EPA-540/1-86-030
Off'ce of Research and Development
Office of Health and Environmental
Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
Superfund
xvEPA
HEALTH EFFECTS ASSESSMENT
FOR PYRENE
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EPA/540/1-86-030
September 1984
HEALTH EFFECTS ASSESSMENT
FOR PYRENE
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, DC 20460
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DISCLAIMER
This report has been funded wholly or In part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. II has been subject to the Agency's peer and adminis-
trative review, and It has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
11
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with pyrene.
All estimates of acceptable Intakes and carcinogenic potency presented 1n
this document should be considered as preliminary and reflect limited
resources allocated to this project. Pertinent toxlcologlc and environ-
mental data were located through on-Hne literature searches of the Chemical
Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The
basic literature searched supporting this document 1s current up to
September, 1984. Secondary sources of Information have also been relied
upon In the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The fol-
lowing Office of Health and Environmental Assessment (OHEA) sources have
been extensively utilized:
U.S. EPA. 1980a. Ambient Water Quality Criteria for Polynuclear
Aromatic Hydrocarbons. Environmental Criteria and Assessment
Office, Cincinnati, OH. EPA 440/5-80-069. NTIS PB 81-117806.
U.S. EPA. 1981. Hazard Profile on PAH. Prepared by the Environ-
mental Criteria and Assessment Office, Cincinnati, OH, OHEA for the
Office of Solid Waste and Emergency Response, Washington, DC.
The Intent In these assessments 1s to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited 1n
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the Interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemlcal(s) addressed.
Whenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer 1s not the endpolnt of concern).
The first, the AIS or acceptable Intake subchronlc, Is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (I.e., for an Interval that
does not constitute a significant portion of the Hfespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants 1n ambient air or water where lifetime exposure Is
assumed. Animal data used for AIS estimates generally Include exposures
with durations of 30-90 days. Subchronlc human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
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The AIC, acceptable Intake chronic, 1s similar In concept to the ADI
(acceptable dally Intake). It 1s an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the llfespan [see U.S. EPA (1980b) for a discussion
of this concept]. The AIC 1s route specific and estimates acceptable expo-
sure for a given route with the Implicit assumption that exposure by other
routes 1s Insignificant.
Composite scores (CSs) for noncardnogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development Is explained 1n U.S. EPA (1983a).
For compounds for which there 1s sufficient evidence of carc1nogen1c1ty,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980b). Since cancer 1s a
process that 1s not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-j*s have been computed based on oral
and Inhalation data If available.
1v
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ABSTRACT
In order to place the risk assessment evaluation In proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate Inter-
pretation and use of the quantitative estimates presented.
There are essentially no toxlcologlcal data available concerning the
effects of pyrene In animals or man. Existing criteria addressing PAHs as a
class have been established to address the carcinogenic members of this
group. Data are Inadequate to assess the potential carclnogenlclty of
pyrene. Limited short-term $r\ vitro and In vivo testing data have been pri-
marily negative. AIS, AIC or carcinogenic potencies could not be estimated
for this compound.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball was the Project
Officer. The final documents 1n this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1. ENVIRONMENTAL CHEMISTRY AND FATE
2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2.
ORAL
INHALATION
3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.
3.2.
3.3.
3.4.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
4. CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
5. REGUL
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation
OTHER RELEVANT DATA
HEIGHT OF EVIDENCE
UTORY STANDARDS AND CRITERIA . . .
Page
1
2
. . . 2
2
3
3
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3
3
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3
3
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3
4
5
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, , , 5
5
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5
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6
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TABLE OF CONTENTS (cont.)
RISK
6.1.
6.2.
6.3.
•
ASSESSMENT
ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral
6.1.2. Inhalation
ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral
6.2.2. Inhalation
CARCINOGENIC POTENCY (qi*)
6.3.1. Oral
6.3.2. Inhalation
REFERENCES
Page
9
9
9
9
9
9
9
9
9
9
10
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
AIC Acceptable Intake chronic
AIS Acceptable Intake subchronlc
BCF flic-concentration factor
CAS Chemical Abstract Service
CS Composite score
DNA Deoxyrlbonuclelc acid
PAH Polycycllc aromatic hydrocarbons
TLV Threshold limit value
TWA Time-weighted average
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1. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties and environmental fate of
pyrene (CAS No. 129-00-0) are as follows:
Chemical class: PAH
Molecular weight: 202.24
Vapor pressure: 2.5xlO~6 at 25°C (Mabey et al., 1981)
Water solubility: 0.132 mg/kg at 25°C (Wise et al., 1981)
Log octanol/water
partition coefficient: 4.88 (U.S. EPA, 1980a)
BCF: 2800 (U.S. EPA, 1980a)
Half-life In air: 2 hrs->2 days (estimated)
The half-life value for pyrene In the atmosphere has been estimated from
the observed decomposition of soot-adsorbed pyrene (58%) In artificial smog
(Falk et al., 1956) and the photodecomposltlon study of Korfmacher et al.
(1980). No estimated value for the half-life of pyrene In the aquatic
media could be located 1n the available literature; however, photolysis of
dissolved pyrene In the aquatic phase and adsorption onto participate matter
with subsequent sedimentation may be the Important processes. Blodegrada-
tlon of partlculate-sorbed pyrene 1s likely to be an Important removal pro-
cess from sediment In the aquatic environment. (Callahan et al., 1979).
The fate of pyrene 1n soil Is not known with certainty, but blodegrada-
tlon Is believed to be the most significant removal process (Santodonato et
al., 1981). Based on Its high soil adsorption coefficient (KQC= 84,000)
(Kenaga and Goring, 1980) and low water solubility, this compound Is not
likely to leach significantly from soils, particularly from soils con-
taining high organic carbon content.
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
2.1. ORAL
Mitchell and Tu (1979) reported that an aqueous suspension of pyrene was
poorly absorbed from the gut of male Fischer 344 rats.
2.2. INHALATION
Mitchell and Tu (1979) reported rapid pulmonary absorption of a pyrene
aerosol (300-500 vg/l of air) by male Fischer 344 rats. Widespread tis-
sue distribution was seen after 60 minutes of exposure.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. Pertinent data regarding the subchronlc oral toxldty of
pyrene In humans and experimental animals could not be located In the avail-
able literature.
3.1.2. Inhalation. Pertinent data regarding the subchronlc Inhalation
toxlclty of pyrene In humans and experimental animals could not be located
In the available literature.
3.2. CHRONIC
3.2.1. Oral. Pertinent data regarding the chronic oral toxlclty of
pyrene 1n humans and experimental animals could not be located In the avail-
able literature.
3.2.2. Inhalation. Holland et al. (1980) administered uncharacterlzed
oil shale containing PAH, Including pyrene, to Syrian golden hamsters by
Inhalation of 50 mg resplrable shale dust/m3 for 4 hours/day, 4 days/
week. The authors reported Interim results Indicating that shale dust
caused little pulmonary epithelial or flbrotlc reaction, but that retorted
shales caused Inflammation accompanied by flbrosls. Because of the unchar-
acterlzed nature of the test material. It Is not possible to quantify these
or future data from this study for use In risk assessment.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenlclty of pyrene fol-
lowing oral administration could not be located 1n the available literature.
3.3.2. Inhalation. Weaver and Gibson (1979) exposed pregnant rats to
graded airborne concentrations of uncharacterlzed oil shale containing PAH,
Including pyrene, on days 6-15 of gestation. No treatment-related terato-
genlc effects were observed during examination of fetuses obtained by
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Caesarean section on day 20 of gestation. Because of the uncharacterlzed
nature of the test material, 1t Is not possible to quantify the data from
this study for use In risk assessment.
3.4. TOXICANT INTERACTIONS
Pertinent data regarding the toxicant Interactions of pyrene could not
be located 1n the available literature.
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4. CARCINOGENICITY
4.1. HUNAN DATA
4.1.1. Oral. Pertinent data regarding the carcinogenic effects of oral
exposure to pyrene In humans could not be located 1n the available
literature.
4.1.2. Inhalation. Pertinent data regarding the carcinogenic effects of
Inhalation exposure to pyrene In humans could not be located In the avail-
able literature.
4.2. BIOASSAYS
4.2.1. Oral. Pertinent data regarding the carcinogenic effects of orally
administered pyrene to experimental animals could not be located In the
available literature.
4.2.2. Inhalation. Pertinent data regarding the carcinogenic effects of
Inhalation exposure to pyrene 1n experimental animals could not be located
In the available literature.
4.3. OTHER RELEVANT DATA
Pyrene was negative In the reverse mutation assay with Salmonella typhl-
mur1 urn (LaVole et a!., 1979; Nagao and Suglmura, 1978); In mammalian cell
mutagenesls assays In the presence of a metabolizing enzyme system (Maher
and McCormlck, 1978); In the Escher1ch1a coll WP2/WP100 rec assay 1n the
presence or absence of exogenous mammalian activation (Mamber et al., 1983);
and 1n the L51F8Y/TK assay with or without a mammalian metabolic activation
system (Amacher and Turner, 1982).
Pyrene significantly Induced unscheduled DNA synthesis 1n cultured rat
hepatocytes (Althous et al., 1982). Chen (1983) reported that pyrene binds
to DNA; at least two binding sites were Identifiable.
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4.4. WEIGHT OF EVIDENCE
The carclnogenlclty of oral or Inhalation exposures of humans or animals
to pyrene have not been evaluated. When applied dermally, pyrene Is
regarded as a noncardnogen (Santodonato et al., 1981; U.S. EPA, 1981).
Pyrene was Ineffective as a complete carcinogen when applied to the skin of
mice (LaVole et al., 1979). Mouse skin Is known to be highly sensitive to
the effects of carcinogenic PAH. Pyrene 1s not an effective tumor Initiator
for mouse skin (Wood et al., 1980).
IARC (1983) reported that there was Insufficient evidence regarding the
carcinogenic risk to humans and experimental animals associated with oral or
Inhalation exposure to pyrene. Applying the criteria for evaluation of the
overall weight of evidence for the carcinogenic potential for humans pro-
posed by the Carcinogen Assessment Group of the U.S. EPA (Federal Register,
1984), pyrene 1s most appropriately designated a Group D - Not Classified
chemical.
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5. REGULATORY STANDARDS AND CRITERIA
Exposure criteria and TLVs have been developed for PAH as a class, as
well as for several Individual PAHs. The OSHA has set an 8-hour TWA concen-
tration limit of 0.2 mg/m3 for the benzene-soluble fraction of coal tar
pitch volatlles (anthracene, benzo[a]pyrene, phenanthrene, acrldlne, chry-
sene, pyrene) (Code of Federal Regulations, 1981). NIOSH (1977) recommends
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 In workers. NIOSH (1977)
also recommends a celling limit for exposure to asphalt fumes of 5 mg air-
borne part1culates/m3 of air.
Environmental quality criteria, which specify concentration limits
Intended to protect humans against adverse health effects, have been recom-
mended for PAH In ambient water. The U.S. EPA (1980a) has recommended a
concentration limit of 28 ng/l for the sum of all carcinogenic PAHs 1n
ambient water. This value Is 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 PAHs are
equal In potency to benzo[a]pyrene. On the basis of the animal bloassay
data, dally consumption of water containing 28 ng/i of carglnogenlc PAHs
over an entire lifetime 1s estimated to keep the lifetime risk of cancer
development below one chance In 100,000.
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The EPA has not recommended an ambient water quality criterion for non-
carcinogenic PAHs as a class. The U.S. EPA (1980a) acknowledged that data
suitable for quantitative risk assessment of noncarclnogenlc PAHs are
essentially nonexistent.
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. The lack of subchronlc oral data precludes the derivation
of an oral AIS for pyrene.
6.2.1. Inhalation. The lack of subchronlc Inhalation data precludes the
derivation of an Inhalation AIS for pyrene.
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. The lack of chronic and subchronlc oral data precludes the
derivation of an oral AIC for pyrene.
6.2.2. Inhalation. The lack of chronic and subchronlc Inhalation data
precludes the derivation of an Inhalation AIC for pyrene. U.S. EPA (1983b)
reviewed the Inhalation studies of Holland et al. (1980) In hamsters and
Weaver and Gibson (1979) In pregnant rats and concluded that data were
Insufficient for computation of a CS for pyrene.
6.3. UNIT CARCINOGENIC RISK (q *)
6.3.1. Oral. The lack of oral carclnogenlclty data precludes the deriva-
tion of a unit carcinogenic risk for pyrene.
6.3.2. Inhalation. The lack of Inhalation carclnogenlclty data precludes
the derivation of a unit carcinogenic risk for pyrene.
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8. REFERENCES
Althous, F.R., S.D. Lawrence, G.L. Sattler, D.G. Longfellow and H.C. Pilot.
1982. Chemical quantification of unscheduled DNA synthesis In cultured
hepatocytes as an assay for the rapid screening of potential chemical car-
cinogens. Cancer Res. 42(8): 3010-3015.
Amacher, D.E. and G.N. Turner. 1982. Mutagenlc evaluation of carcinogens
and noncarclnogens In the L5178Y/TK assay utilizing postmltochondrlal frac-
tions (S9) from normal rat liver. Mutat. Res. 97(1): 49-65.
Callahan, M.A., N.W. Sllmak and N.W. Gabel, et al. 1979. Water-Related
Environmental Fate of 129 Priority Polluntants. Vol. II. U.S. EPA, Office
of Water Planning and Standards, Office of Water and Waste Management, Wash-
ington, DC. EPA-440/4-79-0295.
Chen, F.M. 1983. Binding of pyrene to DNA, base sequence specificity and
Us Implication. Nucleic Adds Res. 11(20): 7231-7250.
Code of Federal Regulations. 1981. OSHA Safety and Health Standards. 29
CFR 1910.1000.
Falk, H.L., I. Markul and P. Rotln. 1956. Aromatic hydrocarbons. IV.
Their fate following emission Into the atmosphere and experimental exposure
to washed air and synthetic smog. A.M.A. Arch. Ind. Health. 13: 13-17.
(Cited In Santodonato et al., 1981)
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Federal Register. 1984. Environmental Protection Agency.' Proposed
guidelines for carcinogenic risk assessment. FR 49: 46294-46299.
Holland, L.M., W.d. Spall and L.L. Garcia. 1980. Inhalation toxicology of
oil shale - related materials. Health ImpHc. New Energy Technol. (Park
City Environ. Health Conf.). p. 515-526. (CA 94(7): 423052)
IARC (International Agency for Research on Cancer). 1983. Polynuclear
Aromatic Compounds, Part I, Chemical, Environmental and Experimental Data.
ITK IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals
to Humans. WHO, IARC, Lyon, France. Vol. 32.
Kenaga, E.E. and C.A.I Goring. 1980. Relationship between water solubil-
ity, soil sorptlon, octanol/water partitioning and concentration of chemi-
cals 1n biota. In: Aquatic Toxicology, J.G. Eaton, P.R. Parrlsh and A.C.
Hendrlcks, Ed. ASTH, Philadelphia, PA. p. 78-115. ASTM STP 707.
Korfmacher, W.A., E.L. Wehry, G.Mamantox and D.F.S. Natusch. 1980. Resis-
tance to photochemical decomposition of polycycllc aromatic hydrocarbons
vapor-adsorbed on coal fly ash. Environ. Scl. Technol. 14: 1094-1099.
LaVole, E., et al. 1979. A comparison of the mutagenlclty, tumor-Initiat-
ing activity and complete carclnogenlclty of polynuclear aromatic hydrocar-
bons. In: Polynuclear Aromatic Hydrocarbons, P.W. Jones and P. Leber, Ed.
Ann Arbor Science Publishers, Inc., Ann Arbor, MI. p. 705-721. (Cited In
U.S. EPA, 1981)
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•I '
Mabey, H.R., O.H. Smith and R.T. Podoll. 1981. Aquatic Fate Process Data
for Organic Priority Pollutants, U.S. EPA, Monitoring and Data Support Dlv.,
Office of Water Regulation and Standards, Washington, DC. EPA 440/4-81-014.
Maher, V.M. and 3.J. McCormlck. 1978. Mammalian Cell Mutagenesls by Poly-
cycllc Aromatic Hydrocarbons and Their Derivatives. In: Polycycllc Hydro-
carbons and Cancer. 2. Molecular and Cell Biology, H.V. Gelboln and P.O.P.
Ts'o, Ed. Academic Press, Inc., NY. p. 137-160. (Cited In U.S. EPA, 1981)
Mamber, S. W., W., V. Bryson and S.E. Katz. 1983. The Escherlchla coll
WP2/WplOO rec assay for detection of potential chemical carcinogens. Mutat.
Res. 119(2): 135-144.
Mitchell, C.E. and K.W. Tu. 1979. Distribution, retention and elimination
of pyrene In rats after Inhalation. J. . Toxlcol. Environ. Health.
5: 1171-1179. (Cited In U.S. EPA, 1981)
Nagao, M. and T. Suglmura. 1978. Mutagenesls: Mlcroblal Systems. In:
Polycycllc Hydrocarbons and Cancer. 2. Molecular and Cell Biology, H.V.
Gelboln and P.O.P. Ts'o, Ed. Adademlc Press, Inc., NY. p. 99-122. (Cited
1n U.S. EPA, 1981)
NIOSH (National Institute of Occupational Safety and Health). 1977.
Criteria for a Recommended Standard...Occupational Exposure to Coal Tar
Products, U.S. DHEW, PHS, CDC, Rockvllle, MD. Pub. No. 78-107.
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Santodonato, 0., P. Howard and D. Basu. 1981. Health and Ecological
Assessment of Polynuclear Aromatic Hydrocarbons. Pathotox Publishers, Inc.,
Park Forest South, IL.
U.S. EPA. 1980a. Ambient Water Quality Criteria for Polynuclear Aromatic
Hydrocarbons. U.S. EPA, Environmental Criteria and Assessment Office,
Cincinnati, OH. EPA 440/5-80-069. NTIS PB 81-117806.
U.S. EPA. 1980b. Guidelines and Methodology Used In the Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45:79347-79357.
U.S. EPA. 1981. Hazard Profile on PAH. Prepared by the Environmental Cri-
teria and Assessment Office, Cincinnati, OH, OHEA for the Office of Solid
Waste and Emergency Response, Washington, DC.
U.S. EPA. 1983a. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Toxldty Data. Prepared by the Environmental
Criteria and Assessment Office, Cincinnati, OH, OHEA for the Office of Solid
Waste and Emergency Response, Washington, DC.
U.S. EPA. 1983b. Reportable Quantity for Pyrene. Prepared by Environ-
mental Criteria and Assessment Office, Cincinnati, OH, OHEA for the Office
of Solid Waste and Emergency Response, Washington, DC.
Weaver, N.K. and R.L. Gibson. 1979. The U.S. oil shale Industry: A health
perspective. Am. Ind. Hyg. Assoc. J. 40(6): 460-467.
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Wise, S.A., W.3. Bonnett, F.R. Guenther and H.E. May. 1981. A relationship
between /versed-phase C10 liquid chromatographlc retention and the shape
lo
of polycycllc aromatic hydrocarbons. J. Chromatogr. Sc1. 19: 457-465.
Wood, A.W., et al. 1980. Mutagenlclty and tumor-Initiating activity of
cyclopenta [c,d]pyrene and structurally related compounds. Cancer Res.
40(3): 642. (Cited In U.S. EPA, 1981)
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