Environmental Protection
Agency July, 1987
EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS PROFILE
FOR PHENANTHRENE
Prepared for
OFFICE OF SOLID HASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati. OH 45268
DRAFT: DO NOT CITE OR QUOTE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 Us 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 1n the
section titled "Appendix: Literature Searched." The literature search
material 1s 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 1s defined as the amount of a chemical to which
humans can be exposed on a dally 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 tox1c1ty and cardno-
genlclty are derived. The RQ 1s used to determine the quantity of a hazard-
ous substance for which notification 1s required In the event of a release
as specified under CERCLA. These two RQs (chronic tox1c1ty and carclnogen-
UHy) represent two of six scores developed (the remaining four reflect
1gnHab1l1ty, reactivity, aquatic toxldty and acute mammalian toxlclty).
The first draft of this document was prepared by Syracuse Research
Corporation under EPA Contract No. 68-03-3228. 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.
111
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EXECUTIVE SUMMARY
Phenanthrene Is a colorless solid at ambient temperatures. It 1s
soluble 1n a number of organic solvents Including ethanol, benzene, toluene,
carbon dlsulflde and ethyl ether (Verschueren, 1983; Wlndholz, 1983), but
practically Insoluble In water (Pearlman et al., 1984). The aqueous
solubility of phenanthrene decreases slightly with the Increase of Ionic
strength and decreases greatly with the lowering of water temperature
(Whltehouse, 1984). It 1s susceptible to oxidation by ozone, perloxldes and
other oxidizing agents (NAS, 1972). Although this compound Is not currently
produced or Imported Into the United States (IARC, 1983; USITC, 1984; SRI.
1986), between 1.1 and 11.0 million pounds of It was produced by two U.S.
companies In 1977 (U.S. EPA, 1977). Phenanthrene 1s produced by fractional
distillation of high-boiling coal.-tar oil and the subsequent purification of
the crystalline solid (Hawley, 1981). This compound 1s 'used for the
production of dyestuffs, explosives and drugs. It can also be used for the
synthesis of phenanthrenequlnone (Hawley, 1981).
The fate and transport of phenanthrene 1n surface waters depends on the
nature of the water. The three processes that are likely to be Important
for the loss of phenanthrene from water are photolysis, blodegradatlon and
volatilization. In very shallow, fast flowing and clear water, both
photolysis and volatilization may be Important processes. The half-life of
phenanthrene 1n such waterbodles may be <1 day (Zepp and Schlotzhauer, 1979;
Lyman et al., 1982). On the other hand, In deep eutrophlc ponds, blodegra-
datlon may be the most Important process for aquatic phenanthrene. Based on
Its blodegradatlon half-life In estuarlne water (Lee and Ryan, 1983), the
1v
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half-life of the compound 1n deep eutrophlc ponds may be >36 days. Phenan-
threne will moderately bloconcentrate 1n aquatic organisms. A steady-state
bloconcentratlon factor of 374 has been estimated for phenanthrene 1n
Daphnla pulex (Southworth et al., 1978).
In air, phenanthrene 1s expected to be present both In the vapor and the
partlcle-sorbed phase, although the vapor phase 1s likely to predominate
(Thrane and Hlkalsen, 1981). The photochemical reaction of partlcle-sorbed
or gas-phase state phenanthrene 1n the atmosphere will not be Important
compared with Us other chemical reactions (Behymer and H1tes, 1985;
Korfmacher et al., 1980). The half-lives for the vapor phase chemical
reactions of phenanthrene with 0 and HO radical are estimated to be ~6
O
hours each (Atkinson, 1985; Butkovlc et al., 1982); however, these chemical
reactions will be slower for partlcle-sorbed phenanthrene In the atmosphere
(Santodonato et al., 1981). The long-range transport of phenanthrene
observed by iunde and Bjoerseth (1977) Indicates that partlcle-sorbed
phenanthrene may have a half-life of the order of days.
The fate and transport of phenanthrene 1n soils 1s not well documented.
Both blodegradatlon and unknown chemical reactions will decrease phen-
anthrene 1n soils (Bossert et al., 1984). In sandy loam soil, the half-life
of phenanthrene could be as high as 35 days (Bossert et al., 1984).
Phenanthrene may not leach from most soils because of Its high soil sorptlon
coefficient (G1le et al., 1982). Leaching of phenanthrene may occur 1n
sandy soils that have low sorptlve capacities and 1n soils from waste
disposal sites that have been depleted of phenanthrene-utnizlng and
cometabol1z1ng microorganisms by high concentrations of toxic chemicals.
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Phenanthrene Is widely distributed In the aquatic environment and has
been detected in Industrial effluents, runoff waters, surface water and
sediments, groundwater and drinking water. Phenanthrene concentrations of
~70 yg/8. were detected In the wastewater from an unspecified tire
manufacturing plant (Jungclaus et a!., 1976). Cole et al. (1984) reported
Phenanthrene In urban runoffs from five U.S. cities at a concentration range
of 0.3-10.0 vg/8.. The frequency of detection of phenanthrene In runoff
water from 15 U.S. cities was 12%. Phenanthrene was detected at trace
levels In water from the Delaware River north of Philadelphia (Hltes, 1979).
•
Unseparated anthracene/phenanthrene derived from various sources and at
concentrations <6.46.4 mg/kg was detected 1n a sediment sample from an
estuary between England and Wales (John et al., 1979). Phenanthrene at a
concentration <0.78 mg/8. was reported 1n groundwater 1n the vicinity of a
wood treatment plant In Pensacola, FL (Goerlltz et al., 1985). This com-
pound has been detected In drinking water In the United States and elsewhere
In the world. The median concentration of phenanthrene In finished water
from 11 U.S. water supplies was 5 ng/8.. Assuming this value as the
average concentration of phenanthrene 1n U.S. drinking water, and a dally
human consumption of 28. of drinking water, the average dally Intake of
phenanthrene for an adult In the United States Is estimated as 10 ng.
Some of the known sources of phenanthrene In the atmosphere are vehicu-
lar emissions, coal and oil burning, wood combustion, coke plants, aluminum
plants, Iron and steel works, foundries, ferroalloy plants, municipal
Incinerators, synfuel plants and oil shale plants (Santodonato et al., 1981;
Dalsey et al., 1986; Gammage, 1983). The atmospheric concentration of
phenanthrene in a Soderberg aluminum reduction plant In Norway was reported
to be <454 vg/m3 (Bjoerseth et al., 1978). Phenanthrene exists 1n the
v1
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ambient air 1n cities around the world at various concentrations (L1gock1 et
al., 1985; Keller and Bldleman, 1984; Karlckhoff et al., 1979; Yamasak! et
al., 1982). Although data for phenanthrene was limited, Grosjean (1983)
estimated that the levels of other PAHs 1n Los Angeles air did not signifi-
cantly change during the last decade. The median concentration of atmo-
spheric phenanthrene 1s estimated to be 14 ng/m3 from the available atmo-
spheric levels of five U.S. locations. Assuming this value as the average
phenanthrene concentration 1n U.S. air, and that an adult Inhales 20 m3
air/day, the average dally Inhalation Intake of phenanthrene for a U.S.
Individual 1s estimated to be 280 ng.
Phenanthrene has been reported to be present 1n oysters and fishes
collected from contaminated waters and 1n liquid smoke, smoked foods and
charcoal-broiled steaks (Fazio and Howard, 1983). Marcus and Stokes (1985)
reported the concentration of phenanthrene 1n oysters collected from contam-
inated waters 1n South Carolina ranged from not detected to 76.5 yg/1.
Fishes collected from contaminated U.S. waters were reported to contain
<20-100 yg/kg of combined phenanthrene/anthracene (DeVault, 1985). Until
data on the levels of this compound 1n total diet composites used by an
average Individual 1n the United States are available, 1t 1s not possible to
estimate the human dietary Intake of phenanthrene.
The data base for the aquatic toxlclty 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 yg/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 D. pulex
(Trucco et al., 1983). This result conflicts with the only chronic toxlclty
study available (Gelger and Bulkema, 1982), 1n which no toxic effects or
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reproductive success or survival of I), pulex occurred at 110
Aquatic plants appeared to be less sensitive to phenanthrene than fish and
Invertebrates, with EC5_ values for Inhibition of photo- synthesis ranging
from 870 yg/5L 1n N. paleo (Mlllemann et al.t 1984) to 100% saturation In
S. caprlcornutum (G1dd1ngs, 1979). B1oconcentrat1on and residue monitoring
data Indicated wide variability In potential for phenanthrene accumulation
1n various species (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).
•
Pertinent data regarding the absorption, distribution and excretion of
phenanthrene could not be located 1n the available literature as cited In
the Appendix. PAHs are, 1n general, highly I1p1d-soluble, however, and are
absorbed readily from the gastrointestinal tract and lungs. Metabolites of
phenanthrene Identified 1n \j± vivo and 1_n vitro studies Indicate that
metabolism proceeds by epoxldatlon at the 1-2, 3-4 and 9-10 carbons (Boyland
and Wolf, 1950; Boyland and S1ms, 1962; S1ms, 1970; Chaturaplt and Holder,
1978; Nordqvlst et al., 1981). trans-D1hydrod1hydroxyphenanthrenes
(dlhydrodlols) are the primary products, with the 9,lO-d1hydrod1ol being the
major metabolite.
Phenanthrene did not Induce mammary tumors In rats when administered 1n
single 200 mg oral treatments (Muggins and Yang, 1962) and was not tumor 1-
genlc to mice when administered In single subcutaneous Injections (Stelner,
1955; Grant and Roe, 1963) or three Intraperltoneal Injections to neonates
(Buenlng et al., 1979). The results of these studies were negative, but
should be regarded as Inconclusive because the studies are Inadequate for
evaluation of carclnogenlclty because of limited treatment schedules.
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Phenanthrene did not produce skin tumors 1n mice In an Inadequately reported
skin painting study (dose and application schedule not reported) (Kennaway,
1924). Several mouse skin Initiation-promotion assays using phenanthrene
have been conducted. Phenanthrene was active as a tumor Initiator In one
study In which TPA was used as the promoter (Scrlbner, 1973), but was
Inactive In the other 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 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 responses. Phenanthrene was
reported not to be mutagenlc In the His reversion assay using Salmonella
typhlmurlum tester strains TA100, TA98, TA1535, TA1537 and TA1538 when
assayed with or without liver metabolic activation (McCann et al., 1975;
Wood et al., 1979; Buecker et al., 1979; LaVole et al., 1981; Florin et al.,
1980; Dunkel et al., 1984). One study reported phenanthrene to be mutagenlc
In Salmonella tester stain TA100 when assayed 1n the presence of a high
concentration of liver S9 (Oesch et al., 1981) and another study found
phenanthrene to be positive In the new frameshlft sensitive tester strain
Salmonella typhlmurlum TA97 (Sakal et al., 1985). Negative results were
reported In the forward mutation assay using Salmonella typhlmurlum TH677
(Kaden et al., 1979; Selxas et al., 1982).
Phenanthrene was reported to Induce gene mutations In human
lymphoblastold TK6 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 1n Chinese hamster V79 cells Yn_ vitro
1x
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(Huberman an Sachs, 1979). IntraperHoneal 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 In Chinese hamster V79-4 cells treated ^n
vitro with phenanthrene 1n 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 vitro, and yeast
(I.e., differential growth Inhibition, DNA repair and mltotlc recombination
tests) (HcCarrol et al., 1981; Rosenkranz and Polrler, 1979; Lake et al.,
1978; Probst et al., 1981; Simmon, 1979).
Neoplastlc transformation was not Induced 1n mouse prostate C3HG23
cells, C3H/10T1/2 clone 8 mouse embryo flbroblasts, Syrian hamster embryo
cells, mouse BALB/3T3 cells or guinea pig fetal cells by In vitro treatment
with phenanthrene or In hamster embryo cells following IntraperUoneal
Injection of phenanthrene 1n pregnant females (Quarles et al., 1979;
Marquardt et al., 1972; Plenta et al., 1977; Kakunaga, 1973; Evans and
DIPaolo, 1975; Peterson et ali, 1981).
Data regarding teratogenlcHy or other reproductive effects, or the
chronic or subchronlc toxldty of phenanthrene, could not be located In the
available literature. Single 1ntraper1toneal Injections of 150 mg/kg
produced evidence of slight hepatotoxldty 1n rats (Yoshlkawa et al., 1985);
these Included gross congestion and distinct lobulatlon and small Increases
In the activities of SGOT and serum GGTP.
Data were Insufficient to derive an RfD, RQ, q * or F factor for phen-
anthrene. This chemical was placed In EPA Group D, that Is, not classified,
and no direct ranking under CERCLA 1s possible.
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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 3
2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES 4
2.1. WATER 4
2.1.1. Photodegradatlon 4
2.1.2. Chemical Reactions 4
2.1.3. B1odegradat1on 5
2.1.4. Volatilization 8
2.1.5. Adsorption 8
2.1.6. B1oconcentrat1on 9
2.2. AIR 9
2.3. SOIL 11
2.4. SUMMARY 12
3. EXPOSURE 14
3.1. WATER 14
3.2. AIR 17
3.3. FOOD 18
3.4. SUMMARY 18
4. PHARMACOKINETCS 23
4.1. ABSORPTION 23
4.2. DISTRIBUTION 23
4.3. METABOLISM 23
4.4. EXCRETION 24
4.5. SUMMARY 24
5. EFFECTS 25
5.1. CARCINOGENICITY 25
5.2. MUTAGENICITY 29
5.3. TERATOGENICITY 30
5.4. OTHER REPRODUCTIVE EFFECTS 31
5.5. CHRONIC AND SUBCHRONIC TOXICITY 31
5.6. OTHER RELEVANT INFORMATION 31
5.7. SUMMARY. 31
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TABLE OF CONTENTS (cont.)
Page
6. AQUATIC TOXICITY 34
6.1. ACUTE 34
6.2. CHRONIC 34
6.3. PLANTS 34
6.4. RESIDUES 37
6.5. SUMMARY. 42
7. EXISTING GUIDELINES AND STANDARDS 43
7.1. HUMAN 43
7.2. AQUATIC 44
•8. RISK ASSESSMENT 45
9. REPORTABLE QUANTITIES . 48
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC
TOXICITY 48
9.2. WEIGHT OF EVIDENCE AND POTENCY FACTOR (F=1/ED10)
FOR CARCINOGENICITY 48
10. REFERENCES 51
APPENDIX: LITERATURE SEARCHED. . . 76
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LIST OF TABLES
No.
3-1
3-2
3-3
5-1
6-1
6-2
6-3
Title
Concentrations of Phenanthrene In U.S. Finished and
Distributed Waters
Ambient Atmospheric Levels of Phenanthrene 1n Various
World Locations
Phenanthrene Levels 1n Different Foods
Dermal and Injection Cardnogenlclty Assays of
Phenanthrene
Acute Toxlclty of Phenanthrene to Aquatic Organisms
Bloconcentratlon Data for Phenanthrene 1n Aquatic
Organisms
Monitoring Data for Phenanthrene 1n Aquatic Organisms ....
Page
16
19
20
26
35
38
40
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
BCF Bloconcentratlon factor
BUN Blood urea nitrogen
CAS Chemical Abstract Service
DMSO Dimethyl sulfoxlde
DNA Deoxyrlbonuclelc acid
EC5Q Concentration effective to 50% of recipients
GGTP Gamma glutamyl transpeptldase
K Soil sorptlon coefficient
K Log octanol/water partition coefficient
LC5Q Concentration lethal to 50% of recipients
LD Dose lethal to 50% of recipients
LDH Lactate dehydrogenase
MED Minimum effective dose
PAH Polycycllc aromatic hydrocarbons
ppm Parts per million
RfD Reference dose
RQ Reportable quantity
RV, Dose-rating value
RV Effect-rating value
SGOT Serum glutamlc oxaloacetlc transamlnase
SGPT Serum glutamlc pyruvlc transamlnase
TLV Threshold-limit value
TPA 12-0-Tetradecanoylphorbol-13-acetate
TWA Time-weighted average
x1v
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
Phenanthrene 1s a member of a class of chemicals called polycycllc
aromatic hydrocarbons (PAH). The structure, empirical formula, molecular
weight and CAS Registry number for this chemical are as follows:
Empirical formula: C^N-m
Molecular weight: 178.22
CAS Registry number: 85-01-8
1.2. PHYSICAL AND CHEMICAL PROPERTIES
Phenanthrene 1s a colorless crystalline solid at ambient temperatures.
It 1s practically Insoluble 1n water but 1s soluble 1n a number of organic
solvents Including ethanol, benzene, toluene, carbon dlsulflde and ethyl
ether (Verschueren, 1983; Wlndholz, 1983). The relevant physical properties
\
of phenanthrene are listed below:
Melting point:
Boiling point:
Density at 25°C:
Water solubility:
distilled water at 25°C
distilled water at 25°C
distilled water with
36.5% salinity at 25.3°C
distilled water at 4.6°C
101°C
340°C
1.179 g/cm'
1.28 mg/8.
1.10 mg/8.
1.00 mg/8.
0.36 mg/8.
Santodonato
et al., 1981
Santodonato
et al., 1981
Wlndholz, 1983
Pearlman
et al., 1984
Whltehouse,
1984
Whltehouse,
1984
Whltehouse,
1984
0861 p
-1-
05/20/87
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Log Kow: 4.45-4.57 Mackay et al.,
1985; Miller
et al., 1985
Vapor pressure: 6.8xlO~* ram Hg Santodonato
et al., 1981
5.2xlO~* to 8.3xlO"« Bldleman, 1984
mm Hg at 25°C
Henry's Law constant: 9.5xlO~5 atm-mVmol"1
(estimated based on
solubility of 1.28 mg/l
and vapor pressure of
5.2xlO~« mm Hg)
It can be concluded from the above tabulated data that the solubility of
phenanthrene 1n water decreases slightly with the Increase 1n salt content.
The solubility, however, 1s greatly dependent upon the water temperature.
PAHs are reactive chemically and 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
According to the TSCA production file (U.S. EPA, 1977), two U.S. com-
panies produced between 1.1 and 11.0 million pounds of phenanthrene 1n 1977.
Currently, 1t- 1s neither commercially produced nor Imported Into the United
States (IARC, 1983; USITC, 1984; SRI, 1986). Phenanthrene Is produced by
fractional distillation of high-boiling coal-tar oil. The distillate 1s
crystallized and the phenanthrene 1s purified by recrystalUzatlon from
alcohol (Hawley, 1981).
1.4. USE DATA
Phenanthrene can be used 1n the production of dyestuffs, explosives and
drugs. It can also be used for the synthesis of phenanthrenequlnone
(Hawley, 1981).
0861p -2- 10/23/86
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1.5. SUMMARY
Phenanthrene 1s a colorless solid at ambient temperatures. It 1s
soluble In a number of organic solvents Including ethanol, benzene, toluene,
carbon disulflde and ethyl ether (Verschueren, 1983; Wlndholz, 1983), but
practically Insoluble 1n water (Pearlman et al., 1984). The aqueous
solubility of phenanthrene decreases slightly with the Increase of Ionic
strength and decreases greatly with the lowering of water temperature
(WhHehouse, 1984). Phenanthrene Is susceptible to oxidation by ozone,
perloxldes and other oxidizing agents (NAS, 1972). Although this compound
Is not currently produced or Imported Into the United States (IARC, 1983;
USITC, 1984; SRI, 1986), between 1.1 and 11.0 million pounds of H was
produced by two U.S. companies In 1977 (U.S. EPA, 1977). Phenanthrene Is
produced by fractional distillation of high-boiling coal-tar oil and the
subsequent purification of the crystalline solid (Hawley, 1981). This
compound.can be used for the production of dyestuffs, explosives and drugs.
It can also be used for the synthesis of phenanthrenequlnone (Hawley, 1981).
0861p -3- 05/20/87
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2. ENVIRONMENTAL FATE AND TRANSPORT PROCESSES
2.1. MATER
2.1.1. Photodegradatlon. The photodegradatlon of phenanthrene 1n water
by natural sunlight was studied by Zepp and Schlotzhauer (1979). The near-
surface half-life for direct photochemical transformation of phenanthrene at
40° N latitude by midday, midsummer sun was estimated to be 8.4 hours.
Because of light attenuation and sediment-water partitioning, the photolysis
rate decreases with the Increase of water depth and suspended sediment
concentration. The photolysis half-life of phenanthrene 1n river water 5 m
deep with a suspended sediment concentration of 20 mg/j. during a summer
day at 40° N latitude was estimated to be 69 days (Zepp and Schlotzhauer,
1979). Zepp and Schlotzhauer (1983) showed that certain green and blue-
green algae found 1n many natural waters, accelerate the phototransformatlon
of several compounds, probably through sensitized photoreactlon. In the
case of phenanthrene, only one of six species of algae slightly accelerated
the sunlight-Induced photoreactlon, but all the other five species slightly
lowered the phototransformatlon rate. Therefore, the presence of algae may
not significantly affect the phototransformatlon of phenanthrene 1n most
natural waters.
2.1.2. Chemical Reactions. The rate of oxidation of phenanthrene with
singlet oxygen (102) was reported by Zepp and Schlotzhauer (1979).
Assuming the near surface steady-state concentration of singlet oxygen In
natural waters In summer to be 6xlO"12 M, these authors estimated the
half-life for this reaction to be 10* hours. (The source of the rate
constant value used 1n determination of the half-life 1s not clear.)
Therefore, this reaction was concluded not to be a significant
fate-determining process for phenanthrene 1n water. The reaction of
0861p -4- 05/20/87
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phenanthrene with ozone was reported by Kuo and Barnes (1985) and Butkovlc
et al. (1983). The rate of this reaction was reported to be higher In
neutral solution than 1n strongly addle solution, and the rate was- enhanced
at higher temperatures. The rate constants for this reaction at 25°C and a
pH of 1 and 7 were reported to be (1.33-1.94)xl04 and (1.57-4.75)xlO«
l/mol-sec, respectively. At an ozone concentration of 10~* M, these
correspond to half-lives of <1 second. Therefore, the ozone reaction may be
Important for compl-ete oxidation of phenanthrene 1f ozonatlon 1s used as a
method of disinfection of drinking water.
2.1.3. B1odegradat1on. The b1odegradab1!1ty of phenanthrene has been
studied with pure cultures of microorganisms, mixed microorganisms and 1n
natural water and sediments. Several pure cultures of microorganisms
Including FlavobacteMum sp., Pseudomonas aeruqlnosa. Pseudomonas putlda.
Be1jer1nck1a sp., Pseudomonas sp., Alcallqenes faecalls. Achromobacter sp.,
Aeromonas sp. and Nocardla sp. (Kobayashl and RHtman, 1982; Sh1ar1s artd
Cooney, 1983; Fuhs, 1961; Klyohara et al., 1982; McKenna, 1977; Gibson,
1977; Cernlglla, 1981; Ribbons and Eaton, 1982) degraded phenanthrene.
Although these pure culture studies do not simulate environmental conditions
for blodegradatlon, they are useful 1n establishing blodegradatlon pathways
of chemicals. The proposed pathway for mlcroblal catabollsm of phenanthrene
Is shown 1n Figure 2-1.
The blodegradabUHy of phenanthrene with mixed microorganisms was
studied by several Investigators. Thorn and Agg (1975) reported that
phenanthrene 1s biodegradable by biological sewage treatment, provided that
suitable acclimatization can be achieved. WHh settled domestic wastewater
as mlcroblal Inoculum and a static-culture flask-screening procedure, 100%
of the phenanthrene was found to be biodegradable 1n 7 days at an Initial
0861p -5- 05/20/87
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H
OH
COOH
Ph«n«nthr«n«
3,4-Dihydroxy-
phcn&nthrcne
1-Hydroxy-a-
n*phth«ic *cid
Rerononas so
CHO
2-Carboxybenzaidehyd«
OOH
'COOH
o-Phthalle acid
COOH
Protocatechuic acid
l,C-Dlhydroxy-
.OH
Saiicyaldohyda
,OH
'COOH
Salicylic acid
OH
'OH
CtUchol
FIGURE 2-1
Proposed Pathway for M1crob1al Degradation of Phenanthrene
Sources: Cern1gl1a, 1981; Van der Linden and Thljsse, 1965;
McKenna and Kalllo, 1965
086 Ip
-6-
10/23/86
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concentration of 5 ppm (Tabak et al., 1981). Lutln et al. (1965) used
activated sludge from three municipal treatment plants as mlcroblal Inoculum
and the Warburg method for the estimation of the rate of b1oox1dat1on.
Phenanthrene was reported to be biodegradable with all three activated
sludges. The removal of phenanthrene 1n a municipal facility using
activated sludge was reported to be 91% at an Influent concentration of 3.2
yg/SL, but the removal was 0% at an Influent concentration of 3 yg/SL
In an Industrial facility using aerated lagoon treatment (Patterson and
Kodukala, 1981).
The blodegradabUHy of phenanthrene with natural waters (Lee and Ryan,
1983; Sherrlll and Sayler, 1980) has also been reported. The blodegradatlon
of phenanthrene 1n water 1s controlled by the temperature, state of acclima-
tization of the microorganisms and Its concentration. The blodegradatlon
rates were linearly higher as the temperature was raised from 15-37°C.
Phenanthrene blodegradatlon was virtually not detected -at the extreme
temperatures of 5 and 45°C {Sherrlll and Sayler, 1980). Similarly, higher
blodegradatlon rates were observed with microorganisms acclimatized with
PAH, possibly phenanthrene (Sherrlll and Sayler, 1980; Lee and Ryan, 1983).
The acclimatization time for phenanthrene-degradlng microorganisms was
probably <3 days (Sherrlll and Sayler, 1980). Higher concentrations of
phenanthrene were found to Increase the blodegradatlon rates. Increasing
the phenanthrene concentration from 100-1000 yg/s. Increased the relative
blodegradatlon rate 3-fold (Sherrlll and Sayler, 1980). The optimum concen-
tration at which phenanthrene may be toxic to the microorganisms was not
reported. The half-life for phenanthrene blodegradatlon 1n water was
reported to be 12 days 1n fresh water at 25°C (Sherrlll and Sayler, 1980)
and 19-36 days In estuarlne water at 27-28°C (Lee and Ryan, 1983).
0861p -7- 05/20/87
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2.1.4. Volatilization. Using the liquid and gas-phase exchange coeffi-
cients for computing the overall liquid-phase mass transfer coefficient,
Lyman et al. (1982) estimated the half-life of evaporation for phenanthrene
from water 1 m deep to be 31 hours at a wind speed of 3 m/sec and a water
current of 1 m/sec. The volatility of phenanthrene from a laboratory-scale
waste stabilization pond was reported by Davis et al. (1983). Although the
experimental volatilization half-life was 300 hours, the predicted half-life
from the same pond by the L1ss and Slater model was 2.1 hours. The authors
concluded that the sorptlon of phenanthrene onto biota and silt was respon-
sible for the difference between the experimental and predicted half-life
values (the predictive models do not consider the effect of sorptlon on
volatilization). From their waste stabilization pond study, Davis et al.
(1983) estimated that only 0.2% of the applied phenanthrene dose was lost by
volatilization; losses of 93.5 and 3% were due to degradation and
sedimentation, respectively. The remainder was lost 1n the effluent .or
remained 1n the water column as residual.
2.1.5. Adsorption. The adsorption of phenanthrene to suspended partlcu-
late matter and sediment can be predicted from Its K . The K value
oc oc
for phenanthrene 1s estimated to be 23,000 (Karlckhoff et al., 1979). This
1s Indicative of the possibility of strong sorptlon of phenanthrene onto
suspended particles and sediments 1n water. As 1n the case of anthracene
(estimated K of 26,000} where the removal through adsorption constitutes
only negligible to 18% (Southworth, 1979) of the overall removal processes,
the contribution of sorptlon 1n water 1s expected to be low 1n the case of
phenanthrene as well. In their model waste stabilization pond study, Davis
et al. (1983) estimated that only 3% of total phenanthrene removal was
attributable to sedimentation.
0861p -8- 05/20/87
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2.1.6. Bloconcentratlon. The BCF for phenanthrene In algae (species
unspecified) was reported to be 4552 (Davis et al., 1983). Southworth et
al. (1978) examined the bloaccumulatlon potential of several PAH Including
•
phenanthrene 1n Daphnla pulex. a representative component of the aquatic
food web. A 24-hour BCF of 325 was reported for phenanthrene 1n filtered
spring water. Using uptake and elimination rates, these authors estimated a
steady-state BCF of 374 for phenanthrene. The bloconcentratlon of phenan-
threne 1n aquatic organisms may be species-dependent. Species that contain
mlcrosomal oxldase/mlxed function oxldase activity that allows metabolism of
the parent compounds will tend to lower the BCF (Santodonato et al., 1981).
It was also reported by McCarthy (1983) that the BCF for hydrophoblc organic
pollutants are considerably less In natural water than measured values In
laboratories using particle-free water because of nonavailability of sorbed-
state compounds for uptake by organisms.
2.2. AIR
The fate and transport of phenanthrene 1n the atmosphere Is less docu-
mented than Us water fate. The reactivity of atmospheric phenanthrene will
depend on the state In which 1t exists In the atmosphere. The reactivity of
vapor phase phenanthrene 1s expected to be faster than 1n the adsorbed state
(Santodonato et al., 1981). Thrane and Mlkalsen (1981) suggest that phenan-
threne will be present predominantly 1n the vapor phase In the atmosphere.
The heterogenous reaction of gas-phase 0_ and NO- with phenanthrene
coated on sodium chloride was reported by Nlessner et al. (1985).
0861p -9- 05/20/87
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The heterogenous reaction of phenanthrene was negligible with NO-, but
reaction with 03 was significant. The reaction with 03 produced the
following products:
CHO COOH COOH
The atmospheric half-life of phenanthrene resulting from reaction with
03 was reported by Butkovlc et al. (1983). Assuming the rate constant for
this reaction as 1.5x10* l/mol-sec (the same as In water) and the tropo-
spherlc 03 concentration as 2xlO~* H In clear air, these authors esti-
mated a half-life of 6 hours. The rate constant for the gas phase reaction
of phenanthrene with HO radical at 25°C was reported to be 34xlO~12
cm3/molecule-sec (Atkinson, 1985). If the concentration of HO radical In
the atmosphere 1s assumed to be 10* radicals/cm3, the half-life of this
reaction 1s -6 hours.
Korfmacher et al. (1980) reported that phenanthrene was resistant to
photodecomposltlon 1n cyclohexanone solution. When phenanthrene vapors
adsorbed on fly ash were Irradiated with a xenon Tamp for 3.3 hours, no
significant decomposition was observed (Korfmacher et al., 1980). The
photodegradatlon of particle-bound phenanthrene was found to be highly
dependent on the substrate to which 1t was adsorbed (Behymer and Kites,
1985). For example, the half-lives of phenanthrene Irradiated with medium
pressure mercury arc lamps In a rotary photoreactor were 150, 40, 49 and
>1000 hours when the adsorption media were silica gel, alumina, fly ash and
carbon black, respectively. Therefore, 1t can be concluded that photodegra-
datlon of phenanthrene 1n the atmosphere will be less significant than Us
reactions with 0. and HO radical.
O
0861p -10- 05/20/87
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The removal of atmospheric phenanthrene through wet and dry deposition
can also occur. Elsenrelch et al. (1981) reported that In the Great Lakes
ecosystem both dry deposition of the vapor and particle-bound phenanthrene
and wet deposition through rain and snow occurred; dry deposition, however,
was found to be more Important. Llgockl et al. (1985) concluded from their
•
experimental observation that particle scavenging was less Important than
gas scavenging of atmpspherlc phenanthrene. The half-lives for these
physical removal mechanisms were not provided In either study. The removal
of atmospheric phenanthrene through these physical processes appear to be
less significant than Us removal through chemical processes. Finally,
Lunde and Bjorseth (1977) reported that the concentration of phenanthrene 1n
air trajectories that originated from Western Europe (polluted air) con-
tained >8 times more phenanthrene than air samples with trajectories from
»
northern Norway or stationary air from southern Norway (less polluted air).
This result suggests that phenanthrene 1s capable of undergoing long-
distance transport In the atmosphere.
2.3. SOIL
The fate of phenanthrene 1n soils 1s even less documented than Its fate
1n the atmosphere. Predictions, however, can be made from the knowledge of
Us fate In water. The three processes that are Important 1n the loss of
phenanthrene from water are photolysis, blodegradatlon and volatilization.
Because of light attenuation and scattering, photolysis cannot be an Impor-
tant process 'for the loss of phenanthrene beyond the surface layer of soils.
Bossert et al. (1984) Incorporated oily sludge containing phenanthrene 1n a
sandy loam soil and observed the loss of phenanthrene In sterile and non-
sterile soils. Because multiple applications of sludge to soil were made at
various Intervals with Intervening nonappHcatlon periods, 1t Is difficult
to estimate from the data the degradation half-life of phenanthrene In soil.
0861p -11- 10/23/86
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On the basis of the loss of the chemical after Us first application In non-
sterile soil, the overall degradation half-life Is estimated to be -35 days.
The authors concluded from sterilized and nonsterHlzed soil studies that
both blodegradatlon and undefined chemical processes accounted for the
observed loss In phenanthrene concentrations. The chemical processes were
responsible for <50% of the loss. The loss of phenanthrene from volatili-
zation was speculated to be Insignificant.
The leaching of phenanthrene from soil to groundwater depends on the
soil characteristics. The K for phenanthrene was estimated to be 23,000
(KaMckhoff et al., 1979), Indicating that phenanthrene will be strongly
adsorbed to most soils and degrade before H reaches groundwater. The
terrestrial microcosm experiment performed by 61le et al. (1982) predicted
that leaching of phenanthrene from soil to groundwater will not normally
occur. Leaching of phenanthrene may occur In sandy soil that has a low
•sorptlve capacity and 1n soils from waste disposal sites that have been
depleted of phenanthrene-utlUzIng and cometabo!1z1ng microorganisms.
2.4. SUMMARY
The fate and transport of phenanthrene 1n surface waters depends on the
nature of the water. The three processes that are likely to be Important
for the loss of phenanthrene from water are photolysis, blodegradatlon and
volatilization. In very shallow, fast-flowing and clear water, both
photolysis and volatilization may be Important processes. The half-life of
phenanthrene 1n such waterbodles may be <1 day (Zepp and Schlotzhauer, 1979;
Lyman et al., 1982). On the other hand, In deep eutrophlc ponds, blodegra-
datlon may be the most Important process for aquatic phenanthrene. Based on
Us blodegradation half-life 1n estuarlne water (Lee and Ryan, 1983), the
0861p -12- 05/20/87
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half-life of the compound 1n deep eutrophlc ponds may be >36 days. Phenan-
threne will moderately bloconcentrate 1n aquatic organisms. A steady-state
bloconcentratlon factor of 374 has been estimated for phenanthrene In
Daphnla pulex (Southworth et al., 1978).
In air, phenanthrene Is expected to be present both In the vapor and the
partlcle-sorbed, although the vapor phase 1s likely to predominate (Thrane .
and Mlkalsen, 1981). The photochemical reaction of partlcle-sorbed or gas-
phase state phenanthrene 1n the atmosphere will not be Important compared
with Us other chemical reactions (Behymer and HHes, 1985; Korfmacher et
al., 1980). The half-lives for the vapor phase chemical reactions of
phenanthrene with 0_ and HO radical are estimated to be ~6 hours each
(Atkinson, 1985; Butkovlc et al., 1982); however, these chemical reactions
will be slower for partlcle-sorbed phenanthrene 1n the atmosphere
(Santodonato et al., 1981). The long-range transport of phenanthrene
observed by Lunde and Bjorseth (1977) Indicates that partlcle-sorbed phenan-
threne may have a half-life of the order of days.
The fate and transport of phenanthrene 1n soils 1s not well documented.
Both blodegradatlon and unknown chemical reactions will degrade phenanthrene
1n soils (Bossert et al., 1984). In sandy loam soil, the half-life of phen-
anthrene could be as high as 35 days (Bossert et al., 1984). Phenanthrene
may not leach from most soils because of Its high soil sorptlon coefficient
(G1le et al., 1982). Leaching of phenanthrene may occur 1n sandy soils that
have low sorptlve capacities and 1n soils from waste disposal sites that
have been depleted of phenanthrene-ut1!1z1ng and cometabol1z1ng microorgan-
isms by high concentrations of toxic chemicals.
0861p -13- 05/20/87
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3. EXPOSURE
3.1. WATER
Phenanthrene Is widely distributed In the aquatic environment. It has
been detected 1n Industrial effluents. In run-off water, In surface water
and sediments, 1n groundwater and 1n drinking water. Phenanthrene at a con-
centration of -70 yg/i was detected 1n the wastewater from an unspeci-
fied tire manufacturing plant (Jungclaus et al., 1976). Concentrations of
Phenanthrene 1n the secondary effluent from a Scandanavlan sewage treatment
plant were reported to range from 72-117 ng/i (Kveseth et al., 1982). The
aqueous effluents from unspecified coke plants reportedly contained <30-1300
ng/l of phenanthrene (GMest, 1980; Walters and Luthy, 1984). The U.S.
EPA has detected phenanthrene at a frequency of 5% 1n -1288 effluents
collected since 1980 from different sources, with a median concentration of
<10 v9/5. (Staples et al., 1985). Phenanthrene was also detected In
urban runoff waters. The annual Inputs of phenanthrene by urban runoff to
the upper Narragansett Bay, RI, watershed were estimated to be 1.7, 2.1,
32.4 and 32.2 kg/year from residential, commercial, Industrial and highway
runoffs, respectively (Hoffman et al., 1984). Cole et al. (1984) detected
phenanthrene In urban runoffs from five U.S. cities at a concentration range
of 0.3-10.0 vg/l and at a frequency of 12%. Phenanthrene was detected
at trace levels 1n water from a small segment of the Delaware River north of
Philadelphia (HHes, 1979). The U.S. EPA has collected 865 ambient water
samples since 1980 and has detected phenanthrene In 5% of these samples,
with a median concentration of <10 vQ/t (Staples et al., 1985). Phenan-
threne was also reported 1n surface water 1n England (Fielding et al.,
1981). Several Investigators reported the detection of phenanthrene 1n
surface water sediments and attempted to establish the sources and modes of
0861p -14- 10/23/86
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transportation of this compound In water (Jungclaus et al., 1978; Boehm and
Farrfngton, 1984; Sportstol et al., 1983; Windsor and HHes, 1979; Eadle et
al., 1982; Tan and Helt, 1981). Unseparated anthracene/phenanthrene derived
from various sources and at concentrations as high as 6.4 mg/kg were
reported In sediment samples from an estuary between England and Wales (John
et al., 1979).
Rostad et al. (1985) qualitatively detected phenanthrene in groundwater
from a coal tar waste aquifer In St. Louis Park, MM. Goerlltz et al. (1985)
monitored groundwater from several sites 1n the vicinity of a wood treatment
plant at Pensacola, FL, and reported phenanthrene concentrations as high as
0.78 mg/i; however, phenanthrene was not detected 1n groundwater beyond a
depth of 18 m. Phenanthrene has been detected In drinking water 1n the
United States and elsewhere In the world. Kveseth et al. (1982) detected
phenanthrene 1n tap water from Scandinavia In. the concentration range' of
0.2-64 ng/l. In Tsukuba, Japan, the concentration of phenanthrene 1n tap
water was reported to be 0.34-1.41 ng/i (Shlralshl et al., 1985). Tap
water from KUakyushu, Japan, contained concentrations of combined phenan-
threne/anthracene at 1.7 yg/l (Shlnohara et al., 1981). The concentra-
tion of phenanthrene 1n drinking water from Ottawa was reported to be
>0.5-1.1 ng/l (Benolt et al., 1979). The combined concentrations of
anthracene/phenanthrene (unseparable) 1n Canadian drinking water derived
from the Great Lakes reportedly ranged between 0.6 and 1269 ng/fc (Williams
et al., 1982). The highest concentration was obtained In the water from
Sault Ste Marie collected during the summer. Fielding et al. (1981)
monitored 14 treated water samples In England and qualitatively detected
phenanthrene In 7 of these samples. The concentrations of phenanthrene
detected In several U.S. finished and distributed waters (passed through
transmission /distribution pipes) are given 1n Table 3-1.
0861p -15- 10/23/86
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TABLE 3-1
Concentrations of Phenanthrene 1n U.S. Finished
and Distributed Waters (ng/fc)*
City
Cape Glrardeau, MO
Cincinnati, OH
Colorado Springs, CO
Columbus, OH
Jefferson Parish, LA
Ludlow, MA
Miami, FL
New Orleans, LA
Portland, OR
Seattle, WA
Standlsh, ME
Wheeling, WV
Finished
5
10
3
3
14
2
14
NR
8
2-10
5
4
Distributed
NR
NR
29
17
NR
3 .
NR
14
3300
32
57
NR
*Source: Sorrell et al., 1980
NR = Not reported
0861 p
-16-
05/20/87
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The distributed water from some cities (e.g., Portland, OR) shows much
higher concentrations of phenanthrene than the treated water because phenan-
threne Is leached from the coating materials of the distribution pipes.
Assuming the average concentration of phenanthrene In U.S. drinking water to
be the same as the median value of the concentration of the finished water
given In Table 3-1 (5 ng/l), and that human consumption of drinking water
Is 2 8,/day, the average dally Intake of phenanthrene for an adult 1n the
United States Is 10 ng.
3.2. AIR
The sources of PAH Including phenanthrene In the atmosphere are vehicu-
lar emissions, coal and oil burning, wood combustion, coke plants, aluminum
plants. Iron and steel works, foundries, ferroalloy plants and municipal
Incinerators (Santodonato et a!., 1981; Oalsey et a!., 1986; Gammage, 1983).
More -recent sources of phenanthrene may be synfuel and oil shale plants.
The atmospheric concentration of phenanthrene In an aluminum reduction plant
(Soderberg) In Norway was reported to be as high as 454 yg/ma (Bjoerseth
et a!., 1978). Personnel sampling of the Soderberg plant showed partlculate
phenanthracene concentration of none detected for tappers to 60.4 yg/m3
for pin pullers (Bjoerseth et a!., 1978). The concentrations of atmospheric
combined anthracene/phenanthrene Inside a Solvent Refined Coal Pilot plant
facility at Fort Lewis, WA, was reported to vary between 1.8 and 43.2
vg/m3 (Gammage, 1983). Personal air samples taken In the coal prepara-
tion area of the plant showed combined anthracene/phenanthrene concentra-
tions of none detected to 15.7 yg/m3 (Gammage, 1983). The simulated
Incineration of polyvlnylchlorlde at temperatures between 800°C and 950°C
was qualitatively shown to produce phenanthrene (Hawley-Fedder et al.,
1984). The concentrations of phenanthrene In the atmosphere of woodheated
saunas varied from 2.3-122 yg/m3 (Hasanen et al., 1984).
0861p -17- 10/23/86
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The ambient atmospheric levels of phenanthrene In various locations
around the world are shown In Table 3-2. Although suitable data were not
available for phenanthrene, Grosjean (1983) estimated that the levels of
other PAHs In the air In Los Angeles did not significantly change during the
last decade. Assuming that the mean levels of phenanthrene concentration 1n
urban U.S. air 1s similar to the median value of all the U.S. ambient atmo-
spheric levels (H ng/ma) given In Table 3-2, and that an adult Inhales 20
mVday, the average dally Inhalation Intake of phenanthrene for a U.S.
Individual would be 280 ng.
3.3. FOOD
Phenanthrene reportedly Is present In oysters, liquid smoke, smoked
foods and charcoal-broiled steaks (Fazio and Howard, 1983). The levels of
phenanthrene detected 1n different foods are given In Table 3-3. Because
data on the- levels 1n total diet composites used by an Individual 1n the
United States are not available. It Is not possible to estimate the human
Intake of phenanthrene through food consumption.
3.4. SUMMARY
Phenanthrene Is widely distributed 1n the aquatic environment and has
been detected 1n Industrial effluents, runoff waters, surface water and
sediments, groundwater and drinking water. Phenanthrene concentrations of
~70 vg/l were detected 1n the wastewater from an unspecified tire
manufacturing plant (Jungclaus et al., 1976). Cole et al. (1984) reported
phenanthrene 1n urban runoffs from five U.S. cities at a concentration range
of 0.3-10.0 vg/l. The frequency of detection of phenanthrene In runoff
water from 15 U.S. cities was 12%. Phenanthrene was detected at trace
levels In water from the Delaware River north of Philadelphia (H1tes, 1979).
0861p -18- 10/23/86
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TABLE 3-2
Ambient Atmospheric Levels of Phenanthrene In Various World Locations
Location
Portland, OR
Columbia, SC
Savannah River
plant, SC
Gainesville, FL
Jacksonville, FL
Osaka, Japan
Osaka, Japan
Budapest. Hungary
Years
Sampled
1984
1981-1982
1981-1982
NRa
NRa
1977-1978
1981-1982
1971-1972
Phenanthrene
Concentration
(ng/m3)
27
14 to >140
6 to >14
10
20
52. 1-294. 5b
0.79-2.64
(1.63)C
3.8-17.4
(10)C
Reference
Llgockl et al.,
1985
Keller and
Bldleman, 1984
Keller and
Bldleman, 1984
Kerkhoff et al.,
1985
Kerkhoff et al.,
1985
Yamasakl et al.,
1982
Hatsumoto and
Kashlmoto, 1985
Kertsz-SaMnger
and Morlln, 1975
aThe year of sampling was not reported but appears to be 1982.
bComb1ned anthracene/phenanthrene values
cMean concentration values
0861 p
-19-
10/23/86
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TABLE 3-3
Phenanthrene Levels In Different Foods
Food
Phenanthrene
Concentration
(vg/kg)
Reference
Oysters from Arkansas and
Galvaston Bay
Coffee roasted dark and
very dark
Roasted coffee soots
Electric-broiled Japanese
horse mackerel
Gas-broiled Japanese horse
mackerel
NO
NO
130-300
1-9
8-11
Fazio and Howard, 1983
Fazio and Howard, 1983
Fazio and Howard, 1983
Fazio and Howard, 1983
Fazio and Howard, 1983
Charcoal-broiled steaks
Barbecued ribs .
Fish (U.S.)
Mussel (Greece)
(M. qalloprovlnclalls)
Fresh water fish
(preserved) from Nigeria
Mussel composite (U.S.)
(M. edulls and M. callfornlanus)
Oyster (Crassostrea vlrqlnlca)
from South Carolina
21
58
<20 to 100*
9
9-189.3
7.9-32*
ND-76.5
Fazio and Howard,
Fazio and Howard,
DeVault, 1985
loslf Idou et al .,
1983
1983
1982
Afolabl et al., 1983
Galloway et al.,
Marcus and Stokes
1985
1983
•
*Comb1ned anthracene/phenanthrene levels
ND = Not detected
0861 p
-20-
05/20/87
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Unseparated anthracene/phenanthrene derived from various sources and at
concentrations <6.46.4 mg/kg was detected In a sediment sample from an
estuary between England and Wales (John et al., 1979). Phenanthrene at a
concentration <0.78 mg/8. was reported In groundwater 1n the vicinity of a
wood treatment plant 1n Pensacola, FL (Goerlltz et al., 1985). This com-
pound has been detected In drinking water In the United States and elsewhere
In the world. The median concentration of phenanthrene In finished water
from 11 U.S. water supplies was 5 ng/i. Assuming this value as the
average concentration of phenanthrene 1n U.S. drinking water, and a dally
human consumption of 2 l of drinking water, the average dally Intake of
phenanthrene for an adult In the United States Is estimated as 10 ng.
Some of the known sources of phenanthrene 1n the atmosphere are vehicu-
lar emissions, coal and oil burning, wood combustion, coke plants, aluminum
plants. Iron and steel works, foundries, ferroalloy plants, municipal
Incinerators, synfuel plants and oil shale plants (Santodonato et al., 1981;
Dalsey et al., 1986; Gammage, 1983). The atmospheric concentration of
phenanthrene 1n a Soderberg aluminum reduction plant In Norway was reported
to be <454 vg/m3 (Bjoerseth et al., 1978). Phenanthrene exists 1n the
ambient air 1n cities around the world at various concentrations (Llgockl et
al., 1985; Keller and Bldleman, 1984; KaMckhoff et al., 1979; Yamasakl et
al., 1982). Although data for phenanthrene was limited, Grosjean (1983)
estimated that the levels of other PAHs 1n Los Angeles air did not signifi-
cantly change during the last decade. The median concentration of atmo-
spheric phenanthrene 1s estimated to be 14 ng/m3 from the available atmo-
spheric levels of five U.S. locations. Assuming this value as the average
phenanthrene concentration 1n U.S. air, and that an adult Inhales 20 m3
air/day, the average datly Inhalation Intake of phenanthrene for a U.S.
Individual Is estimated to be 280 ng.
0861p -21- 05/20/87
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Phenanthrene has been reported to be present 1n oysters and fishes
collected from contaminated waters and 1n liquid smoke, smoked foods and
charcoal-broiled steaks (Fazio and Howard, 1983).' Marcus and Stokes (1985)
reported the concentration of phenanthrene 1n oysters collected from contam-
inated waters 1n South Carolina ranged from not detected to 76.5 vQ/l-
Fishes collected from contaminated U.S. waters were reported to contain
<20-100 vg/kg of combined phenanthrene/anthracene (DeVault, 1985). Until
data on the levels of this compound 1n total diet composites used by an
average Individual 1n the United States Is available, H 1s not possible to
estimate the human dietary Intake of phenanthrene.
0861p -22- 10/23/86
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4. PHARMACOKINETICS
4.1. ABSORPTION
Pertinent data regarding the gastrointestinal or pulmonary absorption of
phenanthrene could not be located 1n the available literature as cited 1n
the Appendix. Data from other structurally related PAHs suggest, however,
that phenanthrene 1s absorbed readily from the gastrointestinal tract (Rees
et al., 1971) and lungs (Kotln et al., 1969; Valnlo et al., 1976). In
general, these compounds are highly I1p1d-soluble and can pass across
epithelial membranes (U.S. EPA, 1980a).
4.2. DISTRIBUTION
Pertinent data regarding the distribution of phenanthrene could not be
located In the available literature as cited 1n the Appendix.
4.3. METABOLISM
Evidence from _l£ vivo and Jm vitro studies Indicate that metabolism of
phenanthrene occurs by epoxldatlon at the-1-2, 3-4 and 9-10 carbons, with
trans-dlhydrodlhydroxyphenanthrenes (dlhydrodlols) as primary metabolites
and the 9,10-dlhydrodlol as.the major metabolite.
Phenanthrene-9,10-, -1,2- and -3,4-dlhydrodlol were Identified unaltered
or as glucuronlc acid conjugates In the urine of rats and rabbits that were
given 1ntraper1toneal Injections of phenanthrene (Boyland and Wolf, 1950;
Boyland and Sims, 1962). The glucuronlc add conjugates of 1-, 2-, 3- and
4-hydroxyphenanthrene, 1,2-dlhydroxyphenantnrene and 3,4-dlhydroxy-
phenanthrcne were also Identified 1n these urines (Boyland and S1ms, 1962).
The above metabolites as well as phenanthrene-9,10-ox1de and 1,2-d1ol-3,4-
epoxlde were detected in Vn vLltr_o studies with guinea pig, rat and mouse
liver preparations (Sims, 1970; Chaturaplt and Holder, 1978; Nordqvlst et
al., 1981).
0861p -23- 05/20/87
-------
4.4. EXCRETION
Metabolites of phenanthrene have been detected In the urine of Intra-
perltoneally treated rodents as Indicated In Section 4.3. Additional Infor-
mation regarding the elimination of phenanthrene could not be located In the
available literature as cited In the Appendix.
4.5. SUMMARY
Pertinent data regarding the absorption, distribution and excretion of
phenanthrene could not be located 1n the available literature as cited In
the Appendix. PAHs are, 1n general, highly Upld-soluble, however, and are
absorbed readily from the gastrointestinal tract and lungs. Metabolites of
phenanthrene Identified 1n ^n vivo and jji vitro studies Indicate that
metabolism proceeds by epoxldatlon at the 1-2, 3-4 and 9-10 carbons (Boyland
and Wolf, 1950; Boyland and S1ms, 1962; S1ms, 1970; ChaturapU and Holder,
1978; Nordqvlst et al., 1981). . trans-D1hydrod1hydroxyphenanthrenes
(dlhydrodlols) are the primary products, with the 9,10-dlhydrodlol as the
major metabolite.
0861p -24- 10/23/86
-------
5. EFFECTS
5.1. CARCINOGENICITY
Single oral doses of 200 mg phenanthrene (purity unspecified) 1n sesame
oil vehicle were administered by gavage to ten 50-day-old female Sprague-
Dawley rats {Hugglns and Yang, 1962). The rats were examined for develop-
ment of mammary tumors by palpation for 60 days following treatment. No
mammary tumors were observed. Tissues other than the mammary gland were not
examined as this was a comparative study of mammary tumor Induction.
Mammary tumors occurred 1n 100/4 of 700 rats that were administered 20 mg
7,12-d1methylbenz[a]anthracene under the same conditions.
Phenanthrene has been tested for cardnogenldty In an Inadequately
reported skin application study with mice {dose and schedule not specified)
(Kennaway, 1924), 1n several mouse skin Initiation-promotion assays, In
single subcutaneous Injection studies with adult (Stelner, 1955) or newborn
(Grant and Roe, 1963) mice and In a three-Injection Intraperltoneal study
with newborn mice (Buenlng et al., 1979) (Table 5-1). The results of the
skin application and Injection studies were negative, but Interpretation 1s
complicated by the Inadequate reporting and single- or three-Injection
protocols. Phenanthrene was active as a tumor Initiator In one study In
which TPA was used as the promoter (Scrlbner, 1973), but 1t was Inactive In
other studies with TPA as a promoter (Wood et al., 1979; LaVole et al.,
1981), with croton oil as a promoter (Salaman and Roe, 1956; Roe, 1962),
with benzo[a]pyrene and croton oil as promoters (Roe and Grant, 1964) and
Inactive as a promoter with benzo[a]pyrene used as an Initiator (Roe and
Grant, 1964). Phenanthrene was also not active when used as an Initiator by
subcutaneous Injection with croton oil promotion by skin application (Roe,
1962).
0861p -25- 10/23/86
-------
TABU 5-1
Dermal and Injection Carcinogenic Ily Assays of Phenanthrene
o
CD
cr>
Route
Skin
Species/Strain
mouse/NR
No.VSex
100/NR
Purity
NR
Treatment
dose and application
Duration
9 months
Effects/Comments
No skin tumors
Reference
Kennaway, 1924
mouse/S
20/NR
NR
mouse/albino
i
IVJ
mouse/CD-I
10/H,
10/F
30/F
high
mouse/Swiss
Ha/ICR
mouse/Charles
River CD-I
20/F
TLC
purified
>99.5X
30/F
>98*
schedule not specified;
90% solution In benzene
0.3 ml of 1BX solution 25 weeks
In acetone 3 times/week
for 10 applications;
starting 25 days later,
16 weekly applications
of croton all In acetone
JO.3 flft): 1 of 0.17*. 2
of 0.065* and 15 of 0.17X
300 ng In acetone on 24 weeks
days 0, 2, 6 and B;
weekly application of
0.25 ml of 0.1X croton
oil In acetone from day
21 for 20 weeks
single application of 10 35 weeks
pmol In benzene,, fol-
lowed 1 week later with
applications of 5 yinol
TPA, 2 times/week for
34 weeks
100 tfl of 1.0* solution NR
In acetone 10 times on
alternate days; starting
10 days later, applica-
tions of 2.5 «g TPA, 3
times/week for 20 weeks
single application of 36 weeks
10 pmol In acetone;
starting 1 week later,
applications of 16 nmol
TPA, 2 times/week for
35 weeks
In
In
Skin paplllomas
5/20 {12 total
tumors) vs. 4/19
co.ntrols treated only
with croton oil
(4 total tumors)
Skin paptllomas In
4/19 vs. 2/20 In
controls treated only
with croton oil
Skin paplllonas In
12/30 (40X) vs. 0/30
In controls treated
with 10 iitml TPA
alone; 100X survival
No skin tumors; high
Incidence of tumors
Induced by benzofaj-
pyrene
Skin paplllomas In
5/30 «. 2/30 1n
controls treated with
acetone only; Inci-
dences were 4/29 vs.
2/30 In a second
Identical experiment
Salaman and
Roe, 1956
Roe, 1962
Scrlbner, 1973
LaVote et al.
1981
Hood et al.,
1919
CD
cr>
-------
TABLE 5-1 (cant.)
o
00
Route
Species/Strain No.VSex
Purity
Treatment
Duratton
Effects/Conments
Reference
Skin
mouse/NR
NR/NR
mouse/NR
NR/NR
NR
nwuse/NR
NR/NR
NR
Subcutaneous
mouse/CSIBl
mouse/stock
albino
40/mixed
10 H,
10 F
NR
unspecified Initiating 1 year
dose of benio[a]pyrene
followed by applications
of 5* phenanthrene In
unspecified solvent, 3
tines/week for 1 year
unspecified Initiating NR
dose of benzo[a]pyrene
followed by 12 applica-
tions of 5X phenanthrene
In unspecified solvent;
application schedule not
reported
1? unspecified appllca- NR
tlons of 5% phenanthrene
In unspecified solvent
followed by a single un-
specified dose of benzo-
(a)pyrene and weekly
applications of 0,1%
croton oil In acetone for
an unspecified duration
single Interscapular In-
jection of 5 mg In trl-
caprylln
300 tig In 3X aqueous
gelatin on days 0, 2, 4,
6 and 8; once weekly
with O.ZS M 0.1X
croton oil In acetone
from day 21 for 20 weeks
No skin tumors; pri-
mary report not
available
No skin tumors
Roe and Grant,
1964
Roe and Grant,
1364
No skin tumors
Roe and Grant,
1964
28 months
?4 weeks
No local tumors;
27/40 surviving at
4 months
Skin papHlomas >n
3/17 treated vs. 2/20
In controls treated
with acetone only
Stelner, 1955
Roe, 1962
ro
CO
03
CJ>
-------
TABLE 5-1 (cent.)
o
en
Route
Species/Strain Mo.VSex
Purity
Treatment
Duration
Effects/Comments
Reference
Subcutaneous
neonatal mouse/ 60/mlxed high
stock albino
40 ug tn 1% aqueous
gelatin, single Injec-
tion
62 weeks
Intraperitoneal
neonatal mouse/
Blu-HA (1CR)
Swiss-Webster
100/mlxed >98X
35 ug on day 1, 70 ^g
on day 8 and 140 i>g
on day 15; OMSO vehicle
36-40 weeks
CO
I
Incidences of pulmo-
nary adenomas, hepa-
tomas and skin papH-
lomas comparable with
two solvent control
groups; 10 mice/group
sacrificed after 52
weeks; similar results
In experiments of same
design In which phenan-
threne (20 or 40 j»g) was
mixed with benzo[a]pyrene
(20 or 40 ug)
Grant and Roe,
1963
Pulmonary adenomas tn
6/35 (17XJ vs. 9/59
(15X) In OMSO con-
trols; Incidences In
survivors at 42 weeks
of age; major organs
examined grossly and
those with suspected
pathology were examined
hlsiologlcally
Buentng
et al., 1979
•Numbers In treated and control (If used) groups unless specified otherwise.
o
•"x.
!S3
CD
o>
-------
5.2. MUTA6ENICITY
Phenanthrene has been tested In numerous mutagenldty and other
short-term assays with generally negative responses. The discussion that
follows Is not a comprehensive review of all the published literature
regarding the mutagenlcHy of phenanthrene, but a review of selected
articles that provides a representative assessment of Us mutagenlc
potential. The reader may wish to refer to other reviews on the
mutagenlcHy of phenanthrene (IARC. 1983; N1sh1, 1984; Brookes, 1977).
Phenanthrene was reported not to be mutagenlc 1n the His4" reversion
assay using Salmonella typhlmuMum tester strains TA100, TA98, TA1535,
TA1537 and TA1538 when assayed with or without liver metabolic activation
(McCann et al., 1975; Wood et al., 1979; Buecker et al., 1979; LaVole et
al., 1981; Florin et al., 1980). In a mutagenlcHy test program on the
tnterlaboratory reproduclbUHy of chemicals tested 1n the standard Ames
•
assay, phenanthrene was found to be predominantly negative 1n tester strains
TA98, TA100, TA1535, TA1537, TA1538 and 1n Escher1ch1a coll WP2 uvrA by four
different laboratories when assayed with or without various rodent liver S9
mixes (Dunkel et al., 1984). However, one study reported phenanthrene to be
mutagenlc 1n Salmonella tester strain TA100 when assayed 1n the presence of
a high concentration of liver S9 (Oesch et al., 1981). Phenanthrene also
showed a positive response on Salmonella typhlmurtum TA97 (Sakal et al.,
1985). TA97 Is a new frameshlft strain that 1s similar to and appears to be
more sensitive than TA1537. Negative results were reported 1n the forward
mutation assay using Salmonella typh1mur1um TM677 (Kaden et al., 1979;
Selxas et al., 1982).
Phenanthrene was reported to Induce mutation to trlfluorothymldlne
resistance 1n human lymphoblastold TK6 cells U) vitro In the presence of a
metabolic activation system (Barfknecht et al., 1981), but was reported to
0861p -29- 07/24/87
-------
be negative For the Induction of 8-azogualne and ouabaln resistance 1n
Chinese hamster V79 cells in vitro (Huberman and Sachs, 1979).
IntraperHoneal 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 a!., 1979). Sister
chromatld exchanges and chromosome aberrations were not produced 1n Chinese
hamster V79-4 cells treated j_n vitro with phenanthrene 1n the presence of
exogenous metabolic activation (Popescu et al., 1977).
Phenanthrene did not produce positive responses 1n other assays
Indicative of DNA damage with bacteria (Bacillus subtnis recVrec",
Escherlchla coll polAVpolA"), mammalian cells U» vitro (unscheduled DNA
synthesis 1n human foreskin epithelial cells and primary rat hepatocytes),
and yeast (mltotlc recombination 1n Saccharomyces cerevlslae D3) (McCarrol
et al., 1981; Rosenkranz and Polrler, 1979; Lake et al., 1978; Probst et
al., 1981; Simmon, 1979).
5.2.1. Cell Transformation Studies. Neoplastlc transformation was not
Induced In mouse prostate C3HG23 cells, C3H/10T1/2 clone 8 mouse embryo
flbroblasts, Syrian hamster embryo cells, mouse BALB/3T3 cells or guinea pig
fetal cells by \n_ vitro treatment with phenanthrene or In hamster embryo
cells following IntraperHoneal -Injection of' phenanthrene In pregnant
females (Quarles et. al., 1979; Marquardt et al., 1972; Plenta et al., 1977;
Kakunaga, 1973; Evans and DIPaolo, 1975; Peterson et al., 1981).
5.3. TERATOGENICITY
Pertinent data regarding the teratogenlclty of phenanthrene could not be
located In the available literature as cited In the Appendix.
0861p -30- 07/24/87
-------
5.4. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding the other reproductive effects of phenanthrene
could not be located 1n the available literature as cited In the Appendix.
5.5. CHRONIC AND SUBCHRONIC TOXICITY
Pertinent data regarding the effects of chronic or subchronlc exposure
to phenanthrene could not be located In the available literature as cited In
the Appendix.
5.6. OTHER RELEVANT INFORMATION
A single dose 1ntraper1toneal LD.Q of 700 mg/kg has been reported for
mice (Simmon, 1979). A single Intraperltoneal Injection of 150 mg/kg
phenanthrene dissolved 1n DMSO produced gross pathological alterations In
the livers of six male Sprague-Dawley rats after 24 and 72 hours (Yoshlkawa
et al., 1985); these Included congestion and a distinct lobular pattern.
Gross effects 1n other unspecified tissues were not Indicated. Small but
significant Increases In SGOT and serum GGTP levels were observed 24 but not
72 hours after treatment, and effects on SGPT and serum LDH, bH1rub1n,
glucose, BUN and creatlne were not Indicated.
5.7. SUMMARY
Phenanthrene did not Induce mammary tumors 1n rats when administered In
single 200 mg oral treatments (Muggins and Yang, 1962) and was not tumorl-
genlc to mice when administered 1n single subcutaneous Injections (Stelner,
1955; Grant and Roe, 1963) or three Intraperltoneal Injections to neonates
(Buenlng et al., 1979). The results of these studies were negative, but
should be regarded as Inconclusive concerning cardnogenlclty because of
limited treatment schedules.
0861p -31- 07/24/87
-------
Phenanthrene did not produce skin tumors In mice In an Inadequately reported
skin painting study (dose and application schedule not reported) (Kennaway,
1924). Several mouse skin Initiation-promotion assays with phenanthrene
have been conducted. Phenanthrene was active as a tumor Initiator In one
study 1n which TPA was used as the promoter (Scrlbner, 1973), but was
Inactive In the other studies In which TPA was used as the promoter (Wood et
al., 1979; LaVole et a!., 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 as an Initiator by subcutaneous
Injection with croton oil promotion by skin application (Roe, 1962).
Phenanthrene has been tested 1n numerous mutagenlclty and other short-
term assays with generally negative results. Positive responses occurred 1n
S. typhlmurlum 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 when tested with activation In other
studies. Phenanthrene also Induced mutation to trlfluorothymldlne resist-
ance 1n human lymphoblastold TK6 cells in vitro (Barfknecht et al., 1981)
and sister chromatld exchanges 1n hamster bone marrow cells Jm vivo (Bayer,
1978; Roszlnsky-Kocher et al., 1979). Phenanthrene did not produce chromo-
some aberrations or mlcronuclel In hamster bone marrow cells in vivo, sister
chromatld exchanges or chromosome aberrations In hamster bone marrow cell i£
vitro. DNA damage 1n bacteria or mammalian cells in vitro, mltotlc recombi-
nation In yeast, mutation to 8-azoguanlne and ouabaln resistance In hamster
V79 cells in vitro or neoplastlc transformation In various mouse, hamster
and guinea pig systems.
0861p -32- 07/24/87
-------
Data regarding teratogenlclty or other reproductive effects, or the
chronic or subchronlc toxlclty of phenanthrene, could not be located In the
available literature as cited In the Appendix. Single Intraperltoneal
Injections of 150 mg/kg produced evidence of slight hepatotoxlclty In rats
(Yoshlkawa et al., 1985); these Included gross congestion and distinct
lobulatlon and small Increases In the activities of SGOT and serum GGTP.
0861p -33- . 07/24/87
-------
6. AQUATIC TOXICITY
6.1. ACUTE
The available Information concerning acute toxldty of phenanthrene to
aquatic organisms Is presented 1n Table 6-1. Rainbow trout, Salmo qalrd-
ner.V. were the most sensitive fish species tested, with concentrations as
low as 1-4 vg/s. causing some mortality of eggs and larvae (Black et al.,
1983). Eggs and larvae of largemouth bass, Hlcropterus salmoldes. were also
quite sensitive, experiencing 32X mortality at 68 vg/i (Black et al.,
1983). Among Invertebrates, the lowest reported lethal concentration was
100 vg/l, the 96-hour LC5Q for Daphnla pulex (Trucco et al., 1983).
6.2. CHRONIC
The only data concerning the chronic toxldty of phenanthrene were
provided by Gelger and Bulkema (1982), who exposed JD. pulex to phenanthrene
for their lifetime (-50 days). Daphnla exposed to 360 jig/I had fewer
broods/animal; fewer live young/brood and delayed maturation. There were no
statistically significant effects on Daphnla exposed to 110 vg/l.
6.3. PLANTS
Bastlan and Toetz (1982) reported that the standing crop of the blue-
green alga, Anabaena flos-aquae, was reduced by phenanthrene at 96% satura-
tion but not <48% saturation. G1dd1ngs (1979) found that a 100% saturated
phenanthrene solution Inhibited photosynthesis In the green alga, Selenas-
trum caprlcornutum. Mlllemann et al. (1984) reported 4-hour EC5Q values
for Inhibition of photosynthesis of 940 and 870 jig/l 1n S. caprlcornutum
and the diatom, NUzschla palea. respectively. Hutchlnson et al. (1980)
reported EC5Q values of 945 and 1212 vg/l for Inhibition of photo-
synthesis In the green algae, Chlamydomonas angulosa and Chlorella vulgarls.
respectively.
0861p -34- 07/24/87
-------
o
CO
0*
TABLE 6-1
Acute ToxIcHy of Phenanthrene.to Aquatic Organisms
Species
Concentration
Effect
Reference
co
U1
I
FISH
Sea lamprey
Pftromyzon roarlnus
Rainbow trout
Salmo galrdnerl
Largemouth bass
Hlcropterus salmoldes
Bluegill
Lepomls macrochlrus
5000
5000
40
30
1-4
250
180
68
5000
nonlethal, 24 hours
lethal, 12 hours
96-hour LCgQ, eggs and larvae
27-day LC5Q, eggs and larvae
mortality, eggs and larvae
7-day LCgrj, eggs and larvae
96-hour LCjQ, eggs and larvae
32% mortality, eggs and larvae
lethal, 12 hours
Applegate et a!,, 1957
Applegate et al., 1957
Black et al., 1983
milemann et al., 1984
Black et al., 1983
HHIemann et al., 1984
Black et al., 1983
Black et al., 1983
Applegate et al., 1957
00
CRUSTACEANS
Water flea
Daphnla roagna
Mater flea
AmpMpod
Gammarus minus
700
1160
843
960-1280
100
460
48-hour
48-hour
LC50
48-hour
96-hour LC5Q
48-hour
Hlllemann et al., 1984
Bobra et al., 1983
Eastmond et al., 1984
*<
Gelger and Bulkema, 1982
Trucco et al., 1983
milemann et al., 1984
-------
o
CD
TABLE 6-1 (cont.)
Species Concentration Effect
INSECTS
3
Reference >
•5
fi
Nidge
Chlronomus tertians
MOLLUSCS
Marine snail
Llttorlna llttorea
Mussel
Mytllus edulls
ANNELIDS
Polychaete
Neanthes arenaceodentata
PROTOZOA
dilate
Colpldlum colpoda
dilate
Tetrahymena ell lot 1
490
40
600
48-hour LC§0
Hlllemann et a!., 1984
lysosome lablllzatlon, 3 days Moore et al., 198S
50-200 decreased lysosomal stability Moore and ferrar, 1985
96-hour
Rossi and Neff, 1978
saturated nontoxlc, saturated solution
saturated nontoxlc, saturated solution
Roger son et al., 1983
Rogerson et al., 1983
00
-------
6.4. RESIDUES
Data from bloconcentratlon experiments wHh phenanthrene are presented
In Table 6-2. The highest reported BCF was 23,800 for the alga, S. caprl-
cornutum (Casserly et al., 1983). In some species, uptake from food may
also be an Important route of accumulation. Such species Include D_. pulex
(Trucco et al., 1983) and the benthlc amphlpod, Pontoporela hoyj (Eadle et
al., 1983).
Once Inside the organism, phenanthrene tends to accumulate In certain
tissues. In fish, the liver seems to be the principal site of accumulation
(Solbakken et al., 1979, 1982). In the horse mussel, Hodlola modlolus.
phenanthrene accumulated In the hepatopancreas and kidney {Palmork and
Solbakken, 1981).
Bony fishes tend to metabolize and eliminate phenanthrene more quickly
than other aquatic organisms (Gerhart et al., 1981; Solbakken and Palmork,
1981). The primary metabolite formed by flounder, Platlchthys flosus, and
rainbow trout, S. qalrdnerl. was !,2-d1hydro-l,2-d1hydroxyphenanthrene
(Solbakken and Palmork, 1981). Fathead minnows, Plmephales promelas. elimi-
nated phenanthrene rapidly, with no detectable residues remaining after 24
hours depuration (Gerhart et al., 1981). D. maqna eliminated phenanthrene
somewhat more slowly, with an Initial elimination half-time of 9 hours
(Eastmond et al., 1984). D. pulex eliminated 80-92% of Its body burden 1n
24 hours of depuration (Trucco et al., 1983).
Phenanthrene monitoring data are presented 1n Table 6-3. In some cases,
aquatic organisms can accumulate body burdens of phenanthrene In the ppm
range and, therefore, could be an Important route of exposure If consumed by
humans. Dunn and Fee (1979) pointed out that lobsters, Homarus amerlcanus.
0861p -37- . 07/24/87
-------
CD
CP
TABLE 6-2
Bloconcentratlon Data for Phenanthrene In Aquatic Organisms
CJ
00
o
-j
V.
ro
*
00
Species
FISH
Fathead minnow
Plmephales promelas
CRUSTACEANS
Water flea
Daphnia magna
Water flea
Daphnia pulex
MOLLUSCS
Clam
Macoma Inguinata
Mussell
Mytllus edulls
Concentration BCF
NR 3,100-5,100
NR 1.000-12,000
60 600
NR 325
NR 1,032-1,424
NR 10.3
0.2
0.3 68
1.9 81
Remarks
28-day BCF
14-day BCF
peak BCF, 20-30 hours
24-hour BCF
24-hour BCF
7-day BCF, water
7-day BCF, sediment
8-hour BCF
8-hour BCF
Reference
Carlson
et al., 1979
Gerhart
et al., 1981
Eastmond
et al., 1984
Southworth
et al., 1978
Trucco
et al., 1983
Roesljadl
et al., 1978.
Hansen
et al., 1978
-------
o
CO
TABLE 6-2 (cont.)
to
-------
TABLE 6-3
0
co
o<
•o
i
o
1
Species
FISH
White sucker
Catostomus commersoni
English sole
Parophrys vetulus
CRUSTACEANS
Brown shrimp
Penaeus aztecus
Lobster
Homarus americanus
Monitoring Data for Phenanthrene In Aquatic
Location Tissue
eastern Lake Erie stomach
contents
Puget Sound stomach
contents
central Gulf of Mexico whole body
eastern Canada, whole body
Atlantic Ocean
Organisms
Concentration
(ng/g)
23-43
56-1400
10
32
Reference
Maccubbin
et al.. 1985
Mallns
et al.. 1985
Nulton and
Johnson, 1981
Dunn and Fee,
1979
CO
MOLLUSCS
Mussell
Mytil us edulis
Periwinkle
Littorina littorea
Limpet
Patella vulgata
Norway, polluted areas whole body 41-792
Norway, polluted areas whole body 115-258
Norway, polluted areas whole body 55-2542
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
-------
o
00
TABLE 6-3 (cent.)
o
V.
ro
^
00
Species
MISCELLANEOUS INVERTEBRATES
Starfish
Asterlas rubens
Sponge
Hallchondrla panlcea
Polychaetes
(unspecified)
PLANTS
Bladder wrack
Fucus veslculosus
Toothed wrack
Fucus serratus
Knotted wrack
Ascophyllum nodosum
Lamlnarla saccharina
Ceramlum rubrum
Location
Norway,
Norway,
New York
Norway,
Norway,
Norway,
Norway,
Norway,
polluted areas
polluted areas
bight
polluted areas
polluted areas
polluted areas
polluted areas
polluted areas
Tissue Concentration
(ng/g)
whole body 32-50
whole body 71
whole body ND-14
whole body 31-325
whole body 109-146
whole body 45-431
whole body 87
whole body 34
Reference
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
Farr ington
et al., 1986
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
Knutzen and
Sortland, 1982
ND = Not detected
-------
maintained in 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 In Impounded lobsters.
6.5. SUMMARY
The data base for the aquatic toxlclty of phenanthrene Is 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 yg/8, (Black et
a!., 1983). Among the nine Invertebrate species tested, the lowest reported
lethal concentration was 100 yg/1, the 96-hour LCcn for D. pulex
3U ~ -
(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 D, pulex occurred at 110 iig/s..
Aquatic plants appeared to be less sensitive to phenanthrene than fish and
Invertebrates, with EC,-n values for Inhibition of photosynthesis ranging
from 870 yg/t In N. paleo (MITIemann et al., 1984) to TOOK saturation In
S. caprlcornutum (Glddlngs, 1979). Bloconcentratlon and residue monitoring
data Indicated wide variability In potential for phenanthrene accumulation
In 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
-------
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/m3 of air.
U.S. EPA (1980a) recommended a concentration limit of 28 ng/8. for the
sum of all carcinogenic PAH In 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 1n 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 noncarclnogenlc PAH are essentially nonexistent, and an
ambient water quality criterion has not been recommended.
0861 p -43- 07/24/87
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7.2. AQUATIC
Guidelines and standards for the protection of aquatic bl.ota from the
effects of phenanthrene In particular could not be located In the available
literature as cited In the Appendix; however, U.S. EPA (1980b) noted that
acute toxldty to saltwater life occurred at concentrations as low as 300
ng/l of polynuclear aromatic hydrocarbons In general and would occur at
lower concentrations 1n 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 carclnogenlclty 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
tumor 1 gen 1dty of phenanthrene was also evaluated 1n single-treatment (40
yg or 5 mg) subcutaneous (Stelner, 1955; Grant and Roe, 1963) and three-
treatment (35, 70 and 140 vg at weekly Intervals) IntraperHoneal (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 cardno-
genlclty. Phenanthrene reportedly did not produce skin tumors 1n mice In an
Inadequately reported study 1n which the dose and application schedule was
not specified (Kennaway, 1924). Phenanthrene was active as a tumor Initi-
ator In one study In which TPA was used as the tumor promoter (Scrlbner,
1973), but was Inactive In other mouse skin Initiation-promotion studies In
which TPA was used as the promoter (Wood et a!., 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 1n 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; Ounkel
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 In the presence of a high concentration of liver S9 (Oesch et al.,
1981) and another study reporting a positive response 1n the new frameshlft
tester strain TA97 with liver metabolic activation (Sakal et al., 1985).
Phenanthrene was reported to Induce gene mutations In human lymphoblastold
cells in vUro 1n 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 in vitro (Huberman and Sachs,
1979). IntrapeMtoneal Injection of phenanthrene Into Chinese hamsters
produced sister chromatld exchanges, but no chromosome aberrations or
mlcronuclel 1n 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 j£ vitro with phenanthrene
1n 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 vitro, and yeast (1»e.,
differential growth Inhibition, DNA repair and mltotlc recombination tests)
(McCarrol et al., 1981; Rosenkranz and Polrier, 1979; Lake et al., 1978;
Probst et al., 1981; Simmon, 1979).
The oral, subcutaneous, IntrapeMtoneal and dermal carclnogenlclty
studies of phenanthrene are Inadequate for evaluation of carclnogenlclty
because of deficiencies In treatment schedules and reporting. Phenanthrene
was active as an Initiator 1n 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[ajpyrene as the
Initiator. Mutagenlclty and clastogenlclty (sister chromatld exchange) of
phenanthrene was reported In several assays, but the preponderance of data
0861p -46- 07/24/87
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from numerous short-term genotoxIcHy tests Is negative. The available
evidence 1s therefore Inadequate to evaluate the cardnogenldty of
phenanthrene.
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 RfD
(formerly ADI) 1s therefore precluded, as It was at the time of an earlier
health effects assessment for phenanthrene (U.S. EPA, 1984).
QB&lp -47- 07/24/87
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9. REPORTA8LE QUANTITY
9.1. REPORTABLE QUANTITY (RQ) RANKING BASED ON CHRONIC TOXICITY
Information regarding the chronic or subchronlc toxlclty, teratogenlcHy
or other reproductive effects of phenanthrene could not be located !n the
available literature as cited In the Appendix. Calculation of an RQ ranking
for phenanthrene based on chronic toxlclty 1s therefore precluded, as It 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/ED1()) FOR CARCINOGENICITY
Rhenanthrene has been tested for cardnogenlclty In a single-treatment
(200 ing) gavage study In which rats were examined for development of mammary
tumors for 60 days following treatment (Muggins and Yang, 1962). The
tumorIgenlcity of phenanthrene was also evaluated 1n single-treatment (40
pg or 5 mg) subcutaneous (Stelner, 1955; Grant and Roe, 1963) and three-
treatment (35, 70 and 140 ^g at weekly Intervals) Intraper Honeal (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 cardnogenlclty. Phenanthrene
reportedly did not produce skin tumors In mice In an Inadequately reported
study 1n which a dose and application schedule was not specified (Kennaway,
1924), As detailed In Table 5-1, phenanthrene was active as a tumor Initi-
ator In one study In which TPA was used as the tumor promoter (Scrlbner,
1973), but was Inactive In 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
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 1n numerous mutagenlclty and other short-
term assays with generally negative results. These Include assays for DNA
repair, rautagenesls and clastogenlclty In bacterial and mammalian cells J_n
vitro and Jj| vivo and neoplastlc transformation In mammalian cells.
Positive responses occurred 1n S. typhlmurjum strain TA100 In the presence
of a high concentration of metabolic activation preparation (Oesch et a!.,
1981), but not 1n strains TA100, TA98, TA1535, TA1537, TA1538 or TM677 with
activation In other studies. Phenanthrene also Induced mutation to
trlfluorothymldlne resistance In human lymphoblastold TK6 cells ^n vitro
(Barfknecht et a!., 1981) and sister chromatld exchanges In hamster bone
marrow cells In vivo (Bayer, 1978; Roszlusky-Kocher et a!., 1979).
The oral, subcutaneous, Intraperltoneal and dermal carclnogenlclty
studies of phenanthrene are Inadequate for evaluation of carclnogenlclty
because of the differences In 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 1n other
studies that used the same or different promoters or benzofajpyrene as the
Initiator. Mutagenlcity and clastogenlclty (sister chromatld exchange) of
phenanthrene was reported 1n several assays, but the preponderance of data
from numerous short-term genotoxlclty tests Is negative. The available
evidence 1s therefore Inadequate to evaluate the carclnogenlclty of
phenanthrene.
0861p -49- 07/24/87
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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 1s 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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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
TQXBACK 76
TOXBACK 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
These searches were conducted In April, 1986. In addition, hand searches
were made of Chemical Abstracts (Collective Indices 6 and 1), and the
following secondary sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hygienlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hygienlsts).
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.O. 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.
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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 Wiley and
Sons, NY. p. 3817-5112.
Grayson, M. and D, Eckroth, Ed. 1978-1983. K1rk-0thmer 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., H.R. Mabey., S.T. L1u, T.H. Chow and H.L. Johnson.
1984. Data aqulsltlon for environmental transport and fate screen-
Ing for compounds of Interest !n the Office of Solid Waste. EPA
600/6-84-010. NTIS PB84-2439Q6. SRI International, Henlo 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 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, OC.
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 Relnhold Co., NY.
Hlndholz, M., Ed. 1983. The Herck 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.
0861p -77- 07/24/87
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In. addition, approximately 30 compendia of aquatic toxlcity 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 Toxldty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxlcity Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Oept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, 3.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
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