TECHNICAL REPORT DATA
(fuut rt»d Instntcttora on the rtvmt before completing)
REPORT NO.
EPA/600/8-88/011
3. RECIPIENT'S ACCESSION HO.
PB88-17951Q
. TITLE AND SUBTITLE
Health Effects Assessment for Acenaphthylene
B. REPORT DATE
B. PERFORMING ORGANIZATION CODE
. AUTHOR(S)
B. PERFORMING ORGANIZATION REPORT NO
ft. PERFORMING ORGANIZATION NAME AND ADDRESS
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
TZ. SPONSORING AGENCY NAME AND ADDRESS
13. TYPE OF REPORT AND PERIOD COVERED
'Environmental Criteria and Assessment Office
Office of Research and Development
li.S. Environmental Protection Agency
Cincinnati. OH 45268 __
14. SPONSORING AGENCY CODE
EPA/600/22
SUPPLEMENTARY NOTES
This report summarizes and evaluates information relevant to a preliminary interim
assessment of adverse health effects associated with specific chemicals or compounds.
The Office of Emergency and Remedial Response (Superfund) uses these documents in
preparing cost-benefit analyses under Executive Order 32991 for decision-making under
CERCLA. All estimates of acceptable intakes and carcinogenic potency presented in
this document should be considered as preliminary and reflect limited resources
allocated to this project. The intent in these assessments is to suggest acceptable
exposure levels whenever sufficient data are available. The interim values presented
reflect the relative degree of hazard associated with exposure or risk to the
chemical(s) addressed. Whenever possible, two categories of values have been
estimated for systemic toxicants (toxicants for which cancer is not the endpoint of
concern). The first, RfD$ or subchronic reference dose, is an estimate of an exposure
level that would not be expected to cause adverse effects when exposure occurs during
a limited time interval. The RfD is an estimate of an exposure level that would not
be expected to cause adverse effects when exposure occurs for a significant portion
of the lifespan. For compounds for which there is sufficient evidence of
careinbgenicity, qi*s have been computed, if appropriate, based on oral and
inhalation data if available.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS
c. COSATi Field/Group
U.S. BivlroTiineirtal Protection Agency
E-^Ti--n 5, Library (5PL-]6)
£vO S. Dearborn ?t:-oot, lioois 1670
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1BL DISTRIBUTION STATEMENT
19. SECURITY CLASS (This Rtport)
21. NO. OF PAGES
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EPA ?«• 222CM (R««. 4-77) PREVIOUS BOITIOM i» OMOLCTK
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EPA/600/8-88/011
May, 1987
HEALTH EFFECTS ASSESSMENT
FOR ACENAPHTHYLENE
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI. OH 45268
U.S. Environmental Protection Ar
Region 5, Library "'
2'30 S. Dearborn
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DISCLAIMER
This document has been reviewed In accordance with the U S
Environmental Protection Agency's peer and administrative review policies
and approved for publication. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
1V
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PREFACE
4
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with acenaph-
thylene. All estimates of acceptable Intakes and carcinogenic potency
presented In this document should be considered as preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-line literature searches of the
TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The basic
literature searched supporting this document Is current up to Hay, 1986.
Secondary sources of Information have also been relied upon In the prepara-
tion of this report and represent large-scale health assessment efforts that
entail extensive peer and Agency review. The following Office of Health and
Environmental Assessment (OHEA) sources have been extensively utilized:
U.S. EPA. 1980a. Ambient Water Quality Criteria Document for
Polynuclear Aromatic Hydrocarbons. Prepared by the Office of
Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Water Regula-
tions and Standards, Washington, DC. EPA 440/5-80-069. NTIS PB
81-117806.
U.S. EPA. 1980b. Hazard Profile for Acenaphthylene. Prepared by
the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of
Solid Waste, Washington, DC.
U.S. EPA. 1983. Reportable Quantity Document for Acenaphthylene.
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.
The Intent 1n 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.
Nevertheless, 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
systemic toxicants (toxicants for which cancer Is not the endpolnt of
concern). The first, RfD$ (formerly AIS) or subchronlc reference dose. 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 1s assumed. Animal data used for RFD§ 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. These
values are developed for both Inhalation (RfD§j) and oral (RfD$o)
exposures.
111
-------
t The RfD (formerly AIC) Is similar 1n concept and addresses chronic
exposure. It 1s an estimate of an exposure level that would not be expected
to cause adverse effects when exposure occurs for a significant portion of
the Ufespan [see U.S. EPA (1980a) for a discussion of this concept]. The
RfD 1s route-specific and estimates acceptable exposure for either oral
(RfOg) or Inhalation (RfDj) with the Implicit assumption that exposure
by other routes Is Insignificant.
Composite scores (CSs) for noncardnogens have also been calculated
where data permitted. These values are used for ranking reportable quan-
tities and the methodology for their development Is explained 1n U.S. EPA
(1983).
For compounds for which there Is sufficient evidence of carclnogenldty
RfD$ and RfO values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980a). Since cancer 1s a
process that Is not characterized by a threshold, any exposure contributes
an Increment of risk. For carcinogens, q-|*s have been computed, 1f appro-
priate, based on oral and Inhalation data 1f available.
1v
-------
ABSTRACT
Data sufficient for risk assessment were not available for acenaph-
thylene; therefore, no risk assessment values were derived. A Russian
Inhalation study where rats were exposed to acenaphthylene dust suggests a
carcinogenic role for this compound (Rotenberg and Mashblts, 1965). The
lungs appear to be a target organ for acenaphthylene by either Inhalation
(Rotenberg and Mashblts, 1965; Reshetluk et al., 1970) or oral (Rotenberg
and Mashblts, 1965) exposure. Continued mutagenlclty testing and short-term
animal cardnogenlclty assays to clarify the carcinogenic role of acenaph-
thylene are recommended as a first step In the testing of acenaphthylene.
-------
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. Or. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and John Helms (Office of
Toxic Substances) was the Project Officer. The final documents In 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 the following:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by the
following:
Bette Zwayer, Jacky Bohanon and Kim Davidson
Environmental Criteria and Assessment Office
Cincinnati, OH
vl
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TABLE OF CONTENTS
Page
1.
2.
3.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . . .
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
3.2. CHRONIC
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.4. TOXICANT INTERACTIONS
. . 1
, , 4
. . 5
. . 5
. . 5
5
. . 6
. . 7
. . 7
5
ft
7.
4.1. HUMAN DATA ,
4.2. BIOASSAYS ,
4.2.1. Oral ,
4.2.2. Inhalation ,
4.3. OTHER RELEVANT DATA
4.4. WEIGHT OF EVIDENCE
REGULATORY STANDARDS AND CRITERIA
RECOMMENDATIONS
REFERENCES
8
8
8
8
8
8
10
11
12
V11
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LIST OF ABBREVIATIONS
CAS Chemical Abstract Service
CS Composite score
Kow Octanol/water partition coefficient
LD5Q Dose lethal to 50X of recipients
MED Minimum effective dose
NOEL No-observed-effect level
PAH Polycycllc aromatic hydrocarbon
ppm Parts per million
RV,j Dose-rating value
RVe Effect-rating value
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1. ENVIRONMENTAL CHEMISTRY AND FATE
Selected physical and chemical properties and environmental fate of
acenaphthylene are presented In Table 1-1.
Acenaphthylene Is widely distributed 1n the environment. In air.
acenaphthylene will be present partly In the vapor phase and partly In the
sorbed state onto aerosol particles. Acenaphthylene adsorbed to partlcu-
lates could potentially travel great distances before ultimately being
removed by rainfall or dry deposition (NRC, 1983; Pankow et a"!., 1984).
Acenaphthylene In the vapor phase Is expected to undergo direct photolysis
or oxidation by reaction with hydroxyl radicals or ozone (estimated oxida-
tion half-life -1 hour) (HSDB, 1986; NRC, 1983; U.S. EPA, 1986a). In water,
acenaphthylene will be present partly 1n solution and partly as sorbed onto
suspended particles and sediments. The dissolved portion may undergo rapid
hydrolysis and significant blodegradatlon (Callahan et al., 1979). The
adsorbed portion may persist for years In sediments (Bjoerseth et al.,
1979). Based on the relatively high log K value, acenaphthylene 1s
expected to strongly adsorb to soil, thus persisting In the upper few
centimeters. In soil. It may undergo blodegradatlon.
Human exposure data specific for acenaphthylene could not be located 1n
the available literature. U.S. EPA (1980a), however, reviewed monitoring
studies In which total PAH content of groundwater varied from 0.003-0.04
jig/l and total PAH content of surface water ranged from 0.24-2.5
vg/i. In finished drinking water from 15 U.S. cities, total PAH content
ranged from 0.3-138.5 ng/l. with samples from only two cities >10 ng/t
(Basu and Saxena, 1977; 1978). The other major sources of oral exposure of
humans to PAH Is through food. Borneff (1977) estimated this contribution
0082H -1- 12/03/86
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TABLE 1-1
Selected Physical and Chemical Properties
and Environmental Fate of Acenaphthylene
CAS number:
Chemical class:
Molecular weight:
Vapor pressure:
Mater solubility:
Log octanol/water
partition coefficient:
Bloconcentratlon factor:
Half-lives In
Air:
Hater:
Soil:
208-96-8
polycycllc aromatic
hydrocarbon
152.20
10~8 to 10~2 mm Hg
at 20°C (estimated)
3.93 mg/i at 25°C
(estimated)
4.07 (estimated)
18.0 green mussels
(Perna verldls)
NA
NA
NA
Callahan et al., 1979
Callahan et al., 1979
Callahan et al., 1979
Hungspreugs et al., 1984
NA = Not available
0082h
-2-
12/03/86
-------
at ~3-4 mg total PAH/year. These data do not Indicate what proportion of
total PAH content of water and food 1s acenaphthylene, so 1t 1s not possible
to estimate human Intakes of acenaphthylene alone. The data reviewed and
presented by U.S. EPA (1980a) Imply that acenaphthylene may be a small pro-
portion of the total PAH content of water and food, since this compound 1s
not listed by name In tables that present levels of the more abundant PAHs.
Overall, human exposure to acenaphthylene may be expected to occur by
both oral and Inhalation routes and H Is Impossible to predict which route
may be the more Important.
0082h -3- 09/03/86
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
Pertinent data regarding the absorption of acenaphthylene following oral
or Inhalation exposure could not be located In the available literature.
0082h -4- 09/03/86
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. In a Polish study reported 1n an abstract, Knobloch et al.
(1969) administered acenaphthylene orally to rats at a dose of 0.6 g/kg for
40 days. Treatment-related effects observed were considerable body weight
loss, changes In renal function, changes In the peripheral blood pattern and
Increased serum amlnotransferase activities.
In a Russian study (Rotenberg and Mashblts, 1965), acenaphthylene In oil
was administered orally to white mice at a dose 1/10 the LD5Q [LOrQ =
1760 (range of 2800 to 1100) mg/kg] every other day for 2 months. Treated
mice showed a significant lag In weight gain as compared with controls.
Hlstopathologlcal examination of organs showed signs of stasis 1n the paren-
chymatous organs and albuminoid degeneration of the liver. The most severe
changes were observed In the lungs, which showed hemorrhage with destruction
of the Interalveolar septa and focal bronchial pneumonia. Purulent foci
were observed In Isolated cases, and bronchogenlc lung cancer was diagnosed
1n one mouse. Further details of this study were not provided.
3.1.2. Inhalation. In a Russian study (Rotenberg and Hashblts, 1965),
acenaphthylene was administered to white rats Intratracheally In a sunflower
oil solution or by blowing acenaphthylene powder Into the trachea. The
dosing regimen used was not provided. The pulmonary tracts of animals
sacrificed 1 month after the experiment began showed signs of tracheobron-
chH1s and hyperemla, edema and necrosis of the epithelium In the trachea
and bronchi with the formation of ulcers. No further details of this study
were available.
0082h -5- 09/03/86
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In an additional study reported by Rotenberg and Mashblts (1965). white
rats were exposed to acenaphthylene dust at 0.5-1.25 mg/rn3 for 4 hours/day
for 4 months. After 3 weeks of exposure, a delay In weight gain and a
tendency toward decreased blood pressure were observed. Hlstopathologlcal
examination revealed various degrees of malignancy In the lungs of almost
all treated rats. Focal bronchitis and perlbronchUls with bronchlollzatlon
of the alveolar and metaplasia of the bronchial epithelium were observed 1n
the mildest cases. Advanced cases showed desquamatlon of the bronchial and
alveolar epithelium, paplllar growths In the epithelium and. In three rats.
Isolated regions of carcinoma 1n the form of strands of epithelial cells.
Further details of this study were not provided.
In a Russian study by Reshetluk et al. (1970), -100 white male rats were
exposed to vapors of acenaphthylene at a concentration of 18±2.5 mg/m3, 4
hours/day, 6 exposures/week for 5 months. In exposed rats, reflexes of the
upper airways were altered and an Increase 1n the concentration of nucleic
acids In the liver was observed. Hlstopathologlcal examination of the lungs
revealed aspeclflc pneumonia as the major pathology of Inhalation exposure
to acenaphthylene. Changes observed In the lungs Included desquamatlon of
the cells 1n the alveolar epithelium and focal bronchitis accompanied by
hyperplasla and metaplasia of the bronchial epithelium. No signs of malig-
nant growth were observed In this study. No further details of this study
were available.
3.2. CHRONIC
Pertinent data regarding the toxic effects of acenaphthylene following
chronic oral or Inhalation exposure could not be located In the available
literature.
0082H -6- 12/03/86
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" 313. TERATOGEHICITY AND OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding teratogenlc and other reproductive effects
following oral or Inhalation exposure could not be located In the available
literature.
3.4. TOXICANT INTERACTIONS
Without providing details, Reshetluk et al. (1970) stated that Inhala-
tion of naphthalene caused an Increase In the sensitivity of rats to a
single Inhalation exposure of acenaphthylene at 7 mg/m3. Observations
recorded Include an Increase In oxygen "composition" (as written by
translator — probably should read "consumption") (60%), an Increase In body
(0.6*0.2°) and skin temperature (0.4+0.2°), an Increase In blood peroxldase
activity (38%), and decreases 1n blood sugar concentration (10%) and
ascorbic acid In the lungs (33%).
0082H -7- 12/03/86
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4. CARCINOGENIC1TY
4.1. HUMAN DATA
Pertinent data regarding the carcinogenic potential of acenaphthylene In
humans following oral or Inhalation exposure could not be located In the
available literature.
4.2. BIOASSAYS
4.2.1. Oral. Pertinent data regarding the oncogenlcHy of acenaphthylene
In orally exposed animals could not be located 1n the available literature.
4.2.2. Inhalation. Rotenberg and Mashblts (1965) reported "various
degrees of malignancy11 In the lungs of almost all of an unspecified number
of rats exposed to acenaphthylene dust at 0.5-1.25 mg/m3 for 4 hours/day
for 4 months. Further details were not provided. In another Russian study
with male white rats, hlstopathologlcal lesions Including hyperplasla and
metaplasia of the bronchial epithelium, but no signs of malignancy, were
reported following Inhalation of acenaphthylene vapors at 18 mg/m3, 4
hours/day, 6 days/week for 5 months (Reshetluk et a!., 1970).
4.3. OTHER RELEVANT DATA
Acenaphthylene has tested negative for reverse mutations In Salmonella
typhlmuMum strains TA1537 and TA1538 with S-9 metabolic activation
(Gatehouse, 1980) and 1n strains TA98 and TA100 with and without S-9 from
3-methylcholantrene Induced rats (Florin et al., 1980). Acenaphthylene was
mutagenlc In S. typhlmurlum strain TM677 with S-9 metabolic activation
(Kaden et al.. 1979).
4.4. WEIGHT OF EVIDENCE
Acenaphthylene has not been evaluated for Mr> carclnogenlclty In humans
and has not been adequately studied for Us carcinogenic activity 1n
0082H -8- 01/20/87
-------
animals; therefore, H can be placed In IARC Group 3 and In EPA Group 0, not
classified, according to the CAG classification scheme (U.S. EPA, 1986b).
Given Us structural realtlonshlp to known carcinogenic PAHs, however,
prudent public health policy would dictate minimizing exposure until more Is
known about the health hazards.
0082h -9- 01/20/87
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5. REGULATORY STANDARDS AND CRITERIA
No standards or criteria are available for acenaphthylene alone. The
U.S. EPA (1980a) derived ambient water quality criteria for PAH based upon
the excess cancer risk associated with benzo(a)pyrene, a known animal
carcinogen. For excess cancer risks of 10-s, 10-« and 10-7, these
criteria are 28.0, 2.8 and 0.28 ng/i, respectively, for consumption of
6.5 g of aquatic organism and 2 I of water/day. Based on consumption of
aquatic organisms alone, these criteria are 311.0, 31.1 and 3.11 ng/i,
respectively.
0082h -10- 01/20/87
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6. RECOMMENDATIONS
Because of the lack of data for the carclnogenlcHy and threshold
tox1c1ty of acenaphthylene, risk assessment values cannot be derived.
Acenaphthylene Is a PAH, a class of chemicals that Includes known
carcinogens. In a Russian study, malignancies 1n the lungs of rats were
associated with Inhalation exposure to acenaphthylene dusts (Rotenberg and
MashbHs, 1965). CarclnogenlcHy testing of acenaphthylene should be a
priority. MutagenlcHy studies of acenaphthylene have been negative In S.
typhlmurlum strains TA1537, TA1538, TA98 and TA100 (Gatehouse, 1980; Florin
et al., 1980), but positive In strain TM677 (Kaden et al., 1978).
If adequate testing Indicates that acenaphthylene Is not carcinogenic,
effort should be made to determine thresholds for noncardnogenlc toxldty.
Exposure data specifically for acenaphthylene could not be located, but
assuming exposure similar to other PAHs, both oral and Inhalation routes of
exposure may be of concern. From the Russian studies (Rohenberg and
MashbHs, 1965; Reshetluk et al., 1970), the lungs appear to be the target
organ; additional studies may define this further. Continued mutagenldty
testing, particularly In eukaryotlc systems, and short-term animal assays
may be useful to qualitatively estimate the oncogenldty of this compound.
0082h -11- 01/20/87
-------
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HSOB (Hazardous Substance Data Bank). 1986. No. 2661. On-Llne.
Hungspreugs, M., S. SUplpat, C. Tonapong, R.F. Lee, H.L. Wlndom and K.R.
Tenore. 1984. Heavy metals and polycycllc hydrocarbon compounds In benthlc
• I*
-------
U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Polynuclear
Aromatic Hydrocarbons. Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of Water Regulations and Standards, Washington, DC. EPA
-------
HSDB (Hazardous Substance Data Bank). 1986. No. 2661. On-Une.
Hungspreugs, M., S. Sllplpat, C. Tonapong, R.F. Lee, H.L. Wlndom and K.R.
Tenore. 1984. Heavy metals and polycycllc hydrocarbon compounds In benthlc
organisms of the upper gulf of Thailand. Marine Poll. Bull. 15(6): 213-218.
Kaden, O.A., R.A. HHes and W.G. ThUly. 1979. HutagenlcHy of soot and
associated polycycllc aromatic hydrocarbons to Salmonella typhlmurlum.
Cancer Res. 39(10): 4152-1459.
Knobloch, K., et al. 1969. Acute and subacute toxldty of acenaphthene and
acenaphthylene. Med. Pracy. 20: 210. (Cited In U.S. EPA, 1983)
NRC (National Research Council). 1983. Polycycllc aromatic hydrocarbons.
Evaluation of sources and effects. Natl. Acad. Press, Washington, DC.
p. 3-7.
Pankow, J.F., L.H. Isabella and W.E. Asher. 1984. Trace organic compounds
1n rain. I. Sampler design and analysis by adsorption/thermal desorptlon
(ATD). Environ. Sc1. Techno!. 18: 310-318.
Reshetluk, A.L., E.I. Talaklna and P.A. En'lakova. 1970. Toxlcologlc
assessment of cenaphthene and acenaphthylene. Gig. Tr. Prof. Zabol. 14(6):
46-47.
Rotenberg, lu.S. and P.O. MashbHs. 1965. Toxlcologlc aspects of acenaph-
thylene. G1g. Tr. Prof. Zabol. 9(9): 53-54.
0082h -13- 01/20/87
V ? feviromental
-------
U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Polynuclear
Aromatic Hydrocarbons. Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of Water Regulations and Standards, Washington, DC. EPA
440/5-80-069. NTIS PB 81-117806.
U.S. EPA. 1980b. Hazard Profile for Acenaphthylene. Prepared by the
Office of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Solid Haste, Washington,
DC.
U.S. EPA. 1983. Reportable Quantity Document for Acenaphthylene. 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. 1986a. Graphical Estimations Modeling System (GEMS). Fate of
Atmospheric Pollutants (PAP) Data Base. U.S. EPA, Office of Toxic Sub-
stances. Washington, DC. On-Hne.
U.S. EPA. 1986b. Guidelines for Carcinogenic Risk Assessment. Federal
Register. 51(185): 33992-34003.
0082h -14- 02/09/87
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