene
0.020
0.01
Habs et al., 1980
Chrysene
0.0044,
0.001
Wynder and
Hoffmann, 1959
Dibenz[a,h]anthracene
1.11
1.0
Wynder and
Hoffmann, 1959
lndeno[1,2,3-cd]pyrene
0.055b
0.1
Habs et al., 1980;
Hoffmann and
Wynder, 1966
aModel was P(d)=1-exp[-a(1+bd)2] for all but indeno[1,2,3-cd]pyrene
bSimple mean of relative potencies (0.021 and 0.089) the latter of which was derived
using the one-hit model.
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REFERENCES
Bingham, E. and H.L. Falk. 1969. Environmental carcinogens - The modifying effects
of cocarcinogens on the threshold response. Arch. Environ. Health 19: 779-783.
Brune, H., R. Deutsch-Wenzel, M. Habs, S. Ivankovic and D. Schmahl. 1981.
investigation of the tumorigenic response to benzo[a]pyrene in aqueous caffeine
solution applied orally to Sprague-Dawley rats. J. Cancer Res. Clin. Oncol. 102:153-
157.
Bryan, W.R. and M.B. Shimkin. 1943. Quantitative analysis of dose-response data
obtained with three carcinogenic hydrocarbons in strain C3H male mice. J. Natl.
Cancer Inst. 3:502-531-.
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risk associated with exposure to mixtures of polycyclic aromatic hydrocarbons. Interim
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a
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X
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Pfeiffer, E.H. 1977. Oncogenic interaction of carcinogenic and noncarcinogenic
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Wynder, E.L. arid D. Hoffman. 1959. A study of tobacco carcinogenesis. VII. The
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