United States
Environmental Protection
1=1 m m Agency
EPA/690/R-07/028F
Final
7-29-2007
Provisional Peer Reviewed Toxicity Values for
Perylene
(CASRN 198-55-0)
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

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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
NAAQS
National Ambient Air Quality Standards
NOAEL
no-ob served-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-ob served-effect level
OSF
oral slope factor
p-IUR
provisional inhalation unit risk
p-OSF
provisional oral slope factor
p-RfC
provisional inhalation reference concentration
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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
Hg
microgram
|j,mol
micromoles
voc
volatile organic compound
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PROVISIONAL PEER REVIEWED TOXICITY VALUES FOR
PERYLENE (CASRN 198-55-0)
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.
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
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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
Perylene (CASRN 198-55-0; molecular weight = 252.3) is a polycyclic aromatic
hydrocarbon (PAH) with 5 fused, 6-membered rings. Synonyms for perylene include
dibenz[de,kl]anthracene and peri-dinaphthalene (IARC, 1998). Isomers of perylene include
benzo[a]pyrene and benzo[e]pyrene. Perylene, like other polycyclic aromatic hydrocarbons
(PAH), is formed during the combustion or pyrolysis of carbon-containing materials including
coal and mineral oils (IARC, 1983; ATSDR, 1995). Demonstration of PAH formation in high
temperatures include observations that concentrations of PAHs in lubricating oils increase with
continued use at high temperatures (e.g., Apostoli et al., 1993).
This paper evaluates available information on carcinogenic and non-carcinogenic health
effects in humans and animals exposed orally and by inhalation to perylene. Classification of
perylene in the U.S. EPA (2005) cancer weight-of-evidence scheme is considered, as well as
potential derivation of a cancer oral slope factor, a cancer inhalation unit risk, subchronic and
chronic oral RfD, and subchronic and chronic inhalation RfC.
Neither a reference dose (RfD) nor a reference concentration (RfC) were available for
perylene in the Integrated Risk Information System (IRIS) database (U.S. EPA, 2007) or the
Health Effects Assessment Summary Tables (HEAST; U.S. EPA, 1997). There was no Agency for
Toxic Substances and Disease Registry (ATSDR) Toxicological Profile on perylene (ATSDR,
2007). Health assessments for perylene were not available from other major sources, including
CalEPA (2007), the National Toxicology Program (NTP, 2007), or the World Health
Organization (WHO, 2007). Occupational exposure limits were not available from the American
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Conference of Industrial Hygienists (ACGIH) (2007), National Institute for Occupational Safety
and Health (NIOSH) (2005) or Occupational Safety and Health Administration (OSHA) (2007).
Perylene was not listed on HEAST (U.S. EPA, 1997), the Chemical Assessments and Related
Activities (CARA) lists (U.S. EPA, 1991, 1994) or the Drinking Water Health Advisories list
(U.S. EPA, 2006). Perylene had not been studied by NTP (2007), and was not among the 17
PAHs discussed in the ATSDR (1995) Toxicol ogical Profile for Poly cyclic Aromatic
Hydrocarbons or the 15 PAHs discussed in the U.S. EPA (1990) Drinking Water Criteria
Document for Poly cyclic Aromatic Hydrocarbons. IARC (1998), however, prepared a review of
the carcinogenicity and mutagenicity of perylene.
Searches of TOXLINE were conducted (1983-1991 in May, 1991; 1991-September 1995
in August, 1995; 1981-1991 and after September, 1995 in January 1996 and June 2007) to
identify reports of studies with health effects data for perylene. A CASRN and synonym
strategy was employed using oral, inhalation, and cancer terms in the searches. Searches of
CANCERLINE (1991- 1995 in August, 1995; 1981-1995 in January, 1996; and 1995-2007 in
June 2007) also were conducted, as were searches of the RTECS, TSCATS, MEDLINE, CCRIS,
DART, GENETOX, EMIC, EMICBACK and ETICBACK databases.
REVIEW OF PERTINENT DATA
Human Studies
Studies directly examining the toxicity or carcinogenicity of perylene in humans were not
located. Perylene has been present in the environment as a component of complex PAH-
containing combustion product mixtures, several of which are known or suspected to be
carcinogenic in humans (e.g., coal tars, soot, and tobacco smoke and products; see IARC, 1983,
1998). However, results from studies of these mixtures were inadequate to evaluate the toxicity
or carcinogenicity of perylene or other individual PAH components.
Animal Studies
No studies were located regarding cancer or noncancer effects in animals after oral or
inhalation exposure. Available cancer bioassays in animals were limited to mouse studies with
dermal exposure or i.p. injection.
Data from several tumor assays following dermal exposure are summarized in Table 1.
In a skin tumor initiation assay, Van Duuren et al. (1970) applied single doses of 800 jag
perylene (purified by recrystallization) in 200 [xL benzene to the clipped dorsal skin of a group of
20 female ICR/Ha Swiss mice, six- to eight-weeks old. No skin tumors were found during a 58-
60 week observation period. Another group of 20 mice received single dermal doses of perylene
at the same level. These were followed, beginning 2 weeks later, by three times per week
application of 2.5 jag 12-O-tetradecanoylphorbol-13-acetate (TPA) in 0.1 mL acetone during the
58-60 week observation period. Skin papillomas were found in 3/20 mice in the perylene/TPA
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TABLE 1: Tumor data from dermal application of perylene
Species and
Study Type
Exposure
Critical Effects
Comments
Reference
Mouse
Dermal
Carcinogenicity
Twice weekly dermal
application of 60 |iL for
up to 82 weeks
No significant increase
in skin tumors
Examinations apparently
limited to application site
Hortonand Christian, 1974
Mouse
Dermal
Carcinogenicity
Single 800 |ig dermal
dose followed by 58-60
weeks of observation
No significant increase
in skin tumors
Examinations apparently
limited to application site
Van Duuren et al., 1970
Mouse
Skin Tumor Initiation
Single 800 |ig dermal
dose followed by thrice
weekly application of
TPA for 58-60 weeks
No significant increase
in skin tumors
Examinations apparently
limited to application site
Van Duuren et al. 1970
Mouse
Skin Tumor Initiation
Single 1 mg dermal dose
followed by thrice weekly
application of TPA for 25
weeks
No significant increase
in skin tumors or tumors
at other sites
Skin tumors were evaluated
histologically and animals
were examined for visible
tumors at other sites
El-Bayoumy et al., 1982
Mouse
Dermal
Carcinogenicity11
Thrice weekly dermal
application of 1%
perylene for 1 year
No significant increase
in skin tumors
Study poorly reported as an
abstract
Anderson and Anderson 1987
Mouse
Skin Tumor
Promotiond
Single 300 |ig dermal
dose of benzo(a)pyrene
followed by thrice weekly
dermal application of 1%
perylene for 1 year
No significant increase
in skin tumors compared
to treatment without
benzo(a)pyrene
initiation.
Study poorly reported as an
abstract
Anderson and Anderson 1987
Mouse (Strain A)
Lung Tumor
Initiation11
Thrice weekly i.p.
injection of 200, 500 or
1000 mg/kg perylene for 8
weeks followed by 16
weeks of observation
No significant increase
in lung adenomas in
Strain A mouse model
system for detection of
tumor initiation.
Study poorly reported as an
abstract
Anderson and Anderson 1987
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group compared with 0/20 in an acetone control group and 1/20 in a TPA control group. The
report did not mention a benzene control group. Differences in tumor incidence between the
perylene group and either of the control groups were not statistically significant, using the Fisher
Exact test conducted for this document, andp=0.05 as the criteria of significance.
Horton and Christian (1974) applied 60 [jL of a 0.15% solution of perylene (purified by
recrystallization) in decalin twice weekly for up to 82 weeks to the dorsal skin of 20 male C3H
mice, beginning at two months of age. At 52 weeks, 16/20 of the mice had survived without
showing skin tumors. Details were not provided regarding the 4 mice that died during the first
52 weeks. During the following 30 weeks, no skin tumors developed in the 16 mice that
survived 52 weeks. A decalin-only control group was not included, but in a group of 20 mice
treated with a 50:50 mixture of dodecane and decalin twice weekly for up to 82 weeks, 2/13
mice that survived at least 52 weeks developed skin papillomas, although no carcinomas were
found.
El-Bayoumy et al. (1982) compared the mouse skin tumor initiation activities of several
PAHs, including perylene and benzo[a]pyrene. Test compounds (> 99% pure by HPLC analysis)
were dissolved in acetone and applied in 10 doses, every other day, to the shaved backs of
groups of 20 Crl/CD-1(ICR)BR female mice. The total initiation dose was 1 mg/mouse for
perylene and 0.05 mg/mouse for benzo[a]pyrene. Ten days after initiation, 2.5 jag
tetradecanoylphorbol acetate (TPA) in 0.1 mL acetone was applied three times weekly for 25
weeks, after which the animals were autopsied. At autopsy, skin tumors were examined
histologically and animals were examined for visible tumors at other sites. One non-skin tumor
was found in the vehicle control group (acetone initiation and TPA promotion). In the group
given initiating doses of 1 mg perylene/mouse, 5% (1/20) had skin tumors with an average 0.1
skin tumors per mouse. Skin tumors were reported to be predominately squamous cell
papillomas. This tumorigenic response was identical to that in the vehicle control group. In the
group initiated with benzo[a]pyrene (0.05 mg/mouse), 90% (18/20) had skin tumors with an
average 7.1 skin tumors/mouse. These results suggest that the perylene might not be
tumorigenic in mouse skin.
Anderson and Anderson (1987) applied 1% perylene to mouse skin tree times per week
for one year. No increase in the rate of skin tumors was reported in this abstract. Likewise,
among mice similarly treated with perylene following a single 300 |ig dermal dose of
benzo(a)pyrene they reported no significant increase in skin tumors compared to treatment
without benzo(a)pyrene initiation. Finally, among mice injected (i.p.) three times weekly for
eight weeks with 200-1000 mg/kg perylene, and observed for 16 additional weeks, they reported
no increase in lung adenomas.
In summary, no statistically significant tumorigenic responses to perylene were found in
two mouse-skin tumor-initiation assays (Van Duuren et al., 1970; El-Bayoumy et al., 1982) or in
an 82-week mouse skin complete carcinogenicity assay (Horton and Christian, 1974).
Comparison of the skin tumor initiation activity of perylene with that of its isomer,
benzo[a]pyrene, suggested that if perylene is tumorigenic in mouse skin, its potency is much less
than that of benzo[a]pyrene (El-Bayoumy et al., 1982). Animal cancer bioassays in other animal
species or examining routes of exposure other than dermal or intraperitoneal were not located.
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Other Studies
The animal data discussed in the previous section and the supporting data discussed in
this section suggest that, if perylene is carcinogenic or genotoxic, its potency is likely to be much
less than that of its isomer, benzo[a]pyrene, one of the most potent carcinogenic PAHs studied to
date.
In the presence of rat liver metabolic activation systems ("S9") from rats pretreated with
the poly chlorinated biphenyl, Aroclor 1254, perylene produced mutagenic effects in numerous
Salmonella typhimurium reverse mutation assays using a 2-fold increase in reversion rate as the
criteria of mutagenicity. The results from the various laboratories, however, did not consistently
identify the same strains as being responsive to perylene (Anderson and Styles, 1978; Kaden et
al., 1979; LaVoie et al., 1979; Florin et al., 1980; Ho et al., 1981; DeFlora et al., 1984; Sakai et
al., 1985; Carver et al., 1985). One laboratory, Salamone et al. (1979), found that, in the
presence of S9 activation, perylene concentrations up to 1000 [j,g/plate did not increase the rate
of reverse mutations in any of 5 tested strains (TA98, TA100, TA1535, TA1537, TA 1538), by
the two-fold increase criteria.
Sakai et al. (1985) reported that perylene at concentrations up to 50 [j,g/plate increased
reverse mutations at the histidine locus only in the presence of S9 activation, in strain TA97 but
not in strains TA98 or TA100. In contrast, LaVoie et al. (1979) and Ho et al. (1981) reported
that perylene was mutagenic at the same locus at 10 [j,g/plate in strain TA100 and at 5 [j,g/plate in
strain TA98, respectively, both in the presence of S9 activation only. Anderson and Styles
(1978) found that 100 jag perylene/plate, in the presence of S9 activation, increased reverse
mutations at the histidine locus by 10-fold, compared with negative control conditions, in strain
TA1535 and 4-fold at 4 [j,g/plate, in strain TA100. However, they found no mutagenic activity in
strains TA1538 or TA98 at concentrations up to 2500 [j,g/plate. DeFlora et al. (1984) found that
perylene in the presence of S9 activation increased reverse mutations compared with negative
control conditions in strains TA1538, TA98, TA1537, but not in strains TA97 or TA1535.
Florin et al. (1980) found that perylene in the presence of S9 activation significantly increased
reverse mutations in strain TA98, but not in strain TA100. Carver et al. (1985, 1986) found
perylene-induced mutagenic activity at 50 [j,g/plate with S9, in strains TA98 and TA100, and
found that the degree of activity increased with increasing concentrations of S9.
Comparison of the mutagenic activities of perylene and benzo[a]pyrene in Salmonella
typhimurium reverse mutation assays suggested that the mutagenic potency of perylene might be
less than that of benzo[a]pyrene (Florin et al., 1980; DeFlora et al., 1984; Carver et al., 1985).
Florin et al. (1980) reported that an optimal mutagenic dose of benzo[a]pyrene, 0.003
[j,mol/plate, produced 235 revertants/plate in strain TA98, whereas an optimal dose of perylene,
0.025 [j,mol/plate, produced 91 revertants/plate in the same strain. DeFlora et al. (1984) reported
that the mutagenic potency of benzo[a]pyrene, measured as the number of revertants in the most
sensitive strain divided by the corresponding dose of compound (nmole/plate), was
approximately 9-fold greater than that of perylene (185 versus 21 revertants/nmole). Carver et
al. (1985) found that 1.0 jag benzo[a]pyrene/plate, in the presence of 15 [xL S9, produced
reversion rates similar to those produced by 50 jag perylene/plate in the presence of 240 [oL S9.
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In contrast to the S. typhimurium reverse mutation results, Penman et al. (1980) reported that a
40 micromolar ([j,mol) concentration of perylene in the presence of S9 produced forward
mutation rates for 8-azaguanine resistance in S. typhimurium strain TM677 that were similar to
those produced by 40 [j.mol benzo[a]pyrene under similar conditions (approximately 30 versus
43 "induced mutant fraction x 105" for perylene and benzo[a]pyrene, respectively).
Hera and Pueyo (1988) found that at concentrations up to 400 nmol perylene/plate, in the
presence of S9, did not significantly increase the reversion rate of histidine-locus mutations in S.
typhimurium strain TA97, but significantly increased the frequency of L-arabinose-resistant
mutants in strain BA9 in the presence of a high concentration of S9.
Kaden et al. (1979) reported that 1 nmol perylene/mL was mutagenic in the presence of
metabolic activation at the 8AGs/8AGr locus in S. typhimurium strain TM677.
Mersch-Sundermann et al. (1992) found no evidence for perylene genotoxicity in
Escherichia coli PQ37 using the SOS Chromotest for DNA damage, in the presence or absence
of S9 activation. This assay indirectly measured DNA damage by measuring induction of the
SOS-DNA repair system. In contrast, benzo[a]pyrene, in the presence of S9 activation,
markedly induced the SOS-DNA repair system in E. coli PQ37. von der Hude et al. (1988)
reported similar results comparing perylene and benzo[a]pyrene in the same SOS chromotest
with E. coli PQ37.
In in vitro assays, Popescu et al. (1977) found that incubation of Chinese hamster V79
cells for 24 hours inlO [j,g/mL perylene did not induce sister chromatid exchanges (SCE).
However, chromosome aberrations were found in more cells treated with perylene than in
control cells, but a statistical analysis was not conducted. Sirianni and Huang (1978) examined
SCE frequencies in Chinese hamster V-79 cells that were contained in diffusion chambers
implanted in the peritoneal cavities of mice; V-79 cells were examined for SCE frequencies 22
hours after intraperitoneal injection of a test compound. 25-150 |ig Perylene/g mouse body
weight) did not significantly increase SCE frequencies in the V-79 cells compared with V-79
cells implanted in mice without injection of a test compound. In contrast, injection of 25-150 jag
benzo[a]pyrene/g mouse body weight, produced statistically significant, dose-related increases in
SCE frequencies in V-79 cells.
Crespi and Thilly (1984) compared the abilities of perylene and benzo[a]pyrene to induce
6-thioguanine-resistant mutations in a human lymphoblast cell line, AHH-1. Incubation of the
cells in benzo[a]pyrene concentrations > 3 [jmol for 24 hours significantly increased the mutant
frequency compared with control conditions. In contrast, incubation of the cells in medium
containing up to 20 (iinol perylene for 48 hours did not produce statistically significant increases
in the mutation frequency.
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DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC ORAL RfD
VALUES FOR PERYLENE
No studies were located regarding non-carcinogenic effects in humans or animals after
oral exposure to perylene. Due to the lack of data, no RfDs were derived for perylene.
DERIVATION OF PROVISIONAL SUBCHRONIC AND CHRONIC INHALATION RfC
VALUES FOR PERYLENE
No studies were located regarding non-carcinogenic effects in humans or animals after
inhalation exposure to perylene. Due to the lack of data, no RfC was derived for perylene.
PROVISIONAL CARCINOGENICITY ASSESSMENT FOR PERYLENE
Weight-of-Evidence Classification for Perylene
No studies were located examining associations between cancer and exposure of humans
to perylene. Perylene is a component of several complex mixtures containing PAHs, including
tobacco smoke and soot, that are demonstrated human carcinogens. However, the available data
did not determine what role, if any, perylene played in the carcinogenic responses to these
mixtures. Thus, there were inadequate human data to assess the carcinogenicity of perylene.
Data examining the potential for perylene to produce cancer in animals were restricted to
several mouse skin tumor assays that found no perylene-induced increases in incidence of skin or
distant site tumors. U.S. EPA guidelines (2005) indicated that, in order to classify data from
animal studies as providing no evidence of carcinogenicity, no increased incidence of neoplasms
should be found in at least two-well designed and well-conducted animal studies of adequate
power and dose in different species. Thus, the available animal data for perylene were not
sufficient to classify them as providing no evidence of carcinogenicity. Alternatively, the animal
data were classified as providing inadequate evidence. Additional well-conducted testing in
other animal species with long-term exposure, preferably via oral and inhalation exposure, is
necessary to provide reasonable assurance as to whether perylene may or may not be
carcinogenic in animals or humans.
The genotoxicity of perylene was tested in several short-term genotoxicity assays in
bacteria and in in vitro mammalian systems. Although perylene induced genotoxic effects in
several of these test systems, comparisons of perylene genotoxic potency with that of its
carcinogenic isomer, benzo[a]pyrene, generally found perylene to be a less potent genotoxic
agent.
Following U.S. EPA (2005) guidelines for compounds with inadequate human data and
inadequate animal data, perylene was classified as having inadequate information to assess
carcinogenic potential.
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Quantitative Estimates of Carcinogenic Risk for Perylene
Due to inadequate information to assess carcinogenic potential, a quantitative cancer risk
estimate for neither an oral slope factor nor an inhalation unit risk could be derived for perylene.
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Anderson, R.S. and L.M. Anderson. 1987. Lack of effect of perylene as an inititator of lung
tumors or as a promoter of skin tumors. Fed. Proc. 46:746
Apostoli, P., M. Crippa, M.E. Fracasso, D. Cottica and L. Alessio. 1993. Increases in polycyclic
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Carver, J.H., M.L. Machado and J.A. MacGregor. 1985. Petroleum distillates suppress in vitro
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Crespi, C.L. and W.G. Thilly. 1984. Assay for gene mutation in a human lymphoblast line,
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DeFlora, S., P. Zanacchi, A. Camoirano, C. Bennicelli and G.S. Badolati. 1984. Genotoxic
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test. Mutat. Res. 133:161-98.
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Florin, I., L. Rutberg, M. Curvall and C.R. Enzell. 1980. Screening of tobacco smoke
constituents for mutagenicity using the Ames' test. Toxicology. 18:219-32.
Hera, C. and C. Pueyo. 1988. Response of the L-arabinose forward mutation assay of
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