ECAO-CIN-P277
July, 1987
EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS PROFILE
FOR PYRENE
Prepared for
OFFICE OF SOLID WASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
flop
V, Library3' Pr°tectl°n AgOft#T: DO NOT CITE OR QUOTE
NOTICE
This document Is a preliminary draft. It has not been formally released
by the U.S. Environmental Protection Agency and should not at this stage be
construed to represent Agency policy. It Is being circulated for comments
on its technical accuracy and policy implications.
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DISCLAIMER
This report 1s an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
Health and Environmental Effects Profiles (HEEPs) are prepared for the
Office of Solid Waste and Emergency Response by the Office of Health and
Environmental Assessment. The HEEPs are intended to support listings of
hazardous constituents of a wide range of waste streams under Section 3001
of the Resource Conservation and Recovery Act (RCRA), as well as to provide
health-related limits for emergency actions under Section 101 of the Compre-
hensive Environmental Response, Compensation and Liability Act (CERCLA).
Both published literature and information obtained from Agency program
office files are evaluated as they pertain to potential human health,
aquatic life and environmental effects of hazardous waste constituents. The
literature searched and the dates of the searches are included in the
section titled "Appendix: Literature Searched." The literature search
material is current through November, 1985.
Quantitative estimates are presented provided sufficient data are
available. For systemic toxicants, these include Reference doses (RfDs) for
chronic exposures. An RfD is defined as the amount of a chemical to which
humans can be exposed on a daily basis over an extended period of time
(usually a lifetime) without suffering a deleterious effect. In the case of
suspected carcinogens, RfDs are not estimated in this document series.
Instead, a carcinogenic potency factor of q-|* Is provided. These potency
estimates are derived for both oral and inhalation exposures where possible.
In addition, unit risk estimates for air and drinking water are presented
based on Inhalation and oral data, respectively.
Reportable quantities (RQs) based on both chronic toxicity and carclno-
genlclty are derived. The RQ Is used to determine the quantity of a hazard-
ous substance for which notification is required In the event of a release
as specified under CERCLA. These two RQs (chronic toxicity and carcinogen-
icity) represent two of six scores developed (the remaining four reflect
ignltability, reactivity, aquatic toxicity and acute mammalian toxicity).
The first draft of this document was prepared by Syracuse Research
Corporation under EPA Contract No. 68-03-32P8. The document was subse-
quently revised after reviews by staff within the Office of Health and
Environmental Assessment: Carcinogen Assessment Group, Reproductive Effects
Assessment Group, Exposure Assessment Group, and the Environmental Criteria
and Assessment Office In Cincinnati.
The HEEPs will become part of the EPA RCRA and CERCLA dockets.
ill
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EXECUTIVE SUMMARY
Pure pyrene is a colorless solid at ambient temperatures. The presence
of tetracene, a common Impurity, gives yellow color to pyrene. It Is fairly
soluble In organic solvents Including ethanol, ethyl ether and benzene
(Wlndholz, 1983; Weast, 1980), but is almost Insoluble In water (Pearlman et
a!., 1984). Chemically, pyrene Is susceptible to oxidation by ozone,
peroxides and other oxldants (NAS, 1972). Currently, pyrene 1s neither
commercially produced nor Imported Into the United States (SRI, 1986). It
can be Isolated from coal tar or from the products of destructive
hydrogenatlon of coal (Wlndholz, 1983). There Is no known commercial use of
pyrene (IARC, 1983).
If released to the aquatic environment, adsorption to partlculate
organic matter and sediments In water will be an Important environmental
fate process based on measured sediment K values and widespread monitor-
ing of pyrene In ambient sediments. In the dissolved state In the water
column, direct photolysis may be significant, as the average photolytlc
half-life of pyrene near the surface at 40°N latitude has been estimated to
be -1.1 hours in June and 3.1 hours In January (Zepp and Schlotzhauer,
1983). In deep, turbid water, photolysis may not be an Important process.
Mlcroblal degradation data (Walker and Colwell, 1975) suggest that pyrene
may be susceptible to blodegradatlon in natural water. Mlcroblal oxidation
of PAH requires oxygen and will not proceed in anoxlc sediments or water
(U.S. EPA/NIH, 1986). In clear and shallow water, blodegradatlon will not
be Important. It will, however, be an Important process In slow moving,
deep and turbid waters. Volatilization may have some significance in
shallow, rapidly flowing rivers. Bloaccumulation potential appears to be
1v
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dependent on the organism being considered. Hydrolysis 1s not expected to
be Important. The detection of a nearly constant concentration of pyrene 1n
sediment cores of a remote forest "lake (Tan and Heit, 1981) Indicate that
pyrene 1s very persistent under anaerobic and dark conditions. If released
to the atmosphere, pyrene will exist in both vapor and particulate-adsorbed
phases; monitoring data (Ligocki et al., 1985a,b; Yamasaki et al., 1982)
suggest that the vapor-phase may dominate. Vapor-phase pyrene appears to be
susceptible to relatively rapid decomposition by direct photolysis or
reaction with photochemically produced HO radical. Adsorption of pyrene to
partlculates containing a high carbon content significantly attenuates
photolysis and other chemical oxidation reactions (Behymer and Hites, 1985;
Valerlo and Lazzarotto, 1984; Yokley et al., 1986; Santodonato et al.,
1981), and may therefore permit the long-range atmospheric transport (Lunde
and Bjoerseth, 1977). Pyrene may be physically removed from the atmosphere
by wet and dry deposition (Llgocki et al., 1985a,b; Tan and Heit, 198-1). If
released to soil, pyrene may be susceptible to biodegradatlon under aerobic
conditions. Under most conditions, H Is not expected to leach or vola-
tilize significantly and may persist in soils.
Human exposure to pyrene occurs primarily through the inhalation of
tobacco smoke and polluted air and by the Ingestion of contaminated food and
water (IARC, 1983). Pyrene occurs ubiquitously as a product of Incomplete
combustion and occurs naturally In fossil fuels (IARC, 1983). It has been
widely detected 1n drinking water, surface water, groundwater, rainwater and
aquatic sediments (see Tables 3-1 and 3-2), in many foods (Santodonato et
al., 1981; Dennis et al., 1983), and in the general ambient atmosphere (see
Table 3-3). The average dietary intake of pyrene in England is -1.09
yg/day (Dennis et al., 1983); the average intake from drinking water in
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the United States is -2.0 ng/day, while the Inhalation Intake In the United
States is -10-400 ng/day. The presence of pyrene in food Is a result of
contamination from a polluted environment and formation during cooking by
pyrolysls of organic matter (Santodonato et al., 1981; Fazio and Howard,
1983). Emission to the atmosphere results from the combustion of fossil
fuels (oil, coal), wood burning for residential heating, gasoline and dlesel
engine exhaust, and open burning (agricultural burning, forest fires,
structure burning, refuse burning) (NRC, 1983).
Of six species tested, three arthropods were more sensitive to pyrene
than fish or amphibians. LC™ values of 4, 8 and 20 yg/8. were
reported for Daphnla maqna. Artemia salina and Aedes aegypti. respectively.
Like some other PAH, the toxlclty of pyrene Is greatly enhanced by UV light
or sunlight (Kagan et al., 1985). Two algae species were less sensitive to
pyrene than the three arthropods, with EC™ values of 202 and 332 yg/8.
for Inhibition of photosynthesis (Hutchlnson et al., 1980). Reported BCF
values ranged from 72 for rainbow trout (Gerhart and Carlson, 1978) to
36,300 for the alga, Selenastrum capricornutum (Casserly et al., 1983).
Limited gastrointestinal absorption of pyrene was measured 24 hours
after gavage administration of 50 vg pyrene to male rats (Mitchell and Tu,
1977, 1979). Pyrene was detected fluorometrlcally in the gastrointestinal
tract at -50% of the administered dose; no pyrene was detected in the liver,
kidneys, lungs or trachea. An Interpretation of poor gastrointestinal
absorption of pyrene from these data Is supported by detection of pyrene in
the liver and kidneys 24 hours after Inhalation exposure, but complicated by
possible biliary elimination of metabolites since the analytical technique
was not specific for pyrene. Furthermore, the method of administration was
not environmentally relevant. Rapid absorption of Inhaled pyrene by rats is
v1
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Indicated by fluorometrlc detection of pyrene In respiratory tissues, liver
and kidneys 30 minutes after 1-hour exposure to 500 yg/s. pyrene aerosol
(Mitchell and Tu, 1979). Distribution to tissues other than the liver and
kidney was not assessed In the Inhalation study.
I_n_ vivo and jjn vitro studies Indicate that metabolism of pyrene proceeds
by oxidation at the 1-2 and 4-5 bonds, with 1-hydroxypyrene as the principal
metabolite (Boyland and Sims, 1964; Sims, 1970; Jacob et al., 1982; Kelmlg
et al., 1983). The metabolites have been detected as sulfurlc add and
glucuronic acid conjugates In the urine of rats, rabbits and pigs. Urinary
excretion and fecal elimination of pyrene has not been quantHated, but In
limited oral and Inhalation studies with rats, fecal elimination appears to
reflect unabsorbed pyrene, pyrene resulting from mucoclllary clearance or
biliary elimination (Mitchell and Tu, 1979).
Intratracheal Instillation of 3 mg pyrene suspended In saline at weekly
Intervals for 30 weeks did not produce tumors In the respiratory system
(hlstologlc examination) or other tissues (gross examination) In hamsters
observed for life (Sellakumar and Shublk, 1974). Skin tumors were not
Induced 1n mice by twice or three-times weekly dermal application of pyrene
for 1-2 years (Barry et al., 1935; Badger et al., 1940; Wynder and Hoffmann,
1959; Roe and Grant, 1964; Morton and Christian, 1974; Van Duuren and
Goldschmidt, 1976). Mouse skin Initiation-promotion studies Involving
Initiation with benzo[a]pyrene (Roe and Grant, 1964), promotion with croton
oil (Salaman and Roe, 1956) or promotion with TPA (Scrlbner, 1973; Wood et
al., 1980) were negative or Inconclusive (Scrlbner, 1973). Enhancement of
the .dermal carc1nogen1city of benzo[a]pyrene In mice by simultaneous appli-
cation of pyrene has, however, been reported (Goldschmldt et al., 1973; Van
Duuren and Goldschmldt, 1976), Indicating possible cocarcinogeniclty of
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pyrene. Two subcutaneous Injections of. 10 mg pyrene crystals 4 months apart
did not produce local tumors In mice after 12-18 months (Shear and Leiter,
1941).
Pyrene has been tested extensively in mutagenicity and other short-term
assays. Pyrene was mutagenic in some tests with ^. typhimurium in the
presence of metabolic activation preparation (Kaden et al., 1979; Bridges et
al., 1981; Matijasevic and Zelger, 1985; Sakai et al., 1985) and produced
unscheduled DNA synthesis In cultured primary hamster hepatocytes (McQueen
et al., 1983) and human fibroblasts (Robinson and Mitchell, 1981), mutation
in mouse lymphoma L5178Y cells Vn vitro (Jotz and Mitchell, 1981), sister
chromatid exchanges in CHO (Evans and Mitchell, 1981) and V79 (Popescu et
al., 1977) cells in vitro and chromosomal aberrations in Chinese hamster V79
cells In vitro (Popescu et al., 1977). Genotoxidty of pyrene was not
demonstrated In other assays using the same or different indicator organisms
or endpolnts, including morphological transformation in a variety of rat,
mouse, hamster and guinea pig systems.
Pertinent data regarding teratogenldty or other reproductive effects of
pyrene could not be located In the available literature as cited in the
Appendix.
Inhibition of growth and enlarged, fatty livers were reported as effects
in a group of six male rats maintained on diets that contained 2000 ppm
pyrene for as long as 100 days (White and White, 1939). The significance of
these findings 1s uncertain because Incidences were not reported, a small
number of animals was tested, the treatment durations were variable and
unspecified, and control data were not reported. Pertinent data regarding
toxic effects of chronic oral or inhalation exposure to pyrene could not be
located In the available literature as cited in the Appendix.
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A single intraperUoneal Injection of 150 mg/kg pyrene produced minimal
gross swelling and congestion of the liver and Increased serum AST and
blllrubin In rats (Yoshlkawa et al., 1985).
Data were Insufficient to derive an RfD, q * RQ or F factor. Pyrene
is a U.S. EPA Group D chemical; that is, H cannot be classified as to Its
human carcinogenic potential.
ix
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 2
1.4. USE DATA 2
1.5. SUMMARY 2
2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES 4
2.1. WATER 4
2.1.1. Hydrolysis 4
2.1.2. Oxidation 4
2.1.3. Photolysis - 4
2.1.4. Mlcroblal Degradation 5
2.1.5. Volatilization 6
2.1.6. Adsorption 6
2.1.7. Bloconcentratlon. 7
2.1.8. Persistence 7
2.2. AIR . 8
2.2.1. Photolysis 8
2.2.2. Reaction with HO Radical 9
/ 2.2.3. Physical Removal 9
2.3. SOIL 9
2.3.1. Mlcroblal Degradation . 9
2.3.2. Chemical Degradation 10
2.3.3. Adsorption 10
2.3.4. Volatilization 10
2.4. SUMMARY 10
3. EXPOSURE 12
3.1. WATER 12
3.2. FOOD 15
3.3. INHALATION 16
3.4. DERMAL 18
3.5. SUMMARY. 18
4. PHARMACOKINETICS 19
4.1. ABSORPTION 19
4.2. DISTRIBUTION 19
4.3. METABOLISM 20
4.4. EXCRETION 21
4.5. SUMMARY 21
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TABLE OF CONTENTS (cont.)
Page
5. EFFECTS 23
5.1. CARCINOGENICITY 23
5.2. HUTAGENICITY 26
5.3. TERATOGENICITY 28
5.4. OTHER REPRODUCTIVE EFFECTS 28
5.5. CHRONIC AND SUBCHRONIC TOXICITY 28
5.6. OTHER RELEVANT INFORMATION 29
5.7. SUMMARY 30
6. AQUATIC TOXICITY 32
6.1. ACUTE 32
6.2. CHRONIC 32
6.3. PLANTS 32
6.4. RESIDUES 34
6.5. SUMMARY 34
7. EXISTING GUIDELINES AND STANDARDS 38
7.1. HUMAN 38
7.2. AQUATIC 39
8. RISK ASSESSMENT 40
9. REPORTABLE QUANTITIES 43
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC
TOXICITY 43
9.2. WEIGHT OF EVIDENCE AND POTENCY FACTOR (F=1/ED10)
FOR CARCINOGENICITY 44
10. REFERENCES 47
APPENDIX: LITERATURE SEARCHED 71
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LIST OF TABLES
No. Title Page
3-1 Pyrene Monitoring Data for Various Types of Water 13
3-2 U.S. Sediment Monitoring Data for Pyrene 14
3-3 U.S. Air Monitoring Data for Pyrene 1979-1984 17
5-1 Dermal and Injection Carcinogenicity Studies of Pyrene. ... 24
6-1 Acute Toxicity of Pyrene to Aquatic Organisms 33
6-2 Bioconcentration Data for Pyrene in Aquatic Organisms .... 35
6-3 Monitoring Data for Pyrene Residues in Aquatic Organisms. . . 36
9-1 Pyrene: Minimum Effective Dose (MED) and Reportable
Quantity(RQ) 45
xii
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
ALT Alanlne amlnotransferase
AST Aspartate amlnotransferase
BUN Blood urea nitrogen
CAS Chemical Abstract Service
CHO Chinese hamster ovary
DMSO Dimethyl sulfoxlde
DNA Deoxyrlbonuclelc add
ECso Median effective concentration
GGPT Gamma-glutamyl transpeptldase
Koc Soil sorptlon coefficient
Kow Octanol water partition coefficient
Kse(j Sorptlon coefficient between sediment and water
Median lethal concentration
Median lethal dose
LDH Lactate dehydrogenase
MED Minimum effective dose
PAH Polycycllc aromatic hydrocarbons
ppb Parts per billion
ppm Parts per million
ppt Parts per trillion
RQ Reportable quantity
TLC Thin layer chromatography
TLV Threshold limit value
TPA Terephthallc acid
TWA Time-weighted average
UV Ultraviolet
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
The chemical commonly called pyrene 1s also known by the synonym benzo-
(d,e,fJphenanthrene. The structure, empirical formula, molecular weight and
CAS Registry number for this chemical are as follows:
Empirical formula:
-.-.,-
ID IU
Molecular weight: 202.24
CAS Registry number: 129-00-0
Both the numerical and alphabetical numbering system for the substltu-
ents 1n the ring are Indicated 1n the structure above (Santodonato et a!.,
1981).
1.2. PHYSICAL AND CHEMICAL PROPERTIES
Pure pyrene 1s a colorless crystalline solid at ambient temperatures.
The presence of tetracene, a common contaminant, gives yellow color to
pyrene. It Is fairly soluble In organic solvents Including ethanol, ethyl
ether and benzene (Wlndholz, 1983; Weast, 1980), but 1s almost Insoluble 1n
water. A few relevant physical properties of pyrene are listed below:
Melting point:
Boiling point:
Density at 23°C:
Solubility In distilled
water at 25°C:
Solubility In Pacific
seawater at 20°C:
156°C
404°C
1.271 g/cm3
0.129-0.156 mg/j.
0.138 mg/j. (average)
0.065 mg/l
Wlndholz, 1983
Wlndholz, 1983
Wlndholz, 1983
Pearlman et al., 1984
Hashimoto et al., 1984
0866p
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11/12/86
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Log Kou: 4.88-5.22 Ruepert et a!., 1985;
Ogata et a"!., 1984;
Yalkowsky and Valvanl,
1979; Karickhoff, 1981;
Miller et al., 1985
Vapor pressure at 25°C: 6.85xlO"7 mm Hg Santodonato et al., 1981
Henry's Law constant: l.lxlO"5 atm-mVmol Mackay et al., 1982
at 25°C
Chemically, PAH are reasonably reactive. They can undergo substitution
and addition reactions. In addition, these compounds are susceptible to
oxidation by ozone, peroxides and other oxldants (NAS, 1972).
1.3. PRODUCTION DATA
Currently, pyrene Is neither commercially produced nor Imported Into the
United States (SRI, 1986). According to TSCA Inventory of chemical
producers (U.S. EPA, 1977), two companies Imported pyrene Into the United
States In 1977, but their Individual or total Import volume was not
reported. Pyrene occurs In coal tar. It 1s also obtained by the destruc-
*
tlve hydrogenatlon of coal (Wlndholz, 1983).
1.4. USE DATA
There 1s no known commercial use of pyrene (IARC, 1983). Small amounts
of pyrene are used for scientific research (Hawley, 1981).
1.5. SUMMARY
Pure pyrene 1s a colorless solid at ambient temperatures. The presence
of tetracene, a common Impurity, gives yellow color to pyrene. It Is fairly
soluble In organic solvents Including ethanol, ethyl ether and benzene
(Wlndholz, 1983; Weast, 1980), but Is almost Insoluble In water (Pearlman et
al., 1984). Chemically, pyrene 1s susceptible to oxidation by ozone,
peroxides and other oxldants (NAS, 1972). Currently, pyrene is neither
commercially produced nor Imported Into the United States (SRI, 1986; USITC,
0866p -2- 07/27/87
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1984). It can be Isolated from coal tar or from the products of destructive
hydrogenatlon of coal (Wlndholz, 1983). There Is no known commercial use of
pyrene (IARC, 1983).
0866p -3- 07/27/87
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2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES
2.1. WATER
2.1.1. Hydrolysis. Pyrene contains no hydrolyzable functional groups;
therefore, aquatic hydrolysis 1s not expected to be significant (Mabey et
al.t 1981).
2.1.2. Oxidation. The rate constants for the oxidation of pyrene with
photochemlcally produced R0_ radical and aO_ at 25°C have been
estimated to be ~2.2xl04 and 5xl08 fT1 hour'1, respectively (Mabey
et al., 1981). Assuming the R0_ radical and 10? concentrations of
natural water are 10~9 and 10"12 M (Mabey et al., 1981), respectively,
the respective half-lives are -3.6 years and 58 days. These half-lives
apply to the dissolved fraction of pyrene In the water column, and not to
the pyrene that Is adsorbed to suspended partlculates and sediment.
Pyrene reacts readily In aqueous phase with ozone (Butkovlc et al.,
1983), which has Importance 1n water purification plants that use ozone for
disinfection; however, the ozone reaction Is not likely to be important In
natural waters.
2.1.3. Photolysis. In a methanol/ethanol solvent, pyrene exhibits UV
absorption maxima at 305, 318, 333.5, 351.5, 356, 362 and 371.5 nm (1ARC,
1983); similar absorption maxima occur In aqueous solution (Schwarz and
Waslk, 1976). Therefore, direct photolysis in sunlight Is a definite
possibility. Zepp et al. (1984) reported the rate constant for the direct
photolysis of pyrene in aqueous solution to be 1.0 hour"1 at midday
sunlight exposure; this corresponds to a half-life of 41.6 minutes. Based
on data reported by Zepp and Schlotzhauer (1983), the average photolytic
half-life of pyrene near the surface of a clear water body at 40°N latitude
1s -1.1 hours during June and 3.1 hours during January.
0866p -4- 11/12/86
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The dnUi found in Zepp et al. (1984) suggest that direct photolysis of
pyrene in the dissolved state in the water column is a significant trans-
formation process; however,, photolysis .may be significantly attenuated by
pyrene adsorption to suspended particulate matter and sediments.
Thus, the photolytic half-life of pyrene in water will increase as the
turbidity and depth of water increase. In deep and turbid waters, photoly-
sis may not be a significant process.
2.1.4. Mlcrobial Degradation. Tabak et al. (1981) examined the bio-
degradabi1ity of pyrene in a static culture flask-screening procedure using
settled domestic wastewater as microbial inoculum. At 5 ppm concentration,
pyrene was found to be significantly degraded with rapid adaptation, as 71%
of the initial pyrene was degraded in 7 days and 100% was degraded in 7 days
following the addition of a second acclimatized subculture. At 10 ppm,
however, only 11% degraded in 7 days and the degradation rate decreased to
0% in 7 days with 3-week-old subcultures. This result indicated that pyrene
at this concentration was toxic to microorganisms.
Bacteria isolated from Colgate Creek sediment (near the Chesapeake Bay)
and cultured in either oil-contaminated Colgate Creek water or a relatively
oil-free Eastern Bay water for 28 days degraded 19.6-22.4% of added pyrene
in a shake-flask procedure at 20°C (Walker and Colwell, 1975); 2.0-8.2%
degradation was observed using bacteria from Eastern Bay sediment. These
results indicate that biodegradation of pyrene in most natural water will be
slow and that the degradation will be faster with acclimatized micro-
organisms.
PAHs with four or more aromatic rings are degraded slowly by microbes
and biodegradation is considered to be the ultimate fate process in water
0866p 5- Ob/21/87
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(U.S. EPA/NIH, 1986). The concentrations of bacteria and fungi capable of
oxidizing the hydrocarbons are extremely low, however, in all but heavily
polluted fresh and marine waters, and most species cannot use PAH as a sole
carbon source. M1crob1al oxidation of PAH requires oxygen and will not
proceed 1n anoxlc sediments or water (U.S. EPA/NIH, 1986).
2.1.5. Volatilization. The Henry's Law constant for pyrene has been
experimentally determined to be l.lxlO"5 atm-mVmol at 25°C (Mackay et
al., 1982). This value of Henry's Law constant suggests that aquatic
volatilization may have some significance, but Is not likely to be rapid
(Lyman et al., 1982). Based on the method outlined 1n Lyman et al. (1982),
the volatilization half-life from a river 1 m deep, flowing at a speed of 1
m/sec at a wind velocity of 3 m/sec is -4.8 days; volatilization from static
water will be significantly slower. Further, adsorption to sediment Is
expected to attenuate volatilization. Davis et al. (1983) experimentally
determined a pyrene volatilization half-life of 49 days from a laboratory-
scale waste stabilization pond study; loss of pyrene from the pond from
volatilization accounted for only 0.4% of the total transport and fate.
2.1.6. Adsorption. Karickhoff et al. (1979) experimentally examined the
adsorption of pyrene to a variety of river and pond sediments. The follow-
ing average K values, based on the organic carbon content of the
sediments, were determined: sandy sediments, 19,000; coarse silt, 93,000;
medium silt, 130,000; fine silt, 110,000; and clay, 120,000. These KQC
values Indicate that pyrene will be strongly adsorbed onto sediments. The
K . values varied from 9.4 to 3800 and were strongly Influenced by
particle size and organic content. Karickhoff and Morris (1985) found that
several weeks may be required for complete equilibration of pyrene between
sediments and the water column.
0866p -6- 07/27/87
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The K values listed above and the widespread detection of pyrene in
U.S. sediments (Section 3.1.) at concentrations much higher than in water
columns indicate that adsorption to particulate organic matter and sediments-
•
is an important environmental fate process. Movement by sediments is
considered to be an Important transport process for PAH (U.S. EPA/NIH, 1986).
2.1.7. Bioconcentration. The following experimental BCF values have been
reported: 72 (rainbow trout, Salmo qairdneri. 21-day exposure, flowing
conditions) (Spehar et al., 1980); 457- (goldfish, Carassius auratus) (Ogata
et al., 1984); 600-970 (fathead minnow, Pimephales promelas) (Carlson et
al., 1979); 2690 (unspecified species) (Mackay, 1982); 2702 (Daphnia pulex,
24-hour) (Southworth et al., 1978); 13,072 (unspecified algae) (Davis et
al., 1983).
BCF values >1000 are considered significant (Kenaga, 1980). PAH may not
appreciably bloconcentrate in .organisms that have mlcrosomal oxidase, such
as fish, as this enzyme metabolizes PAH (Santodonato et al., 1981). There-
fore, the bloaccumulation potential may be very dependent on the organism
being considered.
2.1.8. Persistence. Tan and Heit (1981) monitored sediment cores taken
from Woods Lake In the remote Adirondack Forest of upstate New York for
various PAH. The following pyrene concentrations (ng/g dry sediment weight)
were found at various depths: 930 (0-4 cm), 290 (4-8 cm), 56 (8-11 cm), 67
(12-17 cm), 37 (24-26 cm), 60 (34-38 cm), 21 (42-44 cm), 89 (50-54 cm) and
16 (80-84 cm). The near constancy In the concentration of pyrene in the
sediment cores deeper than 8 cm indicates that the compound is very persis-
tent, particularly under anaerobic conditions and in the absence of sunlight
prevalent In the deeper cores.
0866p -7- 07/27/87
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2.2. AIR
Pyrene can exist in the ambient atmosphere in both the particulate-
associated form and 1n the vapor-phase. From their ambient air monitoring
data from Portland, OR, Llgocki et al. (1985a,b) reported the mean pyrene
concentration In the vapor-phase to be 6.8 ng/m3, while the mean concen-
tration in the particulate-phase was reported to be 0.53 ng/m3. Yamasakl
et al. (1982) monitored the urban air of a Japanese dty for an entire year
and found the pyrene concentration In the vapor-phase to be ~1 order of
magnitude higher than 1n the particulate phase. The form in which pyrene
exists in the atmosphere has a significant bearing on its environmental
fate. Pyrene in the partlculate-associated form 1s expected to be signifi-
cantly more persistent than vapor-phase pyrene.
2.2.1. Photolysis. Pyrene strongly absorbs environmental UV radiation
and photolyzes quite rapidly in water in the dissolved state (see Section
2.1.3.); therefore, direct photolysis may be expected to be a significant
removal mechanism for pyrene vapor in the atmosphere.
Several investigators have examined the photodegradation of pyrene
adsorbed to particulate materials. Behymer and Hites (1985) examined the
photodegradation of pyrene while adsorbed to various substrates (silica gel,
alumina, flyash, carbon black) by using simulated atmospheric conditions.
The following half-lives were determined: silica gel, 21 hours; alumina, 31
hours; flyash, 46 hours; and carbon black, >1000 hours. Adsorption to
carbon black clearly stabilized the phototransformation. Valerio and
Lazzarotto (1984) found that pyrene photolyzed significantly faster when
adsorbed to inorganic components of air particulates as compared with whole
atmospheric particulate matter containing particulate organic fractions as
well. Yokley et al. (1986) studied the photochemical decomposition of
pyrene adsorbed to various fly ashes, alumina, silica gel and glass. Photo-
0866p -8- ' 07/27/87
-------
transformation proceeded more rapidly wHh the alumina, silica gel or glass
as compared with the fly ashes. The high carbon content of the flyashes was
effective 1n suppressing photolysis.
2.2.2. Reaction with HO Radical. The half-life for the vapor-phase
reaction of pyrene with photochemlcally produced HO radical is -1.12 days at
25°C, assuming an average atmospheric HO radical concentration of 8^105
molecules/cm3 (U.S. EPA, 1986a).
2.2.3. Physical Removal. Removal of pyrene from the atmosphere may occur
by wet and dry deposition. Partlculate-assodated pyrene has been detected
1n rainwater (L1gock1 et al., 1985b). The presence of pyrene In lake
sediments In the Adirondack Forest, NY, has been attributed to physical
deposition (Tan and Helt, 1981). Dissolved pyrene has also been detected In
rainwater (Llgockl et al., 1985a), suggesting that physical removal of vapor
by washout or dissolution Into clouds with subsequent rainfall may be
possible.
Lunde and Bjoerseth (1977) reported that pyrene has been transported In
the atmospheric aerosol from England to Norway, Indicating that long-range
transport of partlculate-phase pyrene occurs. This 1s consistent with the
experimental data Indicating that the persistence of pyrene 1s Increased
when It 1s Is adsorbed to partlculate substrate.
2.3. SOIL
2.3.1. H1crob1al Degradation. Groenewegen and Stolp (1981) examined the
degradation of pyrene In a laboratory soil-water percolation study over a
4-week Incubation period. Significantly more degradation occurred 1n the
units that were not sterilized by HgCl~. The authors attributed the
decline In pyrene concentration in the nonsterlllzed units to biological
breakdown. The microblal data listed in Section 2.1.4. also suggest that
pyrene may be susceptible to blodegradation in soil under aerobic conditions.
0866p -9- 07/27/87
-------
2.3.2. Chemical Degradation. Pertinent data regarding the chemical
degradation of pyrene could not be located In the available literature as
dted In the Appendix.
•
2.3.3. Adsorption. Karlckhoff et al. (1979) reported experimental K
values ranging from 19,000-130,000 and K . values of 9.4-3800 (see
Section 2.1.6.) for various pond and river sediments. Kenaga (1980)
•
reported an experimental soil K value of 84,000. These K values
suggest soil Immobility- (Swann et al., 1983); however, the detection of
pyrene In several groundwaters (Section 3.1.) Indicates that leaching can
occur. This leaching may occur In soils containing low organic 'matter
(e.g., sand) or high porosity. Leaching Is also possible from spill or
waste disposal sites contaminated with materials containing relatively high
concentrations of PAH. In addition, Karlckhoff and Morris (1985) noted that
equilibration of pyrene between sorbed and water-phase may require several
»
weeks; therefore, some movement may occur before equilibrium Is reached.
Pyrene Is not, however, expected to leach 1n soil under most conditions.
2.3.4. Volatilization. Volatilization of pyrene from soils Is not
expected to be an Important process (Sims and Overcash, 1983).
2.4. SUMMARY
If released to the aquatic environment, adsorption to particulate
organic matter and sediments In water will be an Important environmental
fate process based on measured sediment K values and widespread monitor-
ing of pyrene in ambient sediments. In the dissolved state in the water
column, direct photolysis may be significant, as the average photolytic
half-life of pyrene near the surface at 40°N latitude has been estimated to
be -1.1 hours 1n 3une and 3.1 hours in January (Zepp and Schlotzhauer,
1983). In deep, turbid water, photolysis may not be an Important process.
0866p -10- 07/27/87
-------
Mlcroblal degradation data (Walker and Colwell, 1975) suggest that pyrene
may be susceptible to blodegradatlon 1n natural water. Mlcroblal oxidation
of PAH requires oxygen and will not proceed in anoxlc sediments or water
(U.S. EPA/NIH, 1986). In clear and shallow water, blodegradatlon will not
be Important. It will, however, be an Important process In slow moving,
deep and turbid waters. Volatilization may have some significance In
shallow, rapidly flowing rivers. Bloaccumulatlon potential appears to be
dependent on the organism being considered. Hydrolysis 1s not expected to
be Important. The detection of a nearly constant concentration of pyrene In
sediment cores of a remote forest lake (Tan and He1t, 1981) Indicates that
pyrene 1s very persistent under anaerobic and dark conditions. If released
to the atmosphere, pyrene will exist In both vapor and partlculate-adsorbed
phases; monitoring data (Llgockl et a!., 1985a,b; Yamasakl et al., 1982)
suggest that the vapor-phase may dominate. Vapor-phase pyrene appears to be
susceptible to relatively rapid decomposition by direct photolysis or
reaction with photochemlcally produced HO radical. Adsorption of pyrene to
partlculates 'With a high carbon content significantly attenuates photolysis
and other chemical oxidation reactions (Behymer and HHes, 1985; Valeric and
Lazzarotto, 1984; Yokley et al., 1986; Santodonato et al., 1981), and may
therefore permit the long-range atmospheric transport (Lunde and Bjoerseth,
1977). Pyrene may be physically removed from the atmosphere by wet and dry
deposition (Llgocki et al., 1985a,b; Tan and Heit, 1981). If released to
soil, pyrene may be susceptible to .biodegradation under aerobic conditions.
Under most conditions, 1t Is not expected to leach or volatilize signifi-
cantly and may persist In soils.
0866p -11- 07/27/87
-------
3. EXPOSURE
Human exposure to pyrene occurs primarily through the inhalation of
tobacco smoke and polluted air and by the Ingestlon of contaminated food and
water (IARC, 1983) and smoked fish and meats. Pyrene occurs ubiquitously as
a product of incomplete combustion and occurs naturally 1n fossil fuels
(IARC, 1983).
3.1. WATER
Table 3-1 lists various pyrene monitoring data for drinking water,
groundwater, surface water and rainwater; Table 3-2 lists sediment monitor-
Ing data from various U.S. locations. In an analysis of the U.S. EPA STORET
data base, pyrene was detected in 5.2% of 1271 effluents and 4.0% of 904
surface waters (Staples et al., 1985). Griest (1980) detected pyrene at
concentrations of 23.0 yg/g in the sediment and 4.0 vg/8. 1n the water
of an effluent channel from a coking plant. A pyrene concentration of 10
vg/8. was detected In the wastewater effluent from a tire manufacturing
plant (Jungclaus et al., 1976). Wastewater effluents from two coal coking
plants were found to contain pyrene at levels as high as 480 pg/S.
(Walters and Luthy, 1984). In the preliminary findings of the U.S. EPA
Nationwide Urban Runoff Program, pyrene was detected in the stormwater
runoff from six U.S. cities at levels ranging from 0.3-10 yg/!l (Cole et
al., 1984). Hoffman et al. (1984) detected pyrene In both the partlculate
and soluble phases 1n urban stormwater runoff feeding the Narragansett Bay
watershed.
In general, PAH can be released to water In Industrial and municipal
effluents, atmospheric fallout and precipitation, road run-off (tire wear,
bitumen and asphalt surfaces, cracked lubricating oils) and marine shipping
and harbor oil (Santodonato et al., 1981). Sorrel! et al. (1980) suggested
0866p -12- 07/27/87
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that pyrene and other PAHs may contaminate drinking water supplies as a
result of coal-tar or asphaltlc materials used to line pipes and storage
tanks.
Based on the monitoring data from Table 3-1, the concentration of pyrene
In drinking water may be -1.0 ppt (ng/8.). Assuming an average dally water
Intake of 2.0 I, the Intake of pyrene 1n drinking water Is -2.0 ng/day.
3.2. FOOD
In general, PAH found 1n food are prese-nt as a result of contamination
from a polluted environment or are formed during the cooking process
(Santodonato et a!., 1981; Fazio and Howard, 1983); minute amounts of geo-
chemlcal or blosynthetlc origin may also be present (Fazio and Howard, 1983).
Fazio and Howard (1983) reported the detection of pyrene In the follow-
ing foods: vegetable oils (0.4-5.8 yg/kg), oysters (0.9-6.5 yg/kg), dark
coffee (2-8 yg/kg), horse mackerel (0.2-7.0 yg/kg), charcoal-broiled
steaks (0.9 yg/kg) and barbecued ribs (1.4 vg/kg). Lawrence and Weber
(1984) Identified the following concentrations of pyrene -in Canadian foods:
breakfast cereals (2.2-21 vg/kg), flour (2.6-5.7 yg/kg), skim milk
powder (<0.1-2.1 yg/kg) and cooking oils (<0.1-1.4 vg/kg).
Dennis et al. ('1983) examined total-diet samples of food groups 1n
England and found the following mean pyrene concentrations (1n yg/kg) 1n
the various food groups: cereals (1.85), meat (0.55), fish (0.79), oils and
fats (2.75), fruit and sugar (0.83), vegetables (0.24-1.23), beverages
(0.04) and milk (0.04). Dennis et al. (1983) then estimated the total
pyrene dietary load to be 1.09 yg/person/day. Based on monitoring of
total-diet samples collected 1n the Netherlands, Vaessen et al. (1984)
estimated the median intake of pyrene to be 2.2 yg/person/day.
0866p -15- 05/21/87
-------
3.3. INHALATION
Table 3-3 lists recent (1979-1983) U.S. ambient air monitoring data for
pyrene. It Is possible that the atmospheric load of pyrene has been
generally decreasing over the past 40 years (Santodonato et a!., 1981).
This decrease may be a result of decreases 1n coal consumption for residen-
tial heating and Industrial uses, Improved disposal methods of solid wastes,
restrictions on open burning, and Improved efficiencies for stationary
Incineration and combustion sources with Improvements of pollution control.
The higher atmospheric levels of pyrene in wintertime versus summertime air
in New Jersey (see Table 3-3) may be a reflection of an Increased use of
fossil fuel combustion for heating purposes.
In general, PAHs are emitted to the atmosphere by the combustion of
fossil fuels (oil, coal), 1n exhaust from gasoline and dlesel engines, by
open burning (agricultural burning, forest fires, structure fires, refuse
burning) and by the burning of wood, especially for residential heating
(NRC, 1983).
Pyrene has been identified 1n mainstream cigarette smoke (0.017-27
vg/dgarette), sldestream cigarette smoke (101.1-390 pg/dgarette),
smoke-filled rooms (66 ng/m3), cigar -and pipe smoke, mainstream marijuana
smoke (0.066 vg/dgarette), gasoline engine exhaust, exhaust from burnt
coal and coal-tar (IARC, 1983). The concentration of pyrene detected in
various fly-ash samples ranged from 0.5-120 ng/g (Eiceman et a!., 1981).
Assuming that the approximate average ambient air concentration of
pyrene (gas-phase and particulates) ranges from 0.5-20 ng/m3 (see Table
3-3) and assuming a human air intake of 20 m3/day, the average daily
intake for an adult can be -10-400 ng. Matsumoto and Kashimoto (1985) used
Japanese monitoring data to estimate an average dally Intake of 17 ng in
Japan.
0866p -16- 05/21/87
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3.4. DERMAL
Pertinent data regarding dermal exposure to pyrene could not be located
In the available literature as cited 1n the Appendix.
3.5. SUMMARY
Human exposure to pyrene occurs primarily through the Inhalation of
tobacco smoke and polluted air and by the 1ngest1on of contaminated food and
water (IARC, 1983). Pyrene occurs ubiquitously as a product of Incomplete
combustion and occurs naturally In fossil fuels (IARC, 1983). It has been
widely detected In drinking water, surface water, groundwater, rainwater and
aquatic sediments (see Tables 3-1 and 3-2), In many foods (Santodonato et
a!., 1981; Dennis et al., 1983), and 1n the general ambient atmosphere (see
Table 3-3). The average dietary intake of pyrene 1n England is -1.09
vg/day (Dennis et al., 1983); the average Intake 1n drinking water in the
United States is -2.0 ng/day, while the Inhalation Intake in the United
States is -10-400 ng/day. The presence of pyrene In food 1s a result of
contamination from a polluted environment and formation during cooking by
pyrolysis of organic matter (Santodonato et al., 1981; Fazio and Howard,
1983). Emission to the atmosphere results from the combustion of fossil
fuels (oil, coal), wood burning for residential heating, gasoline and diesel
engine exhaust, and open burning (agricultural burning, forest fires,
structure burning, refuse burning) (NRC, 1983).
0866p -18- 05/21/87
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4. PHARMACOKINETICS
4.1. ABSORPTION
Gastrointestinal absorption of pyrene was evaluated following gavage
administration of 50 pg of pyrene in gelatin-saline solution to two male
Fischer 344 rats (Mitchell and Tu, 1977, 1979). The rats were killed 24
hours later and the gastrointestinal tract and other tissues were removed.
Spectrometrlc analysis for pyrene 1n these tissues showed that the gastro-
intestinal tract contained approximately half of the material that was
administered, but showed no significant Increase of pyrene 1n the lung,
kidney, liver or trachea. These data were Interpreted as suggesting poor
gastrointestinal absorption of pyrene, particularly since pyrene was
detected in the same tissues 24 hours following Inhalation exposure (Section
4.2.). The fluorescence spectra of the major pyrene metabolites, however,
overlap those of pyrene; thus, significant quantities of metabolized pyrene
1n bile can be excreted into the intestine and may not have been detected.
Furthermore administration by gavage of pyrene as a suspension of unknown
particle size does not preclude absorption by a more relevant route. Also,
PAH In general are highly Hpid soluble and are absorbed readily from the
gastrointestinal tract and lungs (U.S. EPA, 1980).
Significant concentrations of pryrene were detected by fluorescence in
the nasal turbinates, trachea, lungs, kidneys and liver of male Fischer 344
rats 30 minutes after exposure to pyrene aerosol (500 yg/i, 0.3-0.8 ym
mass median diameter) for 1 hour (Mitchell and Tu, 1979). Although this
indicates rapid pulmonary uptake of pyrene, data indicating the extent of
uptake were not reported.
4.2. DISTRIBUTION
Rapid distribution of pyrene in rats following inhalation absorption was
Indicated in the study described In Section 4.1. (Mitchell and Tu, 1979) by
0866p -19- 07/27/87
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fluorometMc detection of pyrene in the kidney, liver, carcass and muscle 30
minutes after exposure. Analyses conducted 1, 2 and 4 days after exposure
showed that pyrene was rapidly cleared from these tissues; levels In the
lungs were -65 and 6% of the Initial (30-mlnute) concentrations after 24 and
48 hours, respectively, and concentrations In the liver and kidney were -6
and 14% of the Initial levels, respectively, after 48 hours. Concentrations
1n the gastrointestinal tract 24 hours after exposure were ~4 times higher
than the Initial value, Indicating clearance from the respiratory tract by
mucodllary action. Biliary contribution to gastrointestinal concentrations
was not evaluated, but pyrene was largely cleared from the gastrointestinal
tract after 4 days.
4.3. METABOLISM
Metabolism of pyrene appears to proceed by oxidation at the 1-2 and 4-5
bonds with 1-hydroxypyrene as the principal metabolite. The sulfurlc acid
and glucuronlc acid conjugates of 1-hydroxypyrene, 1,6- and 1,8-dihydroxy-
pyrene and trans-4,5-d1hydro-4,5-d1hydroxypyrene, as well as N-acetyl-S-
(4,5-d1hydro-4-hydroxy-5-pyrenyl)-L-cyste1ne, were detected In the urine of
rats and rabbits that were treated IntraperHoneally with pyrene (Boyland
and Sims, 1964). N-acetyl-S-(4,5-d1hydro-4-hydroxy-5-pyrenyl)-L-cyste1ne
and the corresponding cystelnylglyclne and glutathlone derivatives, the
glucuronic add conjugates of 1-hydroxypyrene and trans-4,5-dihydro-4,5-di-
hydroxypyrene were also detected 1n the bile of Intraperltoneally-treated
rats (Boyland and Sims, 1964). Metabolites Isolated following incubation of
pyrene with rat-liver mlcrosomes Included two uncharacterized trlhydroxy
derivatives (Jacob et a!., 1982) as well as the 1-hydroxy, 1,6-d1hydroxy,
1,8-d1hydroxy and/or 4,5-dihydrodiol derivatives (Jacob et al., 1982; Sims,
1970). 1-Hydroxypyrene has also been detected in the urine of pigs (-14 kg)
that were given single oral doses (1 mg-1 g) of pyrene (Kelmlg et al., 1983).
0866p -20- 07/27/87
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4.4. EXCRETION
The oral and Inhalation experiments with rats (see Sections 4.1. and
4.2.) Indicate that pyrene Is eliminated primarily by the gastrointestinal
tract (Mitchell and Tu, 1979). It appears that gastrointestinal absorption
of pyrene Is relatively poor, that Inhaled pyrene Is cleared to the gut by
mucoclHary action and that absorbed pyrene and Its metabolites are elimi-
nated In the bile. Elimination/excretion was not quantified, as fecal and
urine analyses were not conducted.
4.5. SUMMARY
Poor gastrointestinal absorption of pyrene was suggested from the
results of a study 1n which tissues of two male rats were analyzed 24 hours
after gavage administration of 50 vg pyrene (Mitchell and Tu, 1977, 1979).
Pyrene was detected fluormetrlcally In the gastrointestinal tract at -50% of
the administered dose, but not 1n the liver, kidneys, lungs or trachea.
This Interpretation of poor gastrointestinal absorption of pyrene from these
data Is further supported by detection of pyrene In the liver and kidneys 24
hours after Inhalation exposure, and complicated by possible biliary elimi-
nation of pyrene metabolites Into the Intestinal tract since the analytical
technique was not specific for pyrene. Rapid absorption of Inhaled pyrene
by rats 1s Indicated by fluorometrlc detection of pyrene in respiratory
tissues, liver and kidneys 30 minutes after 1-hour exposure to 500 yg/s.
pyrene aerosol (Mitchell and Tu, 1979). Distribution to tissues other than
the liver and kidney was not assessed in the Inhalation study.
Jm vivo and j_n vitro studies indicate that metabolism of pyrene proceeds
by oxidation at the 1-2 and 4-5 bonds, with 1-hydroxypyrene as the principal
metabolite (Boyland and Sims, 1964; Sims, 1970; Jacob et al., 1982; Kelmig
et al., 1983). The metabolites have been detected as sulfurlc add and
0866p -21- 05/21/87
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glucuronic acid 1n the urine of rats, rabbits and pigs. Urinary excretion
and fecal elimination of pyrene has not been quantltated, but In limited
oral and inhalation studies with rats, fecal elimination appears to reflect
unabsorbed pyrene, pyrene resulting from mucociliary clearance and biliary
elimination (Mitchell and 1u, 1979).
0866p -22- 05/21/87
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5. EFFECTS
5.1. CARCINOGENICITY
Studies evaluating the tumorlgenlc potential of orally-administered
pyrene could not be located in the available literature as cited In the
Appendix.
A finely aggregated dust mixture containing 3 mg of TLC-purified (>99%)
pyrene and an equal amount of hematite (Fe_03, 94% of particles
<1.0 y) suspended in saline was administered to 48 male Syrian golden
hamsters (9-10 weeks old) by intratracheal Instillation at weekly intervals
for 30 weeks (Sellakumar and Shubik, 1974). Ninety untreated hamsters
served as controls. The animals were maintained until natural death or
sacrificed when moribund, and tissue from the lungs, larynx, trachea and
stem bronchi were examined hlstologlcally; other organs were examined if
gross pathology was present. Survival was 50, 25 and 0% after 50, 80 and
120 weeks, respectively, which was comparable with that of the control
group. Respiratory tumors occurred in 1/48 treated hamsters (unspecified
tracheal tumor) and in none of the controls (effective number, 82). Two
malignant lymphomas also occurred in the treated hamsters, but those also
were not treatment-related. A high incidence (39/44) of respiratory tract
(primarily bronchi) carcinomas developed in hamsters that were similarly
treated with dibenz[a,1]pyrene.
CarcinogenlcHy studies Involving dermal application and subcutaneous
Injection of pyrene with mice are summarized 1n Table 5-1. Skin tumors were
not Induced by dermal application of pyrene 2 or 3 times/week for 1-2 years
(Barry et a!., 1935; Badger et a!., 1940; Wynder and Hoffmann, 1959; Roe and
Grant, 1964; Morton and Christian, 1974; Van Duuren and Goldschmidt, 1976).
0866p -23- 05/21/87
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Mouse-skin Initiation-promotion assays Involving Initiation with benzo[a]-
pyrene (Roe and Grant, 1964), promotion with croton oil (Salaman and Roe,
1956) or promotion with TPA (Scrlbner, 1973; Wood et al., 1980) were
negative or Inconclusive (Scrlbner, 1973). Although pyrene does not appear
to be active as a complete carcinogen or Initiator or promoter 1n mouse skin
application studies, enhancement of the dermal carclnogenlclty of benzo[a]-
pyrene In mice by simultaneous application of pyrene has been reported
(Goldschmldt et al., 1973; Van Duuren and Goldschmidt, 1976), Indicating
possible cocarclnogenlclty of pyrene. Two subcutaneous injections of pyrene
crystals (10 mg) moistened with glycerol, 4 months apart, did not produce
local tumors In mice after 12-18 months (Shear and Lelter, 1941), but this
study should be regarded as Inconclusive because of an Inadequate dosing
schedule. Subcutaneous administration of 12 mg pyrene to Strain A mice on
days 18 and 19 of pregnancy did not Increase lung or mammary gland tumor
Incidences 1n the progeny 1 year after weaning (Nikonova, 1977).
5.2. HUTAGENICITY
Pyrene has been tested in numerous mutagenidty and other short-term
assays with equivocal results. The results of assays conducted before 1983
were summarized by IARC (1983) and were not reviewed Independently for this
report. Pyrene was reported to be mutagenlc in Salmonella typhimurium
strains TA97, TA98, TA100, TA1537 and TM677 in the presence of an exogenous
metabolic activating system (Kaden et al., 1979; Bridges et al., 1981;
Mat1jasev1c and Zeiger, 1985; Sakal et al., 1985), but other reports
Indicate nonmutagenlcity in strains TA1535, TA-1537, TA98 and 1A100 (McCann
et al., 1975; LaVole et al., 1979; Ho et al., 1981). Pyrene produced
unscheduled DNA synthesis in cultured primary hamster hepatocytes (McQueen
et al., 1983) and cultured human flbroblast W138 cells (Robinson and
0866p -26- . 07/27/87
-------
Mitchell, 1981), but not in cultured primary mouse hepatocytes (McQueen et
a!., 1983), primary rat hepatocytes, human foreskin epithelial cells or HeLa
cells (IARC, 1983). DNA damage, as Indicated by SfIA gene expression, was
Induced In Escherlchla coll (Qulllardet et al., 1985). Mutation to
trlfluorothymldlne resistance was Induced 1n mouse lymphoma L5178Y cells In
vitro (Jotz and Mitchell, 1981). Sister chromatld exchanges were produced
1n CHO cells (Evans and Mitchell, 1981) and Chinese hamster V79 cells
(Popescu et al., 1977) by pyrene in vitro, but this effect was not observed
In other studies with CHO cells in vitro (IARC, 1983; Darroudi and
Natarajan, 1985), rat liver epithelial ARL 18 cells in vitro (Ved Brat et
al., 1983; IARC, 1983) or mouse bone-marrow cells in vivo (IARC, 1983). In
vivo treatment with pyrene did not produce sperm head abnormalities in mice
(Topham, 1980). Pyrene reportedly produced chromosomal aberrations In
Chinese hamster V79 cells in vitro 1n the presence of a feeder layer
(Popescu et al., 1977), but not in rat liver RL cells in vitro in the
absence of exogenous metabolic activation (Dean, 1981).
Pyrene was not differentially toxic to DNA-repair-profIdent-def 1c1ent
strains of bacteria (Mamber et al., 1983; IARC, 1983) or CHO cells (Hoy et
al., 1984), did not Induce prophage In E_. coli K12 (Mamber et al., 1984),
did not produce DNA single-strand breaks In rat hepatocytes (Sina et al.,
1983), was not mutagenlc to Saccharomyces cerevlsiae or Schizosaccharomyces
pombe yeasts (various endpolnts examined) (IARC, 1983), was not mutagenlc at
the HGPRT locus 1n rat liver ARL18 epithelial cells {Ved Brat et al., 1983),
and did not induce sex-linked recessive lethal mutations In Drosophila
melanoqaster (Valencia and Houtchens, 1981). Pyrene did not Induce growth
in soft agar of rat ARL liver epithelial cells (Shimada et al., 1983), in
pulmonary or peritoneal macrophages from rats treated jjn vivo (Nielsen and
0866p -27- 07/30/87
-------
Anderson, 1986), or 1n Syrian hamster embryo cells, mouse prostate C3H
cells, mouse BALB/C-3T3 cells or guinea pig fetal cells following \r± vivo
treatment (IARC, 1983).
5.3. TERATOGENICITY
Pertinent data regarding the teratogenlclty of pyrene could not be
located 1n the available literature as dted 1n the Appendix.
Weaver and Gibson (1979) exposed pregnant rats to graded airborne
concentrations of uncharacteMzed oil shale containing PAH, including
pyrene, on days 6-15 of gestation. No treatment-related teratogenlc effects
were observed during examination of fetuses obtained by 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.
5.4. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of pyrene could not
be located In the available literature as cite'd in the Appendix.
«
5.5. CHRONIC AND SUBCHRONIC TOXICITY
Six male rats of unspecified strain that weighed 75-85 g were maintained
on diets that contained 2000 ppm pyrene for periods as long as 100 days
(White and White, 1939). Inhibition of growth was observed, but the magni-
tude of the effect was not reported. Autopsies that included hlstological
examinations of the liver, lungs, kidneys, intestines and adrenals were
conducted at the termination, but results were not reported specifically for
pyrene-treated animals. Liver enlargement and fatty appearance were
reported as general findings in "some" animals that were treated with
pyrene, benzpyrene or methylcholanthrene, but the incidence of these effects
in the pyrene-treated rats was not indicated. Interpretation of the results
0866p -28- 07/30/87
-------
of this study is complicated by the small group size, lack of control data,
unreported number of animals, unreported magnitude of depressed weight gain
and food consumption data and unreported Incidence of hepatic alterations.
Holland et al. (1980) administered uncharacterlzed oil shale containing
PAHs, 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 Inflamma-
tion accompanied by flbrosls. Because of the uncharacterlzed nature of the
test material, 1t 1s not possible to quantify these data for use In risk
assessment.
5.6. OTHER RELEVANT INFORMATION
Four-day and 7-day single dose IntraperHoneal LD" s Of 678 and 514
mg/kg, respectively, were determined for pyrene with mice (Salamone et al.,
1981).
A single Intraperltoneal Injection of 150 mg/kg pyrene dissolved in DMSO
produced minimal gross swelling and congestion 1n the livers of 6 male
Sprague-Oawley rats after 24 and 72 hours (Yoshlkawa et al., 1985). Gross
pathologic effects In other unspecified tissues were not Indicated. Small
but significant Increases in serum AST and blUrubin levels occurred 24
hours but not 72 hours after treatment, and significant changes 1n serum
ALT, GGPT, LDH, glucose, BUN and creatlne did not occur.
Pyrene in beeswax pellets was Implanted 1n rat tracheas that had been
Implanted under the dorsal skin of Isogenlc recipients (Topping et al.,
1978). Alterations In the respiratory mucosa developed during an 8-week
observation period, Including goblet-cell and transitional hyperplasla.
0866p -29- . 07/27/87
-------
Intraperltoneal Injection of 20 mg/kg pyrene to CFLP mice on day 18 of
pregnancy did not cause any changes In the activities of lung pyruvate
kinase or lactate dehydrogenase In the offspring when examined on gestation
day 18 or 19 or postpartum days 1, 2, 3, 5, 7, 14, 28 or 35 (Rady et a!.,
1982).
5.7. SUMMARY
Intratracheal Instillation of 3 mg pyrene suspended In saline at weekly
Intervals for 30 weeks did not produce tumors In the respiratory system
(hlstologlc examination) or other tissues (gross examination) 1n hamsters
•*
observed for life (Sellakumar and Shublk, 1974). Skin tumors were not
Induced In mice by twice or three-times weekly dermal application of pyrene
for 1-2 years (Barry et a!., 1935; Badger et al., 1940; Wynder and Hoffmann,
1959; Roe and Grant, 1964; Norton and Christian, 1974; Van Duuren and
Goldschmldt, 1976). Mouse skin Initiation-promotion studies Involving
Initiation with benzo[a]pyrene (Roe and Grant, 1964), promotion with croton
oil (Salaman and Roe, 1956) or promotion with TPA (Scrlbner, 1973', Wood et
al., 1980) were negative or Inconclusive (Scrlbner, 1973). Enhancement of
the dermal cardnogenldty of benzo[a]pyrene In mice by simultaneous appli-
cation of pyrene has, however, been reported (Goldschmldt et al., 1973; Van
Duuren and Goldschmldt, 1976), Indicating possible cocarclnogenlclty of
pyrene. Two subcutaneous Injections of 10 mg pyrene crystals 4 months apart
did not produce local tumors In mice after 12-18 months (Shear and Lelter,
1941).
Pyrene has been tested extensively In mutagenldty and other short-term
assays. Pyrene was mutagenlc In some tests with S. typhlmurlum 1n the
presence of metabolic activation preparation (Kaden et al., 1979; Bridges et
al., 1981; Matljasevlc and Zelger, 1985; Sakal et al., 1985) and produced
0866p -30- 11/12/86
-------
unscheduled DNA synthesis in cultured primary hamster hepatocytes (McQueen
et al., 1983) and human flbroblasts (Robinson and Mitchell, 1981), mutation
In mouse lymphoma L5178Y cells in vitro (Jotz and Mitchell, 1981), sister
chromatld exchanges In CHO (Evans and Mitchell, 1981) and V79 (Popescu et
al., 1977) cells jm vitro and chromosomal aberrations in Chinese hamster V79
cells j_n vitro (Popescu et al., 1977). Genotoxidty of pyrene was not
demonstrated 1n other assays using the same or different Indicator organisms
or endpoints, including morphological transformation in a variety of rat,
mouse, hamster and guinea pig systems.
Pertinent data regarding teratogenlcity or other reproductive effects of
pyrene could not be located In the available literature as cited in the
Appendix.
Inhibition of growth and enlarged, fatty livers were reported as effects
in a group of six male rats maintained on diets that contained 2000 ppm
pyrene for as long as 100 days (White and White, 1939). The significance of
these findings 1s uncertain because Incidences were not reported, a small
number of animals was tested, the treatment durations were variable and
unspecified, and control data were not reported. Pertinent data regarding
toxic effects of chronic oral or inhalation exposure to pyrene could not be
located in the available literature as cited in the Appendix.
A single intraperltoneal Injection of 150 mg/kg pyrene produced minimal
gross swelling and congestion of the liver and Increased serum AST and
billrubln in rats (Yoshikawa et al., 1985).
0866p -31- 07/27/87
-------
6. AQUATIC TOXICITY
6.1. ACUTE
The available data concerning acute toxlclty of pyrene to aquatic organ-
isms are presented In Table 6-1. Of the six species for which there are
data, the three arthropods are the most sensitive, with LC&0 values of 4,
8 and 20 vg/J. for Daphnla maqna. Artemla sallna and Aedes aeqyptl,
respectively (Kagan et a!., 1985).
There Is a wide discrepancy between the Daphnla maqna LCcn value of 4
— —— jju
mg/l (Kagan et a!., 1985) and that reported by Bobra et al. (1983), 1820
vg/SL. This may be due to differences 1n lighting conditions used 1n the
two studies. Like some other PAH (e.g., anthracene and fluoranthene), the
toxlclty of pyrene to aquatic organisms Is greatly enhanced under natural
sunlight or UV light. Pyrene was nontoxlc to the five species tested by
.Kagan et al. (1985) at 1000 vg/8. In the dark; however, under light
sources emitting primarily long-wavelength UV, the LC-- values In Table
6-1 were obtained.
6.2. CHRONIC
Pertinent data regarding chronic toxlclty of pyrene to aquatic organisms
could not be located In the available literature as cited 1n the Appendix.
6.3. PLANTS
The only data concerning effects of pyrene on aquatic plants were
provided by Hutchlnson et al. (1980), who reported EC&0 values of 202 and
332 vg/8. for Inhibition of photosynthesis 1n Chlamydomonas anqulosa and
Chlorella vulgar Is. respectively.
0866p -32- 11/12/86
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TABLE 6-1
Acute ToxicHy of Pyrene to Aquatic Organisms
Species
Concentration
Effect
Reference
FISH
Fathead minnow
(Plmephales promelas)
Sea lamprey
(Petromyzon marlnus)
AMPHIBIANS
Frog (Rana plplens)
CRUSTACEANS
Water flea
(Daphnla magna)
Brine shrimp
(Artemla salIna)
INSECTS
Mosquito (Aedes aeqyptl)
220
5000
140
4
1820
8
20
24-hour LC5Q
24-hour 1050
24-hour LC50
48-hour LC5Q
24-hour LC5Q
24-hour
Kagan
et al., 1985
nontoxlc, 24 hours Applegate
et al.. 1957
Kagan
et al., 1985
Kagan
et al., 1985
Bobra
et al., 1983
Kagan
et al., 1985
Kagan
et al., 1985
0866p
-33-
11/12/86
-------
6.4. RESIDUES
Bioconcentratlon data for five species are presented 1n Table 6-2. The
algae had the highest BCF values, 13,072 and 36,300 (Casserly et a!., 1983;
Davis et al., 1983), and rainbow trout the lowest, 72 (Gerhart and Carlson,
1978). Eadle et al. (1983) noted that sediment can be the principal source
for PAH uptake by benthes such as the amphlpod, Pontoporela hoyl.
Monitoring data for pyrene residues 1n aquatic organisms are presented
in Table 6-3. In general, the highest body burdens were reported for
molluscs from polluted areas In Norway (Knutzen and Sortland, 1982) and the
central Gulf of Mexico (Nulton and Johnson, 1981).
6.5. SUMMARY
Of six species tested, three arthropods were more sensitive to pyrene
than fish or amphibians. LC™ values of 4, 8 and 20 yg/S. were
reported for Daphnla magna. Artemla sallna and Aedes aegyptl, respectively.
Like some other PAH, the toxlclty of pyrene Is greatly enhanced by UV light
or sunlight (Kagan et al., 1985). Two algae species were less sensitive to
pyrene than the three arthropods, with EC™ values of 202 and 332 \iq/l
for inhibition of photosynthesis (Hutchinson et al., 1980). Reported BCF
values ranged from 72 for rainbow trout (Gerhart and Carlson, 1978) to
36,300 for the alga, Selenastrum capMcornutum (Casserly et al., 1983).
0866p -34- 11/12/86
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
Exposure criteria and TLVs have been developed for PAH as a class, as
well as for several Individual PAH. OSHA has set an 8-hour TWA concentra-
tion limit of 0.2 mg/m3 for the benzene-soluble fraction of coal tar pitch
volatiles (anthracene, benzo[a]pyrene, phenanthrene, acridine, chrysene,
pyrene) (OSHA, 1985). 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 1n workers. NIOSH (1977) also recommends a
celling limit for exposure to asphalt fumes of 5 mg airborne partlcu-
lates/m3 of air.
Environmental quality criteria, which specify concentration limits
Intended to protect humans against adverse health effects, have been recom-
mended for PAHs in ambient water. The U.S. EPA (1980) has recommended a
concentration limit of 28 ng/8. for the sum of all carcinogenic PAHs in
ambient water. This value is based on a mathematical extrapolation of the
results from studies wl-th 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 bioassay
data, daily consumption of water containing 28 ng/8. of carcinogenic PAHs
over an entire lifetime is estimated to keep the lifetime risk of cancer
development below one chance in 100,000.
0866p -38- 05/21/87
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The EPA has not recommended an ambient water quality criterion for
noncarclnogenlc PAHs as a class. The U.S. EPA (1980) acknowledged that data
suitable for quantitative risk assessment of noncarclnogenlc PAHs are essen-
tially nonexistent.
7.2. AQUATIC
Guidelines and standards for the protection of aquatic biota from the
toxic effects of pyrene in particular could not be located in the available
literature as cited 1n the Appendix. The U.S. EPA (1980) made the following
conclusions: that acute toxicity of PAH in general to saltwater biota
recurred at concentrations as low as 300 yg/s. and would be expected to
occur at lower concentrations In species more sensitive than those tested;
that acute toxicity of PAH In general to saltwater biota occurred at concen-
trations in species more sensitive than those tested; and that the pyrene
data base at that time was Inadequate to recommend criteria or draw conclu-
sions about chronic toxlcity or acute toxldty freshwater organisms.
0866p -39- 05/21/87
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8. RISK ASSESSMENT
Intratracheal Instillation of 3 mg pyrene suspended in saline at weekly
Intervals for 30 weeks did not produce tumors in the respiratory system
(histologic examination) or other tissues (gross examination) in hamsters
observed for life (Sellakumar and Shubik, 1974). Skin tumors were not
Induced in mice by twice or three-times weekly dermal application of pyrene
for 1-2 years (Barry et al., 1935; Badger et a!., 1940; Wynder and Hoffmann,
1959; Roe and Grant, 1964; Horton and Christian, 1974; Van Duuren and
Goldschmidt, 1976). Mouse skin initiation-promotion studies involving
Initiation with benzo[a]]pyrene (Roe and Grant, 1964), promotion with croton
oil (Salaman and Roe, 1956) or promotion with TPA (Scribner, 1973; Wood et
al., 1980) were negative or inconclusive (Scribner, 1973). Enhancement of
the dermal carclnogenlclty of benzo[a]pyrene in mice by simultaneous appli-
cation of pyrene has, however, been reported (Goldschmldt et al., 1973; Van
Duuren and Goldschmidt, 1976), indicating possible cocarcinogenlcity of
pyrene. Two subcutaneous Injections of 10 mg pyrene crystals 4 months apart
did not produce local tumors In mice after 12-18 months (Shear and Leiter,
1941).
Pyrene has been tested extensively In mutagenicity and other short-term
assays. Pyrene was mutagenic In some tests with S_. typhimuriurn In the
presence of metabolic activation preparation (Kaden et al., 1979; Bridges et
al., 1981; Matijasevic and Zeiger, 1985; Sakal et al., 1985) and produced
unscheduled DNA synthesis in cultured primary hamster hepatocytes (McQueen
et al., 1983) and human fibroblasts (Robinson and Mitchell, 1981), mutation
in mouse lymphoma L5178Y cells in vitro (Jotz and Mitchell, 1981), sister
chromatid exchanges in CHO (Evans and Mitchell, 1981) and V79 (Popescu et
0866p -40- 11/12/86
-------
al., 1977) cells in vitro and chromosomal aberrations In Chinese hamster V79
cells j_n vitro (Popescu et al., 1977). Genotoxldty of pyrene was not
demonstrated 1n other assays using -the same or different Indicator organisms
•
or endpoints, Including morphological transformation 1n a variety of rat,
mouse, hamster and guinea pig systems.
Pertinent data regarding teratogenlclty or other reproductive effects of
pyrene could not be located 1n the available literature as cited In the
Appendix.
Inhibition of growth and enlarged, fatty Hvers were reported as effects
1n a group of six male rats maintained on diets that contained 2000 ppm
pyrene for as long as 100 days (White and White, 1939). The significance of
these findings Is uncertain because Incidences were not reported and control
data were lacking. Information regarding toxic effects of chronic oral or
inhalation exposure to pyrene could not be located 1n the available litera-
ture as cited in the Appendix.
A single intraperitoneal Injection of 150 mg/kg pyrene produced minimal
gross swelling and congestion of the liver and Increased serum AST and
b1lirub1n in rats (Yoshikawa et al., 1985).
As Indicated above, pyrene was not tumorlgenlc when Instilled Into the
trachea of hamsters or applied to the skin of mice. Mouse skin Initiation
promotion studies were negative or Inconclusive. Although pyrene does not
appear to be active as a complete carcinogen or Initiator or promoter In
mouse skin studies, cocarcinogenlcity with benzo[a]pyrene has been reported
in dermal studies with mice. The subcutaneous injection study with mice Is
Inadequate for evaluation of carcinogeniclty because of the limited exposure
schedule. Although genotoxicity of pyrene has been demonstrated 1n several
short-term assays, the available data do not provide evidence that pyrene Is
a procarcinogen.
0866p -41- 07/27/87
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Calculation of an RfD based on the growth Inhibition and fatty livers In
rats (White and White, 1939) 1s precluded by limitation of data quality as
detailed previously, particularly the small number of animals, lack of
control data, unreported Incidence and magnitude of effects. These data
were not evaluated in the U.S. EPA (1984) Health Effects Assessment of
pyrene, which also did not calculate an RfD because of the lack of data.
0866p -42- 05/21/87
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9. REPORTABLE QUANTITIES
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC TOXICITY
Inhibition of growth and enlarged, fatty livers were reported as effects
•
1n a group of six male rats of unspecified strain that were maintained on
diets containing 2000 ppm pyrene for <100 days (White and White, 1939). The
significance of these effects is difficult to ascertain because of defi-
ciencies in experimental design and inadequate reporting. These include the
small group size and lack of an unexposed control group. In addition, the
magnitude of the growth inhibition was not indicated and food consumption
data were not reported. The hepatic effects were reported as general find-
ings in "some" animals that were treated with pyrene, benzpyrene or methyl-
cholanthrene, but the Incidence of these effects in the pyrene-treated rats
was not Indicated.
Holland et al. (1980) administered uncharacterized 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 fibrotic reaction, but that retorted shales caused Inflamma-
tion accompanied by fibrosls.
Weaver and Gibson (1979) exposed pregnant rats to graded airborne
concentrations of uncharacterized oil shale containing PAH, including
pyrene, on days 6-15 of gestation. No treatment-related teratogenic effects
were observed during examination of fetuses obtained by Caesarean section on
day 20 of gestation.
Calculation of an RQ for pyrene based on the growth inhibition or fatty
livers in rats (White and White, 1939) is precluded by the limitations of
data quality as indicated above. Because of the uncharacterized nature of
0866p -43- 05/21/87
-------
the test materials in the inhalation studies with hamsters (Holland et al.,
1980) and rats (Weaver and Gibson, 1979), it Is not possible to quantify
these data for use in deriving an RQ (Table 9-1) to reflect hazard asso-
ciated with exposure to pyrene (U.S. EPA, 1983).
9.2. WEIGHT OF EVIDENCE AND POTENCY FACTOR (F«1/ED1Q) FOR CARCINOGENICITY
Intratracheal Instillation of 3 mg pyrene suspended in saline at weekly
intervals for 30 weeks did not produce tumors In the respiratory system
(histologic examination) or other tissues (gross examination) in hamsters
observed for life (Sellakumar and Shubik, 1974). Skin tumors were not
Induced in mic'e by twice or three-times weekly dermal application of pyrene
for 1-2 years (Barry et al., 1935; Badger et al., 1940; Wynder and Hoffmann,
1959; Roe and Grant, 1964; Horton and Christian, 1974; Van Duuren and
Goldschmidt, 1976). Mouse skin initiation-promotion studies Involving
initiation with benzo[a]pyrene (Roe and Grant, 1964), promotion with croton
oil (Salaman and Roe, 1956) or promotion vith TPA (Scribner, 1973; Wood et
al., 1980) were negative or Inconclusive (Scribner, 1973). Enhancement of
the dermal carcinogenicity of benzo[a]pyrene in mice by simultaneous appli-
cation of pyrene has, however, been reported (Goldschmidt et al., 1973; Van
Duuren and Goldschmidt, 1976), Indicating possible cocarclnogeniclty of
pyrene. Two subcutaneous injections of 10 mg pyrene crystals 4 months apart
did not produce local tumors in mice after 12-18 months (Shear and Leiter,
1941).
Pyrene has been tested extensively in mutagenicity and other short-term
assays. Pyrene was mutagenic in some tests with S. typhimurium in the
presence of metabolic activation preparation (Kaden et al., 1979; Bridges et
al., 1981; Matijasevic and Zeiger, 1985; Sakai et al., 1985) and produced
unscheduled DNA synthesis in cultured primary hamster hepatocytes (McQueen
0866p -44- 05/21/87
-------
TABLE 9-1
Pyrene
Minimum Effective Dose (MED) and ReportabTe Quantity (RQ)
Route:
Dose:
Effect:
Reference:
RVd:
9
RVe:
Composite Score:
RQ: Data are not sufficient to derive an RQ.
0866p -45- 11/12/86
-------
et al., 1983) and human fibroblasts (Robinson and Mitchell, 1981), mutation
1n mouse lymphoma L5178Y cells in vitro (Jotz and Mitchell, 1981), sister
chromatid exchanges in CHO (Evans and Mitchell, 1981) and V79 (Popescu et
al., 1977) cells in vitro and chromosomal aberrations 1n Chinese hamster V79
cells j_n vitro (Popescu et al., 1977). Genotoxiclty of pyrene was not
demonstrated in other assays using the same or different Indicator organisms
or endpoints, including carcinogenic transformation in a variety of rat,
mouse, hamster and guinea pig systems.
Although cocardnogenicity of pyrene with benzo[a]pyrene has been
demonstrated in skin application studies with mice and short-term assays
provide limited evidence of genotoxicity, the available data do not Indicate
that pyrene is a procarcinogen. Carcinogenicity testing of pyrene by the
oral or inhalation routes, however, has not been conducted.
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
proposed by the U.S. EPA (1986b), pyrene is most appropriately designated a
Group D - Not Classified chemical. Direct hazard ranking of pyrene under
CERCLA Is therefore not possible.
0866p -46- 05/21/87
-------
10. REFERENCES
Applegate, V.C., J.H. Howell, A.E. Hall, Jr. and M.A. Smith. 1957.
Toxicity of 4346 chemicals to larval lampreys and fishes. Spec. Sd. Rep.
Fish. No. 207, Fish. Wild!. Serv., USDI, Washington, DC. 157 p.
Badger, G.M., J.W. Cook, C.L. Hewett, et al. 1940. The production of
cancer by pure hydrocarbons. V. Proc. R. Soc. London Ser. B. 129: 439-467.
Barry, G., I.A. Cook, G. Haslewood, C.I. Hewett and E.L. Kennaway. 1935.
The production of cancer by pure hydrocarbons. Part III. Proc. Roy. Soc.
(London). 117: 318-351.
Behymer, T.D. and R.A. HHes. 1985. Photolysis of polyaromatlc hydro-
carbons adsorbed on simulated atmospheric particles. .Environ. Scl. Technol.
19: 1004-1006.
Benolt, P.M., G.L. Lebel and D.T. Williams. 1979. The determination of
polycycllc aromatic hydrocarbons at the ng/s. level in Ottawa tap water.
Int. J. Environ. Anal. Chem. 6: 277-287.
Bobra, A.M., W.Y. Shiu and D. Mackay. 1983. A predictive correlation for
the acute toxicity of hydrocarbons and chlorinated hydrocarbons to the water
flea (Daphnia maqna). Chemosphere. 12(9-10): 1121-1130.
Boehm, P.O. and J.W. Farrington. 1984. Aspects of the polycyclic aromatic
hydrocarbon geochemistry of recent sediments in the Georges bank region.
Environ. Scl. Technol. 18: 840-845.
0866p -47- 11/12/86
-------
Boyland, E. and P. Sims. 1964. Metabolism of polycycllc compounds. The
metabolism of pyrene In rats and rabbits. Blochem. J. 90: 391-398.
Bridges, B.A., E. Zelger and D.B. McGregor. 1981. Summary report on the
performance of bacterial mutation assays. In: Evaluation of Short-Term
Tests for Carcinogens. Report of the International Collaborative Program.
Progress in Mutation Research, F.J. deSerres and J. Ashby, Ed., Vol. 1.
Elsevier/North Holland, NY. p. 49-67.
Brown, R.A. and R.J. Pandrov. 1979. Polynuclear aromatic hydrocarbons In
Baltimore Canyon fish. Environ. Sci. Technol. 13(7): 878-879.
Butkovic, V., L. Klasinc, M. Orhnovic, J. Turk and H. Gusten. 1983.
Reaction rates of polynuclear aromatic hydrocarbons with pzone 1n water.
Environ. Sci. Technol. 17: 546-548. -
Carlson, R.M., A.R. Oyler, E.H. Gerhart, et al. 1979. Implications to the
aquatic environment of polynuclear aromatic hydrocarbons liberated from
northern Great Plains coal. U.S. EPA, Duluth, MN. EPA 600/3-79-093.
Casserly, D.M., E.M. Davis, T.D. Downs and R.K. Guthrie. 1983. Sorptlon of
organlcs by Selenastrum capricornutum. Water Res. 17(11): 1591-1594.
Cole, R.H., R.E. Frederick, R.P. Healy and R.G. Rolan. 1984. Preliminary
findings of the priority pollutant monitoring project of the nationwide
urban runoff program. J. Water Pollut. Control Fed. 56: 898-908.
0866p -48- 11/12/86
-------
Darroudl, F. and A.3. Natarajan. 1985. Cytostatlc drug activity 1n plasma,
a bloassay for detecting mutagenldty of directly and Indirectly acting
chemicals, an evaluation of 20 chemicals. Mutat. Res. 143(4): 263-269.
Davis, E.M., 3.E. Turley, D.M. Casserly and R.K. Guthrle. 1983. Partition-
Ing of selected organic pollutants In aquatic ecosystems. I_n: B1odeter1ora-
tlon 5, T.A. Oxley and S. Barry, Ed. John Wiley and Sons, New York, NY.
p. 176-184.
Dean, B.J. 1981. Activity of 27 coded compounds 1n the RL, chromosome
assay. In: Evaluation of Short-Term Tests for Carcinogens. Report of the
International Collaborative Program. Progress In Mutation Research, F.J.
deSerres and J. Ashby, Ed., Vol. 1. Elsevler/North Holland, NY. p. 570-579.
Dennis, M.J., R.C Massey, D.J. McWeeney, M.E. Knowles and D. Watson. 1983.
Analysis of polycycllc aromatic hydrocarbons 1n UK total diets. Food Chem.
Toxlcol. 21: 569-574.
Dunn, B.P. and J. Fee. 1979. Polycycllc aromatic hydrocarbon carcinogens
1n commercial seafoods. J. FUh. Res. Board Can. 36(12): 1469-1476.
Eadle, B.J., W. Faust, W.S. Gardner and T. Nalepa. 1982. Polycycllc
aromatic hydrocarbons 1n sediments and associated benthos 1n Lake Erie.
Chemosphere. 11: 185-191.
0866p -49- 05/21/87
-------
Eadle, B.J., W.R. Faust, P.P. Landrum, N.R. Morehead, W.S. Gardner and T.
Nalepa. 1983. B1oconcentrat1ons of PAH by some benthlc organisms of the
Great Lakes. Polynucl. Aromat. Hydrocarbons, Int. Symp., M. Cooke, A.J.
Dennis, Ed., Battelle Press, CO. p. 437-449. [CA 99(25):207586k]
Elceman, G.A., R.E. Clement and F.W. Karasek. 1981. Variations in concen-
trations of organic compounds Including PCDDS and polynuclear aromatic
hydrocarbons 1n fly ash from a municipal Incinerator. Anal. Chem. 53:
955-959.
Elder, V.A., B.L. Proctor and R.A. HHes. 1981. Organic compounds found
near dump sites in Niagara Falls, NY. Environ. Sc1. Techno!. 15: 1237-1243.
Evans, E.L. and A.D. Mitchell. 1981. Effect of 20 coded chemicals on
sister chromatid exchange frequencies 1n cultured Chinese hamster cells.
In: Evaluation of Short-Term Tests for Carcinogens. Report of the Inter-
national Collaborative. Program. Progress in Mutation Research, F.J.
deSerres and J. Ashby, Ed., Vol. 1. Elsevier/North Holland, NY. p. 538-550.
Farrington, J.W., S.G. Wakeham, J.B. Llvramento, B.W. Tripp and J.M. Teal.
1986. Aromatic hydrocarbons in New York Bight polychaetes: Ultraviolet
fluorescence analyses and gas chromatography-mass spectrometry analyses.
Environ. Sci. Technol. 20(1): 69-72.
Fazio, T. and J.W. Howard. 1983. Polycycllc aromatic hydrocarbons 1n
foods. Jji: Handbook of Polycyclic Aromatic Hydrocarbons, A. Bjoerseth, Ed.
Marcel Dekker, Inc., New York, NY. p. 461-505.
0866p -50- 05/21/87
-------
Galloway, VI.B., 3.L. Lake, O.K. Phelps, et al. 1983. The mussel watch:
Intel-comparison of trace level constituent determinations. Environ.
Toxlcol. Chem. 2(4): 395-410.
Gerhart, E.H. and R.M. Carlson. 1978. Hepatic mixed-function oxldase
activity In rainbow trout exposed to several polycycllc aromatic compounds.
Environ. Res. 17(2): 284-295.
Goldschmldt, B.M., C. Katz and B.L. Van Duuren. 1973. The cocardnogenlc
activity of non-carcinogenic aromatic hydrocarbons (Abstract No. 334).
Proc. Am. Assoc. Cancer Res. 17: 84.
Goodley, P.C. and M. Gordon. 1976. Characterization of Industrial organic
compounds In water. Kentucky Academy of Science. 37: 11-15.
Great Lakes Water Quality Board. 1983. An Inventory of chemical substances
Identified In the Great Lakes ecosystem. Vol. 1-summary. Report to the
Great Lakes Water Quality Board. Windsor Ontario, Canada, p. 195.
Greenberg, A., F. Darack, R. Markov, P. L1oy and 0. Dalsey. 1985. Poly-
cycllc aromatic hydrocarbons In New Jersey. A comparison of winter and
summer concentrations over a two-year period. Atmos. Environ. 19:
1325-1339.
Griest, W.H. 1980. Multlcomponent polycycllc aromatic hydrocarbon analysis
of Inland water and sediment. In: Hydrocarbon Halo. Hydrocarbon Aquatic
Environ., B.K. Afghan and D. Mackay, Ed. Plenum Press, New York, NY.
p. 173-183.
0866p -51- 05/21/87
-------
Groenewegen, D. and H. Stolp. 1981. Mlcrobial breakdown of polycyclic
aromatic hydrocarbons. In: Decomposition of Toxic and Nontoxic Organic
Compounds In Soil, H.R. Overcash, Ed. Ann Arbor Science Pub!., Ann Arbor,
MI. p. 223-240.
Hashimoto, Y.. K. Tokura, H. Kishi and W.M.3. Strachan. 1984. Prediction
of seawater solubility of aromatic compounds. Chemosphere. 13(8): 881-888.
Hawley, G.G. 1981. The Condensed Chemical Dictionary, 10th ed. Van
Nostrand Reinhold Co., New York, NY. p. 872.
Heit, M. 1985. The relationship of a coal fired power plant to the levels
of polycyclic aromatic hydrocarbons (PAH) in the sediment of Cayuga Lake.
Water Air Soil Pollut. 24: 41-61.
Hites, R.A. 1979. Sources and fates of industrial organic chemicals. A
case study. Proc. Natl. Conf. Munic. Sludge Manage. 8: 107-119.
Ho, C.H., B.R. Clark, M.R. Guerin, B.D. Barkenbus, T.K. Bao and J.L. Epler.
1981. Analytical and biological analyses of test materials from the
synthetic fuel technologies. IV. Studies of chemical structure-mutagenic
activity relationships of aromatic nitrogen compounds relevant to synfuels.
Mutat. Res. 85: 335-345.
Hoffman, E.J., G.L. Mills, J.S. Latimer and J.G. Quinn. 1984. Urban runoff
as a source of polycyclic aromatic hydrocarbons to coastal waters. Environ.
Sci. Techno!. 18: 580-587.
0866p -52- 11/12/86
-------
Holland, L.M., W.D. Spall and L.L. Garcia. 1980. Inhalation toxicology of
oil shale-related materials. Health ImpHc. New Energy Technol., W.N. Rom
and V.E. Archer, Ed. Ann. Arbor Science Publishers, Inc., Ann Arbor, MI.
p. 515-526.
Horton, A.W. and G.M. Christian. 1974. Cocarclnogenlc versus Incomplete
carcinogenic activity among aromatic hydrocarbons. Contrast between
chrysene and benzo[b]tr1phenylene. J. Natl. Cancer Inst. 53: 1017-1020.
Hoy, C.A., E.P. Salazar and L.H. Thompson. 1984. Rapid detection of DNA-
damaglng agents using repair-deficient CHO cells. Mutat. Res. 130(5):
321-332.
Hutchlnson, T.C., J.A. Hellebust, 0. Tarn, D. Mackay, R.A. Mascarenhas and
W.Y. Shiu. 1980. The correlation of the toxldty to algae of hydrocarbons
and halogenated hydrocarbons with their physical-chemical properties.
Environ. Sd. Res. 16: 577-586.
IARC (International Agency for Research on Cancer). 1983. IARC Monographs
on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Pyrene.
In: Polynuclear Aromatic Compounds, Part I. Chemical, Environmental and
Experimental Data. WHO, IARC, Lyons, France. Vol. 32, p. 431-446.
Jacob, J., G. Grimmer, G. Raab and A. Schmoldt. 1982. The metabolism of
pyrene by rat liver mlcrosomes and the Influence of various mono-oxygenase
Inducers. Xenobiotica. 12: 45-53.
0866p -53- 11/12/86
-------
Johnson, A.C., P.P. Larsen, D.F. Gadbols and A.M. Humason. 1985. The
distribution of polycycllc aromatic hydrocarbons 1n the surfldal sediments
of penobscot bay (Maine, USA) 1n relation to possible sources and other
sites world wide. Marine Environ. Res. 15: 1-16.
Jotz, M.M. and A.O. Mitchell. 1981. Effects of 20 coded chemicals on the
forward mutation frequency at the thymldlne klnase locus In L5178Y mouse
lymphoma cells. ITK Evaluation of Short-Term Tests for Carcinogens. Report
of the International Collaborative Program. Progress in Mutation Research,
P.O. deSerres and J. Ashby, Ed. Elsevler/North Holland, NY. Vol. 1,
p. 580-593.
Jungclaus, G.A., L.M. Games and R.A. Hltes. 1976. Identification of trace
organic compounds In tire manufacturing plant wastewaters. Anal. Chem. 48:
1894-1896.
Oungclaus, G.A., V. Lopez-Avlla and R.A. Hites. 1978. Organic compounds 1n
an Industrial waste water. A case study of their environmental Impact.
Environ. Sd. Techno!. 12: 88-96.
Kaden, D.A., R.A. Hltes and W.G. Thllly. 1979. MutagenlcHy of soot and
associated polycycllc aromatic hydrocarbons to Salmonella typhimurium.
Cancer Res. 39: 4152-4159.
Kagan, J., E.D. Kagan, I.A. Kagan, P.A. Kagan and S. Qulgley. 1985. The
phototoxlcity of noncardnogenic polycycllc aromatic hydrocarbons In aquatic
organisms. Chemosphere. 14(11-12): 1829-1834.
0866p -54- 11/12/86
-------
Karlckhoff, S.W. 1981. Seml-eplrical estimation of sorptlon of hydrophobia
pollutants on natural sediments and soils. Chemosphere. 10: 833-846.
Karlckhoff, S.W. and K.R. Morris. 1985. Sorptlon dynamics of hydrophoblc
pollutants 1n sediment suspension. Environ. Toxlcol. Chem. 4: 469-479.
Karlckhoff, S.H., D.S. Brown and T.A. Scott. 1979. Sorptlon of hydrophoblc
pollutants on natural sediments. Water Res. 13: 241-248.
Kelmig, S.D., K.W. K1rby, D.P. Morgan, J.E. Kelser and T.O. Hubert. 1983.
Identification of 1-hydroxypyrene as a major metabolite of pyrene In pig
urine. Xenob1ot1ca. 13(7): 415-420.
Keller, C.D. and T.F. Bldleman. 1984. Collection of airborne polycycllc
aromatic hydrocarbons and other organlcs with a glass fiber filter-
*
polyurethane foam system. Atmos. Environ. 18: 837-845.
Kenaga, E.E. 1980. Predicted bloconcentratlon factors and soil sorptlon
coefficients of pesticides and other chemicals. Ecotoxlcol. Environ.
Safety. 4: 26-38.
Kerkhoff, M.J., T.M. Lee, E.R. Allen, D.A. Lundgren and J.D. Wlnefordner.
1985. Spectral fingerprinting of polycycllc aromatic hydrocarbons 1n
high-volume ambient air samples by constant energy synchronous luminescence
spectroscopy. Environ. Sd. Technol. 19: 695-699.
0866p -55- 11/12/86
-------
Knutzen, 3. and B. Sortland. 1982. Polycycllc aromatic hydrocarbons (PAH)
In some algae and Invertebrates from moderately polluted parts of the coast
of Norway. Water Res. 16(4): 421-428.
Kuntz, K.W. 1984. Toxic contaminants In the Niagara River. 1975-1982.
Technical Bulletin No. 134. Burlington, Ontario.
Kveseth, K., B. Sortland and T. Bonkn. 1982. Polycycllc aromatic hydro-
carbons In sewage, mussels and tap water. Chemosphere. 11: 623-639.
Larsen, P.P., D.F. Gadbols, A.C. Johnson and L.F. Doggett. 1983. Distribu-
tion of polycycllc aromatic hydrocarbons In the surflcial sediments of Casco
Bay, Maine. Bull. Environ. Contam. Toxicol. 30: 530-535.
LaVoie, E., V. Bedenko, N. Hlrota, S.S. Hecht and D. Hoffmann. 1979. A
comparison of the mutagenicity, tumor-initiating activity and complete
cardnogenlclty of polynuclear aromatic hydrocarbons. In: Polynuclear
Aromatic Hydrocarbons, P.M. Jones and P. Leber, Ed. Ann Arbor Science
Publishers, Ann Arbor, HI. p. 705-721.
Lawrence, J.F. and D.F. Weber. 1984. Determination of polycycllc aromatic
hydrocarbons 1n Canadian samples of processed vegetables and dairy products
by liquid chromatography with fluorescence detection. J. Agric. Food Chem.
32: 794-797.
Ligocki, M.P., C. Leuenberger and J.F. Pankow. 1985a. Trace organic
compounds In rain-II. Gas scavenging of neutral organic compounds. Atmos.
Environ. 19: 1609-1617.
0866p -56- 11/12/86
-------
Llgockl, M.P., C. Leuenberger, and J.F. Pankow. 1985b. Trace organic
compounds In rain-Ill. Particle scavenging of neutral organic compounds.
Atmos Environ. 19: 1619-1626.
Lunde, G. and A. Bjoerseth. 1977. Polycyclic aromatic hydrocarbons 1n
long-range transported aerosols. Nature. 268: 518-519.
Lyman, W.J., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical
Property Estimation Methods. McGraw-Hill Book Co., New York. p. 15-16 to
15-29.
Mabey, W.R., 3.H. Smith, T.R. Podoll, et al. 1981. Aquatic Fate Process
Data for Organic Priority Pollutants. U.S. EPA, Monitoring and Data Support
Division (WH 553), Office of Water Regulations and Standards, Washington,
DC. EPA 440/4-82-014.
Maccubbln, A.E., P. Black, L. Trzeclak and J.J. Black. 1985. Evidence of
polynuclear aromatic hydrocarbons In the diet of bottom-feeding fish. Bull.
Environ. Contam. Toxlcol. 34(6): 876-882.
Mackay, D. 1982. Correlation of bloconcentratlon factors. Environ. Sc1.
Technol. 16: 274-278.
Mackay, D., W.Y. Sh1u, A. Bobra, et al. 1982. Volatilization of Organic
Pollutants from Water. U.S. EPA, Athens, GA. EPA 600/53-82-019. NTIS
PB82-230-939.
0866p
-57-
11/12/86
-------
Malins, D.C., M.M. Krahn, M.S. Myers, et al. 1985a. Toxic chemicals 1n
sediments and biota from a creosote-polluted harbor. Relationships with
hepatic neoplasms and other hepatic lesions In English sole (Parophrys
yetulus). Cardnogenesls. 6: 1463-1469.
Malins, D.C., M.M. Krahn, D.W. Brown, et al. 1985b. Toxic chemicals 1n
marine sediment and biota from MukHeo, Washington. Relationships with
hepatic neoplasms and other hepatic lesions In English sole (Parophrys
vetulus). 3. Natl. Cancer Inst. 74(2): 487-494.
Mamber, S.W., V. Bryson and S.E. Katz. 1983. The Escherlchla coll
WP2/WP100 rec assay for detection of potential chemical carcinogens. Mutat.
Res. 119(2): 135-144.
Mamber, S.W., V. Bryson and S.E. Katz. 1984. Evaluation of the Escherlchla
coll K12 Inductest for detection of potential chemical carcinogens. Mutat.
Res. 130(3): 141-152.
Matijasevic, Z. and E. Zelger. 1985. Mutagen1c1ty of pyrene 1n Salmonella.
Mutat. Res. 142(4): 149-152.
Matsumoto, H. and T. Kashlmoto. 1985. Average dally respiratory Intake of
polycycllc aromatic hydrocarbons In ambient air determined by capillary gas
chromatography. Bull. Environ. Contam. Toxlcol. 34: 17-23.
McCann, 0., E. Choi, E. Yamasaki and B.N. Ames. 1975. Detection of
carcinogens as mutagens in the Salmonella/mlcrosome test. Assay of 300
chemicals. Proc. Natl. Acad. Sci. USA. 72: 5135-5139.
0866p -58- 11/12/86
-------
McFall, J.A., W.Y. Huang and J.L. Laseter. 1979. Organics at the air-water
Interface of Lake Pontchartrain. Bull. Environ. Contam. Toxlcol. 22: 80-87.
McQueen, C.A., D.M. Krelser and 6.H. Williams. 1983. The hepatocyte pri-
mary culture/DNA repair assay using mouse or hamster hepatocytes. Environ.
Mutagen. 5: 1-8.
Merrill, E.G. and T.L. Wade. 1985. Carbonized coal products as a source of
aromatic hydrocarbons to sediments from a higher Industrial estuary.
Environ. Scl. Technol. 19: 597-603.
Miller, M.M., S.P. Waslk, G.L. Huang, W-Y Shiu and D. Mackay. 1985.
Relationships between octanol-water partition coefficient and aqueous
solubility. Environ. Sci. Technol. 19: 522-529.
Mitchell, C.E. and K. Tu. 1977. Distribution, retention and elimination of
pyrene in rats following inhalation. Annu. Rep. Inhalation Toxlcol. Res.
Inst. p. 350-355.
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.
NAS (National Academy of Sciences). 1972. Biologic Effects of Atmospheric
Pollutants. Particulate Polycyclic Organic Matter. NAS, Washington, DC.
p. 63-81.
0866p -59- 11/12/86
-------
Nielsen, J.B. and 0. Anderson. 1986. The peritoneal cell carclnogenldty
test. Mutat. Res. 173(2): 153-156.
Nlkonova, T.V. 1977. Transplacental action of benzo[a]pyrene and pyrene.
Bull. Exp. Biol. Med. 84: 1025-1027.
NIOSH (National Institute for Occupational Safety and Health). 1977.
Criteria for a Recommended Standard...Occupational Exposure to Coal Tar
Products, U.S. DHEW, PHS, CDC, Rockvllle, HD. Publ. No. 78-107.
NRC (National Research Council). 1983. Polycycllc Aromatic Hydrocarbons:
Evaluation of Sources and Effects. Natl. Acad. Press, Washington, DC.
Nulton, C.P. and D.E. Johnson. 1981. Aromatic hydrocarbons In marine
tissues from the Central Gulf of Mexico. J. Environ. Scl. Health. Part A.
A16(3): 271-288.
Obana, H., S. Horl, A. Nakamura and T. Kashlmoto. 1983. Uptake and release
of polynuclear aromatic hydrocarbons by short-necked clams (Tapes japonlca).
Water Res. 17(9): 1183-1188.
Ogata, M., K. Fujlsawa, Y. Oglno and E. Mano. 1984. Partition coefficients
as a measure of bloconcentratlon potential of crude oil compounds 1n fish
and shellfish. Bull. Environ. Contam. Toxlcol. 33: 561-567.
0866p -60- 11/12/86
-------
Ohio River Valley Water Sanitation Commission. 1979. Water treatment
process modifications for trlhalomethane control and organic substances In
the Ohio river. Prepared in fulfillment of U.S. EPA Grant R-804615 for
project activities 10/76-8/79. Cincinnati, OH.
OSHA (Occupational Safety and Health Administration). 1985. OSHA Safety
and Health Standards. 29 CFR 1910.1000.
Overton, E.B., S.W. Mascarella, J.A. McFall and J.L. Laseter. 1980.
Organics in the water column and air-water Interface samples of Mississippi
River water. Chemosphere. 9: 629-633.
Pancirov, R.J. and R.A. Brown. 1977. Polynuclear aromatic hydrocarbons in
marine tissues. Environ. Scl. Techno!. 11(10): 989-992.
Pearlman, R.S., S.H. Yalkowsky and S. Banerjee. 1984. Water solubilities
of polynuclear aromatic and heteroaromatlc compounds. J. Phys. Chem. Ref.
Data. 13: 555-562.
Popescu, N.C., D. Turnbull and J.A. DiPaolo. 1977. Sister chromatid
exchange and chromosome aberration analysis with the use of several carcino-
gens and noncarcinogens. Brief communication. J. Natl. Cancer Inst. 59:
289-293.
Prahl, F.G., E. Crecellus and R. Carpenter. 1984. Polycyclic aromatic
hydrocarbons in Washington coastal sediments. An evaluation of atmospheric
and rlverene roots of introduction. Environ. Sd. Techno!. 18: 687-693.
0866p -61- 11/12/86
-------
Qulllardet, P., C. DeBellecombe and M. Hofnung. 1985. The SOS Chromotest,
a colorlmetric bacterial assay for genotoxlns. Validation study with 83
compounds. Hutat. Res. 147(3): 79-95.
Rady, P., I. Arany, E. Uzvolgyl, F. Bojan and P. Kertai. 1982. Transpla-
cental effects of carcinogens and noncarclnogens on activities of pyruvate
klnase and lactate dehydrogenase as well as Isozymic pattern of LDH 1n mouse
lung. Toxicology. 24(3-4): 251-257.
Readman, J.W., R.F.C. Mantoura, M.M. Rhead and L. Brown. 1982. Aquatic
distribution and heterotrophlc degradation of polycycllc aromatic hydro-
carbons (PAH) In the Tamar Estuary. Estuarlne, Coastal. Shelf. Scl. 14:
369-389.
Robinson, D.E. and A.D. Mitchell. 1981. Unscheduled ONA synthesis response
*
of human fibroblasts, WI-38 cells, to 20 coded chemicals. In: Evaluation of
Short-Term Tests for Carcinogens. Report of the International Collaborative
Program. Progress 1n Mutation Research, F.J. deSerres and J. Ashby, Ed.
Elsevler/North Holland, NY. Vol. 1, p. 517-527.
Roe, F.J.C. and G.A. Grant. 1964. Tests of pyrene and phenanthrene for
Incomplete carcinogenic and antlcarclnogenlc activity (Abstract). Br. Emp.
Cancer Campaign. 41: 59-60. (Cited in IARC, 1983)
Rostad, C.E., W.E. Pereira and M.F. Hult. 1985. Partitioning studies of
coal-tar constituents in a two-phase contaminated groundwater system.
Chemosphere. 14: 1023-1036.
0866p -62- 11/12/86
-------
Ruepert, C., A. Grlnusls and H. Covers. 1985. Prediction of partition
coefficients of unsubstltuted polycycllc aromatic hydrocarbons from C10
I o
chromatographlc and structural properties. Chemosphere. 14: 279-291.
Sakal, M., D. Yoshida and S. Mlzusakl. 1985. Mutagenldty of polycycllc
aromatic hydrocarbons and quinones on Salmonella typhlmurlum TA97. Mutat.
Res. 156(1-2): 61-67.
Salaman, M.H. and F.J.C. Roe. 1956. Further tests for tumour-1n1t1at1ng
activity. N,N-D1(2-chloroethyl)-p-am1nophenylbutyr1c add (CB1348) as an
Initiator of skin tumour formation 1n the mouse. Br. J. Cancer. 10:
363-378.
Salamone, H.F., 3.A. Heddle and M. Katz. 1981. Hutagenlc activity of 41
compounds In the Jhi vivo mlcronucleus assay. In: Evaluation of Short-Term
Tests for Carcinogens. Report of the International Collaborative Program.
Progress In Mutation Research, F.J. deSerres and J. Ashby, Ed. Elsevler/
North Holland, NY. Vol. 1, p. 686-697.
Santodonato, 3., P. Howard and D. Basu. 1981. Health and Ecological
Assessment of Polynuclear Aromatic Hydrocarbons. Pathotox Publishers, Inc.,
Park Forest South, IL.
Schwarz, F.P. and S.P. Waslk. 1976. Fluorescence measurements of benzene,
naphthalene, anthracene, pyrene, fluoranthene and benzo(e)pyrene In water.
Anal. Chem. 48: 524-528.
0866p -63- 11/12/86
-------
ScMbner, 3.D. 1973. Brief communication. Tumor Initiation by apparently
noncardnogenlc polycycllc aromatic hydrocarbons. J. Natl. Cancer Inst.
50: 1717-1719.
Sellakumar, A. and P. Shubik. 1974. Cardnogenlclty of different poly-
cycllc hydrocarbons 1n the respiratory tract of hamsters. J. Natl. Cancer
Inst. 53: 1713-1719.
Shear, M.J. and J. Leiter. 1941. Studies In cardnogenesls. XVI. Produc-
tion of subcutaneous tumors on mice by miscellaneous polycycllc compounds.
J. Natl. Cancer Inst. 11: 241-258.
Shlmada, T., K. Furukawa, D.H. Krelser, A. Caweln and G.M. Williams. 1983.
Induction of transformation by six classes of chemical carcinogens In adult
rat liver epithelial cells. Cancer Res. 43(11): 5087-5092.
S1ms, P. 1970. Qualitative and quantitative studies on the metabolism of a
series of aromatic hydrocarbons by rat-liver preparations. Blochem.
Pharmacol. 19: 795-818.
S1ms, R.C. and M.R. Overcash. 1983. Fate of polynuclear aromatic compounds
(PNAS) In soil-plant systems. Residue Reviews. 88: 1-68.
S1na. J.F., C.L. Bean, G.R. Dysart, V.I. Taylor, M.O. Bradley. 1983.
Evaluation of the alkaline elut1on/rat hepatocyte assay as a predictor of
carclnogenic/mutagenlc potential. Mutat. Res. 113(5): 357-391.
0866p -64- 11/12/86
-------
Sorrel!, R.K., H.J. Brass and R. Reding. 1980. A review of the occurrences
and treatment of polynuclear aromatic hydrocarbons 1n water. Environ.
Inter. 4: 245-254.
Southworth, G.R., 3.3. Beauchamp and P.K. Schmleder. 1978. Bloaccumulatlon
potential of polycycllc aromatic hydrocarbons In Daphnia pulex. Water Res.
12: 973-977.
Spehar, R.L., R.W. Carlson, A.E. Lemke, D.I. Mount, Q.H. Pickering and V.M.
Snarskl. 1980. Effects of pollution on freshwater fish. J. Water Pollut.
Control Fed. 52: 1703-1774.
SRI (Stanford Research Institute). 1986. 1986 Directory of Chemical
Producers, United States of America. SRI International, Menlo Park, CA.
Staples, C.A., A. Werner and T. Hoogheem. 1985. Assessment of priority
pollutant concentrations In the United States using STORE! database.
Environ. Toxlcol. Chem. 4: 131-142.
Swann, R.L., D.A. Laskowskl, P.J. McCall, K.VanderKuy and H.J. Dlshburger.
1983. A rapid method for the estimation of the environmental parameters
octanol/water partition coefficient, soil sorptlon constant, water to air
ratio, and water solubility. Res. Rev. 85: 17-28.
Tabak, H.H., S.A. Quave, C.I. Mashnl and E.F. Barth. 1981. Blodegradablllty
studies with organic priority pollutant compounds. J. Water Pollut. Control
Fed. 53: 1503-1518.
0866p -65- 05/21/87
-------
Tan, Y.L. and M. Heit. 1981. Blogenlc and ablogenlc polynuclear aromatic
hydrocarbons in sediments from two remote Adirondack lakes. Geochlm.
Cosmochim. Acta. 45: 2267-2279.
Topham, J.C. 1980. The detection of carcinogen-Induced sperm head
abnormalities in mice. Mutat. Res. 69(1): 149-155.
Topping, D.C., B.C. Pal, D.H. Martin, F.R. Nelson and P. Nettesheim. 1978.
Pathologic changes induced in respiratory tract mucosa by polycyclic hydro-
carbons of differing carcinogenic activity. Am. J. Pathol. 93: 311-324.
U.S. EPA. 1977. Computer print-out of non-confidential production data
from TSCA Inventory. OPTS, CID, U.S. EPA, Washington, DC.
U.S. EPA. 1980. Ambient Water Quality Criteria for Polynuclear Aromatic
Hydrocarbons. Prepared by the Office of Health and Environmental Assess-
ment, 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. 1983. Reportable Quantity for Pyrene. Prepared by the Office of
Health and Environmental Assessment, Environmental Criteria and Assessment
Office, Cincinnati, OH, OHEA, for the Office of Emergency and Remedial
Response, Washington, DC.
0866p -66- 05/21/87
-------
U.S. EPA. 1984. Health Effects Assessment for Pyrene. 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. EPA 540/1-86-030.
U.S. EPA. 1986a. Computer printout: Graphic Exposure Modeling System (GEMS)
EXAMS model. U.S. EPA, Office of Toxic Substances, Washington, DC.
U.S. EPA. 1986b. Guidelines for carcinogenic risk assessment. Federal
Register. 51(185): 3392-34003.
U.S. EPA/NIH. 1986. OHM-TADS (011 and Hazardous Materials Technical
Assistance Data System). April 16, 1986: On-line.
Vaes-sen, H.A.M.G., P.L. Schuller, A.A. Jekel and A.A.H.H. Wllbers. 1984.
Polycycllc aromatic hydrocarbons 1n selected foods. Analysis and occur-
rence. Toxlcol. Environ. Chem. 7: 297-324.
Valencia, R. and K. Houtchens. 1981. Mutagenlc activity of 10 coded com-
pounds in the DrosophUa sex-linked recessive lethal test. In: Evaluation
of Short-Term Tests for Carcinogens. Report of the International Collabora-
tive Program. Progress In Mutation Research, F.J. deSerres and J. Ashby,
Ed. Elsevler/North Holland, NY. Vol. 1, p. 651-659.
Valerlo, F. and A. Lazzarotto. 1984. Role of airborne partlculate matter
components on photochemical degradation of pyrene, benzoanthracene and
benzo(a)pyrene. A preliminary report. Spectrosc. Int. J. 3: 412-415.
0866p -67- 07/27/87
-------
Van Duuren, B.L. and B.M. Goldschmldt. 1976. Cocarclnogenic and tumor-
promoting agents In tobacco carclnogenesls. J. Natl. Cancer Inst. 56:
1237-1242.
Van Noort, P.C.M. and E. Wondergem. 1985. Scavenging of airborne poly-
cyclic aromatic hydrocarbons by rain. Environ. Scl. Technol. 19: 1044-1048.
Varanasl, U., W.L. Relchert, J.E. Stein, D.W. Brown and H.R. Sanbom. 1985.
B1oava1lab1l1ty and blotransformatlon of aromatic hydrocarbons 1n benthlc
organisms exposed to sediment from an urban estuary. Environ. Scl. Technol.
19: 836-841.
Ved Brat, S., C. Tong, S. Teland and G.M. Williams. 1983. Comparison of
sister chromatld exchange and mammalian cell mutagenesls at the hypoxanthlne
guanlne phosphorlbosyl transferase locus 1n adult rat liver epithelial
cells. Ann. N.Y. Acad. Scl. 407: 474-475.
Walker, J.D. and R.R. Colwell. 1975. Degradation of hydrocarbons and mixed
hydrocarbon substrate by microorganisms from Chesapeake Bay. Prog. Water
Technol. 7: 783-791.
Walters, R.W. and R.G. Luthy. 1984. Liquid/suspended solid phase parti-
tioning of polycycllc aromatic hydrocarbon in coal coking waste waters.
Water Res. 18: 795-809.
Weast, R.C., Ed. 1980. CRC Handbook of Chemistry and Physics, 61st ed.
CRC Press, Inc., Boca Raton, FL. p. C-527.
0866p -68- 07/27/87
-------
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.
White, J. and A. White. 1939. Inhibition of growth of the rat by oral
administration of methylcholanthrene, benzpyrene, or pyrene and the effects
of various dietary supplements. J. Biol. Chem. 131: 149-161.
Williams, O.T., E.R. Nestmann, G.L. Lebel, P.M. Benolt, R. Otson and E.G.H.
Lee. 1982. Determination of mutagenlc potential and organic contaminants
of Great Lakes drinking water. Chemosphere. 11: 263-276.
Windholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co., Inc.,
Rahway, NJ. p. 1148-1149.
Wood, A.W., W. Levin, R.L. Chang, et al. 1980. Mutagenldty and tumor-
Initiating activity of cyclopenta(3,d)pyrene and structurally related
compounds. Cancer Res. 40(3): 642-649.
Wynder, E.L. and D. Hoffman. 1959. A study of tobacco carcinogens. VII.
The role of higher polycycllc hydrocarbons. Cancer. 12: 1079-1086.
Yalkowsky, S.H. and S.C. Valvani. 1979. Solubilities and partloning. 2.
Relationships between aqueous solubilities, partition coefficients, and
molecular surface areas of rigid aromatic hydrocarbons. J. Chem. Eng. Data.
24: 127-129.
0866p -69- 07/27/87
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Yamasakl, H., K. Kuwata and H. Miyamoto. 1982. Effects of ambient tempera-
ture on aspects of airborne polycycllc aromatic hydrocarbons. Environ. Scl.
Techno!. 16: 189-194.
Yokley, R.A., A.A. Garrison, E.L. Wehry and G. Mamantor. 1986. Photochemi-
cal transformation of pyrene vapor-deposited on eight coal stack ashes.
Environ. Sc1. Techno!. 20: 86-90.
Yoshlkawa, T., L.P. Ruhr, W. Flory, D. Glamalva, D.F. Church and W.A. Pryor.
1985. Toxlclty of polycycllc aromatic hydrocarbons. I. Effect of phenan-
threne, pyrene and their ozonized products on blood chemistry in rats.
Toxlcol. Appl. Pharmacol. 79(2): 218-226.
Zepp, R.G. and P.P. Schlotzhauer. 1983. Influence of algae on photolysis
rates of chemicals In water. Environ. Scl. Techno!. 17: 462-468.
Zepp, R.G., P.P. Schlotzhauer, M.S. Simmons, G.C. Miller, G.L. Baughman and
N.L. Wolfe. 1984. Dynamics of pollutant photoreactlons 1n the hydrosphere.
Fresenlus Z. Anal. Chem. 319: 119-125.
0866p -70- 11/12/86
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APPENDIX
LITERATURE SEARCHED
This profile is based on data Identified by computerized literature
searches of the following:
GLOBAL
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
CAS online STN International
TOXLINE
TOXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted 1n April, 1986. In addition, hand searches
were made of Chemical Abstracts (Collective Indices 6 and 7), and the
following secondary sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hygienists).
1986. Documentation of the Threshold Limit Value's and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hygienists).
1985-1986. TLVs: Threshold Limit Values for Chemical Substances
and Physical Agents In the Workroom Environment with Intended
Changes for 1985-1986. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2B. John Wiley and
Sons, NY. p. 2879-3816.
0866p -71- 11/12/86
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Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John WHey and
Sons, NY. p. 3817-5112.
Grayson, M. and D. Eckroth, Ed. 1978-1983. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, HA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. WHO, IARC, Lyons, France.
ITII (International Technical Information Institute). 1982. Toxic
and Hazardous Industrial Chemicals Safety Manual for Handling and
Disposal with Toxlclty and Hazard Data. ITII, Tokyo, Japan. 700 p.
Jaber, H.M., W.R. Mabey, S.T. Liu, T.W. Chow and H.L. Johnson.
1984. Data aqulsltlon for environmental transport and fate screen-
Ing for compounds of Interest In the Office of Solid Waste. EPA
600/6-84-010. NTIS PB84-243906. SRI International, Menlo Park, CA.
NTP (National Toxicology Program). 1986. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, N.I. 1979. Dangerous Properties of Industrial Materials, 5th
ed. Van Nostrand Reinhold Co., NY.
SRI (Stanford Research Institute). 1984. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1985. Status Report on Rebuttable Presumption Against
Registration (RPAR) or Special Review Process. Registration Stan-
dards and the Data Call In Programs. Office of Pesticide Programs,
Washington, DC.
U.S. EPA. 1985. CSB Existing Chemical Assessment Tracking System.
Name and CAS Number Ordered Indexes. Office of Toxic Substances,
Washington, DC.
USITC (U.S. International Trade Commission). 1983. Synthetic
Organic Chemicals. U.S. Production and Sales, 1982, USITC Pub!.
1422, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Reinhold Co., NY.
0866p -72- 11/12/86
-------
Windholz, M.. Ed. 1983. The Merck Index. 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
In addition, approximately 30 compendia of aquatic toxldty data were
reviewed. Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Finley. 1980. Handbook of Acute Toxiclty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxicity Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Pimental, D. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0866p -73- 11/12/86
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maintained 1n enclosures made of creosote-treated wood could significantly
Increase their PAH body burden. Phenanthrene levels averaged 32 ng/g In
freshly caught lobsters and 100 ng/g 1n Impounded lobsters.
6.5. SUMMARY
The data base for the aquatic toxldty of phenanthrene 1s limited. The
most sensitive of four fish species tested was the rainbow trout, which
experienced a 10% mortality of eggs and larvae at 1-4 vg/i (Black et
al., 1983). Among the nine Invertebrate species tested, the lowest reported
lethal concentration was 100 yg/l, the 96-hour LC5Q for 0. pulex
(Trucco et al., 1983). This result conflicts with the only chronic toxldty
study available (Gelger and Bulkema, 1982), In which no toxic effects or
reproductive success or survival of £. pulex occurred at 110 yg/l.
Aquatic plants appeared to be less sensitive to phenanthrene than fish and
Invertebrates, with EC™ values for Inhibition of photosynthesis ranging
from 870 yg/i In N. paleo (Mlllemann et al., 1984) to 100% saturation In
S. caprlcornutum (61dd1ngs, 1979). Bloconcentratlon and residue monitoring
data Indicated wide variability In potential for phenanthrene accumulation
1n various species (see Tables 6-2 and 6-3). Bony fishes (teleosts) tended
to metabolize and eliminate phenanthrene more rapidly than other aquatic
organisms (Solbakken and Palmork, 1981).
0861p -42- 07/24/87
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
OSHA set an 8-hour TWA concentration limit of 0.2 mg/m3 for the
benzene-soluble fraction of coal tar pitch volatlles (anthracene, benzo[a]-
pyrene, phenanthrene, acrldlne, chrysene, pyrene) (OSHA, 1985). NIOSH
(1977) recommended 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 airborne part1culates/ma of air.
U.S. EPA (1980a) recommended a concentration limit of 28 ng/l for the
sum of all carcinogenic PAH 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 PAH are equal In potency to benzo[a]pyrene. On the
basis of the animal bloassay data, dally consumption of water containing 28
ng/l of carcinogenic PAH over an entire lifetime Is estimated to keep the
lifetime risk of cancer development <1 chance In 100,000.
U.S. EPA (1980a) acknowledged that data suitable for quantitative risk
assessment of noncardnogenlc PAH are essentially nonexistent, and an
ambient water quality criterion has not been recommended.
0861p -43- . 07/24/87
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7.2. AQUATIC
Guidelines and standards for the protection of aquatic biota from the
effects of phenanthrene In particular could not be located 1n the available
literature as cited 1n the Appendix; however, U.S. EPA (1980b) noted that
acute toxldty to saltwater life occurred at concentrations as low as 300
pg/8. of polynuclear aromatic hydrocarbons 1n general and would occur at
lower concentrations In species more sensitive than tested. U.S. EPA
(1980b) also determined that the data base was Inadequate to recommend
criteria or draw conclusions about chronic or acute toxldty to freshwater
•
biota.
0861p -44- 07/24/87
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8. RISK ASSESSMENT
Phenanthrene has been tested for cardnogenlcHy In a single-treatment
(200 mg) gavage study In which rats were examined for development of mammary
tumors for 60 days following treatment (Muggins and Yang, 1962). The
tumorIgenlclty of phenanthrene was also evaluated In single-treatment (40
vg or 5 mg) subcutaneous (Stelner, 1955; Grant and Roe, 1963) and three-
treatment (35, 70 and 140 »ig at weekly Intervals) Intraperltoneal (Buenlng
et al., 1979) studies with mice. The results of these studies were negative
but should be regarded as Inconclusive (see Table 5-1) because limited
treatment schedules make the studies Inadequate for evaluation of carclno-
genldty. Phenanthrene reportedly did not produce skin tumors In mice 1n an
Inadequately reported study 1n which the dose and application schedule was
not specified (Kennaway, 1924). Phenanthrene was active as a tumor Initi-
ator 1n one study 1n which TPA was used as the. tumor promoter (ScMbner,
1973), but was Inactive 1n other mouse skin Initiation-promotion studies In
which TPA was used as the promoter (Wood et al., 1979; LaVole et al., 1981),
croton oil was used as the promoter (Roe, 1962), benzo[a]pyrene and croton
oil were used as promoters (Roe and Grant, 1964) and benzo[a]pyrene was used
as the Initiator (Roe and Grant, 1964). Phenanthrene also was not active
when used 1n mice as an Initiator by subcutaneous Injection with croton oil
promotion by skin application (Roe, 1962).
Phenanthrene has been tested In numerous mutagenlclty and other
short-term assays with predominant negative responses. Point mutation tests
In bacteria have generally been negative (McCann et al., 1975; Wood et al.,
1979; Buecker et al., 1979; LaVole et al., 1981; Florin et al., 1980; Dunkel
et al., 1984; Kaden et al., 1979; Selxas et al., 1982) with the exception of
one study showing positive results for Salmonella typhlmurlum TA100 when
0861p -45- 07/24/87
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assayed 1n the presence of a high concentration of liver S9 (Oesch et al.,
1981) and another study reporting a positive response In the new frameshlft
tester strain TA97 with liver metabolic activation (Sakal et al., 1985).
Phenanthrene was reported to Induce gene mutations 1n human lymphoblastold
cells In vitro In the presence of a metabolic activation system (Barfknecht
et al., 1981), but was reported to be negative for gene mutations at two
different loci In Chinese hamster V79 cells j£ vitro (Huberman and Sachs,
1979). Intraperltoneal Injection of phenanthrene Into Chinese hamsters
produced sister chromatld exchanges, but no chromosome aberrations or
mlcronuclel In the bone marrow cells (Bayer, 1978; Roszlnsky-Kocher et al.,
1979). Sister chromatld exchanges and chromosome aberrations were not
produced 1n Chinese hamster V79-4 cells treated ^n vitro with phenanthrene
In the presence of exogenous metabolic activation (Popescu et al., 1977).
Phenanthrene did not produce positive responses In other assays Indicative
of DNA damage using bacteria mammalian cells In vUro, and yeast {I.e.,
differential growth Inhibition, DNA repair and m1tot1c recombination tests)
(McCarrol et al., 1981; Rosenkranz and PolMer, 1979; Lake et al., 1978;
Probst et al., 1981; Simmon, 1979).
The oral, subcutaneous, Intraperltoneal and dermal carclnogenlcHy
studies of phenanthrene are Inadequate for evaluation of cardnogen1c1ty
because of deficiencies 1n treatment schedules and reporting. Phenanthrene
was active as an Initiator 1n one mouse skin study that used TPA as the
promoter (ScMbner, 1973), but this effect was not corroborated 1n other
studies that used the same or different promoters or benzo[a]pyrene as the
Initiator. Hutagenldty and clastogenlcHy (sister chromatld exchange) of
phenanthrene was reported In several assays, but the preponderance of data
0861p -46- 07/24/87
-------
from numerous short-term genotoxldty tests 1s negative. The available
evidence Is therefore Inadequate to evaluate the cardnogenlcHy of
phenanthrene.
Information regarding the chronic or subchronlc toxlclty, teratogenlcHy
or other reproductive effects of phenanthrene could not be located In the
available literature as cited In the Appendix. Calculation of an RfD
(formerly ADI) Is therefore precluded, as It was at the time of an earlier
health effects assessment for phenanthrene (U.S. EPA, 1984).
0861p -47- 07/24/87
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9. REPORTABLE QUANTITY
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC TOXICITY
Information regarding the chronic or subchronlc toxldty, teratogenldty
or other reproductive effects of phenanthrene could not be located 1n the
available literature as cited In the Appendix. Calculation of an RQ ranking
for phenanthrene based on chronic toxldty Is therefore precluded, as H was
In an earlier RQ document for phenanthrene (U.S. EPA, 1983) by the lack of
appropriate data.
9.2. HEIGHT OF EVIDENCE AND POTENCY FACTOR (F-1/ED.,0) FOR CARCINOGENICITY
Phenanthrene has been tested for carclnogenlcHy In a single-treatment
(200 mg) gavage study In which rats were examined for development of mammary
tumors for 60 days following treatment (Hugglns and Yang, 1962). The
tumorIgenlcity of phenanthrene was also evaluated In single-treatment (40
jig or 5 mg) subcutaneous (Stelner, 1955; Grant and Roe, 1963) and three-
treatment (35, 70 and 140 yg at weekly Intervals) IntraperUoneal (Buenlng
et a!., 1979) studies with mice. The results of these studies were negative
but should be regarded as Inconclusive because limited treatment schedules
make the studies Inadequate for evaluation of carclnogenlcHy. Phenanthrene
reportedly did not produce skin tumors In mice In an Inadequately reported
study In which a dose and application schedule was not specified (Kennaway,
1924). As detailed 1n Table 5-1, phenanthrene was active as a tumor Initi-
ator In one study 1n which TPA was used as the tumor promoter (Scrlbner,
1973), but was Inactive In other mouse skin Initiation-promotion studies 1n
which TPA was used as the promoter (Wood et al., 1979; LaVole et al., 1981),
croton oil was used as the promoter (Roe, 1962), benzo[a]pyrene and croton
oil were used as promoters (Roe and Grant, 1964) and benzo[a]pyrene was used
0861p -48- 07/24/87
-------
as the Initiator (Roe and Grant, 1964). Phenanthrene also was not active
when used In mice as an Initiator by subcutaneous Injection with croton oil
promotion by skin application (Roe, 1962).
Phenanthrene has been tested In numerous mutagenlclty and other short-
term assays with generally negative results. These Include assays for DNA
repair, mutagenesls and clastogenlclty 1n bacterial and mammalian cells \n_
vitro and \t± vivo and neoplastlc transformation 1n mammalian cells.
Positive responses occurred In £. typhlmurlum strain TA100 1n the presence
of a high concentration of metabolic activation preparation (Oesch et al.,
1981), but not 1n strains TA100, TA98, TA1535, TA1537, TA1538 or TM677 with
activation In other studies. Phenanthrene also Induced mutation to
tr1fluorothym1d1ne resistance In human lymphoblastold TK6 cells in vitro
(Barfknecht et al., 1981) and sister chromatld exchanges 1n hamster bone
marrow cells In vivo (Bayer, 1978; Roszlusky-Kocher et al., 1979).
The- oral, subcutaneous, IntrapfiMtoneal and dermal cardnogenlclty
studies of phenanthrene are Inadequate for evaluation of cardnogenlclty
because of. the differences 1n treatment schedule and reporting. Phen-
anthrene was active as an Initiator In one mouse skin study that used TPA as
the promoter (Scrlbner, 1973), but this effect was not corroborated In other
studies that used the same or different promoters or benzo[a]pyrene as the
Initiator. Mutagenlclty and clastogenlclty (sister chromatld exchange) of
phenanthrene was reported In several assays, but the preponderance of data
from numerous short-term genotoxlclty tests Is negative. The available
evidence Is therefore Inadequate to evaluate the carclnogenlclty of
phenanthrene.
0861p -49- 07/24/87
-------
IARC (1983) reported that there was Insufficient evidence regarding the
carcinogenic risk to humans and experimental animals associated with oral or
Inhalation exposure to phenanthrene. Applying the EPA criteria for
evaluation of the overall weight of evidence for the carcinogenic potential
for humans (U.S. EPA, 1986), phenanthrene Is most appropriately designated a
Group D - Not Classified chemical. Direct hazard ranking of phenanthrene
under CERCLA Is therefore not possible.
0861p -50- 07/24/87
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10. REFERENCES
Afolabl, O.A., E.A. Adesulu and O.L. Oke. 1983. Polynuclear aromatic
hydrocarbons In some Nigerian preserved freshwater fish species. J. Agrlc.
Food Chem. 31: 1083-1090.
Applegate, V.C., J.H. Howell, A.E. Hall, Jr. and M.A. Smith. 1957. Toxlc-
1ty of 4346 chemicals to larval lampreys and fishes. Fish Wlldl. Serv.,
USDI, Washington, DC. Spec. Scl. Rep. - F1sh No. 207.
Atkinson, R. 1985. Kinetics and mechanisms of the gas phase reactions of
the hydroxyl radical with organic compounds under atmospheric conditions.
Chem. Rev. 85: 69-201.
Barfknecnt, T.R., B.M. Andon, W.6.' Thllly .and R.A. HHes. 1981. Soot and
mutation In bacteria and human cells. In: 5th Int. Symp. Chemical Analysis
and Biological F.ate: Polynuclear AromatU Hydrocarbons. Battelle Press,
Columbus, OH. p. 231-242. (Cited In IARC, 1983)
Bastlan, M.V. and D.W. Toetz. 1982. Effect of eight polynuclear hydro-
carbons on growth an Anabaena flosaquae. Bull. Environ. Contain. Toxlcol.
29(5): 531-538.
Bayer, U. 1978. In. vivo Induction of sister chromatld exchanges by three
polyaromatlc hydrocarbons. In: Polynuclear Aromatic Hydrocarbons, Carclno-
genesls, Vol. 3, P.H. Jones, and R.I. Freudenthal, Ed. Raven Press, New
York. p. 423-428. (Cited In IARC, 1983)
0861p -51- 07/24/87
-------
Behymer, T.D. and R.A. HHes. 1985. Photolysis of polycycllc aromatic
hydrocarbons adsorbed on simulated atmospheric participates. Environ. Sd.
Techno!. 19(1): 1004-1006.
Benolt, P.M., G.L. Lebel and D.T. Williams. 1979. The determination of
polycycllc aromatic hydrocarbons at the ng/a level In Ottawa tap water.
Int. J. Environ. Anal. Chem. 6: 277-287.
Bldleman, T.F. 1984. Estimation of vapor pressures for nonpolar organic
compounds by capillary gas chromatography. Anal. Chem. 56: 2490-2496.
BJoerseth, A., 0. BJoerseth and P.E. Fjeldstad. 1978. Polycycllc aromatic
hydrocarbons 1n the work atmosphere. I. Determination In an aluminum
reduction plant. Scand. 3. Work Environ. Health. 4: 212-223.
Black, J.A.. W.J. B1rge, A.G. Westerman and P.C. Francis. 1983. Compara-
tive aquatic toxicology of aromatic hydrocarbons. Fund. Appl. Toxlcol. 3:
353-358.
Bobra, A.M.. W.Y. Sh1u and D. Mackay. 1983. A predictive correlation for
the acute toxldty of hydrocarbons and chlorinated hydrocarbons to the water
flea (Daphnla maqna). Chemosphere. 12(9-10): 1121-1130.
Boehm, P.O. and J.W. Farrlngton. 1984. Aspects of the polycycllc aromatic
hydrocarbon geochemistry of recent sediments In the Georges Bank region.
Environ. Scl. Technol. 18: 840-845.
0861p -52- 07/24/87
-------
Bossert, I., W.M. Kachel and R. Bartha. 1984. Fate of hydrocarbons during
oily sludge disposed In soil. Appl. Environ. Mlcroblal. 47: 763-767.
Boyland, E. and P. Sims. 1962. Metabolism of polycycllc compounds. The
metabolism of phenanthrene In rabbits and rats: Dlhydro-dlhydroxy compounds
and related glucoslduronlc acids. Blochem. J. 84: 571-582.
Boyland, E. and G. Wolf. 1950. Metabolism of polycycllc compounds 6.
Conversion of phenanthrene Into dlhydroxydlhydrophenanthrene. Blochem. J.
47: 64-69.
Brookes, P. 1977. HutagenlcHy of polycycllc aromatic hydrocarbons.
Mutat. Res. 39: 257-284.
Buecker, M., H.R. Glatt, K.L. Platt.-et al. 1979. Mutagenlclty of'phenan-
threne and phenanthrene k-reg1on derivatives. Mutat. Res. 66: 337-348.
Buenlng, M.K., W. Levin, J.M. Karle, H. Yag1, D.M. Jerlna and A.H. Conney.
1979. TumorIgenlclty of bay-region epoxldes and other derivatives of
chrysene and phenanthrene In newborn mice. Cancer Res. 39: 5063-5068.
Butkovlc, V., L. Klaslnc, M. Orhnovlc, J. Turk and H. Gusten. 1983.
Reaction rates of polynuclear aromatic hydrocarbons with ozone In water.
Environ. Sc1. Techno!. 17: 546-548.
0861p -53- 07/24/87
-------
Carlson, R.M. A.R. Oyler, E.H. Gerhart, et al. 1979. Implications to
aquatic environment of polynucelar aromatic hydrocarbons liberated from
northern Great Plains coal. Environ. Res. Lab., U.S. EPA, Duluth, MN. EPA
600/3-79-093. (Cited 1n Spehar et al., 1981)
Casserly, D.M., E.M. Davis, T.D. Downs and R.K. Guthrle. 1983. Sorptlon of
organlcs by Selenastrum caprlcornutum. Water Res. 17(11): 1591-1594.
Cern1gl1a, C.E. 1981. Aromatic hydrocarbons: Metabolism by bacteria, fungi
and algae. Rev. Blochem. Toxlcol. 3: 321-361.
ChaturapU, S. and G.M. Holder. 1978. Studies on the hepatic mlcrosomal
metabolism of (14C)phenanthrene. Blochem. Pharmacol. 27(14>: 1865-1872.
Cole, R.H., R.E. Frederick, R.P. Healy and R.G. Rolan. 1984. Preliminary
findings of the priority pollutant monitoring project of the Nationwide
Urban Runoff Program. 3. Water Pollut. Control Fed. 56(7): 898-908.
Dalsey, O.M., 3.L. Cheney and P.O. L1oy. 1986. Profiles of organic partlc-
ulate emissions from air pollution sources: Status and needs for receptor
source apportionment modeling. J. A1r Pollut. Control Assoc. 36: 17-33.
Davis, E.M., J.E. Turley, D.M. Casserly and R.K. Guthrle. 1983. Partition-
Ing of selected organic pollutants 1n aquatic ecosystems, ^n: B1odeter1ora-
tlon 5, T.A. Oxley and S. Barry, Ed. John Wiley and Sons, New York.
p. 176-184.
0861p -54- 07/24/87
-------
DeVault, D.S. 1985. Contaminants In fish from Great Lakes harbors and
tributary mouths. Arch. Environ. Contam. Toxlcol. 14(5): 587-594.
Dunkel, V.C., E. Zelger, D. Bruslck, et al. 1984. ReproduclbllHy of
mlcroblal mutagenlcHy assays: I. Tests with Salmonella typhlmurlum and
Escher1ch1a coll using a standardized protocol. Environ. Mutagen. 6: 1-38.
Dunn, B.P. and J. Fee. 1979. Polycycllc aromatic hydrocarbon carcinogens
In commercial seafoods. J. Fish. Res. Board Can. 36(12): 1469-1476.
Eadle, B.J., W. Faust, W.S. Gardner and T. Nalepa. 1982. Polycycllc
aromatic hydrocarbons 1n sediments and associated benthos In Lake Erie.
Chemosphere. 11: 185-191.
Eadle, B.J., W.R. Faust, P.F. Landrum, N.R. Horehead, W.S. Gardner and T.
Nalepa. 1983. Bloconcentratlons of PAH by some benthlc organisms of the
Great Lakes. Ijv. 7th Int. Symp. Polynucl. Aromat. Hydrocarbons. Battelle
Press, Columbus, OH. p. 437-449.
Eastmond, D.A., G.M. Booth and M.L. Lee. 1984. Toxlclty, accumulation and
elimination of polycycllc aromatic sulfur heterocycles In Daphnla magna.
Arch. Environ. Contam. Toxlcol. 13(1): 105-111.
E1senre1ch, S.J., B.B. Looney and J.D. Thornton. 1981. Airborne organic
contaminants 1n the Great Lakes ecosystem. Environ. Scl. Technol. 15:
30-38.
0861p -55- 07/24/87
-------
Evans, C.H. and J.A. DIPaolo. 1975. Neoplastlc transformation of guinea
pig fetal cells 1n culture Induced by chemical carcinogens. Cancer Res.
35: 1035-1044.
Farrlngton, J.W., S.G. Wakeham, J.B. Llvramento, B.W. Brlpp and J.H. Teal.
1986. Aromatic hydrocarbons In New York Bight polychaetes: Ultraviolet
fluorescence analyses and gas chromatography/gas chromatography-mass
spectrometry analyses. Environ. Scl. Technol. 20(1): 69-72.
Fazio, T. and 3.W. Howard. 1983. Polycycllc aromatic hydrocarbons In
foods, in: Handbook of Polycycllc Aromatic Hydrocarbons, A. BJoerseth, Ed.
Marcel Dekker Inc., New York. p. 461-505.
Fielding, M., T.M. Gibson, H.A: 3ames, K. McLoughlln and C.P. Steel. 1981.
Organic mlcropollutants In drinking water. Water Res. Cent. p. 21-27.
Florin, I., L. Rutberg, M. Curvall and C.R. Enzell. 1980. Screening of
tobacco smoke constituents for mutagenldty using the Ames' test.
Toxicology. 18: 219-232.
Fuhs, B.W. 1961. The mlcroblal degradation of hydrocarbons. Arch.
Hlkroblol. 39: 374-442. (Ger.)
Galloway, W.B., J.L. Lake, O.K. Phelps, et al. 1983. The mussel watch:
IntercompaMson of trace level constituent determinations. Environ.
Toxlcol. Chem. 2: 395-410.
0861p -56- 07/24/87
-------
Gammage, R.B. 1983. Polycycllc aromatic hydrocarbons In work atmospheres.
ITK Handbook of Polycycllc Aromatic Hydrocarbons, A. Bjoerseth, Ed. Marcel
Dekker Inc., New York. p. 653-707.
Gelger, J.G. and A.L. Bulkema, Jr. 1982. Hydrocarbons depress growth and
reproduction of Daphnla pulex (Cladocera). Can. J. Fish. Aquat. Sc1.
39(6): 830-836.
Gerhart, E.H., R.J. Klukkonen, R.M. Carlson, G.N. Stokes, M. Lukasewycz and
A.R. Oyler. 1981. Hlstologlcal effects and bloaccumulatlon potential of
coal partlculate-bound phenanthrene 1n the fathead minnow, Plmephales
promelas. Environ. Pollut. Ser. A Ecol. B1ol. 25(3): 165-180.
Geyer, H., G. PolHzkl and D. Freltag. 1984. Prediction of ecotoxlcologl-
cal behavior of chemicals: Relationship between n-octanol/water partition
coefficient and bloaccumulatlon of organic chemicals by alga Chlorella.
Chemosphere. 13(2): 269-284.
Gibson, D.T. 1977. Blodegradatlon of aromatic petroleum hydrocarbons. In:
Fate and Effects of Petroleum Hydrocarbons In Marine Organism and Eco-
systems, D.A. Wolfe, Ed. Pergamon Press, New York, NY. p.36-46.
Glddlngs, J.M. 1979. Acute toxldty to Selenastrum caprlcornutum of
aromatic compounds from coal conversion. Bull. Environ. Contam. Toxlcol.
23(3): 360-364.
G1le, J.O., J.C. Collins and J.W. Glllett. 1982. Fate and Impact of wood
preservatives 1n a terrestrial microcosm. J. Agrlc. Food Chem. 30: 295-301.
0861p -57- 07/24/87
-------
GoerlHz, D.F., D.E. Troutman, E.M. Godsy and B.J. Franks. 1985.
Migration of wood-preserving chemicals 1n contaminated groundwater 1n a sand
aquifer at Pensacola, Florida. Environ. Sc1. Techno!. 19(10): 955-961.
Grant, G. and F.J.C. Roe. 1963. The effect of phenanthrene on tumour
Induction by 3,4-benzopyrene administered to newly born mice. Br. J.
Cancer. 17: 261-265.
Grlest, W.H. 1980. Multlcomponent polycycllc aromatic hydrocarbon analysis
of Inland Water and Sediment. In.'- Hydrocarbon and Halogenated Hydrocarbons
1n Aquatic Environment, B.K. Afghan and D. Mackay, Ed. Plenum Press, New
York. p. 173-183.
Grosjean, D. 1983. Polycycllc aromatic hydrocarbons 1n Los Angeles air
from samples collected on Teflon, glass and quartz filters. Environ. Res.
Techno!. Atmos. Environ. 17(12): 2565-2573.
Hansen, N., V.P. Jensen, H. Appelqulst and E. Morch. 1978. The uptake and
release of petroleum hydrocarbons by the marine mussel Hytllus edulls.
Prog. Water Technol. 10(5-6): 351-359.
Hasanen, E., V. Pohjola, H. Pyysalo and K. Wlckstrom. 1984. Polycycllc
aromatic hydrocarbons In Finnish sauna air. Scl. Total Environ. 37:
223-231.
Hawley, G.G., Ed. 1981. The Condensed Chemical Dictionary, 10th ed. Van
Nostrand Relnhold Co., New York. p. 794.
0861p -58- 07/24/87
-------
Hawley-Fedder, R.A., M.L. Parsons and F.W. Karasek. 1984. Products ob-
tained during combustion of polymers under simulated Incinerator conditions.
III. Poly(v1nyl chloride). 3. Chromatogr. 315: 211-221.
Kites, R.A. 1979. Sources and fates of Industrial organic chemicals; A
case study. In.: Proc. 8th Natl. Conf. Munlc. Sludge Manage, p. 107-119.
Hoffman, E.J., G.L. Hills, J.S. Latlmer and J.G. Qulnn. 1984. Urban runoff
as a source of polycycllc aromatic hydrocarbons to coastal waters. Environ.
Sc1. Techno!. 18(8): 580-587.
Huberman, E. and L. Sachs. 1976. Mutability of different genetic loci In
mammalian cells by metabollcally activated carcinogenic polycycllc
hydrocarbons. Proc. Natl. Acad. Sc1. USA. 73: 188-192.
Hugglns, C. and N.C. Yang. 1962. Induction and extinction of mammary
cancer. Science. 137: 257-262.
Hutchlnson, T.C., 3.A. Hellebust, D. Tarn, 0. Mackay, R.A. Mascarenhas and
W.Y. Shlu. 1980. The correlation of the toxlclty to algae of hydrocarbons
and halogenated hydrocarbons with their physical-chemical properties.
Environ. Sc1. Res. 16: 577-586.
IARC (International Agency for Research on Cancer). 1983. IARC Monographs
on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Phenan-
threne. In.: Polynuclear Aromatic Compounds, Part 1, Chemical, Environmental
and Experimental Data. WHO, IARC, Lyon, France. Vol. 32, p. 419-430.
0861p -59- 07/24/87
-------
Ios1f1dou, H.G., S.D. K1l1k1d1s and A.P. Kamarlanos. 1982. Analysis for
polycycllc aromatic hydrocarbons 1n mussels (HytHus galloprovlnclalls) from
the Thermalkos Gulf, Greece. Bull. Environ. Contam. Toxlcol. 28: 535.
John, E.D., M. Cooke and G. Nlckless. 1979. Polycycllc aromatic hydro-
carbons 1n sediments taken from the Severn estuary drainage system. Bull.
Environ. Contam. Toxlcol. 22: 653-659.
Jungclaus, G.A., L.M. Games and R.A. HUes. 1976. Identification of trace
organic compounds In tire manufacturing plant wastewaters. Anal. Chem. 48:
1894-1896.
Jungclaus, G.A., V. Lopes-Avlla and R.A. HUes. 1978. Organic compounds In
an Industrial waste water: A case study of their environmental Impact.
Environ. Scl. Techno!. 12: 88-96.
Kaden, D.A., R.A. HHes and W.G. ThUly. 1979. Mutagen1c1ty of soot and
associated polycycllc aromatic hydrocarbons to Salmonella typh1mur1um.
Cancer Res. 39: 4152-4159.
Kakunaga, T. 1979. A quantitative system for assay of malignant
transformation by chemical carcinogens using a clone derived from BALB/3T3.
Int. J. Cancer. 12:463-474.
KaMckhoff, S.W., O.S. Brown and T.A. Scott. 1979. Sorptlon of hydrophoblc
pollutants on natural sediments. Water Res. 13: 241-248.
0861p -60- 07/24/87
-------
Keller, C.O. and T.F. Bldleman. 1984. Collection of airborne polycycllc
aromatic hydrocarbons and other organlcs with a glass fiber f Uter-polyure-
thane foam system. Atmos. Environ. 18: 834-845.
Kennaway, E.L. 1924. On the cancer-producing factor In tar. Br. Med. 3.
p. 564-567.
Kerkhoff, M.J., T.H. Lee, E.R. Allen, D.A. Lundgren and J.O. Wlnefordner.
1985. Spectral fingerprinting of polycycllc aromatic hydrocarbons In high-
volume ambient air samples by constant energy synchronous luminescence
spectroscopy. Environ. Scl. Technol. 19: 695-699.
Kertsz-Sarlnger, H. and Z. Morlln. 1975. Occurrence of polycycllc aromatic
hydrocarbons In the urban area of Budapest. Atmos. Environ. 9: 831-834.
Klyohara, H., K. Nagao and K. Yana. 1982. Rapid screen for bacteria
degrading water Insoluble solid hydrocarbons on agar plates. Appl. Environ.
Mlcroblol. 43: 454-457.
Knutzen, J. and B. Sortland. 1982. Polycycllc aromatic hydrocarbons (PAH)
In some algae and Invertebrates from moderately polluted parts of the coast
of Norway. Water Res. 16(4): 421-428.
Kobayashl, H. and B.E. RHtmann. 1982. Mlcroblal removal of hazardous
organic compounds. Environ. Sc1. Technol. 16: 170A-182A.
0861p -61- 07/24/87
-------
Korfmacher, W.A., E.L. Wehry, G. Hamantov and D.F.S. Natusch. 1980.
Resistance to photochemical decomposition of polycycllc aromatic hydro-
carbons vapor-adsorbed on coal fly ash. Environ. Sc1. Techno!. 14:
1094-1099.
Kotln, P., H.L. Falk and R. Busser. 1969. Distribution, retention and
elimination of C14-3,4-benzopyrene after administration to mice and rats.
J. Natl. Cancer Inst. 23: 541.
•
Kuo, C.H. and H.M. Barnes. 1985. Reactions of ozone with organic In
aqueous solutions. U.S. EPA, Research Triangle Park, NC. EPA 600/93-85-031.
NTIS PB85-191171.
Kveseth, K., B. Sortland and T. Bokn. 1982. Polycycllc aromatic hydro-
carbons 1n sewage, mussels and tap water. Chemosphere. 11: 623-639.
Lake, R.S., H.L. Kropko, H.R. Prezzuttl, R.H. Shoemaker and H.J. Igel.
1978. Chemical Induction of unscheduled DNA synthesis 1n human skin
epithelial cell cultures. Cancer Res. 38: 2091-2098.
LaVole, E.J., L. Tulley-Freller, V. Bedenko and D. Hoffmann. 1981. Muta-
genldty, tumor-Initiating activity and metabolism of methylphenanthrenes.
Cancer Res. 41(9): 3441-3447.
Lee, R.F. and C. Ryan. 1983. M1crob1al and photochemical degradation of
polycycllc aromatic hydrocarbons 1n estuarlne waters and sediments. Can. J.
Fish Aquat. Sc1. 40: 86-94.
0861p -62- 07/24/87
-------
L1gock1, M.P., C. Leuenberger and J.F. Pankow. 1985. Trace organic
compounds 1n ra1n-II. Gas scavenging of neutral organic compounds. Atmos.
Environ. 19: 1609-1617.
Lunde, G. and A. Bjoerseth. 1977. Polycycllc aromatic hydrocarbons In
long-range aerosols. Nature. 268: 518-519.
Lutln, P.A., J.J. Clbulka and G.W. Malaney. 1965. Oxidation of selected
carcinogenic compounds by activated sludge. Purdue Univ. Eng. Bull., Ext.
Series. 118: 131-145.
Lyman, W.J., H.F. Reehe and D.H. Rosenplatt. 1982. Handbook of Chemical
Property Estimation Methods, Environmental Behavior of Organic Compounds.
McGraw-Hill Book Co., New York. p. 15-24.
Maccubbln, A.E., P. Black, L. Trzedak and J.J. Black. 1985. Evidence for
polynuclear aromatic hydrocarbons In the diet of bottom-feeding fish. Bull.
Environ. Contam. Toxlcol. 34{6): 876-882.
Mackay, 0., S. Paterson, B. Cheung and W.B. Neely. 1985. Evaluating the
environmental behavior of chemicals with a Level III fugaclty model.
Chemosphere. 14: 325-374.
Hallns, O.C., M.M. Krahsn, DM. Brown, et al. 1985. Toxic chemicals 1n
marine sediment and biota from Muklteo, Washington: Relationships with
hepatic neoplasms and other hepatic lesions In English sole (Parophrys
yetulus). J. Natl. Cancer Inst. 74(2): 487-494.
0861p -63- 07/24/87
-------
Marcus, J.M. and T.P. Stokes. 1985. Polynuclear aromatic hydrocarbons In
oyster tissue around three coastal marinas. Bull. Environ. Contam. Toxlcol.
35(6): 835-844.
Marquardt, H., T. Kurokl, E. Huberman, et al. 1972. Malignant
transformation of cells derived from mouse prostate by epoxldes and other
derivatives of polycycllc hydrocarbons. Cancer Res. 32: 716-720.
Matsumoto, H. and T. Kashlmoto. 1985. Average dally respiratory Intake of
polycycllc aromatic hydrocarbons 1n ambient air determined by capillary gas
chromatography. Bull. Environ. Contam. Toxlcol. 34: 17-23.
McCann, J., E. Choi, E. Yamasakl and B.N. Ames. 1975. Detection of carcin-
ogens as mutagen In the Salmonella/mlcrosome test: Assay of 300 chemicals.
Proc. Natl. Acad. Sc1. USA. 72: 5135-5139.
HcCarroll, N.E., B.H. Keech and C.E. Piper. 1981. A mlcrosuspenslon
adaptation of the Bacillus subtllls rec assay. Environ. Mutagen. 3:
607-616.
McCarthy, J.F. 1983. Role of partlculate organic matter In decreasing
accumulation of polynuclear aromatic hydrocarbons by Daphnla magna. Arch.
Environ. Contam. Toxlcol. 12: 559-568.
McKenna, E.J. 1977. B1odegradat1on of polynuclear aromatic hydrocarbon
pollutants by soil and water microorganisms. Presented at the 70th Ann.
Meet, of Am. Inst. Chem. Engineers, New York, Nov. 13-17, 1977.
0861p -64- 07/24/87
-------
McKenna, E.J. and R.E. Kalllo. 1965. The biology of hydrocarbons. Ann.
Rev. M1krob1ol. 71: 181-208.
MUlemann, R.E., W.J. B1rge, 3.A. Black, et al. 1984. Comparative acute
toxldty to aquatic organisms of components of coal-derived synthetic fuels.
Trans. Am. Fish. Soc. 113(1): 74-85.
Miller, H.M., S.P. Waslk, G. Huang, W. Sh1u and D. Mackay. 1985. Relation-
ships between octanol-water partition coefficients and aqueous solubility.
Environ. Scl. Techno!. 19: 522-529.
Moore, M.N. and S.V. Farrar. 1985. Effects of polynuclear aromatic hydro-
carbons on lysosomal membranes In mollusks. Mar. Environ. Res. 17(2-4):
222-225. [CA 104(13):103856d]
Moore, M.N., 3.A. Mayernlk and C.S. Glam. 1985. Lysosomal responses to a
polynuclear aromatic hydrocarbon In a marine snail: Effects of exposure to
phenanthrene and recovery. Mar. Environ. Res. 17(2-4): 230-233.
NAS (National Academy of Sciences). 1972. Biologic effects of atmospheric
pollutants. Partlculate polycycllc organic matter. NAS, Washington, DC.
p. 63-81.
Nlessner, R., D. Klockow, F. Bruynseels and R. van Grleken. 1985. Investi-
gation of heterogeneous reactions of PAHs on particle surfaces using laser
mlcroprobe mass analysis. Int. J. Environ. Anal. Chera. 22(3-4): 281-295.
0861p -65- 07/24/87
-------
NIOSH (National Institute for Occupational Safety and Health). 1977.
Criteria for a Recommended Standard Safety Exposure to Coal Tar Products.
U.S. DHEW, PHS, CDC, Rockvllle, MO. Publ. No. 78-107.
N1sh1, Y. 1984. Relationships of SCE and other biological endpolnts.
Toklshlkorojl Foramu (Toxicology Forum) (Tokyo) 7: 328-343.
Nordqvlst, H., D-.R. Thakker, K.P. Vyas, et al. 1981. Metabolism of
chrysene and phenanthrene to bay-region dlol epoxldes by rat liver enzymes.
Mol. Pharmacol. 19(1): 168-178.
Nulton, C.P. and D.E. Johnson. 1981. Aromatic hydrocarbons 1n marine
tissues from the Central Gulf of Mexico. J. Environ. Scl. Health, Part A.
A16(3): 271-288.
•
Oesch, F., M. Buecker and H.R. Glatt. 1981. Activation of phenanthrene to
mutagenlc metabolites and evidence for at least two different activation
pathways. Mutat. Res. 81(1): 1-10.
OSHA (Occupational Safety and Health Administration). 1985. OSHA Safety
and Health Standards. 29 CFR 1910.1000.
Palmork, K.H. and J.E. Solbakken. 1981. Distribution and elimination of
[9>i«C]-phenanthrene 1n the horse mussel (Modlola modlolus). Bull.
Environ. Contam. Toxlcol. 26(2): 196-201.
Patterson, J.H. and P.S. Kodukala. 1981. B1odegradat1on of hazardous
organic pollutants. Chem. Eng. Prog. 77: 48-55.
0861p -66- 07/24/87
-------
Pearlman, R.S., S.H. Yalkowskl and S. Banerjee. 1984. Water solubilities
of polynuclear aromatic and heteroaromatlc compounds. J. Chem. Ref. Data.
13: 555-562.
•
Peterson, A.R., J.R. Landolph, H. Peterson, C.P. Spears and C.
Heldelberger. 1981. Oncogenlc transformation and mutation of C3H/10T1/2
Clone 8 mouse embryo flbroblasts by alkylatlng agents. Cancer. Res. 41:
3095-3099.
Plenta, R.J., J.A. Polley and W.B. Lebherz, III. 1977. Morphological
transformation of early passage golden Syrian hamster embryo cells derived
from cryopreserved primary cultures as a reliable \n_ vitro bloassay for
Identifying diverse carcinogens. Int. J. Cancer. 19: 642-655.
Popescu, N.C., D. Turnbull and J.A. DIPaolo. 1977. Sister chromatld
exchange and chromosome aberration analysis with the use of several carcino-
gens and noncarclnogens. Brief communication. 0. Natl. Cancer Inst. 59:
289-293.
Probst, G.S., R.E. McMahnon, L.E. H111, C.Z. Thompson, O.K. Epp and S.B.
Neal. 1981. Chemically-Induced unscheduled DNA synthesis In primary rat
hepatocyte cultures: A comparison with bacterial mutagenlclty using 218
compounds. Environ. Mutagen. 3: 11-32.
Quarles, J.M., M.W. Sega, C.K. Schenley and W. Lljlnsky. 1979.
Transformation of hamster fetal cells by nltrosated pesticides 1n a
transplacental assay. Cancer Res. 39: 4525-4533.
0861p -67- 07/24/87
-------
Rees, E.D., P. Mandelstam, J.Q. Lowry and H. Llpscomb. 1971. A study of
the mechanism of Intestinal absorption of benzo(a)pyrene. Blochem. Blophys.
Act. 225: 96-107.
Ribbons, O.E. and R.W. Eaton. 1982. Chemical transformations of aromatic
hydrocarbons that support the growth of microorganisms. In: Blodegradatlon
and Detoxification of Environmental Pollutants, A.M. Chakrabarty, Ed. CRC
Press, Inc. p. 59-84.
Roe, F.J.C. 1962. Effect of phenanthrene on tumour-Initiation by
3,4-benzopyrene. Br. 3. Cancer. 16: 503-506.
Roe, F.J.C. and G.A. Grant. 1964. Tests of pyrene and phenanthrene for
Incomplete carcinogenic and antlcarclnogenlc activity (Abstract). Br. Emp. ,
Cancer Campaign. 41: 59-60. (Cited 1n IARC, 1983)
Roesljadl, G., O.W. Anderson and J.W. Blaylock. 1978. Uptake of hydro-
carbons from marine sediments contaminated with Prudhoe Bay crude oil:
Influence of feeding type of test species and availability of polycycllc
aromatic hydrocarbons. J. F1sh. Res. Board Can. 35(5): 608-614.
Rogerson, A., U.Y. Sh1u, L. Huang, D. Hackay and J. Berger. 1983. Determi-
nation and Interpretation of hydrocarbon toxlclty to dilate protozoa.
Aquat. Toxlcol. 3(3): 215-228.
Rosenkranz, H.S. and L.A. Po1r1er. 1979. Evaluation of the mutagenldty
and DNA-modlfyIng activity of carcinogens and noncarclnogens In mlcroblal
systems. 0. Natl. Cancer. Inst. 62: 873-893.
0861p -68- 07/24/87
-------
Rossi, S.S. and 3.M. Neff. 1978. ToxIcHy of polynuclear aromatic hydro-
carbons to the polychaete Neanthes arenaceodentata. Mar. Pollut. Bull.
9(8): 220-223.
Rostad, C.E., W.E. Perelra and M.F. Hult. 1985. Partitioning studies of
coal-tar constituents In a -two-phase contaminated groundwater system.
Chemosphere. 14(8): 1023-1036.
Roszlnsky-Kocher, G., A. Basler and G. Rohrborn. 1979. Mutagenldty of
polycycllc hydrocarbons V. Induction of slster-chromatld exchanges jjn vivo.
Mutat. Res. 66: 65-67.
Sakal, M. and S. M1zusak1. 1985. Mutagenldty of polycycllc aromatic
hydrocarbons and qulnones on Salmonella typhlmurlum TA97. Mutat. Res. 156:
61-67.
Salaman, M.H. and F.J.C. Roe. 1956. Further tests for tumour-Initiating
activity: n,N-D1(2-chloroethyl)-p-am1nophenylbutyr1c acid (CB1348) as an
Initiator of skin tumour formation In the mouse. Br. 0. Cancer. 10:
363-378.
Santodonato, J., P. Howard and D. Basu. 1981. Health and Ecological
Assessment of Polynuclear Aromatic Hydrocarbons. Pathotox Publishers Inc.,
Park Forest South, IL.
Scrlbner, J.D. 1973. Tumor Initiation by apparently noncarclnogenlc poly-
cycllc aromatic hydrocarbons. J. Natl. Cancer Inst. 50(6): 1717-1719.
0861p -69- 07/24/87
-------
Selxas, G.M., B.M. Andon, P.6. HolUngshead and W.G. Thllly. 1982. The
aza-arenes as mutagens for Salmonella typhlmurlum. Hutat. Res. 102:
201-212.
SherrHl, T.W. and G.S. Sayler. 1980. Phenanthrene blodegradatlon 1n
freshwater environments. Appl. Environ. M1crob1ol. 39: 172-178.
Sh1ar1s, M.P. and J.J. Cooney. 1983. Replica peatlng method for estimating
phenanthrene-utnizlng and phenanthrene-cometabollzlng microorganisms.
Appl. Environ. M1crob1ol. 45: 706.
Shlnohara, R., A. K1do, S. Eto, T. Hor1, M. Koga and T. Aklyama. 1981.
Identification and determination of trace organic substances 1n tap water by
computerized gas chromatography-mass spectrometry and mass fragmentography.
Water Res. 15: 535-542.
Sh1ra1sh1, H., N.H. PUklngton, A. Otsuk! and K. Fuwa. 1985. Occurrence of
chlorinated polynuclear aromatic hydrocarbons In tap water. Environ. Sd.
Technol. 19: 585-589.
Simmon, V.F. 1979. It± vitro assays for recomblnogenlc activity of chemical
carcinogens and related compounds with Saccharomyces cerevlslae 03. J.
Natl. Cancer Inst. 62: 901-909.
S1ms, P. 1970. Qualitative and quantitative studies on the metabolism of a
series of aromatic hydrocarbons by rat-liver preparations. Blochem.
Pharmacol. 19(3): 795-818.
0861p -70- 07/24/87
-------
Solbakken, J.E. and K.H. Palmork. 1981. Metabolism of phenanthrene In
various marine animals. Comp. Blochem. Physlol. C. 70C(1): 21-26.
Solbakken 3.E., K.H. Palmork, T. Neppelberg and R.R. Schellne. 1979.
Distribution of radioactivity 1n coalflsh (Pollachlus vlrens) following
Intragastrlc administration of phenanthrene-9-14C. Bull. Environ. Contam.
Toxlcol. 23(1-2): 100-103.
Solbakken, J.E., A.H. Knap and K.H. Palmork. 1982. Disposition of
(9_i*C)-phenanthrene 1n a subtropical marine teleost (Haemulon sclurus).
Bull. Environ. Contam. Toxlcol. 28(3): 285-289.
Sorrell, R.K., H.J. Brass and R. Reding. 1980. A review of the occurrences
and treatment of polynuclear aromatic hydrocarbons In water. Environ.
Internatl. 4: 245-254. •
Southworth, G.R. 1979. Transport and transportation of anthracene In
natural waters. J_n: Aquatic Toxicology, L.L. Marking and R.A. Klmberle, Ed.
American Society for Testing and Materials, Philadelphia, PA. p. 359-380.
Southworth, G.R., 3.J. Beauchamp and P.K. Schmleder. 1978. B1oaccumulat1on
potential of polycycltc aromatic hydrocarbons In Daphnla pulex. Hater Res.
12(11): 973-977.
Spehar, R.L., A.E. Lemke, Q.H. Pickering, T.H. Roush, R.C. Russo and J.D.
Yount. 1981. Effects of pollution of freshwater fish. J. Water Pollut.
Control Fed. 53: 1028-1076.
0861p -71- 07/24/87
-------
Sporstol, S., N. Gjos, R.G. Llchtenthaler, et al. 1983. Source Identifi-
cation of aromatic hydrocarbons In sediments using GC/MS. Environ. Sc1.
Techno!. 17: 282-286.
SRI (Stanford Research Institute). 1986. 1986 Directory of Chemical
Producers. United States of America. SRI International, Menlo Park, CA.
Staples, C.A., A. Werner and T. Hoogheem. 1985. Assessment of priority
pollutant concentrations In the United States using STORE! database.
Environ. Toxlcol. Chem. 4: 131-142.
Stelner, P.E. 1955. Cardnogenlclty of multiple chemicals simultaneously
administered. Cancer Res. 15: 632-635.
Tabak, H.H., S.A. Quave, C.I. Mashnl and E.F. Barth. 1981. BlodegradabU-
Hy studies with organic priority pollutant compounds. J. Water Pollut.
Control Fed. 53: 1503-1518.
Tan, Y.L. and M. Helt. 1981. Blogenlc and ablogenlc polynuclear aromatic
hydrocarbons In sediments from two remote Adirondack lakes. Geochlm.
Cosmochlm. Acta. 45: 2267-2279.
Thorn, N.S. and A.R. Agg. 1975. The breakdown of synthetic organic com-
pounds 1n biological processes. Proc. R. Soc. Lond. B. 189: 347-357.
Thrane, K.E. and A. Mlkalsen. 1981. High-volume sampling of airborne
polycycllc aromatic hydrocarbons using glass fiber filters and polyurethane
foam. Atmos. Environ. 15: 909-918.
0861p -72- 07/24/87
-------
Trucco, R.G., F.R. Engelhard! and B. Stacey. 1983. ToxIcHy, accumulation
and clearance of aromatic hydrocarbons In Daphnla pulex. Environ. Pollut.,
Ser. A. 31(3): 191-202.
U.S. EPA. 1977. Computer print-out of non-confidential production data
from TSCA Inventory. OPTS, CIO, U.S. EPA, Washington, DC.
U.S. EPA. 1980a. Ambient Water Quality Criteria for Polynuclear Aromatic
Hydrocarbons. Prepared by the Office of Health and Environmental Assess-
ment, Environmental Criteria and Assessment Office, Cincinnati, OH for the
Office of Water Regulations and Standards, Washington, DC. EPA
440/5-80-069. NTIS PB81-117806.
U.S. EPA. 1980b. Fate of toxic and hazardous materials 1n the air environ-
ment. Environmental Sciences Research Laboratory, ORD, U.S. EPA, Research
Triangle Park, NC. EPA 600/3-80-084. NTIS PB80-221948.
U.S. EPA. 1983. Reportable Quantity Document for Phenanthrene. Prepared
by the Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office, Cincinnati, OH for the Office of Solid Waste and
Emergency Response, Washington, DC.
U.S. EPA. 1984. Health Effects Assessment for Phenanthrene. 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. EPA 540/1-86-029.
0861p -73- 07/24/87
-------
U.S. EPA. 1986. Guidelines for Carcinogen Risk Assessment. Federal
Register. 51(185): 33992-34003.
USITC (U.S. International Trade Commission). 1984. Imports of Benzenold
Chemicals and Products, 1983. USITC Publ. 1548, Washington, DC.
Valnlo, H., P. Vollla, 3. Hartlola and 0. Pelkonen. 1976. The fate of
Intratracheally Installed benzo[a]pyrene 1n the Isolated perfused rat lung
of both control and 20-methylcholanthrene pretreated rats. Res. Comm. Chem.
Pathol. Pharmacol. 13: 259-271. (Cited 1n U.S. EPA, 1980a)
Van der Linden, A.C. and G.J.E. Thljsse. 1965. The mechanism of mlcroblol
oxidations of petroleum hydrocarbons. Advanc. Enzymol. 27: 469-546.
Verschueren, R. 1983. Handbook of Environmental Data on Organic Chemicals,
2nd ed. Van Nostrand Relnhold Co., New York. p. 970-972.
Walters, R.W. and R.G. Luthy. 1984. Liquid/suspended solid phase parti-
tioning of polycycllc aromatic hydrocarbon In coal coking waste waters.
Water Res. 18: 795-809.
WhHehouse, B.G. 1984. The effects of temperature and salinity on the
aqueous solubility of polynuclear aromatic hydrocarbons. Mar. Chem. 14:
319-332.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co., Rahway,
NJ. p. 1036.
0861p -74- 07/24/87
-------
Windsor, Jr., J.G. and R.A. HHes. 1979. Polycycllc aromatic hydrocarbons
1n Gulf of Maine sediments and Nova Scotia soils. Geochlm. Cosmochlm. Acta.
42: 27-33.
Hood, A.W., R.L. Chang, W. Levin, et al. 1979. Mutagenlclty and tumorl-
genlclty of phenanthrene and chrysene epoxldes and dlol epoxldes. Cancer
Res. 39: 4069-4077.
Yamasakl, H., K. Kuwata and H. Miyamoto. 1982. Effects of ambient tempera-
ture on aspects of airborne polycycllc aromatic hydrocarbons. Environ. Sc1.
Techno!. 16: 189-194.
Yoshlkawa, T., L.P. Ruhr, W. Flory, D. Glamalva, D.F. Church and H.A. Pryor.
1985. Toxldty of polycycllc aromatic hydrocarbons. I. Effect of phenan-
threne, pyrene, and their ozonized products on blood chemistry 1n rats.
Toxlcol. Appl. Pharmacol. 79(2): 218-226.
Zepp, R.G. and P.P. Schlotzhauer. 1979. PhotoreactlvHy of selected
aromatic hydrocarbons 1n water. ITK Polynuclear hydrocarbons, P.W. Jones
and P. Leber, Ed. Ann Arbor Science Publishers, Inc., Ann Arbor, MI.
p. 141-158.
Zepp, R.G. and P.P. Schlotzhauer. 1983. Influence of algae on photolysis
rates of chemicals In water. Environ. Sc1. Techno!. 17: 462-468.
0861p -75- 07/24/87
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..,.„ APPENDIX
LITERATURE SEARCHED
This profile Is based on data Identified by computerized literature
searches of the following:
GLOBAL
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
CAS online STN International
TOXLINE
TOXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted 1n April, 1986. In addition, hand searches
were made of Chemical Abstracts (Collective Indices 6 and 7), and the
following secondary sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1985-1986. TLVs: Threshold L1mH Values for Chemical Substances
and Physical Agents In the Workroom Environment with Intended
Changes for 1985-1986. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2A. 3ohn Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 28. John Wiley and
Sons, NY. p. 2879-3816.
U.S. Environmental Protection Agency.
Region V, Library
230 South Dearborn Street ^
0861P Chicago, Illinois 60604 -76-^ 07/24/87
-------
Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. 3ohn Wiley and
Sons, NY. p. 3817-5112.
Grayson, M. and D. Eckroth, Ed. 1978-1983. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. WHO, IARC, Lyons, France.
Jaber, H.M., W.R. Mabey, S.T. L1u, T.W. Chow and H.L. Johnson.
1984. Data aqulsltlon for environmental transport and fate screen-
Ing for compounds of Interest 1n the Office of Solid Waste. EPA
600/6-84-010. NTIS PB84-243906. SRI International, Menlo Park, CA.
NTP (National Toxicology Program). 1986. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and 3.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, N.I. 1979. Dangerous Properties of Industrial Materials, 5th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1984. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1985. Status Report on Rebuttable Presumption Against
Registration (RPAR) or Special Review Process. Registration Stan-
dards and the Data Call 1n Programs. Office of Pesticide Programs,
Washington, DC.
U.S. EPA. 1985. CSB Existing Chemical Assessment Tracking System.
Name and CAS Number Ordered Indexes. Office of Toxic Substances,
Washington, DC.
USITC (U.S. International Trade Commission). 1983. Synthetic
Organic Chemicals. U.S. Production and Sales, 1982, USITC Publ.
1422, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, N3.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0861p -77- 07/24/87
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In addition, approximately 30 compendia of aquatic toxlclty data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Pub!. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, D. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0861p -78- 07/24/87
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