v> EPA
United States
Environmental Protection
Agency
Office of Water October 1982
Regulations and Standards (WH-553) * *-» ^ /-x <-x XN r-v
Washington DC 20460 44048502OD
Water
An Exposure
and Risk Assessment for
Benzo[a]pyrene and
Other Polycyclici
Aromatic Hydrocarbons
Volume IV.
Benzo[a]pyrene, Acenaphthylene,
Benz[a]anthracene, Chrysene,
Dibenz[a,h]anthracene,
Benzo[b]fluoranthene,
Benzo[k]fluoranthene,
Benzo[g,h,i]perylene,
lndeno[1,2,3-c,d]pyrene
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DISCLAIMER
This is a contractor's final report, which has been reviewed by the Monitoring and Data Support
Division, U.S. EPA. The contents do not necessarily reflect the views and policies of the U.S.
Environmental Protection Agency, nor does mention of trade names or commercial products
constitute endorsement or recommendation for use.
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REPORT DOCUMENTATION *• «PORT NO. 2.
PAGE EPA-440/4-85-020
4. Tttte and Subtitle
An Exposure and Risk Assessment for Benzo[a]pyrene and Other
Polycyclic Aromatic Hydrocarbons: Volume IV. Benzo[a]pyrene,
Acenaphthylene, Benz [a] anthracene, Benzo [b]Fluoranthene,
7. Author^ Perwak, J.; Byrne, M. ; Coons, S.; Goyer, M.; Harris, J.
(ADL) Cruse, P.; DeRosier, R. : Moss, K. : Wendt. S. (Acurex)
9. Performing Organization Nam* and Address
Arthur D. Little, Inc. Acurex Corporation
20 Acorn Park 485 Clyde Avenue
Cambridge, MA 02140 Mt. View, CA 94042
12. Sponsoring Organization Nam* and Address
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. R*eipi*nf s Accession No.
5. R*port Oat* Final Revision
October 1982
s.
8. Performing Organization R*pt. No.
10. Proj*ct/T*«k/Work Unit No.
11. Contraet(C) or Grant(G) No.
(0 C-6.8-01-616Q
(G, C^68-01-6017
IX Typ* of Report & Period Covered
Final
14.
IS. Supplementary Note*
Extensive Bibliographies
6. Abstract (Limit 200 word*)
This report assesses the risk of exposure to polycyclic aromatic hydrocarbons (PAHs).
This is Volume IV of a four-volume report, analyzing 16 PAHs; it concerns nine of
these: benzo[a]pyrene, acenaphthylene, benz[a]anthracene, benzo[b]fluoranthene,
benzo[k]fluoranthene, benzo[g,h,i]perylene, chrysene, dibenz[a,h]anthracene, and
indeno[l,2,3-c,d]pyrene. This study is part of a program to identify the sources of
and evaluate exposure to 129 priority pollutants. The analysis is based on available
information from government, industry, and technical publications assembled in June of
1981.
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substances. In addition, the fate of PAHs in the
environment is considered; ambient levels to which various populations of humans and
aquatic life are exposed are reported. Exposure levels are estimated and available
data on toxicity are presented and interpreted. Information concerning all of these
topics is combined in an assessment of the risks of exposure to PAHs for various
subpopulations.
7. Document Analyala a. Descriptors
Exposure Effluents
Risk Waste Disposal
Water Pollution Food Contamination
Air Pollution Toxic Diseases
b. Identifiers/Open-Ended Terms
Pollutant Pathways
Risk Assessment
c. COSAT1 Held/Group Q6F 06T
S. Availability Statement
Release to Public
Polycyclic Aromatic Hydrocarbons
Indeno[l,2,3-c,d]pyrene
Benzotg»h,i]perylene
Benzo[b]fluoranthene
Benzo[k]fluoranthene
Dibenz[a,h]anthracene
Chrysene
Acenaphthylene
PAHs
Benzo[a]pyrene
Benz[a]anthracene
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
OpOU«aeurity Class (This Report)
Unclassified
20. Security Class (This Page)
21. No. of Pages
215
22. Price
$19
00
M ANSJ-Z39.181
See Instruction, en ft*vers«
OPTIONAL FORM 272 (4-773
(Formerly NTIS-35)
Department of Commerce
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EPA-440/4-85-020
June 1981
(Revised October 1982)
AN EXPOSURE AND RISK ASSESSMENT FOR BENZO[a]PYRENE AND
OTHER POLYCYCLIC AROMATIC HYDROCARBONS:
VOLUME IV BENZO[a]PYRENE, ACENAPHTHYLENE, BENZ[a]ANTHRACENE,
BaNZOfb]FLUORANTHENE, BENZO[k]FLUORANTHENE
BENZO[g,h,i]PERYLENE, CHRYSENE
DIBENZ[a,h]ANTHRACENE, AND
INDENO[1,2,3-c,d]PYRENE
By
Joanne Perwak, Melanie Byrne, Susan Coons,
Muriel Goyer and Judith Harris
Arthur D. Little, Inc.
U.S. EPA Contract 68-01-6160
Patricia Cruse, Robert DeRosier,
Kenneth Moss and Stephen Wendt
Acurex Corporation
U.S. EPA Contract 68-01-6017
John Segna and Michael Slimak
Project Managers
U.S. Environmental Protection Agency
Monitoring and Data Support Division (WH-553)
Office of Water Regulations and Standards
Washington, D.C. 20460
OFFICE OF WATER REGULATIONS AND STANDARDS
OFFICE OF WATER
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
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FOREWORD
Effective regulatory action for toxic chemicals requires an
understanding of the human and environmental risks associated with the
^anufacture, use, and disposal of the chemical. Assessment of risk
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environmental concentra-
tions. The risk assessment process integrates health effects data
(e.g., carcinogenicity, teratogenicity) with information on exposure.
The components of exposure include an evaluation of the sources of the
chemical, exposure pathways, ambient levels, and an identification of
exposed populations including humans and aquatic life.
This assessment was performed as part of a program to determine
the environmental risks associated with current use and disposal
patterns for 65 chemicals and classes of chemicals (expanded to 129
priority pollutants") named in the 1977 Clean Water Act. It includes
an assessment of risk for humans and aquatic life and is intended to
serve as a technical basis for developing the most appropriate and
effective strategy for mitigating these risks.
This document is a contractors' final report. It has been
extensively reviewed by the individual contractors ?nd by the EPA at
several stages of completion. Each chapter of the draft was reviewed
by members of the authoring contractor's senior technical staff (e.g.,
toxicologists, environmental scientists) who had not previously been
directly involved in the work. These individuals were selected by
management to be the technical peers of the chapter authors. The
chapters were comprehensively checked for uniformity in quality and
content by the contractor's editorial team, which also was responsible
for the production of the final report. The contractor's senior
project management subsequently reviewed the final report in its
entirety.
At EPA a senior staff member was responsible for guiding the
contractors, reviewing the manuscripts, and soliciting comments, where
appropriate, from related programs within EPA (e.g., Office of Toxic
Substances, Research and Development, Air Programs, Solid and
Hazardous Waste, etc.). A complete draft was summarized by the
assigned EPA staff member and reviewed for technical and policy
implications with the Office Director (formerly the Deputy Assistant
Administrator) of Water Regulations and Standards. Subsequent revi-
sions were included in the final report.
Michael W. Slimak, Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
ill
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AN EXPOSURE AND RISK ASSESSMENT FOR BENZO[a]PYRENE AND
OTHER POLYCYCLIC AROMATIC HYDROCARBONS
VOLUME I
1.0
2.0
VOLUME II
3.0
VOLUME III
4.0
VOLUME IV
5.0
SUMMARY
Introduction
Technical Summary
Naphthalene
3.1
3.2
3.3
3.4
3.5
Materials Balance
Fate and Distribution in the Environment
Effects and Exposure—Humans
Effects and Exposure—Aquatic Biota
Risk Considerations
Anthracene, Acenaphthene, Fluoranthene, Fluorene
Phenanthrene, and Pyrene
4.1
4.2
4.3
4.4
4.5
Materials Balance
Fate and Distribution in the Environment
Effects and Exposure—Humans
Effects and Exposure—Aquatic Biota
Risk Considerations
Benzo[a]pyrene, Acenaphthylene, Benz[a]anthracene,
Benzo[b]fluoranthene, Benzo[k]fluoranthene, Benzo-
[g,h,i]perylene, Chtysene, Dibenz[a,h]anthracene,
and Indeno[l,2,3-c,d]pyrene
5.1
5.2
5.3
5.4
5.5
Materials Balance
Fate and Distribution in the Environment
Effects and Exposure—Humans
Effects and Exposure—Aquatic Biota
Risk Considerations
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TABLE OF CONTENTS Pa2e
5
LIST OF FIGURES ix
LIST OF TABLES x
ACKNOWLEDGMENTS xv
1.0 INTRODUCTION ]__!
5.0 BENZO[a]PYRENE, ACENAPHTHYLENE, BENZ[a]ANTHRACENE,
BENZO[b]FLUORANTHENE, 3ENZO[k]FLUORANTHENE,
BENZO[g,h,i]PERYLENE, CHRYSENE, DIBENZ[a,h]ANTHRACENE,
INDENO[l,2,3-c,d]PYRENE 5-1
5.1 MATERIALS BALANCE 5-1
5.1.1 Introduction 5-1
5.1.2 Combustion Sources 5-1
5.1.2.1 Residential Coal Combustion 5-1
5.1.2.2 Wood 5-4
5.1.2.3 Cigarettes 5-4
5.1.2.4 Coal Refuse Piles 5-4
5.1.2.5 Forest Fires 5-6
5.1.2.6 Carbon Black 5-10
5.1.2.7 Agricultural Open Burning 5-12
5.1.2.8 Motor Vehicles 5-12
5.1.2.9 Incinerators 5-12
5.1.2.10 Coal- and Oil-Fired Utility Boilers 5-15
5.1.2.11 Utility and Industrial Internal
Combustion Engines 5-15
5.1.2.12 Gas- and Oil-Fired Residential Heating 5-15
5.1.3 Contained Sources 5-15
5.1.3.1 Coal Tar 5-21
5.1.3.2 Petroleum Sources 5-21
5.1.4 Publicly Owned Treatment Works 5-21
5.1.5 Summary 5-24
5.2 FATE AND DISTRIBUTION IN THE ENVIRONMENT 5-28
5.2.1 Introduction 5-28
5.2.2 Inputs to Aquatic Media 5-28
5.2.2.1 Atmospheric Deposition 5-28
5.2.2.2 Source Identification by PAH
Composition 5-30
5.2.3 Environmental Fate 5-32
5.2.3.1 Basic Physical/chemical Fate 5_32
5.2.3.2 Pathways in the Aquatic Environment 5-32
5.2.3.3 Modeling of Environmental Distribution 5-59
5.2.4 Monitoring Data 5_70
5.2.4.1 STORET Data 5_70
5.2.4.2 Data from Other Sources 5-74
5.2.5 Summary — Ultimate Fate and Distribution 5-84
vii
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TABLE OF CONTENTS (Continued)
Page
5.3 HU1-IAN EFFECTS AND EXPOSURE 5_91
5.3.1 Human Toxicity 5_91
5.3.1.1 Introduction 5-91
5.3.1.2 Pharmacokinetics 5-91
5.3.1.3 Human and Animal Studies 5-92
5.3.1.4 Risk Considerations 5-112
5.3.2 Human Exposure 5-126
5.3.2.1 Introduction
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LIST OF FIGURES
Figure
-^- Page
5-1 Estimated Residential Coal Consumption in 1974 5.3
by State
5-2 Geographic Regions Used to Summarize Survey Data
Within the Coterminous States 5-9
5-3 Geographical Distribution of Residential Fuel
Consumption for Space Heating, 1975 5-16
5-4 Effect of Combustion Temperature on Relative
Abundance of Alkyl Carbon Atoms on Produced
Polynuclear Aromatic Hydrocarbons 5-31
5-5 Distribution of Alkyl Homologs in the Phenanthrene-
Type Series and Pyrene-Type Series in River Water, '
and Air — Charles River, Boston, MA 5-33
5-6 Results of Modeling of the Effect of Suspended
Solids on the Concentration of Benzo[a]Pyrene in
a Partially Mixed River System ' 5-37
Sorption Isot terms for Benzo[a]Pyrene 5-40
Calculated Seasonal and Daily Variation of
Photolysis Half-Life of Benzo[a]Pyrene 5-42
5-9 Sources and Fate of Benzo[a]Pyrene in the Aquatic 5-89
Environments
5-10 Possible Pathways of Benzo[a]pyrene Metabolism 5-93
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LIST OF TABLES
Table
No.
Page
5-1 Estimated Air Emission of BaP Group PAHs, by
Combustion Sources, 1978 5-2
5-2 Estimated Residential Wood Consumption by
State, 1976 5_5
Coal Refuse Fires 5.7
Estimated Net Total Weights of Fuel Consumed
Annually in Prescription Burning on All Ownerships 5-8
5-5 Locations and Capacities of Carbon Black Producers 5-11
5-6 Distribution of Agricultural Open Burning, 1973 5-13
5-7 PAHs Discharged Annually in Used Crankcase Oil 5-14
5-8 PAH Materials Balance: Coal Tar Production and
Distillation, 1978 5-17
5-9 PAHs in Contained Petroleum Sources 5-18
5-10 PAH Emissions: Coke-Oven Doors 5-19
5-11 Water Discharges of BaP Group PAHs: Timber Products, 5-20
1978
5-12 Materials Balance of BaP Group PAHs: Municipal POTWs 5-22
5-13 PAH Concentrations in Municipal POTWs 5-23
5-14 Estimated Environmental Releases of BaP Group PAHs 5-25'
5-15 Evaluation of Air-to-Surface Pathway for
Benzo[a]?yrene 5-29
5-16 Basic Physical/chemical Properties of Ber.zo[al-
Pyrene Group PAHs ' 5-34
5-17 Benzo[a]Pyrene Partition Coefficients for Various
Sorbents 5-38
5-18 Relative Half-Lives of Benzo[a]Pyrene Group PAHs
in Reaction with Major Oxidants 5-45
5-19 Predicted Half-Lives for Benzo[a]Pyrene
Transformation and Removal Processes in
Generalized Aquatic Systems 5-46
x
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LIST OF TABLES (Continued)
Table
-^- Page
5-20 Bioconcentration of Benzo[a]Pyrene in Freshwater
and Saltwater Species 5-47
5-21 Concentrations of Benzo[aJPyrene in Tissues of
Aquatic Organisms 5-49
5-22 Biodegradation Products Reported for the Benzo[a]-
Pyrene Group PAHs 5_53
5-23 Biodegradation Rates of the Benzo[a]Pyrene Group
PAHs: Individual Compound Studies 5-55
5-24 Kinetic Parameters of Biotransformation of
Benz[a]Anthracene and Benzo[a]Pyrene 5-53
5-25 Values of Parameters Used for Calculating the
Equilibrium Distribution of Benzo[a]Pyrene Predicted
by the Mackay Fugacity Model 5_60
5-26 Equilibrium Partitioning of Benzo[aJPyrene Calculated-
Using Mackay's Fugacity Model 5_51
5-27 Input Parameters for EXAMS Modeling of the Fate of
Benzo[a]Pyrene in Generalized Aquatic Systems 5-63
5-28 Molar Absorbtivity for Benzo[a]Pyrene as a Function
of Wavelengths 5-64
5-29 Steady-State Concentrations of Benzo[a]Pyrene in
Various Generalized Aquatic Systems Resulting from
Continuous Discharge 5-65
5-30 The Fate of Benzo[aJPyrene in Various Generalized
Aquatic Systems 5-66
5-31 The Persistence of Benzo[aJPyrene in Various
Generalized Aquatic Systems After Cessation of
Loading 5_68
5-32 Comparison of Results from Mackay's Equilibrium
Model and EXAMS for Benzo[aJPyrene in a Pond System 5-69
5-33 Distribution of Observed Ambient & Effluent Concen-
trations of the Ba? Group PAHs 5-71
XI
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Table
No.
LIST OF TABLES (Continued)
Page
5-34 Number, Detection Limits, and Ranges of Observed
Concentrations in Ambient Water and Sediment for
the Benzo[a]Pyrene Group PAHs — STORET, 1980 5-72
5-35 Distribution of Observed Sediment and Tissue
Concentrations of the BaP Group PAHs 5_ 73
5-36 Concentrations of Benzo[a]Pyrene Group PAHs in
Ambient Water 5-7S
5-37 Levels of PAHs in the Mbnongahela, Ohio, and
Delaware Rivers c -,<•
J— / o
5-38 Levels of Benzo[a]Pyrene Group PAHs in Drinking Water 5-78
5-39 Frequency of Observations of Benzo[a]Pyrene Group
PAHs in Soil and Sediment 5_ 79
5-40 Reported Levels of BaP Group PAHs in Marine Organisms 5- 80
5-41 Reported Levels of Benzo[a]Pyrene Group PAHs in
Air of U.S. Cities 5_ Si
5-42 Concentrations of Benzo[a]Pyrene Group PAHs in the
Air of Selected U.S. Cities, Average of Summer and
Winter Values 5_ 82
5-43 Frequency of Ambient Concentrations of BenzofajPyrene
Group PAHs in Urban Air 5_ 83
5-44 Relationship Between Concentration of Benzo[a]Pyrene
in Air and Distance From Emission Source 5- 35
5-45 Frequency of Ambient Concentrations of Benzo[a]-
Pyrene Group PAHs in Rural Air 5-86
5-46 Calculated Concentrations of Benzo[a]Pyrene and
Related PAEs in Mainstream Cigarette Smoke 5- 87
5-47 Carcinogenic Activity of Benzo[ajPyrene by Various
Exposures c nc
5-48 Incidence of Orally Administered, Benzo[a]Pyrene-
Induced Forestomach Tumors in Mice 5_ 93
xii
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LIST OF TABLES (Continued)
Table
No- Page
5-49 Summary of the Carcinogenic Activity for Other
Polycyclic Aromatic Hydrocarbons in the Benzo[aj-
Pyrene Group 5-100
5-50 Summary of Mutagenic Activity for Compounds
Comprising the Benzo[a]Pyrene Group 5-109
5-51 Carcinogenic Response in CFW Mice Treated with
Benzo[a]Pyrene 5-115
5-52 Carcinogenic Response in CC57 Mice Treated with
Benzo[a]Pyrene 5-116
5-53 Comparison of Dose/Effect Analyses Using Three
Mathematical Models 5-119
5-54 Probable Upper Bounds on Expected Excess Cancers
Per Million Population Due to Benzo[a]Pyrene
Ingestion 5-120
5-55 Probable Upper Bounds on Expected Excess Cancers
Per Million Population Due to Benzo[a]Pyrene
Ingestion 5-121
5-56 Comparison of Dose/Effect Analyses where Effective
Dose is a Power Function 5- 123
5-57 Estimated Human Exposure to the Benzo[ajPyrene
Group PAHs Via Drinking Water 5-127
5-58 Levels of Benzo[a]Pyrene Group PAHs in Food and
Estimated Exposure Via Ingestion of Food 5-128
5-59 Estimated Exposure to Benzo[ajPyrene Group PAHs
Via Inhalation of Ambient Air 5- 139
5-60 Estimated Size of the U.S. Population Exposed to
Ranges of Benzo[a]Pyrene Concentrations in Ambient
Air 5-133
5-61 Estimated Human Exposure to the Benzo[ajPyrene
Group PAHs 5_ ^33
5-62 Summary of Unremarked Observations of Concentrations
of Benzo[ajPyrene Group PAHs in Surface Water and
Sediment — STORET, 1980 5_ 137
xiii
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LIST OF TABLES (Continued)
Table
No- Paae
5-63 Estimated Human Exposure to the Benzo[a]Pyrene
Group PAHs 5_
5-64 Estimated Lifetime Excess Probability of Cancer to
Humans Due to BaP Ingestion at Various Exposure
Levels Based on Three Extrapolation Models 5-143
5-65 Estimated Ranges of Carcinogenic Risk to Humans
Due to BaP Exposure for Various Routes 5-145
A~l Emission Factors 5_ 177
A-2 Fireplace Population ' 5- 173
A-3 PAH Associated with Carbon Black 5_ 179
A-4 PAH Releases from Tire Wear 5_ ISO
A-5 Concentrations of PAHs in Used Crankcase Oils 5- 181
A-6 Municipal Incinerators Release Factors 5_
A-7 Emissions of PAHs from Coal-fired Plants and
Intermediate/Small Oil-fired Units 5_ 133
A-3 Coke-Oven Tar Produced in the United States, Used
by Producers, and Sold in 1978, by State 5-184
A~9 Concentrations of Various PAHs in Coal and Coal
Tar Derivatives 5_ ^35
A-10 PAH Wastewater Discharge: By-product Cokemaking 5- 186
A-ll Concentration of Select PAHs in Petroleum Products 5- 187
A-12 Emissions of PAHs from Petroleum Refining 5- 188
A-13 Emissions of PAHs from Catalyst Regeneration
in Petroleum Cracking 5_ 139
xiv
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ACKNOWLEDGMENTS
The Arthur D. Little, Inc., task manager for the Exposure and
Risk Assessment for the BaP group PAHs was Joanne Perwak. The major
contributors were Melanie Byrne (Aquatic Effects and Exposure), Susan
Coons (Environmental Fate, Murial Goyer (Human Effects) and Joanne
Perwak (Human Exposure); Judith Harris provided significant input to
several chapters of this report. In addition, Kate Scow contributed
to the discussions of biodegradation and aquatic effects, and Janet
Wagner performed the environmental modeling tasks. Documentation of
this report was done by Nina Green; Jane Metzger and Paula Sullivan
were responsible for editing and final report production.
The Materials Balance for the BaP group PAHs (Section 3.1) was
produced by Acurex Corporation, under Contract No. 68-01-6017 to the
Monitoring and Data Support Division (MDSD), Office of Water Regulations
and Standards (OWRS), U. S. Environmental Protection Agency. Patricia
Cruse was the task manager for Acurex, Inc.; other contributors include
Robert DeRosier, Kenneth Moss and Stephen Wendt. Patricia Leslie was
responsible for report production on behalf of Acurex, Inc.
John Segna and Michael Slimak were the EPA project managers for
this assignment.
xv
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1.0 INTRODUCTION
The Office of Water Regulations and Standards (OWRS), Monitoring
and Data Support Division, of the U.S. Environmental Protection Agencv
is conducting a program to evaluate the exposure to and risk of 129
priority pollutants in the nation's environment. The risks to be
evaluated include potential harm to human beings and deleterious effects
on fish and other biota. The goals of the program under which this
report has been prepared are to integrate information on cultural and
environmental flows of specific priority pollutants, to estimate the
likelihood of receptor exposure to these substances, and to evaluate the
risk resulting from such exposures. The results are intended to serve
as a basis for estimating the magnitude of the potential risk and
developing a suitable regulatory strategy for reducing any such risk.
This report, comprised of four separate volumes, provides a summarv
of the available information concerning the releases, fate, distribu-
tion, effects, exposure, and potential risks of the 16 priority pollu-
tants that are polycyclic aromatic hydrocarbons (PAHs). The chemical
structures of these compounds are shown in Figure 1-1.
The number of chemicals considered in this exposure and risk
assessment is appreciable. The possibility of preparing 16 separate
exposure and risk assessment documents was considered and rejected
because it would lead to considerable redundancy and because so little
information was available on some of the individual PAHs. As an
alternative, the 16 PAHs were organized at the onset of the work into
three groups, as indicated in Figure 1-1.
The rationale for the organization into these three specific groups
included considerations of materials balance, chemical properties
related to fate and environmental pathways, and health effects, as
described briefly below.
• Naphthalene is the only one of the 16 PAHs with substantial
U.S. commercial production and with a significant potential
for direct exposure to consumers of a commercial product
(mothballs). It is significantly more volatile and mere water
soluble than any other PAH. It was not anticipated to have
carcinogenic effects in humans.
• Anthracene, acenaphthene, fluorene, fluoranthene, phenanthrene
and pyrene are all imported in rather small quantities for
special commercial uses. These compounds are three- and
four-ring PAHs, with moderately low volatility and water
solubility. The question of their possible carcinogenicity
was expected to require careful review. Most of the informa-
tion pertaining to this group is specific to anthracene.
1-1
-------
THE ANTHRACENE GROUP
COIOTO) (OJDJ CQLJO)
Antlnacene Acenaphthene Fluorene
pgi p_[0j
Phenaiulitene Pyrene Fluoranthene
Ben/o (a) pyreno Acenaphlhylene Benz[a) anthracene
Chryscne
(Q)
Benzo[b]fluoranthene
Benzo[fj,h,ij perylenc
uibenz[a.h] anthracene
Benzo[k| fluoranthene
Indeno [ 1,2.3-c.d ] pyi one
FIGURE 1-1 STRUCTURES OF THE PRIORITY POLLUTANT
POLYCYCLIC AROMATIC HYDROCARBONS
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Benzofajpyrene (3aP) and the eight other PAHs in the third
group have no commercial production or use, except as research
««« ouces. t one exception
(acenaphthylene) , the chemicals in this group have very low
vapor pressures and water solubilities. Several of the PMs
tL in^o* M°UP had,beeU ideatified - carcinogens. Much of
the information regarding this group of compounds is for 3aP.
PAHs III SJTJ'* aUd rlSk assessment f°r ««h of the three groups of
3Q (Volum! m a SSParaue Chapter °f 3 ""^volume report] Chapt^
rh. 1 S } C0ncerns naphthalene; Chapter 4.0 (Volume III) concerns
the anthracene group PAHs; and Chapter 5.0 (Volume IV) conceri the
ben2o[a]pyrene group PAHs. These chapters are bound separately
Potential waterborne routes of exposure are the primary focus of
eX°Se ^ ^f areSSffients b— of the emphasis "of oSs on
water-related pathways. Inhalation exposures a-e a^so
"*** t0 ?laCe the v.t.r-r.l.tP.d exposures I«"
the
Information on environmental releases of the subject PAHs
including the form and amounts released and the receiving
medium at the point of entry into the environment (materials
UcU.H.tlCS
• Description of the fate processes thac transform and/or
transport the compounds from the point of release through
environmental media until exposure of humans and other receo-
tors occurs, and a summary of reported concentrations detected
media * envir0nnent ' with a Particular emphasis on aquatic
• Discussion of the available data concerning adverse health
thr?^ ^ rbJeCt PAHS °n humanS' incl^ing (where known)
the doses eliciting those effects and an assessment of the
likely pathways and levels of human exposure;
* ^view of available data concerning adverse effects on aquatic
biota and the levels of environmental exposure; and
1-3
-------
processes. Since most PAH production is inadvertent rather than
deliberate commercial production, the conventional approach of trving to
balance production versus use and environmental release is not strictly
applicable to these chemicals. Therefore, the materials balance sec-
tions or tnese exposure and risk assessments are focused on estimates of
releases from major sources such as combustion; considerable uncertainty
is associated with most of these estimates.
After an initial review of the three exposure and risk assessments
covering all 16 priority pollutant PAHs, it was determined that one
chemical, benzo[a]pyrene, was of appreciably greater interest to OWRS
than were the other 15 compounds studied. This interest reflects the
more extensive data base available for assessment of environmental fate
and exposure and also the existence of some, although limited, dose-
response data to which various extrapolation models can be applied for
estimation of potential human carcinogenic risk from ingest-'on of BaP
For the other PAHs considered, data on carcinogenic or other long-term
effects were generally limited, nonquantitative, and/or did not indicia
statistically positive results. Table 1-1 presents a summarv of th«
hazard of the 16 priority pollutant PAHs in terms of carcinogenicitv,
based on qualitative review of available information.
For these reasons, the technical summary presented in Volume I is
organized somewha_t differently than the rest of the report (Chapter 3.0-5.0)
(Volumes II-IV). The summary is focused on 'benzo[a]pyrene~as the PAH of
greatest interest. The estimated releases to the environment, environ-
mental fate, monitoring data, human effects and exposure, biotic effects
and exposure, and risk considerations concerning"BaP are presented in
expanded summary form. Abbreviated summaries are then provided for
naphthalene, anthracene group PAHs, and the other PAHs considered.
^Included in the summary volume are critical data and references to
the literature so that this volume may be read and understood by itself
without reference to the separately bound Chapters 3.0-5-0. The latter
volumes contain more extensive compilations of data, more detailed
discussions of the available information and of the interpretations
drawn, and more complete documentation of the multiple literature
sources that were reviewed in the course of this work.
1-4
-------
TABLE 1-1. SUMMARY OF EVIDENCE FOR CARCINOGENICITY OF
PRIORITY POLLUTANT PAEs
PAH
Benzo[ajpyrene
Dibenz[a,h]anthracene
Benz[a]anthracene
Benzo[g,h,i]perylene
Benzo[b]fluoranthene
i
Chrysene
Indeno[1,2,3-c,d]pyrene
Pyrene
Fluoranthene
Benzo[k]fluoranthene
Phenanthrene
Basis
Positive oral carcinogen with
other positive carcinogenic
data.
Positive oral carcinogen with
other positive carcinogenic
data.
Positive oral carcinogen with
other positive carcinogenic
data.
Not tested orally, other posi-
tive carcinogenic or co-car-
cinogenic data.
Not tested orally, other posi-
tive carcinogenic or co-car-
cinogenic data.
Not tested orally, other posi-
tive carcinogenic or co-car-
cinogenic data.
Co-carcinogen or initiator
with negative carcinogen or _in
vivo mutagen.
Co-carcinogen or initiator
with negative carcinogen or in
vivo mutagen.
Co-carcinogen or initiator
with negative carcinogen or in_
vivo mutagen.
Negative in a single carcino
genie study.
Several negative carcinogenic
and mutagenic studies but not
tested orallv.
1-5
-------
TABLE 1-1. SUMMARY OF EVIDENCE FOR CARCINOGENICTY OF
PRIORITY POLLUTANT PAHs (Continued)
Anthracene Negative studies, tested
orally.
Naphthalene Negative studies, tested
orally.
*
No data for evaluation of carcinogenicity were available for
acenaphthene, acenaphthylene, or fluorene.
1-6
-------
5.0 BENZOfalPYRENE, ACENAPHTHYLENE. BENZfalANTHRACENE.
BENZOfblFLUORANTHENE. BENZOfklFLUORANTHENE.
BENZOfg.h.ilPERYLENE. CHRYSENE. DIBENZfa.hlANTHRACEyE.
ID£NOfl.2.3-c.dlPYREXF
5.1 MATERIALS BALANCE
5.1.1 Introduction
This section reviews both published and unpublished data concerning
the production, use, and disposal of the benzo[a]pyrene (BaP) group PAHs
in the United States. Information from the available literature has been
reviewed to present an overview of major sources of environmental re-
leases of these compounds. Annotated tables have been included to aid
data evaluation.
The section is organized according to the major categories of the
sources of releases to the environment. Section 5.1.2 describes the
numerous combustion processes that release the BaP group PAHs; Section
5.1.3 discusses contained sources; and Section 5.1.4 describes the
amounts of these compounds in the influents and effluents of Publicly
Owned Treatment Works (POTWs). Section 5.1.5 is a summary of the
materials balance.
5.1.2 Combustion Sources
Combustion is the major source of PAH releases to the environment.
This section estimates releases of BaP group PAHs from residential heating,
fireplaces, cigarettes, coal refuse piles, wildfire, carbon black manu-
facture, gasoline use, and utility boilers; the emission estimates are
summarized in Table 5-1.
5.1.2.1 Residential Coal Combustion
Residential coal combustion is responsible for a significant fraction
of PAH emissions for the compounds in this group. Since residential
heating units are typically not controlled and are relatively inefficient,
they produce large amounts of PAHs. However, the trend in energy utiliz-
ation for home heating sources suggests a rapidly decreasing reliance on
coal. Whereas coal was used for heating in 2.7% of residences in 1970
it was used in only 0.56% in 1977 (Census 1979). (This trend may have'
reversed in more recent years.) Figure 5-1 shows the estimated distri-
bution of residential coal consumption by state. Emissions from
residential coal combustion (see Table 5-1) were estimated from the
emission factors in Appendix A, Table A-l (EPA 1977a) and the 1978 coal
consumption of 8638 x 10J kkg for residential heating use (DOE 1980).
5-1
-------
Oi
Table 5-1. Estimated Air Emission of Benzo[a]pyrene-Group PAHs by Combustion Source, 1973 (kkg)
Primary Auitllary
Residential Residential Residential
Coal good wood
Combustion Fireplaces Heating Heating Cigarettes
«cenaplitli,l(M ja 400 SOO -,
llen|fluoranthene 20 2 4ft SO
HeiuulVJMuoranthene 20 2 40 SO
Urn 3 40 SO neg
ttenia{t]ffreae |0 2 30 40 neg
Chrysene 20 2 SO 70
l»l>Huii(a.h]
-------
E3 > 100,000 metric tons / yr
^§ 10,000 to 100.000 metric ton s / yr
I 1 < 10,000 metric tons / yr
Figure 5-1. Estimated Residential Coal Consumption in 1974 by State (EPA 1977a
5-3
-------
5.1.2.2 Wood
Wood may be burned in homes in fireplaces or in stoves or furnaces
for primary or for auxiliary heating. Estimated PAH emissions from these
sources are listed in Table 5-1. Fireplaces produce smaller amounts
of PAHs per kg of fuel than does wood combustion in primary heating
units; in addition, fireplaces use less wood overall than is consumed
for heating. The amounts of wood burned in fireplaces, for primary
heating and for auxiliary heating in 1977, were 2.9 x 106 kkg,
6.9 x 106 kkg, and 9.2 x 106 kkg, respectively (see Appendix A, Note 1).
Table 5-2 lists the estimated 1976 wood consumption for residential
burning by state (EPA 1980a). The number of homes heated by wood has
increased by more than 50%, from 794,000 in 1970 to 1,239,000 in 1977
(Census 1979).
Emissions of BaP group PAHs from these sources were calculated
using the emission factors presented in Table A-l (Appendix A) and
1977 wood consumption of 6.9 x 106 kkg and 9.2 x 106 kkg for primary
and auxiliary heating, respectively. The emission factors presented
in Table A-l are averages of those for baffled and nonbaffled wood
stoves (EPA 1980a). Total 1977 wood consumption for primary heating
was obtained from the number of housing units that used wood for primary
heat in 1976 and 1977 (912,000 and 1,239,000) and a proportional ex-
trapolation of the estimated 5.1 x 10& kkg of wood burned in 1976 to
6.9 x 10» kkg for 1977 (EPA 198Qa and Census 1979). Total 1977 wood
consumption for auxiliary heating (9.2 x 106 kkg) was extrapolated from
the 1976 estimate of 8.5 x 106 kkg (EPA 1980a) on the basis of the in-
crease in the number of houses with fireplaces (Appendix A, Note 1).
The estimated wood consumption for each state is shown in Table 5-2.
5.1.2.3 Cigarettes
Although cigarette smoking may be the source of a significant PAH
exposure to individuals, it is a small contributor to national PAH
emissions. Cigarette smoking contributes <1 kkg/yr of each of the
BaP group PAHs to the atmosphere.
The emission factors for cigarette smoking, shown in Table A-l,
were used, along with the number of cigarettes produced (616 x 109)
(USDA 1979) in order to determine the amounts of BaP group PAHs emitted.
The emission factors for the BaP group compounds are all from Neff (1979) .
5.1.2.4 Coal Refuse Piles
Coal refuse piles, impoundments, abandoned mines, and outcrops may
burn through the spontaneous combustion of coal. Because of the relatively
poor air supply and uneven heat distribution, this combustion is in-
efficient and, therefore, produces relatively large amounts of"PAHs.
The estimated 52 x 10° kkg of coal in refuse piles (EPA 1978a) produce
5-4
-------
Table 5-2. Estimated Residential Wood Consumption by State,
1976 (kkg)
State Primary heating
A1 abama
Alaska
Arizona
Arkansas
California
Colorado
Connecticut
Delaware
Florida
Georgia
Hawaii
Idaho
111 inois
Indiana
Iowa
Kansas
Kentucky
Louisiana
Maine
Maryland
Massachusetts
Michigan
Minnesota
Mississippi
Missouri
Montana
Nebraska
Nevada
New Hampshire
New Jersey
New Mexico
New York
North Carolina
North Dakota
Ohio
Oklahoma
Oregon
Pennsyl vania
Rhode Island
SouthCarolina
South Dakota
Tennessee
Texas
Utah
Vermont
Virginia
Washington
West Virginia
Wisconsin
Wyoni ng
Total
150,000
50,000
36,000
280,000
190,000
18,000
22,000
5,000
30,000
310,000
1,000
50,000
29,000
58,000
16,000
24,000
190,000
38,000
180,000
47,000
26,000
76,000
110,000
200,000
330,000
60,000
12,000
15,000
57,000
19,000
120,000
150,000
340,000
3,000
47,000
78,000
290,000
120,000
5,000
190,000
20,000
320,000
87,000
11,000
33,000
280,000
210,000
36,000
91,000
10,000
5,100,000
Fireplaces
34,000
5,000
34,000
21,000
360,000
40,000
29,000
5,000
88,000
46,000
12,000
12,000
120,000
58,000
32,000
26,000
32,000
35,000
16,000
39,000
91,000
97,000
43,000
21,000
55,000
12,000
18,000
10,000
13,000
114,000
69,000
290,000
51,000
7,000
120,000
28,000
38,000 '
190,000
15,000
26,000
7,000
41,000
120,000
13,000
7,000
48,000
58,000
18,000
50,000
6,000
2,700,000
Auxil iary Wood
Stoves
360,000
32,000
26,000
100,000
270,000
61,000
140,000
13,000
210,000
220,000
9,000
19,000
260,000
120,000
63,000
56,000
170,000
84,000
4^0,000
94,000
270,000
410,000
360,000
110,000
230,000
18,000
39,000
8,000
340,000
170,000
25,000
370,000
120,000
14,000
250,000
34,000
250,000
280,000
22,000
62,000
16,000
850,000
290,000
25,000
190,000
110,000
390,000
43,000
210,000
9 .000
8,300,000
Source: EPA 198Ca
5-5
-------
the estimated PAH emissions shown in Table 5-1. The emissions do not
account for burning refuse in impoundments or abandoned mines and out-
crops since the quantity of burning coal is impossible to measure or
estimate (EPA 1978a). It is, however, estimated that only 21% of the
mass present in coal refuse piles is burning at any given time (EPA 1978a).
Table 5-3 presents a distribution of burning coal refuse by state. It is
worth noting that Pennsylvania and West Virginia account for 80% of these
fires. Although the emissions were not estimated, the states of Montana,
Wyoming, Colorado, and New Mexico account for 66% of the approximately
400 burning abandoned mines or outcrops.
From the composition of the particulate polycyclic organic matter
(POM) shown in Table A-l, emissions were calculated based upon a refuse
pile volume of 190 x 106 m3 (2i% Of which is estimated to be burning),"
a density of 1.5 kkg/m3, and a POM emission rate of 1.3 x 10~° kg/kkg-hr
(EPA 1978a). Only particulate emissions were analyzed here; and only
preliminary sampling data are presented. Based upon these assumptions,
the emissions are estimated to be less than 1 kkg. Alternatively, NAS
(1972) gives an unsubstantiated estimate of 340 tons/year of BaP from
coal refuse piles.
5.1.2.5 Forest Fires
Forest fires, either intentional or not (wildfire), are a major source
of PAHs. Unfortunately, the estimates of PAHs produced are based on
data that do not adequately cover the range of situations that may be
termed wildfire. PAH production may be very crudely determined by
using estimates of the amount of fuel burned and an emission factor.
The amount of fuel burned (in terms of both fuel per unit area and
total area burned) is for the most part based upon experienced judg-
ments (EPA 1979a). Emissions factors are based upon laboratory
simulations, which do not test the wide range of fuel type and con-
figurations and may not appropriately simulate the fire intensity,
weather conditions, fuel moisture, etc.
Prescribed burning is a controlled form of open burning used in land
management to achieve specific objectives, which include fire hazard
reduction, disease control, and silviculture, among others. An esti-
mated 36 x 10° kkg (dry weight) of fuel are burned annually, not
including agricultural open burning (Pierovich 1978)(see Section 5.1.2
Table 5-4 presents a breakdown of this fuel usage by region; the
estimated emissions for this source are presented in Table 5-1. These
estimates were calculated from the amount of fuel burned and the
emission factors for forest fires shown in Table A-l (McMahon and
Tsoukalas 1977).
5-6
-------
Table 5-3. Coal Refuse Fires
Amount of 33
State Coal Refuse (10 m )
Alabama 11,000
Colorado 12,000
Illinois 5,000
Kentucky 1,600
Maryland 23
Montana 230
Ohio 1,400
Pennsylvania 84,000
Utah 2,100
Virginia 2,800
Washington 2,300
West Virginia 67,000
Totala 190,000
a) Total does not add due to independent rounding
Source: EPA 1978a
5-7
-------
Table 5-4. Estimated Net Total Weights of Fuel Consumed
Annually in Prescription Burning on All Ownerships
Geographic3
region
Alaska
Eastern
Intermountain
Northern
Pacific
Northwest
Pacific
Southwest
Rocky Mountain
Southern
Southwestern
Total of all
regions
Net annual consumption,
(dry wei
Timber harvesting and
land clearing
residues b
Piles or Broadcast
windrows (unpiled)
0.5
0.1 0.3
6.9 0.7
82.7 6.3
50.4 37.0
20.2 8.2
4.9 1.0
0.9 9.9
12.3 8.3
178.9 71.7
10^ metric
Sht)
Naturally
occurring
understory
vegetation
and litter
0.1
0.5
0.2
114.2
0.3
115.3
tons
Total
of all
categories
0.5
0.5
7.6
89.0
87.4
28.9
6.1
125.0
20.9
365.9
a) See Figure 5-2 for states included in each region
b) Includes precommercial thinning residues as follows: Pacific
Southwest and Rocky Mountain, each <0.1 x 105 metric tons;
Southwestern, 1.1 x 105 metric tons.
Source: Pierovich 1978.
5-8
-------
Figure 5-2. Geographic Regions used to Summarize Survey Data Within
the Coterminous States. (Alaska Region also used in
summarization not shown.)
Source: Pierovich 1978
5-9
-------
Land burned by wildfire each year varies considerably in both the
total area burned and the location of specific sites. On the average
9 X JnlO 2 J= X ^6 aCreS) are burned each year> Although in 1976,° '
2 x 10-^ m^ (5 x 10b acres) were burned (Dahl 1980). The largest
area is burned in the Southeastern section of the country, followed
,Z ^e1South' North Central, Pacific, and Rocky Mountain sections
(Dahl 1980). Emissions estimates are shown in Table 5-1.
The emissions factors for prescribed burning and wildfire in Table A-i
(McMahon and Tsoukalas 1977) are averages obtained from six tests on pine
needles, with differing fuel densities used for heading and backing fires;
hence, these factors cannot provide a very accurate basis for nationwide
emissions estimates. The total amount of fuel burned was estimated by
assuming that 10^ m2 (3 x 106 acres) of land were burned on the average
(Dahl 1980), and that the fuel loading was 2 kg consumed dry weight/m2
(based upon estimates by EPA 1978b). Total quantities of BaP group
PAHs emitted from this source are estimated in Table 5-1.
5.1.2.6 Carbon Black
Carbon black is produced primarily by the furnace process, in which a
liquid hydrocarbon feedstock is incompletely pyrolyzed in a refractory-
lined furnace by burning natural gas. The carbon black particles are
recovered in a baghouse after being cooled by water sprays. The carbon
black is then converted to a marketable product. The principal emission
source from carbon black manufacture is baghouse exhaust *as from the
main process vent. PAHs are present both in the vent gas and on the
carbon black itself (see Appendix A, Note 2 and Tables A-l and A-3) .
For the latter reason, carbon black was banned in food, drugs, and cos-
metics in 1976.
Emissions of PAHs from carbon black manufacture are presented in Table
5-1; Table 5-5 lists the location and capacity of carbon black producers. For
the most part, the emissions during production are negligible (i.e.,
<1 kkg/yr). Larger amounts, however, are contained in/on the carbon
black. These are shown in Table A-3.
The primary use for carbon black is in the elastomers used in auto-
mobile tires (65,0, while other elastomeric uses account for 29% (SRI 1979)
The PAHs present on the carbon black are strongly bound to it and, there-
fore, are not likely to be easily separated from it, except by prolonged
extraction (Locati et al. 1979). An estimate of PAH air emissions from
tire wear, presumably associated with carbon black, is discussed in
Note 2 and presented in Table 5-1 (see Appendix A) . PAHs associated
with carbon black that is transferred to road surfaces are presented
in Table A-4. Although this release presents a possible source of
PAHs in runoff, these PAHs are probably tightly bound to the carbon
black particles .
5-10
-------
Table 5-5. Locations and Capacities of Carbon Black Producers
Company ana Location
Annual Capacity 103 kkg
ASHLAND OIL, INC.
Ashlano Chemical Company, division
Carson Black and Synthetic
Rubber Division
Aransas Pass, Texas
Belpre, Ohio
Iberia, Louisiana
Mojave, California
Shamrock, Texas
Total
CABOT CORPORATION
Big Spring, Texas
Franklin, Louisiana
Rampa, Texas
Villa Platte, Louisiana
Waverly, West Virginia
Total
CITIES SERVICE COMPANY
Chemicals Group
Columbian Chemicals, division
Conroe, Texas
El Dorado, Arkansas
Eola, Louisiana
Mojave, California
Moundsville, West Virginia
Nortn Bend, Louisiana
North Bend, Louisiana
Seagraves, Texas
Jlysses, Kansas
Total
CONTINENTAL CARSON COMPANY
(owned oy Continental Oil Company
80* ana *'itco Chemical Corporation,
0%)
J.M.
Sakersfield, California
Phemx City, Alabama
Ponca City, Oklahoma
Sunray, Texas
Westlake, Louisiana
Total
HUBER CORPORATION
Baytown, Texas
Sorger, Texas
Sorger, Texas
Total
PHILLIPS PETROLEUM COMPANY
Rubber Chemicals Division
Sorger, Texas
Orange, Texas
Toledo, Ohio
Total
SID RICHARDSON CARBON COMPANY
Addis, Louisiana
Sig Spring, Texas
Total
74
45
120
30
50
320"
110
100
24
110
74
420
7
32
24
71
71
25
40
_23
370
TOTAL
35
23
61
43
55
217
117
62
19
198
130
61
39
230
46
54
96
1,350
Totals may not add aue to rounding
Source: SSI 1980.
5-11
-------
5.1.2.7 Agricultural Open Burning
Agricultural open burning involves burning of crop residues for residue
removal, field sanitation, or preparation of farmlands for cultivation.
Wastes that may be burned include a wide variety of residues, including
rice straw, orchard prunings, potato vines, and bagasse, among others
Although PAH formation is dependent upon fuel type, among the many other
variables, the emissions in Table 5-1 were calculated based upon wood
burning (forest fire; see Table A-l, Appendix A), and an estimated
total of 13 x 10 kkg dry weight of burned material (EPA 1977b).
Table 5-6 lists the estimated distribution of open burning by state.
5.1.2.8 Motor Vehicles
Motor vehicles that burn gasoline are ubiquitous sources of PAHs, al-
though emissions control devices for hydrocarbons in exhaust gas and from
the crankcase reduce the amount emitted at efficiencies up to 99% (Gross 1977}
PAHs released by motor vehicles are either emitted in the exhaust or
dumped along with the used crankcase oil. Estimated PAH emissions from
exhaust gas are presented in Table 5-1 (see Appendix .A, Note 3) .
Although crankcase controls reduce hydrocarbon emissions from the vehicle
PAHs still reside in the crankcase oil and may be released to either land'
or water if the oil is disposed of haphazardly. Table 5-7 presents estimates
of the PAHs contained in these releases. (See Appendix As Note 3 and Table A-5,
5.1.2.9 Incinerators
PAH releases from municipal and commercial incinerators are estimated
to be negligible (<1 kkg/yr). Releases were calculated for municipal
incinerators using the release factors in Table A-6 (Davies 1976) for 104
plants with an average capacity of 385 kkg/day when operating at full
capacity (EPA 1978b).
Releases for commercial incinerators were assumed to be similar to
those from municipal incinerators. Even when the higher emission factors in
Table .A-6 are used, calculated emissions of any given PAH were ne»li-
gible without controls. The incinerators were assumed to number 100 000
units, firing 3 hours/day, 260 days/year at an average capacity of 0.1 kkg/hr
(EPA 1978b).
5-12
-------
Table 5-6. Distribution of Agricultural Open Burning, 1973
State
Alabama
Arizona
Arkansas
California
Colorado
Delaware
Florida
Georgia
Hawaii
Idaho
Kansas
Kentucky
Louisiana
Maine
Maryl and
Massachusetts
Michigan
Minnesota
Mississippi
Missouri
Montana
Nebraska
Nevada
New Mexico
North Carolina
North Dakota
Ohio
Oklahoma
Oregon
Pennsylvania
South Carolina
South Dakota
Tennessee
Virginia
Washington
Wisconsin
Wyoming
National Total
Area burned
10 7 m2/yr
36.
4.5
26.
309.
32.
0.1
109.
39.5
44.7
4.8
243.
13.
142.
15.
0.6
0.6
21.
61.2
138.
40.5
34.
67.6
0.8
0.5
138.
97.
32.
36.
107.
15.
8.
59.
14.
9.5
57.
32.
7.3
1995.
Amount of crop
residue burned
103 kkg/yr
161
20
115
2,075
143
2
1,716
883
1,175
22
544
58
1,904
33
7
3
93
274
617
181
152
303
5
2
619
438
142
161
479
69
38
265
61
43
256
145
34
13,238
Source: EPA 1977b.
5-13
-------
Table 5-7. BaP Group PAHs Discharged Annually in Used Crankcase Oil (kkg)
PAH Discharge
Benzo[a]anthracene 2
Benzo[k]fl uoranthene 3
Benzo[ghi]perylene 3 ,
Benzo[a]pyrene negD
Chrysene 2
a) Releases gc presumably to POTWs and landfills. No recycling
is assumed.
b) Negligible is <1 kkg.
Source: Peake and Parker 1980 and Tanacredi 1977.
See Note 3, Appendix A. '
5-14
-------
5.1.2.10 Coal- and Oil-fired Utility Boilers
Table 5-1 summarizes PAH emissions from coal- and oil-fired utility
boiler units. The estimates of total PAHs released to the environment '
are based upon the emission factors averaged from Table A -7 and a
total coal and oil consumption for electricity generation of 4.8 x 108
and 7.8 x 10' kkg per year, respectively (Monthly Energy Review 1980).
These emissions are uncontrolled releases calculated from 1967 emis-
sions factors, and are probably lower today with the use of baghouses or
electrostatic precipitator units. Further, the emission factors for oil
are for small- or intermediate-sized units, and thus serve as an upper
limit of the PAH releases from higher capacity plants.
5.1.2.11 Utility and Industrial Internal Combustion Engines
Stationary internal combusion engines are used for electricity gen-
eration, oil and gas transmission, natural gas processing, and oil and
gas production and exploration. These engines are either gas turbines
or reciprocating engines and are fueled with either oil or gas. Table
5-1 presents the estimated amount of PAHs emitted from these sources in
1978 as estimated by EPA (1979d) .
5.1.2.12 Gas- and Oil-fired Residential Heating
Table 5-1 lists PAH emissions from oil-fired residential heating units
as estimated by EPA (1979e). Although a large fraction of residences'
provide space heat with gas, gas-fired units emit negligible amounts of
PAHs. Figure 5-3 presents the geographic distribution of oil and gas
used for residential heating in 1975 (EPA 1979e).
5.1.3 Contained Sources
This section presents information, primarily in tabular format, on sources
of BaP group PAHs from which these compounds are not specifically isolated.
Delineation of all such "inadvertent sources" of PAH releases is indeed a
monumental task because of the omipresent nature of petroleum- and
coal-derived oils, fuels or solvents that contain at least small amounts
of PAHs. The major sources discussed here are summarized in two tables:
Coal Tar Production and Distillation (Table 5-8) and Petroleum Sources
(Table 5-9); supporting data and related information are presented in
Tables 5-10 and 5-11 and Appendix A.
It is important to comment on the quality of available data in this sec-
tion. Specifically, concentrations of the various PAHs in crude oils "coal or
coal and petroleum products are highly variable, depending upon the geo-
graphic source and method of processing. Furthermore, as subsequent°cal-
culations are based on these concentrations, they can be considered as
estimates only, at the order of magnitude level of reliability.
5-15
-------
HI*
Cn
I
M
CT>
*-T KUHTM HHTHAL
CAS I2»J
OIL «OJ
OIMIH J2 MIOOLC All Aril iC
aouTH CtHTHAL OIL i»
CAS S»J OTHtH iT
OIL i
6A5 381
OIL 10*
OTHfM T
OTIItH »
Figure 5-3. Geocjy^aphical Oistribution of Residential Fuel ConsuinpLion for Space Heating, 1975, 10lb J/yr (EPA 1979e)
-------
Table 5-8. PAH Materials Balance: Coal Tar Production and Distillation, 1978 (kkg/yr)a
Ln
I
Tar Used By Producers - Sold for Refining
Production Refining/ fuel Others Quantity On Hano
Topping Dec. 31
Acenaph-tWt^t. Ood»\a avjaLVo.v.iO
Benzo(a)anthracene ntit. }
Benzo(a)pyrene *~n ig 13 1.3, qq i».i.
Chrysene. ic^^ooo ^MOQ \*7c& i^o 3noo ff<*o
Indenopyrenes (^no A*\OL. cvx>aUo.to»t>)
Total
Coal -Tar
Pitch c
8
8
8
Total
Environmental Releases
Coal -Tar AirfLand Water f
Creosote
OiH
9
/ 1
Q °'4
^o" 0
-------
Table 5-9. PAIIs in Contained Petroleum Sources, (kkg/yr)a
I
M
00
PAH
Acenaphthylene
tlenzo[a]anthracene
Ben/o[b]f 1 uoranthene
Benzo[k]fl uoranthene
Benzo[ghi ]peryl ene
Benzo[a]pyrene
Chrysene
Diben/o[a,h]anthracene
Ideno[l ,2,3-cd]pyrene
Crude Oild
340,000
trace
<4,200
<4 ,200
17
840
<84 ,000
Inputb
Gasoline6
250
170
170
170
Environmental l(eleasesc
Diesel Fuelf
3
0.9
2
20
Oil Spills
Water
10
neg
(ieg
neg
neg
neg
3
Land
neg 9
neg
neg
neg
neg
neg
neg
neg
neg
Gasoline
Water
neg
neg
neg
neg
Petroleum
Spills Refinery Wastes
Land Airh Water Land
neg
neg 5
neg 3 neg
neg
a) Blanks indicate data not available.
b) See Table A- 11 for PAH concentrations.
c) See Appendix A., Note 4, for derivations
d) Based on 8.4 x 10° kkg of crude oil consumed (Guerin 1978).
e) Based on 7.4 x 106 bbl/day consumed (Oil and Gas Journal 1979); 42 gal/bbl; 0.73 kg/1.
f) Based on 3.4 x 1010 1/yr; 0.865 kg/1.
g) Less than one kkg.
h) Based on data in Table A-13, 4.985 x 106 bbl/day feed for catalytic cracking, 0.887 x 106 bbl/day for catalytic
hydrocracking (Oil and Gas Journal 1979), 42 gal/bbl.
-------
Table 5-10. PAH Emissions: Coke-Oven Doors
Emission Rate
(mg/hr/oven)a
Yearly Emission
(kkg/yr)b
Chrysene
Indenopyrene
Benzoperylene
Benzopyrene
16
6
6
16
1.0
0.4
0.4
1.0
Total
3.0
a) EPA 1977e
b) Based on 1300 kkg coke produced per typical coke oven battery of 58
ovens; 160,000 kkg/day typical capacity for total by-product coke-
making industry (resulting in a total of 123 batteries); 365 day,
24 hour operation; emission data in first column, EPA 1979f.
5-19
-------
Table 5-11. Water Discharges of Benzo[a]pyrene Group PAHs: Timber Products, 1978 (kkg/yr)'
Ul
I
PAH
Acenaphthylene
Benzo[a]anthracene
Benzo[b]f 1 uoranthene
Benzo[k]fl uoranthene
Benzo[ghi ]peryl ene
Benzo[a]pyrene
Chrysene
Dibenzo[a,h]anthracene
In«Jeno[l ,2,3-cd]pyrene
Input
6,900
neg
neg
neg
neg
neg
0.4
neg
neg
Raw
Discharge
Concentration Quantity^
(mg/£)
0.68
0.85
0.39
0.45
0.05
0.36
0.69
0.007
0.18
5
6
3
3
neg
2
5
neg
1
Treated
Concentration
(mg/t)
0 05
0.43
0.31
0.03
0.01
0.04
0.90
ND
0.02
Discharge
Quantity11
npn
3
2
npu
neg
neg
npd
neg
neg
a) See Table 5-8, coal-tar creosote.
b) Based on 56# of 476 total plants using creosote or mixture thereof, 350 day/yr,
75,500 liters/day/plant, assumed to go to POTU.
Source: CPA, 1979J.
-------
5.1.3.1 Coal Tar
Coal tar is the heavy distillate fraction from the destructive distil-
lation (coking) of coal. The distribution of coke-oven tar production
in the U.S., PAH concentrations, and environmental releases (Tables 5-10.
A-8, and A-9) have been combined to provide the information
presented in Table 5-8. Naphthalene (see Section 3.1), present in the
largest concentration in coal tar, is the only PAH compound warranting
recovery and isolation in large amounts. Anthracene is also isolated,
but to a lesser extent and usually in crystals which form during cre-
osote oil recovery (see Section 4.1). Creosote oil is used in the wood
preserving industry. Information on PAH concentrations in creosote oil
and wastewater discharges during use are presented in the previously
mentioned tables and Table 5-11, respectively. Of a total of 224 wood
preserving plants responding to EPA's data collection protocol, two
reported direct discharge, 47 reported discharge to POTWs and the re-
mainder reported self-contained no-discharge operations (mostly evapo-
ration with some oil irrigation or treated effluent recycle; EPA 1979g).
i
Besides creosote, other principal tar products containing PAHs are
pitch and refined tar, used in a variety of applications ranging from road
materials and electrodes to shampoos. Coal tar and tar products are
also used as fuel (see Table 5-8), either by producers (e.g., iron and
steel plants) or distillers.
5.1.3.2 Petroleum Sources
The other fossil fuel source containing appreciable amounts of PAHs
is petroleum. The concentration and emissions data in Appendix Tables A-ll,
A-12 and A-13 have been combined for use in the summary Table 5-9.
Only spills and petroleum refinery environmental releases are presented
here; gasoline combustion has been covered in Section 5.2.1 with other
combustion sources. As mentioned previously, the type of crude feed-
stock determines its chemical composition and, therefore, the composition
of specific waste streams. Other variables include pollution controls,
age of the processes used (level of technology), and operational practices
and control. It has been estimated that a total of 0.1 kkg benzo[a]pyrene
is released in solid waste streams industry-wide from petroleum refining
(EPA 1976). The air emissions also listed in Table 5-9 are specifically
from petroleum catalytic cracking, which accounts for over 50% of the
annual oil feed to refineries (Oil and Gas Journal 1979); the remainder
is used for catalytic reforming, for which emissions factors were
not available.
5.1.4 Publicly-Owned Treatment Works
Input of PAHs to POTWs is largely dependent upon variations in indus-
trial discharges feeding the POTWs and the types of industry in a particular
municipality. A recent EPA study of 20 urban POTW facilities with secondary
treatment and varying feed conditions produced a materials balance of P4Hs
shown in Table 5-12.
5-21
-------
Table 5-12. Materials Balance of Benzo[a]pyrene Group PAHs: Municipal POTWs (kkg/yr
Environmental Releases
PAH Inputb ATrc Waterd Land6
^(
Chrysene
Indeno[l ,2,3-c,d]pyrene
Benzo[ajpyrene
Benzo[b]fl uoranthene
Benzo[k]f 1 uoranthene
Benzo[ghi]perylene
Dibenzo[a,h]anthracene
Benzo[a]anthracene
Acenaphthylene
7.3
3.7
3.7
3.7
3.7
11
3.7
7.3
ND
MA
3.7
3.7
0.7
3.7
11
3.7
NA
NA
3.7
ND^
UD
ND
ND
ND
ND
3.7
3.7
9 1
negh
neq
3
neg
neg
neg
9.1
neg
a) All values rounded to two significant figures.
b) Based on influent concentrations shown in Table 5-13,
liters per day total POTW flow.
c) Difference between input and water and land.
d) Based on secondary effluent concentrations shown in Table 5-13,
101! I/day total POTW flow.
e) Based on wet sludge concentrations shown in Table 5-13,
6x10° metric tons dry sludge generated/yr, wet sludge 95*
water (by weight).
f) Not available.
g) Not detected.
h) <1 kkg.
5-22
-------
Table. 5-13. PAH Concentrations in Municipal POTWs (yg/1)
PAH
Acenaphthylene
Benzo[a]anthracene
Benzo[b]f 1 uoranthene
Benzo[k]fl uoranthene
Benzo[ghi]perylene
Benzo[a]pyrene
Chrysene
Dibenzo[a,h]anthracene
Indeno[l ,2,3-c,d]pyrene
Infl uent
ND
0.2
0.1
0.1
0.3
0.1
0.2
0.1
0.1
2° Effluent
0.1
0.1
ND
ND
ND
ND
0.1
ND
ND
Raw SI udge
3
76
25
2.5
0.6
3.9
76
0.2
0.2
a) Average values.
Source: EPA 1980d
5-23
-------
The materials balance in Table 5-12 was constructed using a total
POTW flow of approximately 1011 I/day (EPA 1978c) and the average concen-
trations of the various PAHs in influent, effluent and sludge, presented
in Table 5-13. For purposes of these calculations, influent and effluent
flow rates are assumed to be equal, i.e., water losses from sludge removal
and evaporation are small compared with influent flows. With these assump-
tions, an estimated 70 kkg of PAHs were discharged to water from POTWs in
1978, while there was an input of 590 kkg in influent. Of aquatic releases
from POTWs, 11 kkg are attributed to BaP group PAHs.
PAHs discharged in sludge can be estimated from the PAH concentrations
in sludge and the quantity of dry sludge produced annually: 6.0 x 106 kkg
(EPA 1979i). Wet sludge is assumed to be 95% water by weight. As ocean
dumping of sludge is mandated to cease by 1981, and if one assumes that
more stringent air quality standards curb incinerator use (EPA 1979j) ,
the 25 kkg of the BaP group of PAHs contained in sludge are assumed to be
discharged to land.
PAHs released to the atmosphere were estimated by the difference
from the above calculations (influent loading - effluent and sludge
loading). On this basis, an estimated 30 kkg of these PAHs were released to
the atmosphere from POTWs in 1978.
5.1.5 Summarv
As shown in Table 5-14, the largest amount, 96% (2700 kkg) of the
Of tLr^eaS\S °f BaP.gr°U? PAHs <2800 kk§>' is emitted to the atmosphere.
.
r u emissions> Combustion (Table 5-1) is the source of
of Jf trl i Sr°UP PAHS released' Of the various compounds, relea.es
of acenaphthylene are much greater than the other PAHs in this ^roup .
Aquatic discharges that have been identified (37 kkg total) are chiefly
the result of oil/gas spills and POTWs (Tables 5-9 and 5-12, respectively)
£ t0 C°al tar Production
5-24
-------
Tcible 5-14. Estimated Environmental Releases of BaP Group PAHs (kkg/yr) (Continued)
I
to
Chrysene
combustion3
crankcase oil disposal
coal tar production
contained petroleum sources'
timber products
tire wear
POTW
Total :
Dibenzo[a,h]anthracene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
PO'l W
Total :
Indeno[l,2,3-c,d]pyrene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
POTW
Total :
Air
340
3
Water
340
40
Land
1
2
neg
_
10
Surface
3
3
_4
10
POTW
1
2
neg
40
130
neg
1
130"
neg
neg
neg
neg
neg
neg
neg
neg
2
necj
1
neg
neg
neg
Total
340
2
10
3
neg
Jl
370
40
neg
neg
40
130
neg
neg
neg
2
T30"
-------
5.2 FATE AND DISTRIBUTION IN THE ENVIRONMENT
5.2.1 Introduction
This section describes the fate processes that determine the
ultimate distribution of 3aP and the other related PAHs in the aquatic
environment and, therefore, the opportunities for water-borne exposure
to humans and other biota. Much of the information presented pertains
specifically to BaP; however, since the properties and fate characteris-
tics of this compound are similar to those of the other compounds
in the group, the behavior of BaP in the environment is believed to be
a good model. In addition, some information concerning benz[a]anthracene
is presented from a major study of the fate of organics in the en-
vironment (Smith et_ al. 1978) .
Section 5.2.2 presents an overview of the environmental loading of
BaP to the aquatic media, both direct releases to surface water and
deposition from the atmosphere. In Section 5.2.3, physical/chemical
properties of the BaP group PAHs are summarized in order to identify
the processes that transform and transport the chemical upon its release
to the environment (Section 5.2.3.1). Section 5.2.3.2 discusses the
interplay of fate processes that determines the major pathways of BaP
in aquatic environmental media.
Modelling efforts were undertaken based upon environmental loadings
estimated in Section 5.1, in order to characterize the fate and distri-
bution of BaP in specific environmental scenarios; these are discussed
in Section 5.2.3.3. Monitoring data from STORET and a limited number of
other surveys are summarized in Section 5.2.4 to provide indications of
concentrations of_BaP group PAHs actually detected in aquatic media.
Finally, Section 5.2.5 summarizes those aspects of the fate and ultimate
environmental distribution of BaP having the greatest significance for
the water-born exposure of humans and other biota.
5.2.2 Inputs to Aquatic Media,
5.2.2.1 Atmospheric Deposition
Data presented in Section 5.1 indicate that direct releases of BaP
to surface waters are negligible; atmospheric emissions of BaP from
combustion sources were estimated to be approximately 173 kkg in 1978
(Section 5.1). Atmospheric BaP may be transported to the aquatic
environment indirectly via wet and/or dry deposition. These physical
removal mechanisms are expected to be significant for BaP; Cupitt (1980)
suggests an atmospheric residence time (time required for BaP to be
reduced to 1/e of its original value) of approximately 8 days.
The air-to-surface transport pathway has been evaluated for BaP and
is detailed in Appendix B; the results of that analysis are summarized
in Table 5-15. Under ambient conditions in either rural or urban areas,
virtually all of the BaP is adsorbed onto aerosols. The deposition
5-28
-------
Table 5-14. Estimated Environmental Releases of BaP Group PAMs (kkg/yr)
01
i
Aceritiphthylene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources6
timber products
tire wear
POTW
Total:
Benzo[a]anthracene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
POTW
Total:
Benzo[b]fluoranthene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
POTW
Total:
a)
b)
c)
d)
See Table 5-1.
See Table 5-7.
Blanks mean data not available;
neg means <1.
See Table 5-8.
Air
930
9
940'
210
1
210
Land
c
10
neg
Water
Surface
10
10
POTW
10
neg
Total
930
40
10
10
neg
_
"20
neg
neg
neg
10
_
980
340
1
340"
1
2
neg
9
10
2
neg
4
6
1
2
3
6
340
2
7
neg
3
13
360
210
_
"220
e) See Table 5-9.
f) See Table 5-11.
g) See Table A-4, air releases included in combustion
h) See Table 5-12.
-------
Table 5-1/1. Estimated Environmental Releases of BaP Group PAIIs (kkg/yr) (Continued)
Ul
I
Benzo[k]fluoranthene
combustion9 .
crarikcase oil disposal
coal tar production
contained petroleum sources'
timber products
tire wear
POTW
Total :
Benzo[ghi]perylene
combust ion
crarikcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
POTW
Total:
Benzo[a]pyrene
combustion
crankcase oil disposal
coal tar production
contained petroleum sources
timber products
tire wear
POTW
Total :
Air
210
_
210
310
160
2
3
1
_4
170
Land
1.5
neg
Pig.
2
1.5
neg
5
8
11
330
neg
7
neg_
9
neg
6.6
neg
1
burl
*
neg
m
neg
neg
neg
neg
0.
neg
neg
1
Water
ace POTW
1.5
neg
2
1.5
neg
2
neg
9 0.7
neg
1
Total
210
3
neg
neg
4
220
310
3
neg
5
neq
15
11
340
160
neg
4
3
neg
2
4
170
-------
TABLE 5-15. EVALUATION OF AIR-TO-SURFACE PATHWAY
FOR BENZO[a]PYRENE
Adsorbed fraction of
airborne mass
Rural
0.99
Urban
Dry deposition Velocity
(cm/sec)
Precipitation scavenging
ratio:
/ng/1 (water )\
Ug/m3 (air) I
6x10'
6xl04-1.2xlO:)a
Percent of atmospheric
emissions deposited
- dry deposition
- wet deposition
- total
22
4
26
19
4-7
23-26
aDepends on distance from combustion source.
5-29
-------
parameters for BaP vary only slightly from rural to urban environments,
since they are highly dependent upon vapor/aerosol partitioning. As
shown in Table 5-15, approximately 26% of atmospheric BaP will be
deposited on the surface. The analysis indicates that dry deposition
of BaP adsorbed onto atmospheric aerosols accounts for most of the re-
moval; wet deposition is less significant by a factor of from three to
five, depending upon the extent of equilibrium achieved in the combustion
plume.
On the basis of total annual atmospheric emissions of 170 kkg for 1978
(Section 5.1), approximately 44 kkg may have been deposited on the surface
of the U.S. Some of the fallout will land on surface waters. If approxi-
mately 2% of the total area of the continental U.S. is surface water (U.S.
Bureau of the Census 1980), direct deposition onto aquatic systems would
have amounted to less than 1 kkg.
A fraction of the remaining fallout deposited on land would be
transported ultimately to aquatic systems via surface runoff. Data
cited by Neff (1979) suggest that 500 kkg/yr of BaP are deposited on
surface waters worldwide (including oceans) and that 118 kkg/yr end
up in aquatic systems via surface runoff. These ratios indicate that
surface runoff would deposit much less than 1 kkg of BaP in U.S. waters
each year. The local effects of surface runoff, especially near combustion
sources, could still be significant. The BaP adsorbed to surface particles
is tightly bound and would probably be carried along with these particles
in runoff. However, there are insufficient data to estimate the importance
of this pathway.
5.2.2.2 Source Identification by PAH Composition
Sediments have an integrating effect on patterns of PAH input over
time and supply geographical information when current patterns, sediment
origins, and settling rates are known (Dunn and Stich 1976). It should,
however, be mentioned that the composition in sediment does not always
directly reflect the original PAH composition at the source. Partitioning
between the sediment and aqueous phases may be different for parent PAHs
and alkylated PAHs within an aromatic series, since solubility in water
decreases as the number of alkyl carbons increases (Armstrong et al.
1977).
Information on whether the origin of PAHs in water is atmospheric
deposition from combustion sources or direct discharge can be gained
from studying the PAH composition in the sediments. The extent of
alkylation of PAH mixtures has been shown to be highly dependent upon
the combustion temperatures (Bluiaer 1976) . The number of alkyl carbons
on PAHs formed during combustion of fuel (400°C-2000°C) is generally
0-2; at the low temperatures at which petroleum was formed over geologic
time (100°C-150°C), PAHs with 2-4 alkyl carbons are most common
(Figure 5-4) .
5-30
-------
Ui
OJ
60 2 4 60 2 4 60
NUMBER OF ALKYL CARBONS ON AROMATIC RINGS
HIGH TEMPERATURE
(-2,000' C.)
MEDIUM TEMPERATURE
(-800*-400* C.)
LOW TEMPERATURE
(-150--10CTC.)
Source: Blumcr (1976)
FIGURE 5-4
EFFECT OF COMBUSTION TEMPERATURE ON RELATIVE
ABUNDANCE OF ALKYL CARBON ATOMS ON PRODUCED
POLYNUCLEAR AROMATIC HYDROCARBONS
-------
Furthermore, it has been reported that the distribution of homologs
in PAHs measured in soils and marine sediments varies little over a wide
range of depositional environments. Homologs extending to at least seven
alkyl carbons occurred in all samples and all PAH series. However,
within a PAH series, the unsubstituted hydrocarbons were the most abun-
dant with the intensities of isomeric homologs, decreasing nearly two-
fold with each additional carbon atom (Blumer and Youngblood 1975). In
one study of PAH composition of sediment, a semilog plot of abundance
vs. number of alkyl carbons was found to produce a straight line with a
highly negative slope (Hase and Hites 1977). These data are presented
in Figure 5-5, along with similar measurements for river water and air
particulates. The authors postulated that the steep slope characteristic
of urban air particulates was changed to the more gradual slope of the
sediments due to the differential solubilities and partitionings of
parent PAHs and their alkyl homologs. After airborne particulates are
deposited on soil or water, the lower homologs continuously fractionate
into the water phase, thereby increasing the relative abundance of the
alkylated species in the sediment. The slope of the airborne particulate
plot is intermediate between those of water and sediment, and this led
the authors to the conclusion that the main source of the aquatic load
of PAHs is anthropogenic, airborne PAHs produced during combustion.
It should be noted that industrial effluents containing PAHs would
undergo similar fractionation (Lewis 1975, Armstrong _et _al. 1977). PAH
profiles from petroleum sources show that parent compounds of each series
are less abundant than the alkylated forms. The fact that the unsubsti-
tuted PAHs are the most abundant homolog (despite higher aqueous solu-
bility) in sediment from non-industrial areas further indicates that the
major source of PAHs in sediment is generally a combustion source rather
than direct contamination by fossil fuels. Sediment known to be
contaminated with fossil fuels exhibited an elevated concentration of
four- and five-ring PAHs (due to lower water solubility) similar to that
in the uncontaminated sediments, but also contained a much higher
proportion of alkylated compounds (Youngblood and Blumer 1975).
5.2.3 Environmental Fate
5.2.3.1 Basic Physical/chemical Properties
The physical/chemical properties that are relevant to the fate and
distribution of the BaP group PAHs are summarized in Table 5-16. The
properties of all of these PAHs, exclusive of acenaphthylene, are quite
similar; the properties of acenaphthylene more closely resemble the
compounds discussed in Chapters 3.0 and 4.0 of this report.
5.2.3.2 Pathways in the Aquatic Environment
This section examines the details of the fate pathways of BaP in
the aquatic environment. The major processes for removal from the water
5-32
-------
10,000 :
3000
Q
1000
300
100
I
WATER
14 IS 14 17
CARBON NUMBER
B
10,000
u 3000
o
1000
300
|_ RIVER
WATER
16
17
RIVER —
SEDIMENT:
\ AIR PARTICIPATES •
IS
19
20
CARBON NUMBER
Source: Hase and Hites (1977).
Note: Data are normalized such that the unsubstituted species is 10,000 units in each case; A-pyrene,
B-phenanthrene.
FIGURE 5-5 DISTRIBUTION OF ALKYL HOMOLOGS IN THE PHENANTHRENE-TYPE SERIES
AND PYRENE-TYPE SERIES IN RIVER WATER, AND AIR - CHARLES RIVER,
BOSTON, MA
5-33
-------
TAHI.K 5-16. BASIC I'HYblCAL/CIUMlCAL PUOPIJtriES OF bKN?.(j{u)l'VKL,li; CRIxlP Mils
"B K(|t , 25*C
ioust jut at 25
(uim M Vi*ul«->
i (pyrene Acenjptttliyletie
f luur.inlliene
l>«ryU-iie Chryaeae
Aliblt^v t JL tun BdP
** ~ BjA
'"r""la C2« "12 C12 "8 C,8 B,2
"" 2M.W- 152. 2. c „,.„'
"•I"., r,. CO m" ,J2b lM_ii/h
u.,ui,,K ft. Cc)
5xlO-9(20'C)lv lo-J-102(2o*C)h SxlU'1'(2U>i:)h
W«l«r S.,l,J,lllly 0.0038s 3.9jb 0 005 7(211* )''
0.00911
I«K *.„, 25'c 6.0Ba 3.7?" 5.bla-1'
»"' "kF »8.l«.lPr CHr dB.hA U.2.1-c.d|-
C20 H12 C2« «12 C22 "12 C18 "l2 C22 II, t
«2.32C 252.32' 276. 3«c 22g.28c 278.36° 276. J4C
I67-16B1' 2l7b J22b 256>> 270b |6^ s-lo*1'
ixlO-'l>.1.1 <£l j|. (Wl)
(19/41.
-------
column are reviewed first, i.e., volatilization and sedimentation; the
transformation and degradation pathways for BaP in solution are then
described. Finally, biodegradation and its role in determining the
ultimate fate of PAHs, especially in sediment, are considered.
Volatilization
Benzo[a]pyrene has a vapor pressure of 5 x 10 torr at 25°C and a
Henry's law constant of 4.8 x 10" ^ mQ — , and these properties suggest
that volatilization will not be an important pathway for this compound
in the environment. When the role of volatilization in removing BaP and
benzo [a] anthracene from the aquatic environment was studied, these two
high-molecular-weight PAHs were not rapidly volatilized. With maximum
wind (4 m/sec) and current velocity (1 m/sec) , half-lives due to vola-
tilization were 150 hours for benzo [a] anthracene and 430 hours for BaP,
compared with 3.2 hours for naphthalene and 16 hours for anthracene
(Southworth 1979). The variability of volatilization was also examined;
for both of these PAHs, a ten-fold increase in current velocity roughly
doubled volatilization, while a ten-fold increase in wind velocity
increased volatilization five-fold. These larger PAHs appear to be much
less sensitive to changes in current velocity and slightly more sensi-
tive to wind velocity changes when compared with lower-molecular
weight PAHs.
In a separate study of the environmental fate of these PAHs, the
volatilization half-lives were determined to be 89 hours for benz[a]an-
thracene and 22 hours for BaP under conditions of rapid stirring
(Smith et_ al. 1978). In the same study, volatilization half-lives were
calculated using a one-compartment model:
Volatilization Half-life (hours)
River Eutrophic Eutrophic Oligotrophic
Pond Lake Lake
benzo[a]pyrene 140 350 700 700
benz[a]anthracene 1000 1000 1000 1000
For these compounds, volatilization is a slow process in comparison with
the degradation pathways, such as photolysis, discussed below. Further-
more, most of these larger PAHs will be found sorbed onto sediment, and
volatilization of sorbed material is presumed to be very slow
(Smith et_ _al. 1978). Another study of fate and transport of radio-
labeled BaP, conducted in a laboratory model ecosystem (Lu ej: al. 1977)
failed to detect any radioactivity in traps; this supports the premise
that volatilization is not a significant fate process for BaP.
5-35
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As shown in Section 5.2.3.1, most of the other PAHs in this group
exhibit vapor pressures and Henry's law constants that are fairly close
to those for BaP and benzo[a]anthracene and would be expected to act
similarly with respect to volatilization. Acenaphthylene, on the other
hand, will volatilize more rapidly as indicated by its vapor pressure
and Henry's law constant.
Adsorption, Sedimentation, and Solubilization
Partition coefficient and solubility data suggest that BaP in the
aquatic environment is likely to be adsorbed onto sediment and biota.
Concentrations (in rivers, ponds and lakes) predicted from a one-
compartment model show that the expected concentrations of BaP and
benzo[a]anthracene on sediments and suspended solids are greater than
the dissolved concentrations by a factor of more than 10^ (Smith et al.
1978). This is expected since the partition coefficients for all of the
PAHs in this group range from 5.61 to 7.66, with the exception of
acenaphthylene at 3.72.
The patterns of buildup and decline of BaP in pond, river,iand lake
simulations were also analyzed by Smith et al. (1978). These predictions are
shown in Figure 5-6 for a river system. In all aquatic systems modeled,
the concentrations of dissolved BaP rapidly approached steady-state
before and after the discharge ceased; sediment concentrations changed
very slowly (see Figure 5-6). Cessation of the discharge was shown to
cause a 100-1000-fold decrease in dissolved BaP concentrations (solution).
Continuous desorption from sediments is sufficient to maintain a low
concentration of BaP in the water column, roughly equal to the background
level in groundwaters (Suess 1976, Andelman and Snodgrass 1974). The
authors obtained similar results in modeling of benzo[a~!anthracene
(Smith et _al. 1978).
BaP sorption onto sediments was shown to be strongly cor-
related with the organic carbon content of the sediment and not
related to the cation exchange capacity (Smith jit al. 1978). Since
calcium montmorillonite clay (0.06% carbon) displayed some affinity for
BaP, it seems likely that BaP sorption involves weak interaction with
solid surfaces, as well as strong binding to organic matter. Sorption
onto bacterial cells was also investigated, and very high sorption
coefficients were obtained. These results are in agreement with other
data indicating that PAHs will preferentially sorb onto organic and
biological material (Southworth 1977). Sorbent data and partition
coefficients for BaP are presented in Table 5-17.
It appears that very little of the BaP in aquatic systems will be
found in solution, and this compound can be expected to accumulate in the
sediments of placid lakes and reservoirs. River-borne BaP, however,
will be transported to the ocean, where inshore and alongshore currents
combine to restrict suspended matter to continental areas and spread
the PAHs almost uniformly along the coastal regions. In these areas,
continuous resuspension and transport via wave action and currents have
5-36
-------
8 x 10 e—^. L. -* jsmj—jrvu
- .**£~^-f=>— — -
1 =-
a * 10
•» -
0123
Source: Smith et al. (1978).
10
FIGURE 5-6 RESULTS OF MODELING OF THE EFFECT OF SUSPENDED SOLIDS
ON THE CONCENTRATION OF BENZOla] PYRENE IN A PARTIALLY
MIXED RIVER SYSTEM
5-37
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TABLE 5-17. BENZO[a]PYRENE PARTITION COEFFICIENTS
FOR VARIOUS SORBENTS
Sorbent
Ca-montmorillonite
-Clay
Des Moines River
Sediment
Coyote Creek
Sediment
Searsville Pond
Sediment
Mixed Bacteria
(dry wt. equivalent
to 97 mg/1)
Total Organic
Carbon (%)
0.06
0.6
1.4
3.8
Carbon Exchange
Capacity
(meq/lOOg)
69
10.5
13.5
34.5
Partition
Coefficient
Kp
1. 7xlOA
3.5xl04
7.6xl04
1.5xl05
3-4x10
Source: Smith et al. 1978.
5-38
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been observed (Gross 1970). PAHs have been identified in coastal waters
adjacent to or distant from developed areas (Mallet 1961); coastal
plankton have also been found to contain significant amounts of BaP,
whereas plankton from the open ocean were uncontaminated (DeLima-Zanghi
1968). Both of these observations indicate that physical transport
along the coast is an important fate process for adsorbed PAHs.
The fate of adsorbed PAHs in the water column is influenced by a
number of factors; duration of PAH exposure to sunlight will largely
determine the extent of photo-oxidation (discussed below). The
duration of exposure is partially controlled by particulate sedi-
mentation and resuspension. It has been estimated that estuarine
sediment a few millimeters deep is recycled through the water column
daily, and that the top 2 cm are recycled annually. Particulates less
than 0.5 mm in diameter may reside in the water column for 200-600 years.
It has also been postulated that it will take 500-1000 years to bury a
single layer of particulate. These data are relevant to determining
the fate of adsorbed PAHs since much of this material will ultimately
find its way to the coastal regions (Gross 1970).
The low solubility and high Kow for BaP do not necessarily mean
that all BaP is sorbed; many natural waters and industrial effluents
also contain appreciable amounts of organic material that may increase
the solubility of BaP. PAHs could be solubilized by incorporation into
micelles if a critical micellar concentration is reached. The concen-
tration of detergents, such as linear alkylbenzene sulfonate, must reach
10-50 mg/1 before significant solubilization of BaP occurs; detergent
concentrations of 0.1-1.0 mg/1, which are probably closer to environ-
mental concentrations, have no effect on BaP (Bohm-Gasol and Kruger
1965, Il'nitskil and Ershova 1970, Il'nitskil _et _al. 1971).
Another mechanism for solubilization of PAHs in water exists as a
result of the presence of other organic compounds not associated with
colloid or micelle formation. With some specific organic mediators,
such as butyric and lactic acids, organic solvents, and nitrogen-
containing organics, the extent of solubilization has been reported
to be proportional to the concentration of the mediator or the square
of its concentration (Neff 1979). However, naturally occurring dissolved
organic matter (humic acids, fulvic acids, etc.) in seawater appeared to
have no effect on solubility of phenanthrene and anthracene (Boehm and
Quinn 1973) and may have little effect on PAH solubility, in general.
Sorption of PAHs and other chemicals to natural sediments and bio-
genous materials has been shown to be a reversible equilibrium process
(Smith e± _al. 1978). Elevated particulate PAH concentrations are gener-
ally accompanied by elevated concentrations of dissolved PAHs as shown
in Figure 5-7 for BaP. These data do suggest an exchange between
adsorbed and dissolved states, and further indicate that there may be
a significant amount of BaP in solution, particularly in heavily contami-
nated systems.
5-39
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too
Sorsvillt Pond Sediment. K
160.000
75500
Coyote Creek Sediment. K
• DCS Momes River Sediment. K_ •» 35.000
6 Calcium Montmorillomte Clay, K
0.1
0.3 0.4 0.5 0.6 0.7
CONCENTRATION OF BaP IN SUPERNATANT
AT EQUILIBRIUM
ng ml Ippb)
Source: Smith et al. (1978).
FIGURE 5-7 SORPTION ISOTHEMS FOR BENZO[a] PYREIME
5-40
-------
The larger-molecular-weight PAHs discussed in this section, partic-
ularly BaP, will tend to adsorb onto particulate matter and will ulti-
mately accumulate in the sediment due to sedimentation; half-lives in
sediments are expected to be on the order of a few years (White and
Vanderslice 1980). Chemical degradation pathways for BaP dissolved in
aquatic environments are discussed below; however, these are generally
less important as fate processes than sedimentation.
Chemical Degradation
In oxygenated water, photolysis of BaP by light with wavelengths
in the solar region gives a mixture of three quinones, as shown below.
B
Several authors (Andelman and Suess 1970, Smith _et_ _al. 1978, NAS
1972, Stevens and Algar 1968, Neff 1979) have suggested that direct
photo-oxidation of PAHs is a major oxidation pathway in water. This
reaction is postulated to be mediated by singlet oxygen formed by
energy transfer from the electronically excited aromatic molecule in
its triplet state. However, contrasting evidence has recently been
reported (Zepp and Scholtzhauer 1979), suggesting that neither mole-
cular oxygen nor singlet oxygen is the exclusive mediator in any of
the major photochemical reactions of the PAHs.
The half-life for direct photolysis of BaP in sunlight> as a func-
tion of the time of day was calculated by the procedure of Zepp and
Cline (1977) using a quantum yield of 8.9xlO~4 and the measured UV
spectrum of BaP (Smith et _al. 1978). Their results are presented in
Figure 5-8. (These data were obtained from BaP in a solution of 20%
acetonitrile in pure water.) The calculated half-life of 1.2 hours
for midday photolysis in winter is in close agreement with the measured
results of 1.1 hours and 0.7 hours. Similar experiments with benz[a]-
anthracene yielded a half-life of 2 hours for that compound.
5-41
-------
7 -
I «
I
MEASURED -j
/ (WINTER)
AM
PM
6
6
7
5
3 9 10
432
TIME OF DAY
11
1
12 NOON
Source: Smith et^aU1978).
FIGURE 5-8 CALCULATED SEASONAL AND DAILY VARIATION OF
PHOTOLYSIS HALF-LIFE OF BENZOfa] PYRENE
5-42
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Benzo[a]pyrene in natural waters or pure water containing humic
acid exhibited slower rates of photolysis than in similar experiments
conducted in pure water (Smith _e_t_ a_l. 1978). The rate of photolysis
of BaP in the presence of humic acid was five times slower than photol-
ysis in pure water; natural water caused an intermediate, but definite
retardation of BaP photolysis. A light-screening effect is probably
not entirely responsible since absorbance of natural waters at 366 nm
is less than 0.02: the 0.11 absorbance of the humic acid solution
should only reduce the photolysis rate by 13%. The authors speculated
that substances present in natural waters may quench a BaP excited state,
singlet oxygen, or any excited state complex occurring in the reaction.
Another possible cause is formation of a complex of BaP with natural
organic or inorganic substances in solution, which may alter the re-
activity of ground state BaP itself. Evidence for this mechanism was
found in that only 50% of the 270 ng/ml of BaP in solution with 30
yg/inl of humic acid could be recovered from aqueous solution by hexane
extraction (Smith _et_ _al. 1978).
Inhibition of photolysis was also observed when BaP was adsorbed
onto Kaolinite clay (McGinnis and Snoeyink 1974); products formed
during photolysis are thought to be responsible. Mechanisms by which
such effects occur may include competitive reactions of the oxidizing
agent(s) formed with the organic matrix. Similar results were obtained
in studies of BaP dissolved in acetone and adsorbed onto calcium car-
bonate (Andelman and Suess 1970).
In another study, BaP adsorbed onto calcite particles in water was
exposed to illumination roughly equivalent to one-fourth of the winter
solar radiation at the earth's surface (Suess 1972). Half-lives of
BaP were 15 hours when the water sample was exposed to atmospheric air,
11 hours under oxygen atmosphere, and 35 hours under helium atmosphere.
These results indicate a dependence of BaP degradation on oxygen concen-
tration in water; no oxidation was observed in the absence of sunlight.
Again, all of these half-lives are significantly longer than the
photolysis half-life of 1-2 hours predicted above.
Benzo[a]pyrene suspended in the water column as a condensed parti-
culate was shown to decompose rapidly under normal daylight conditions
(McGinnis and Snoeyink 1974), the rate of decomposition being governed
by particle size. For particulates 1.5 mm in diameter, the reaction
exhibited first-order kinetics until 55-65% of total BaP was decomposed;
at this point, a residual was left that was not affected by an increase
in radiant energy. Apparently the decomposition products formed a
protective barrier, preventing further reaction of the residual BaP.
The authors postulated that in particulate of greater than 0.4-mm
diameter a residual would remain. Benzo[a]anthracene did not exhibit
this effect; after a threshold of sunlight had been attained, the
reaction went to completion, presumably due to the solubility of the
decomposition products.
5-43
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The free radical oxidation of BaP was studied under experimental
laboratory conditions at 50°C in order to obtain a first-order rate
constant of 5.7x10-5 sec"1 (Smith _e_t al. 1978). Extrapolating these
data to 25°C, this rate corresponds to a second-order rate constant
of 1.86x10-3 M-! sec-1; using Smith's estimate of lb"10 M R02 « the half-
life was calculated to be 4.3 days (^100 hours). This half-life is
considerably shorter than that estimated by Radding et_ al. (1976). How-
ever, the fact that both are relatively long suggests free radical
oxidation of BaP is not competitive with photolysis and adsorption
under environmental conditions.
A number of authors have studied the oxidation of PAHs by chlorine
(Perry and Harrison 1977) and ozone (Il'nitskii et_ al. 1968) and the
data havp been summarized by Radding et al. (1976). The data in Table 5-18
indicate that oxidation by chlorine and ozone may be significant
fate processes when these oxidants are available in sufficient quantities,
such as in water treatment plants. The products of aqueous chlorination
of PAH solutions are not fully known.
Predictions of the fate of BaP in natural waters, based on studies
performed under laboratory conditions using pure water or organic
solvents, must be made with caution since there may be numerous factors
affecting the photo-oxidation rate. The half-lives for individual
transformation and removal processes were calculated for various water
systems using a one-compartment model (Smith et _al., 1978), and are
shown in Table 5-19. Chemical degradation due to photolysis is clearly
the major transformation pathway for BaP in solution, since the half-
lives are at least an order of magnitude smaller than the half-lives
for other pathways. Sorption rates were not measured, but were postu-
lated to be at least 100 times faster than photolysis rates; therefore,
it is probable that most of the BaP is removed to the sediments.
Biological Fate
Analyzing the exposure and bioavailability of PAHs to aquatic
organisms requires an examination of the disposition of these compounds
in the biological compartments of the environment. The considerations
discussed here include bioaccumulation in aquatic organisms, both as
seen in the laboratory and in the field, biotransfonnation, and bio-
degradation.
Bioaccumulation
The uptake and bioaccumulation of BaP have been investigated by
several authors, using both laboratory model ecosystem studies
and predictions based on the octanolrwater partition coefficient
(Kow ^ 6) and water solubility (0.0038 tag/I of BaP. A wide range
of bioconcentration data has resulted; some of the data are presented
in Table 5-20. As shown, there are significant differences in bio-
5-44
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Ul
I
01
TABLE 5-18. RELATIVE HALF-LIVES OF BENZO[a]PYRENE GROUP PAHs IN REACTION
WITH MAJOR OXTDANTS
Half-life (hours) in Reaction with
Compound
Benzofa] pyrene
I5tmz[a Janthracene
Dibenzanthracene a
R°2' Singlet
10"10 M Oxygen
2.4 x 105 5
10
Ozone (water) Ozone (air)
10~4 M 2xlO~9 M
1.05 870
0.45 370
0.42 340
C12 HO*
Cl/2 % 0.5hr LJ/2^ 10 1
for for
all PAHs all PAHs
Isomer not specified.
Source: Radding et al. (1976)
-------
TABLE 5-19. PREDICTED HALF-LIVES FOR BENZO[a]PYRENE TRANSFORMATION
AND REMOVAL PROCESSES IN GENERALIZED AQUATIC SYSTEMS
Half-life (hours)
Process
Photolysis
Oxidation
Volatilization
Biodegradation
Hydrolysis
River
3.0
>340
140
>104
NA
Eutrophic
Pond
7.5
>340
350
>104
NA
Eutrophic
Lake
7.5
>340
700
>104
NA
Cligotrophic
Lake
1.5
>340
700
>104
NA
Source: Smith et al. (1978).
5-46
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TABLE 5-20. BIOCONCENTRATION OF BENZO[a]PYRENE IN FRESH-
WATER AND SALTWATER SPECIES
Species
Alga,
Oedogonlum cardiacum
Snail,
Physa sp.
Cladoceran,
Daphnia pulex
Mosquito,
Culex pipiens
quinquefasciatus
Mosquitofish,
Gambusia affinis
Bioconcen-
Duration tration Factor Reference
Freshwater Soecies
3 days
3 days
3 days
3 davs
5,258a Lu et__al. (1977)
82,231a Lu et al. (1977)
3 days 134,248a Lu _et al. (1977)
11,536* Lu et al. (1977)
930
Lu et al. (1977)
Clam,
Rangia cuneata
Clam,
Rangia cuneata
Eastern oyster,
Crassostrea virginica.
Mudsucker
Gillichthys mirabills
Tidepool sculpin,
Oligocottus maculosus
Sand dab,
Citharichthys stigmacus
Saltwater Species^
24 hours 8.66
24 hours
14 days
96 hours
1 hour
1 hour
236
242
0.048
0.13
0.02
Neff et al. (1976a)
Neff et al. (1976b)
Couch _et_ al_. (in press)
Lee et al. (1972)
Lee et al. (1972)
Lee et al. (1972)
ecosystem concentration factor.
5-47
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concentration factors (BCFs) among species and over time, Ba? accumulated
to high levels (BCFs of 900-134,000) over 3 days in freshwater organisms
but to much lower levels (0.02-242 BCF) in marine biota in less than
3 days.
The rates of BaP uptake and depuration have been investigated in a
microcosm study using freshwater insect larvae (midges), Daphnia, peri-
phvton (diatoms), and bluegill sunfish. Organisms were exposed to
C-w-labeled BaP at a concentration of 1.0 yg/1 for 8 hours, and the
rate of depuration was determined. In periphyton, accumulation was
linear over time, surface-area dependent, and diffusion-limited.
Daphnia had high uptake and depuration rates, perhaps due to their
large surface area/volume ratio; very little biotransformation occurred
in^Daphnia, however. In the midges (Chironomus riparius). greater than
50% of the BaP was transformed into polar compounds in 1 hour, and 10%
of the accumulated BaP was associated with the exo-skeleton. Biocon-
centration factors derived for these insects were 950 (steady state) and
150 (based on BaP analysis). Half-lives of BaP in the four species tested
ranged from 5.3-8.5 days (Leversee et al. 1980). From these and several1
other studies, there is evidence that considerable variation exists in
uptake and depuration rates and in the levels found in various types of
tissues, even with the same species and compound.
Several investigations of the accumulation of BaP by biota from
sediment and water in the natural environment have been reported.
Experiments on the uptake of hydrocarbons, including BaP, from con-
taminated sediments by marine organisms showed that deposit feeders
(the clam Macoma inquinata and sipunculid Phascolosoma agassizii)
generally accumulated the compound to a greater extent than the
suspension feeder (the clam Protothaca staminea). Experiments with
the deposit-feeding clam M^_ inquinata, however, indicate that con-
pounds directly associated with particulate matter in sediment were
less available for uptake than those released from sediment in the
surrounding seawater. Concentration factors for uptake from sediment
were <0.2, while those from seawater were 10-1349. This work indicated
that the PAHs present in interstitial water may be a prime source of
contamination for benthic infauna and probably accounted for much of
the uptake fay the sediment-feeding organisms (Roesijadi _et al. 1978).
Numerous studies have examined the PAH content of aquatic
organisms in relation to the environment in which the organisms
reside. Data are presented in Table 5-21 that show the range of
BaP levels in various species from different locations. In general,
but not always, organisms sampled from coastal regions near major
industrial or domestic point sources of PAH (e.g., Norfolk, VA harbor)
contained higher BaP concentrations than organisms from more remote
areas (Neff 1979). Benzo[a]pyrene concentrations in various aquatic
organisms from several locations in the U.S. and southern Canada
ranged from approximately <0.1 yg/kg (dry weight) to as high as
5000 yg/kg. In most cases, the organisms contained low (0-20 yg/kg range)
5-48
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TABLE 5-21. CONCENTRATIONS OF BEN20[a]PYRENK IN TISSUES OF AQUATIC ORGANISMS
Organism
Cod (Gadus sp. )
Menhaden
Anchovy and smelt
Flounder (unidentified)
Shrimp (Penaeus^ aztecui?)
Clam (unidentified)
Crab (unidentified)
Crab (Cellinectes _sap_idus)
Soft-shell clam (Mya arenarla)
Butter clam (Saxidomas glganteus)
Oyster (Crassostrea virginica)
Crassostrea gigas
Gaper clam (Tresus capax)
Location
BaP
dry wt)
Holsteinborg, Greenland 15
Atlantic, 40 km off Toms River
New Jersey, USA < 10
Raritan Bay, New Jersey, USA 6.0
San Diego Bay, California, USA up to 5000
Long Branch, New Jersey, USA
Soutli of Long Island, New York
USA, 40-27'N 73°06'W
<8
<4
<4
1.2
<0.4
Pa lac 1 os, Texas, USA
Chincoteague, Virginia, USA
Darien, Connecticut, USA
Raritan Bay, New Jersey, USA 12
Chesapeake Bay, Virginia, USA <2.0
Tillamook Bay, Oregon, USA 1.2
Alsea Bay, Oregon, USA <0.4
Coos Bay, Oregon, USA 1.32-26.64
Coos Bay, Oregon, USA 1.16- 4.20
Norfolk Harbor, Virginia, USA 20-60
Long Island Sound, USA 8.0
Chincoteague, Virginia, USA 1.2
Tillamook Bay, Oregon, USA <0.4
Tillamook Bay, Oregon, USA 0.64-12.8
Netarts Bay, Oregon, USA <0.4
Yaquina Bay, Oregon, USA 1.0-2.24
Alsea Bay, Oregon, USA 0.4
Coos Bay, Oregon, USA 0.56-2.04
Reference
Mallet et al. (1963)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Lee e^ al_. (1972)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Mix et al. (1977)
Mix e£ aK (1977)
Mix e£ £l. (1977)
Mix e£ al. (1977)
Cahnmann and Kuratsune (1957)
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Mix et^ al. (1977)
Mix et_ al. (1977)
Mix e^ ai. (197/)
Mix et aJL. (1977)
Mix et^ al. (1977)
Mix et al. (1977)
-------
TABLE 5-21. CONCENTRATIONS OF BENZOlaJPYRENE IN TISSUES OF AQUATIC ORGANISMS (Continued)
Organism
Mussel
Mytilus edulis
BaP
Ui
I
Ul
o
M. edulis and M. californeanus
M. californeanus
Location
dry wt)
Falmouth, Massachusetts USA
Little Sippewissett <2
Wild Harbor 2
Tillamook Bay, Oregon, USA <0.4-67.4
Yaquina Bay, Oregon, USA 0.48-120.8
Alsea Bay, Oregon, USA <0.4
Vancouver, B.C., Canada
outer harbor 8 + 1.2
wharf, marina and dock areas 72 +
168 -t
19.6
24
inner harbor
Vancouver marina area
(May'74) 7.6+0.4
(Sept '74) 7.2 + 0.4
wharf area on rock and cables
(May '74) 52 + 21.2
(Sept '74) 156 + 29.2
ereosoted pilings
(May '74) 272 + 52
(Sept '74) 532 + 76
25 stations between
Bodega Head and San Diego,
California, USA <0.4-32.8
West coast of Vancouver
Island, British Columbia, 0.4 + 0.4
Canada
Reference
Pancirov and Brown (1977)
Pancirov and Brown (1977)
Mix et, aK (1977)
Mix et, al_. (1977)
Mix e^ al. (1977)
Dunn and Stich (1975)
Dunn and Young (1976)
Dunn and Stich (1975)
-------
BaP concentrations, except for animals collected from severely polluted
areas or from the immediate vicinity of marina (creosoted pilings) or
fish processing facilities (Mix e_t_ al. 1979). Fish from San Diego Bay,
a large shipping port, contained up to 5000 ug/kg BaP (dry weight) (Lee
et^al. 1972).
Several species of bivalve mollusks (clams) from Oregon estuaries
were sampled for levels of BaP. The maximum concentrations found were
in the range of 15-30 ng/g (ppb). However, specimens from Coos Bay,
the most heavily industrialized bay on the Oregon Coast, did not contain
significant levels of BaP overall, except for the softshell calm Mya
arenaria (Mix et al. 1977).
One report of BaP accumulation by mussels following an oil spill
in a coastal area indicated that after 11 days, Mytilus edulis contained
approximately 55 ug/kg BaP (Bories _et _al. 1976).
Biotransformation
The process of biotransformation and the resultant metabolites of
BaP and other PAHs in aquatic organisms have been studied fairly exten-
sively. It is known that enzymatic activity in the excretory systems —
i.e. hepatopancreas, intestine, etc — of these organisms, facilitates
the metabolizing of PAHs and excretion of water-soluble products. The
extent to which animals are able to remove PAHs enzymatically from their
tissues varies among species. Some marine organisms, primarily the
invertebrates including starfish, sea anemones, oysters, and ctenophores,
have been found to have very low or non-existent enzyme activity related
to hydrocarbon metabolism. One explanation may be that organisms that
pass large volumes of water across their tissues have not developed the
enzyme mechanisms important in the toxification/detoxification system
(Lee _et al. 1977). Most of the teleost fish studied so far (including
flounder, mackerel, trout, salmon, cunner, and sheepshead) and some
members of the Phyla Arthropoda and Annelida are able to metabolize
PAHs to polar compounds (Neff 1979). Such metabolic activity has not
been detected in several species of marine algae (Payne 1977).
Microbial Biotransformation
Some of the members of the BaP group of PAHs are subject to micro-
bial breakdown; on the whole, though, biodegradation is slower and not
as extensive in this group as in the lower-molecular-weight PAHs. In a compara-
tive study of the relative biodegradability of approximately 42 different
polynuclear aromatic hydrocarbon compounds, McKenna and Heath (1976) found
no significant biodegradation of compounds with more than three rings..
5-51
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Within the BaP group, biodegradation rate data were available for
only BaP, benz[a]anthracene, chrysene, and dibenz[a,h]anthracene.
Within this group, the rate and extent of degradation is variable.
Since structural factors such as ring number and molecular geometry
influence biodegradation, there is danger in extrapolating from even
relatively similar compounds to compounds for which no data are
available. Other influences include environmental fate character-
istics of the compounds, such as adsorption, solubility, vaporization,
and other competitive transformation reactions (if any). Most of the
biodegradation studies on PAHs are laboratory investigations, commonly
conducted in simplified systems with the goal of eliciting biodegrada-
tion. Under environmental conditions, persistence may be longer than
that measured in laboratory studies due to influences of external
factors usually controlled for in the laboratory. As noted in
Section 3.2.3.4, these environmental factors may include availability
of oxygen, soil solution pfi, and the presence of natural humic
polymers.
Microorganisms act on PAHs by removing one cyclic unit at a time
(Alexander 1977). This is supported by an observed inverse relation-
ship between ring number and degradation rate.l Presumably a process
analogous to that described for anthracene (Section 4.2.3.4)
(Alexander 1977) occurs in the breakdown of the BaP group.
Presented in Table 5-22 are reported biodegradation products
derived from the breakdown of two members of the group: BaP and
benz[a]anthracene. The products are primarily intermediates in the
multistap pathway of reactions leading to eventual complete minerali-
zation. Gibson et al. (1975) isolated a mutant strain of the bacterium,
Beijerinckia, which converted benz[a]anthracene to four isomeric
dihydrodiols. (However, this study had limitations. For example,
it was not possible to confirm whether the first step in biodegrada-
tion was removal of one ring from the molecule.) No other data were
available on other group members.
It must be mentioned, however, that other factors such as substituent
type and size, interfere with this relationship. Malaney did not
find a direct relationship between ring number and biodegradability
(Malaney et al. 1967).
5-52
-------
TABLE 5-22. BIODEGRADATION PRODUCTS REPORTED FOR THE
BENZO[a]PYRENE GROUP PAHs
PAH
3enzo[a]pyrenee
Benz[a]anthracene3
Degradation Products
cis-9 , 10-dihydroxy-9 , 10-dihydro-
b enz o [ a ]
cis-l,2-dihydroxyl-l,2-dihydro-
benzo[a]anthraceneb
Fungi.
'Tentative identification.
Source: Gibson (1976).
5-53
-------
The rate of biodegradation is quite variable for the Ba?
group of PAHs. Table 5-23 presents quantified rates of biodegradation
reported for the BaP group in soil, freshwater, and estuarine systems.
Due to the variety of test methods, analytical techniques, microbial
species, and data analyses used in biodegradation testing, it is
difficult to compare the results from the different tests reported
in Table 5-23.
A total of nine studies was available on BaP; five of these studies
found no degradation, two found minimal degradation, and two found rela-
tively rapid degradation, as much as 86% in 5 days. Degradation of
acclimated populations was generally faster than that of unacclimated
ones. The addition of naphthalene, or especially phenanthrene, signif-
icantly increased biodegradation (McKenna and Heath 1976), apparently
due to cometabolism. The results of five studies on benz[a]anthracene
are similar to those found for BaP; in some cases no degradation occurred,
but in one study as much as 41% was lost in 1 week. The addition of
other PAHs again resulted in an increase in degradation. The one study
available on chrysene found a moderate rate of decay, as much as 59%
in 1 week. The sole study on dibenz[a]anthracene found negligible
degradation for the compound alone, but a significantly higher rate in
the presence of phenanthrene (McKenna and Heath 1976). No biodegrada-
tion data were available for acenaphthylene, benzo[bjfluoranthene,
benzo[k]fluoranthene, benzo[g,h,ijperylene, or ideno[l,2,3-c,d]pyrene.
A study on biodegradation of BaP and benz[a]anthracene in estuarine
sediment populations found that the presence of a polychaete worm species
increased the rate of degradation, possibly due to its role in sedi-
ment mixing or metabolism of the substances. Degradation was greatest
in populations associated with large-grain-size sediment and higher in
the surface than in subsurface sediment layers. Approximately 50% of
the initial benz[a]anthracene concentration was degraded after 30 weeks
in fine sand without the polychaete worm. Mo long-term measurements
were reported for BaP (Gardner _et_ _al. 1979).
There is other evidence that BaP and benz[a]anthracene are not
readily degradable by microbial populations. Biological treatment in
wastewater treatment is reported to be ineffective at removing PAHs from
waste streams (Andelman and Snodgrass 1974). Smith _et_ al. (1978) were
unable to isolate enrichment microbial cultures capable of degrading
either compound; however, the authors allowed that under environmental
conditions such microbes may exist.
The turnover time and transformation rate of PAHs in both acclimated
and unacclimated stream populations (Schwall and Herbes 1978) provide
a good estimation of the environmental persistence of these compounds,
as well as the importance of microbial adaptation (see Table 5-24).
The turnover time in acclimated populations ranged from 417 days for
benzo[a]anthracene to more than 3.5 years for BaP. Turnover times in
non-acclimated populations were significantly greater by at least an
5-54
-------
TABLE 5-23. BIODEGRADATION RATES OF THE BENZOja ]PYRENL CROUP PAHs:
INDIVIDUAL COMPOUND STUDIES
Ul
I
Ul
Ul
Test Type/Population Origin
Static flask
(wastewater population)
Static flask
(wastewater population)
Freshwater populations -
enrichment shake flask,
also using naphthalene
In culture
Adapted soil populations
of Pseudomonas aeruginosa
and Escherischla coll
Salmonella typhimurium,
Aerobacter aarogenes.
Escherlschla coll,
Saccharomyces cerevlsiae
Mycobactcrium flavum
M. rubrum, M. lactlcolum.
M. smeginatls. Bacillus
megateriurn, Bacillus
sphaerlcus
Compound Tested
Benz[a]anthracene
Chrysene
Benzo[a]pyrene
Benz[a]anthracene
Benzo[a]pyrene
Benzofa]pyrene
Bcnzofa Jpyrcne
Results
Inconsistent degradation over
month period of acclimation from
0% degraded to 41% degraded In one
week at 5 mg/1
59% lost at 5 mg/1 and 38% at 10 mg/1
at one week in acclimated culture
No degradation observed in 6-week
period
No degradation observed in 6-week
period
90% taken up from medium, 10-26%
metabolized
Species accumulate compound but
little metabolized. Can take up as
much as 1 to 2 x ]Q~10 ug/cell
(E. coll).
M. rubrum and M. flavum metabolized
50% of compound in 4 days. Other
species accumulated the compound
(no mention of biodegradation)
Reference
Quave et ajl.
(1980T
Quave et^ al.
(1980)
Colwe11 and Sayler
(1978)
Colwell and Sayler
(1978)
Lorbacher et^ al.
(1971)
Moore and Harrison
(1965)
Poglazova, ej^ al .
(1966, 1976a7bT
-------
TABLE 5-23. BIODEGRADATION RATES OF THE BENZOfajPYRENE GROUP PAHs:
INDIVIDUAL COMPOUND STUDIES (Continued)
I
Ul
Test Type/Population Origin
Coastal estuary sediment
populations (3 types) with
and without presence of
polychaete worm, Capltella
capltata
Soil bacteria from benzo-
pyrene contaminated area
and from non-contaminated
Bacteria in power plant
and coke over wastewater
14
evolution with
sea water population
from treated area
Compound Tested
Benzo[a]pyrene
Benz|a]anthracene
Benzofajpyrene
Benzo[a]pyrene
benz[a]anthracene
benzo[a]pyrene
Results
Experiment
Fine sand
Fine sand
& C_. capitata
Med. sand
Med. sand
4 £. capitata
Marsh sed.
Marsh sed.
& C. Capitata
% removed
in 1 week
BaP
1.2
2.4
1.4
3.0
0.84
BaA
1.5
2.7
1.8
3.0
1.4
1.98 1.8
Acclimated population metabolized
(75-86% of compound in 5 days;
non-acclimated population 48-59%
in same period
Metabolized <15% of compound
Not degraded
Not degraded
Reference
Gardner et al_.
(1979)
Shabad (1978)
Shabad (I971a,b)
Shabad et aj_.
(1971b)
Poglazova
(1972)
Lee et al.
(1978) "
al
-------
TABLE 5-23. BIODEGRADATION RATES OF TOE BENZO[aJPYRENE GROUP PAHs:
INDIVIDUAL COMPOUND STUDIES (Continued)
Test Type/Population Origin
CO.
14
evolution from
contaminated stream
sediment population
Shake flasks with
natural water
populations
Compound Tested
benz[a]anthracene
[C ] benz[a]pyrene
Benzo[a]pyrene
Benz[a]anthracene
Dibenz[a,h Janthracene
Results
No measurable transformation
in 26 days
Percent main compound (column 2)
remaining at A weeks
+ naphthalene + phenanthrene
83.5
58.3
92.7
38.3
33.8
32.9
Reference
Schwall and llerbes
(1978)
McKenna and Heath
(1976)
ui
I
Negligible degradation was observed
for each compound alone.
-------
I
Oi
00
TABLE 5-24. KINETIC PARAMETERS OF BIOTRANSFORMATION OF BENZfuIANTHRACENE
AND BENZOfaJPYRENE
Rate Constant k (1/h) Turnover Time3
Transformation Rate ((ig/g/hr)
Compound Contaminated Uncontaminated Contaminated Uncontamluated Contaminated Uiicontamtnated
BenZ[a)anthracene 1.0 x 10~A 4.0 x ]0~6 417 days 28.5 years 1.2 x 10~5 <4 x 10~8
Benzotajpyrene <3 x l(f5 <3 x lO'5 3.5 years 57 years <2 x lo"6 <3 x 10~7
Turnover rate = 1/k
Transformation rate = k x concentration
Source: Schwall and lierbes (1978).
-------
order of magnitude: an estimated 28.5 years and 57 years, respectively.
How applicable these aquatic turnover times are for soil systems is
unknown. However, the turnover time for the acclimated population
could be comparable to that of a well-acclimated soil population.
In another small-scale biodegradation study using acclimated stream
populations, the degradation time of PAHs increased 30-100 times for
each additional ring from naphthalene to benz[a]anthracene (Schwall and
Herbes 1978). In a static flask study of several PAHs (Quave e_t al_. 1980),
a considerable variation was observed over a four-ring range. Accli-
mation was required for all but benz[a]anthracene; for some compounds
10 mg/1 of the compound was inhibitory (Quave et_ al. 1980).
Thus the benzo[a]pyrene group of PAHs is relatively resistant, as
a class, to biodegradation, especially in comparison with lower-ringed
aromatics. Most biodegradation studies are too short-term to quantify
the half-lives for persistence of most of these PAHs. In some cases,
half-lives on the order of weeks were reported; however, in general,
PAHs with three rings or more were presistent on the order of months
or longer. No information at all was available for acenaphthylene,
benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[g,h,i]perylene, and
ideno[l,2,3-c,d]pyrene.
5.2.3.3 Modeling of^ Environmental Distribution
Mackay Model
The Mackay equilibrium partitioning model (Mackay 1979) described
in Section 3.2, was utilized for BaP. The values for the input parameters
used in the Mackay model and the predicted distribution of BaP are
given in Tables 5-25 and 5-26. Benzo[a]pyrene has a large adsorption
coefficient for soil or sediment and a very low water solubility and
vapor pressure. These characteristics suggest very little partitioning
into the air or water with most of the BaP concentrated in the sediments.
The differences in partitioning among the solid phases are a result of
the relative amounts of each in the model ecosystem. The concentrations
of material in the air and water compartments are significantly lox^er
than those in the solid phases, while the concentration in the aquatic
biota is somewhat higher. The number of moles predicted to reside in
each compartment is directly proportional to the total number of moles
in the whole system.
The Mackay model predicts that 99.9% of the BaP load to the system
will reside in the sediment compartment. Less than 0.1% will be present
in the water column, and less than 0.001% will partition to the
atmosphere. Dibenz[a,h]anthracene, benz[a]anthracene, benzo[g,h,ij-
perylene, indenofl,2,3-c,d]pyrene all have physical properties similar to
5-59
-------
TABLE 5-25. VALUES OF PARAMETERS USED FOR CALCULATING THE EQUILIBRIUM
DISTRIBUTION OF BENZO[a]PYRENE PREDICTED BY THE MACKAY
FUGACITY MODEL
Chemical-Specific Parameters (25°C) ;
Henry's Law Constant (atm m3/mole) 4.8 x 10- 7
Adsorption Coefficients:
Suspended Solids Ic26 x 10*
Sediment ^ 26 x 104
Biota (0.2 x KOW) 2.2 x 105
Total Amount in System (kg) jja
Compartment-Specific Parameter (25°C) :
Air
f eau 1 x 10* m2
dePth 3 x 10 3 m
volume 3 x 1Q2 m3
Water
f e\ 1 x 10* m2
depth 2m
volume 2 x 1Q4 ffi3
biomass content ^29
suspended solids 30
Sediment
f ea 1 x 10* m2
dePth 5 x 10-1 m
volume 5 x 10 3 m3
biomass content 50.018/m3
wet sediment density 1.858/cm3
(sediment dry weight = (100 x wet weight) /137)
a
The load to the MacKay model was assumed to be equal to the
total pond accumulation predicted by EXAMS.
5-60
-------
TABLE 5-26. EQUILIBRIUM PARTITIONING OF 3ENZO[a]PYRENE
CALCULATED USING MACKAY'S FUGACITY MODEL
Partitioning at Equilibrium
Compartment
Air
Water
Suspended Solids
Sediment
Aquatic Biota
Biotic Sediment
Moles
2.95 x 10
1.02 x 10
3.88 x 10
43.65
2.91 x 10
2.82 x 10
-4
-2
-3
-2
-3
Concentration
2.48 x 10~4 yg/m3
0.13 yg/1
1.628 mg/kg
1.628 mg/kg
28.38 mg/kg
28.38 mg/kg
Percent
0.007
0.0235
0.0089
99.89
0.0666
0.0065
5-61
-------
those of benzo[a]pyrene, and would be expected to be partitioned into the
various environmental compartments in the same manner. The benzo-
fluoranthenes have larger vapor pressures and Henry's law constants,
suggesting they might partition into air to a somewhat greater extent
than the other compounds in this group. Acenaphthylene has physical
properties more closely resembling naphthalene and anthracene,
and atmospheric partitioning for this compound would be expected to
be greater than for BaP.
EXAMS
The U.S. EPA EXAMS (Exposure Analysis Modeling System) model
(U.S. EPA 1890b), described in Section 3.1 was run for BaP. All six
EXAMS environments (pond, eutrophic lake, oligotrophic lake, river,
coastal plain river and turbid river) were modelled using the ecosystem
parameters that are provided with the model. The input parameters for
BaP are given in Table 5-27. Any variables not in the table were set
to zero, since these variables (such as hydrolysis) were generally not
considered important for BaP. Photolysis is an important fate process
for these PAHs, thus the absorption spectrum was included as input
(Table 5-28).
A loading rate of 0.1 kg/hour was specified for the BaP calculations.
However, in some environments this loading would cause a concentration
of benzo[a]pyrene in the input stream that was greater than the maximum
water solubility of the compound. When this type of overloading occurs,
the EXAMS model automatically decreases the loading to a physically
allowable level. Once the concentration of BaP is below the maximum
solubility level, the maximum concentrations and accumulations are
proportional to the loading, and the self-purification times and dis-
posal rates remain unaffected. As shown in Table 5-29, the loading
rates for the relatively static aquatic systems (ponds and lakes) were
reduced by the model to 3.6xlO~2 kg/day or lower. The load to the
rivers was allowed to remain at 2.4 kg/day due to the fact that rapid
dilution prevented BaP concentrations above solubility levels. The
materials balance (Section 5.1) suggests that a maximum
loading would be approximately 3xlO~2 kg/day. Therefore, the concen-
tration estimates for the pond and lakes are reasonable, but the
actual river concentrations would be expected to be lower than the
EXAMS estimates, shown in the following tables, by a factor of 80.
Table 5-29 summarizes the BaP concentrations predicted for the
simulated environments under steady-state conditions. Concentrations
in water are generally lO^-lO^ times lower than concentrations in
sediment and biota. The steady-state accumulation of BaP is highest
in those environments with a higher biomass, i.e.. coastal river,
eutrophic lake and pond. The distribution and fate of BaP in the
aquatic systems are presented in Table 5-30. In the oligotrophic lake,
about 81% of the BaP load remains in the sediment, while more than 94%
of the load in the rest of the environments resides in the sedinent.
5-62
-------
TABLE 5-27. INPUT PARAMETERS FOR EXAMS MODELING OF THE FATE OF
BENZO[a]PYRENE IN GENERALIZED AQUATIC SYSTEMS
Explanation
— ' - Value
Molecular weight 252.0
Ratio volatilization: 0.3760
re-aeration rate
Henry's Law constant 4.8 x 10
Quantum yield in water (at 313 nm) 8.9 x 10~4
Absorption spectra See Table 5-28
Aqueous solubility (nig/1) 3.8 x 10~^
Partition coefficient for 1.89 x 10"3
Octanol:H20 partition coefficient 1.1 x 10
1 9
Second-order biolysis rate constant: 3.0 x 10 ~
in sediment and in the water column
Increase in biolysis rate constant 2.0
for 10°C increase in temperature
Source: SRI (1980).
5-63
-------
TABLE 5-28. MOLAR ABSORBTIVITY FOR BENZO[a]PYRENE AS \
FUNCTION OF WAVELENGTHS
interval
1
2
3
4
5
6
7
8
9
'10
11
12
13
14
15
16
17
18
19
Center of Interval (nm)
297.5
300.0
302.5
305.0
307.5
310.0
312.5
315.0
317.0
320.0
323.1
330.0
340.0
350.0
360.0
370.0
380.0
390.0
400.0
Molar Absorb tivitv (Icm/mole/'
46,600
27,700
13,900
6,670
4,840
3,970
3,870
3,650
3,730
3,570
3,650
5,400
8,330
12,300
18,100
19,680
21,910
15 , 160
2,100
Source: Smith et al. (1978).
5-64
-------
TABLE 5-29. STEADY-STATE CONCENTRATIONS OF BENZO[a]PYRENE IN VARIOUS GENERALIZED AQUATIC
SYSTEMS RESULTING FROM CONTINUOUS DISCHARGE3
Maximum Concentrations
Ul
1
ON
Ol
Water
Loading Dissolved
System (kg/hr) (mg/1)
Pond 6.2xlO-5 2.2xlO"4
Eutrophic 1.5xlO~3 1.6xlO~4
Lake
Oligotrophic l.SxlO"3 3.2xlO"5
Lake
River 0.1 4.1xlO~5
Turbid 0.1 1.3xlO"5
River
Coastal 0.1 7.4xKT4
RJver
Maximum in
Water Sediment
Total Deposits
(mg/1) (mg/kg)
1.2xlO-3 16
1. 7xlO-3 4.3
3.4xlO"4 0.11
1.5x10""'' 0.33
1.2xlO"4 0.09
1.9x10-3 xg
Total Total
Steady-State Daily
Plankton Benthos Accumulation Load
(V"g/g) (MR/8) (kg) (kg/day)
43 43 11 1.5x10-3
30 30 59 3.6xlO-2
6.1 0.3 0.047 3.5xlO"2
7.8 1.4 6.2 2.4
2.4 1.2 1.9 2.4
140 37 290 2.4
AJI data simulated by EXAMS (U.S. EPA 1980b) model (see text for further information).
-------
TABLE 5-30. THE FATE OF BENZO[a]PYRENE IN VARIOUS GENERALIZED AQUATIC SYSTEMS*
Percent Distribution
Percent Lost by Various Processes
Residing in
Water at
System Steady-State
Ol
cr>
Pond
Eutrophic Lake
Ollgotrophlc Lake
River
Turbid River
Coastal River
0.24
1.85
18.75
2.17
5.63
0.56
Residing in
Sediment at
Steady-State
99.76
98.15
81.25
97.83
94.37
99.44
Transformed
Transformed by
by Chemical Biological
Process Process
68.79 0
95.10 0.05
99.97 0
0.04 0
0 0
2.89 0
Lost TJme for
by Other System Self-
Volatilized Processes Purification0
0.16 31.03
0.21 4.64
0.02 0.01
0 99.96
0 100
0.02 97.08
69 years
25 years
393 days
95 days
89 days
376 days
All data simulated by the EXAMS (U.S. EPA 1980b) model . See text for further information.
Including loss through physical transport beyond system boundaries.
r»
Estimate for removal of ca. 97% of the toxicant accumulated in system. Estimated from the results of
the half-lives for the toxicant in bottom sediment and water columns, with overall cleansing time
weighted according to the pollutant's initial distribution.
-------
The ultimate fate of BaP in these systems is controlled primarily by
chemical processes in the static systems, and physical transport'
beyond the system boundaries for the river systems. Volatilization
and biological degradation are negligible processes for BaP.
The EXAMS estimates for the persistence of BaP upon cessation
of loading in the aquatic environments are given in Table 5-31. The
fastest system to purify itself of the BaP load is the turbid river:
8.93% is lost within one day: Table 5-30 indicates a self-purification
time of 89 days due to physical transport. The other river systems
show similar purification characteristics, although somewhat slower.
Of the pond and lake systems, the oligotrophic lake exhibits the lowest
persistence of BaP. Within 24 days 30% of the accumulated BaP will
be lost. Chemical degradation processes control the fate of BaP in
the oligotrophic lake, probably due to the high rate of photolysis
in the clear waters and the fact that almost 20% of the BaP is residing
in the water column and available for absorption of sunlight. The
pond and eutrophic lake require much longer time periods for removal
of BaP, and have self-purification times of 69 years and 25 years,
respectively. Chemical transformation appears to account for the'
ultimate fate of BaP in these systems. However, the waters of the
pond and eutrophic lake are not clear and photolysis will be slower
than in the oligotrophic lake. Furthermore, more than 98% of the BaP
resides in the sediment of these systems, where light penetration is
extremely low.
Comparison of Mackay and EXAMS Models
The Mackay model used is simply a partitioning model, whereas EXAMS
utilizes kinetic data to predict the fate of the compound after
partitioning. Therefore, the models are not directly comparable.
The EXAMS pond environment was taken to be the best system r.o compare
with the Mackay model, since there is very little transport across
system boundaries. The load to the Mackay model was assumed to be
equal to the total pond accumulation predicted by EXAMS, 11 kg.
Table 5-32 summarizes the concentration and distribution data
predicted by the two models. The percentages of distribution pre-
dicted by the two models agree quite well; the estimated concentrations
are also in agreement within an order of magnitude. The most important
conclusion from these data is that there will be very little Ba? in
the dissolved state, and most of the aquatic load will be removed to
the sediment.
5-67
-------
TABLE 5-31. THE PERSISTENCE OF BENZOfajPYRENE IN VARIOUS
GENERALIZED AQUATIC SYSTEMS AFTER CESSATION
OF LOADINGS
System
Pond
Eutrophic
Lake
Time
Period
(days)
1460
2190
% Lost
from Water
19.02
71.93
% Lost
from Sediment
18.17
56.26
/o
Lost
from
Total
System
18.18
56.55
Oligotrophic
Lake
River
Turbid River
Coastal River
24
92.63
16.01
30.36
3.5
1
168
94.57
98.21
87.52
11.74
3.6
78.67
13.54
8.93
•78.27
All data simulated by the EXAMS (U.S. EPA 1980b) model.
See text for further information.
5-68
-------
TABLE 5-32. COMPARISON OF RESULTS FROM MACKAY'S EQUILIBRIUM MODEL AND
EXAMS FOR BENZO[a]PYRENE IN A POND SYSTEM
EXAMS Results
(Pond: l.SxlO'3 kg/day loading,
11 kg steady-state accumulation)
Maximum Concentrations
Water (Total) 0.2 ug/1
Water Biota 43 ing/kg
Sediment Biota 43 mg/kg
Sediment 16 mg/kg
% in Water
% in Sediment
Steady-State
Accumulation
0.24
99.76
Mackay Results
(11 kg in system)
Concentrations
Water (dissolved) 0.13 ug/1
Suspended Solids 1.6 mg/kg
Water Biota 28.4 mg/kg
Sediment Biota 28.4 ing/kg
Sediment 1.6 mg/kg
Percent of Chemical per Compartment
3
in water
% in Sediment
0.1
99.9
Includes BaP dissolved in water, adsorbed on suspended solids, and
in aquatic biota compartment.
5-69
-------
5.2.4 Monitoring Data
5.2.4.1 STORE!
Ambient and Effluent
As Table 5-33 indicates, observations i
[a, h] anthracene, and indeno-
the rfp
"
~uu» remark^ fT" ** d,istribution °f effluent concentra-
I--LWU& , remarked and unremarkp^ fn-r i-v,^ v r i
_S_ediment and So-ll
r-«tad. The distriution
I'T^l^fcT^ "or
L8/ks d™of"s
"
5-70
-------
TABLE 5-33. DISTRIBUTION OF OBSERVED AMBIENT AND EFFLUENT CONCENTRATIONS OF THE
BENZOfa]PYRENE CROUP PAHs
Number of Ambient Observations*
Ul
M
Compound
Benzo[a]pyrene
Acenaphtliylene
Benz|a]anthracene
Benzo[b]fluoranthene
Benzo|k]fluoranthene
Benzo[g,h,i]perylene
Chrysene
Dtbenz[a,h]anthracene
Indeno[1,2,3-c,d]pyrene
Remarked Data
Total f
Obs.
All
423
34 7
236
354
407
246
416
e 404
il
41
46
41
41
39
37
47
50
45
1.1-10
281
326
268
154
194
128
184
108
121
Cone. (uR/1)
10.1-100 100.
80
38
35
41
113
230
15
237
222
1-1000
9
13
3
4
8
13
12
>1000
4
4
8
4
IInr*»maT-Wr>rl Hn 1- n
Total 9
Obs.
0
6
5
0
5
0
1
0
0
Cone. (MR/1)
Si 1.1-10 10.1-100 100.1-1000 >1000
6
1 2 2
3 2
1
Number of Effluent Observations
Remarked Data
Total #
Benzol a] pyrene
Acenaphtliylene
henzfajanthracene
Benzofb] fluoranthene
Benzol k] fluoranthene
Benzol g.h.ijperylene
Chrysene
I) j benz f a ,h ] an th racene
luderio [ 1, 2, 3-c, d] pyrene
Obs.
667
575
559
512
659
677
508
564
666
Si
290
196
190
215
325
296
188
J80
282
1.1-10
335
362
352
287
320
305
315
305
303
Cone. (uR/1)
10.1-100 100.1-1000 >1000
42
17
17
10
14
76
5
73 6
81
Total it
Obs.
4
8
4
2
2
3
7
2
6
Si 1.1-10
2 1
4 4
1
1
2
2 I
5
Unremarked Data
Cone. (uR/1)
10.1-100 100.1-1000
1
1 l
>1000
1
3
1
1
3
as of December 1, 1980, except data for Dlbenzfa ,h]anthracene, which are as of November 20, 1980.
'Data as of April 9, 1980.
Source: U.S. EPA (1980c).
-------
Ul
I
^
Ambient Water (tig/1)
Total No. Observations
Unremarked
Remarked
Maximum Detection
Limit
Range of Unremarked
Observations
Benzofa]-
pyrene
411
0
411
800
Acenaph-
tliyleiie
429
6
423
640
0.01-0.12
ut:ii£ ( a J-
anthra-
cene
352
347
400
1-400
f luoran-
thene
236
236
25
- BenzofkJ-
fluoran-
thene
359
5
354
1000
320-1500
Benzo-
pervlene
407
0
407
1600
Chrysene
247
1
246
25
0.02
Dibenz Tndeno-
fa.hjan- fl,2,3-c,dj
416
0
416
1600
404
0
404
1600
Sediment (gg/kg— dry weiphi-}
Total No. Observations
Unremarked
Remarked
Maximum Detection
Limit
Range of Unremarked
Observations 0
125
11
11.4
10000
.02-1400
125
12
113
10000
0.002-93
116
12
104
10000
6.2-340
109
13
96
JOOOO
121
12
109
10000
3.4-310 0.9-1300 4.
123
5
118
10000
3-40.9 0
102
11
91
10000
.06-120 15
130
2
128
JOOOO
. 7-2600
117
5
112
10000
1-35.8
a»ata as of November 20, 1980, except for Dibenz f a,,, Janthracene, which are as of Decker 1, 1980.
Source: U.S. EPA (I980c).
-------
TABLE 5-35. DISTRIBUTION OF OBSERVED SEDIMENT AND TISSUE CONCENTRATIONS OK
THE BENZO[a]PYRENE GROUP PAHs.
Ben20[ajpyrene
Acenaphthalene
Benz[alanthracene
Benzo[b]fluoranthene
Benzofkjfluoranthene
BenzoIg,h,i|perylene
Chrysene
Olbenz |a,li]antliracene
Indeno[1,2,3-c,d]pyrene
Number of Sediment Observations
Total //
Obs.
114
113
104
96
109
118
91
128
112
Remarked Data
il
30
28
21
28
28
Jb
28
36
29
Cone. (Mg/kg-dry wt.
1.1-10 10.1-100 100.
2
1
]
I
I -1000
19
18
16
17
21
12
13
18
16
>1000
65
65
61
50
60
70
50
74
66
Total //
Obs.
11
12
12
13
12
5
11
2
5
Hi
iremarked fiafn
Cone. (Mg/kg-dry wt.)
<1 1.1-10 10.1-100 100.1-ionn >innn
2
1
3
1
1
1
1
6
2
2
2
3
2
2
5 2 1
5
5 2
2 y
4 4 i
2
6 2
x 1
2
Benzo(ajpyrene
Acenaphthylene
Benz|a]anthracene
Benzo [b] fluorantliene
Benzo [kj fluorantliene
Benzo fg,h,i]pcrylene
Chrysene
Dihenz(a ,h]anthracene
Indeno{] ,2 , 3-c,d]pyrene
Total II
Obs.
72
72
72
72
72
73
68
73
70
*1
io
12
10
10
10
9
9
9
J.O
Cone
1.1-10
62
60
62
62
62
56
58
55
51
N_ufflb_er_aL_Tis.sue Observa 1 1 ons
. ^g/kg-wet wt.)
10.1-100 100.1-1000 >1000
8
1
9
9
Total //
Obs.
0
I
0
o
0
0
2
0
0
• r. — Unremarked Data
Cone. (mg/kg-wet wt.)
*•! 1.1-10 10.1-100 100.1-1000 >1000
]
2
Source: U.S. EPA (1980c)
-------
Fish Tissue
As shown in Table 5-35 , most concentrations for the benzo[a]pyrene
group in fish tissue are remarked. The exceptions are observations for
acenaphthylene, with one unremarked observation no higher than 1 mg/kg
(wet weight), and chrysene, with two unremarked observations no higher
than 1 mg/kg. The distribution indicates that, in general, roughly 15%
/ t±ss"e0!amPles are analyzed with detection limits not
l ™/ HS(n§' af? 85% °f thS tlme the detection limits are between
i.l mg/kg and 10 mg/kg-wet wt.
5.2.4.2 Data From Other Sources
Ambient and Effluent Water
White and Vanderslice (1980) have thoroughly reviewed literature
reports of concentrations of PAHs in ambient waters. The results of
their review are presented as frequency distributions of reported con-
centrations in Table 5-36. The data show that levels are almost always
less than 1 ug/1, and commonly less than 0.01 ug/1, suggesting that
actual levels are probably much less than the 10 ug/1 detection limit
generally reported in the STORET data base.
A 1978 study by Basu and Saxena (1978) reports concentrations of
BaP and of total PAHs in river waters that serve as municipal drinking
water supplies. Their results are summarized in Table 5-37. The higher
levels found in Monongahela probably result from coking operations in the
area.
? inn Snod§rass <1974> hav* reported BaP concentrations of
2-300 ug/1 in aqueous effluents from industrial operations such as
shale oil recovery, oil refining coke byproduct recovery, and acetylene
manufacture. The fact that the upper end of this range exceeds the BaP
water solubility suggests that total (dissolved plus suspended) PAHs
were being analyzed.
Davies et al. (1976) reported that levels of BaP group PAHs in the
spent scrubber water of a British municipal refuse incinerator were on
the order of 0.03-0.64 ug/1. These direct aqueous discharges represented
only a small (< U) percentage of the total estimated PAH emissions from
this facility, compared with stack gas (approximately 10%) and ash
(approximately 90%) emissions of PAHs.
A systematic study of sources of priority pollutants to POTWs in
Cincinnati, St. Louis, Atlanta, and Hartford (Levins et al. 1980)
reported no detectable levels of BaP or other PAHs in this" group in raw
wastewater from residential, commercial, or industrial urban areas, at
4-10 yg/1 detection limits.
Drinking Water
Basu and Saxena (1978) investigated levels of BaP group PAHs in
several United States municipal drinking water supplies. The results
5-74
-------
TABLE 5-36. CONCENTRATIONS OF BKNZ()[a|FYRENE CROUP 1'Alls IN AMBIENT WATER
I
^j
Ol
River Water
Benzo[ a jpyrene
Benz[a Janthracene
Benzo[b]f luoranthene
Benzofkjfluoranthene
Benzo[g,h, 1 Iperylene
Chrysene
lndeno(l,2,3-c,d]pyrene
Total
No. of
Observal ions
Benzofajpyrene
Uenzo[b]f luoranthene
Benzo[k]fluorantliene
lienzo[g,h,i Jperylene
jiroundwater
BcMizofaJpyrtme
Benz[a]anthraceno
Bcnzo [ I) ] f luoranthene
Bonzo[g,||, ijperylene
J' ?H ?. i £ i t!*iiPJl
Kenzo|a]pyrcne
Bt-iiK [a )antlir<-)cene
Bonzofb] f luoranthene
I5enzo[k J f luoranthene
Reit£n[g,h, i ]|)t-rylene
Source;: White and Vanderslice (1980).
17
i
5
12
13
]
12
6
2
/»
4
3
1
2
2
Ijijndjcaj
1
I
1
1
2
2
4
4
3
7
6
1
6
2
I
1
2
1
0.1-1
5
1
2
4
Range _
> 10
-------
TABLE 5-37. LEVELS OF PAHs IN THE MONONGAHELA, OHIO,
. AND DELAWARE RIVERS
Concentration (ng/1)
BaP Total PAH
Monongahela, PA 42-77 600-660
Ohio, WV 5.6 58
Delaware, PA 4.1 350
Source: Basu and Saxena (1978).
5-76
-------
reported for tap water in selected locations in New York, Pennsylvania,
West Virginia, and Louisiana are given in Table 5-38. The highest value
reported in this survey was 0.004 yg/1 for benzo[g,h,i]perylene. However,
most values were less than 0.001 yg/1.
Levins et al. (1980) reported no detectable levels of the BaP group
PAHs in tap water samples from Cincinnati, St. Louis, Atlanta, and
Hartford (detection limit of 4-10 yg/1).
Sediment and Soil
Heit (1979) has reported BaP concentrations of 6-305 yg/g (dry
weight) in sediment samples collected at depths ranging from 0-55 cm
from a lake near Los Angeles, CA. The largest concentration corresponds
to a sample taken at a depth of 27-29 cm; this value was almost a factor
of 10 above the concentrations at the other depths. Samples of other
western lake sediments from rural areas showed BaP levels generally
below the 2 yg/g detection limit in this study.
Giger and Blumer (1974) and Kites _et al. (1977) have documented the
BaP levels in marine sediments in the vicinity of the 1969 oil spill
near West Falmouth, MA. BaP concentrations of 370 yg/kg and 340 yg/kg
dry weight of sediment were observed in 1969 and 1970, respectively.
Sediment core samples showed apparent historical levels of 380 yg/kg
(in 1900) and 26 yg/kg (in 1850). By contrast, a parallel examination
of Charles River, MA, sediment by Kites et_ al. (1977) showed a BaP level
of 8000 yg/kg dry weight of sediment.
A research group at Research Triangle Institute (White and Vanderslice
1980) has reviewed reported data on PAH levels in soils. The results of
that review for the BaP group PAHs are summarized in Table 5-39.
Fish Tissue
Shellfish tissue taken from estuarine waters indicated a higher
level of BaP than those taken from marine environments (Pancirov and
Brown 1977, Mix e_t aJ.. 1976). Table 5-40 summarizes readily available
data on the BaP group PAHs in edible marine organisms from a number of
U.S. locations.
Air
Benzo[a]pyrene has been monitored in air in urban and
industrial areas. Table 5-^1 summarizes concentration ranges for
BaP and related PAHs in U.S. urban air as cited in the U.S. EPA
Criteria Document (U.S. EPA 1980a). Table 5-42 presents some earlier
data, also from the Criteria Document, that illustrates the variability
of PAH levels in different cities. Table 5-43 presents the frequency
distribution of observations of BaP group PAHs in urban air, based upon
the compilation of White and Vanderslice (1980).
5-77
-------
Ul
I
CO
TABLE 5-38. LEVIES OF BENZOfaJPYRENE GROUP PAIIs IN DRINKING WATER
Location of
Water Supply System
Concentration data_Jor_Treated DrinkingWater" (ne/L)
Benzo ~ "
Benzofa] Benzojk]
~^._ i-r-_r ~j*»w
Syracuse, NY
Buffalo, NY
Pittsburgh, PA
Huntlngton, WV
Endicott, NY
llaminundsport, NY
Philadelphia, I'A
Unidentified
Lake George, NY
New Orleans, LA
^^_ i\«iw water aource £
Lake Skaneatelas (uncontaminal ed)
Lake Erie (contaminated with
industrial discharge)
Monongahela River (contaminated
with coke oven effluent)
Ohio River (downstream from
coke oven plants)
Croundwater (uncontaminated)
Keuka Lake (contaminated with
agricultural waste)
Delaware River (contaminated
with municipal waste)
Uncontaminated upland water
Lake George (contamination
from recreational sources)
Mississippi River (contaminated
with industrial discharges)
ia"'P"nK Date pyrene fluoranthene jjerylene — "i-.^-c.u,
12/16/76 0.3 0.4 0.4
12/26/76 0.2 0<7
1/19/77 0.4 0.2 0.7 1>2
1/20/77 0.5 0.2 2.5 1 2
2/22/77 0.2 — 2.9 Q?
2/28/77 0.3 01 10
1.9 0.9
3/5/77 0.3 / o
* A • /
3/17/77 0.5 0.7 i.8 2.2
3/26/77 0-3 o.l 2.6 o.9
5/1/77 1.6 0.6
of
Source: Basu arid Saxona (1978).
-------
TABLE 5-39. FREQUENCY OF OBSERVATIONS OF BEN?.0{a]PYRENE GROUP I'AHb IN SOU. AND SEDIMENT
Sample/PAH
Rural Soil
Benzo[a]pyrene
Benz[a]anthracene
Benzo ( b ] f luorantheuc
Benzo [ k ] f luoran thene
Benzo[g,h,l JperyJene
Indeno[l,2,3-c,d]pyrene
Urban Soil
Bcnzo[a]pyrene
Benz[a]anthracene
Benzo[k]fluoranthene
Benzo[g,h.i ]perylene
Chrysene
Marine Sediments
Benzo[a]pyrcne
Benz[a]anthracene
Benzo [g,h,i]perylene
Chrysene
Soil Near Industrial Sources
Total
No. of
Observations
52
3
3
3
6
3
23
2
2
2
2
17
2
2
2
No. Observations in Indicated Concentration (|ig/kg) Range
0.01-0.1 0.1-1.0 1-10 10-100 100-1000 1000-10,000 10,000-100,000
3 3 19 23 4
3
3
2 1
3 3
2 1
177 7 1
1 1
1 1
} I
1 1
34 6
411
1 1
1 i
Benzofa jpyrene
13
Source: White and Vanderslice (1980).
-------
TABLE 5-40. REPORTED LEVELS OF BENZO[a]PYRENE GROUP PAHS
IN EDIBLE MARINE ORGANISMS
Location of Sample
Long Island Sound
Chincoteague, VA
Black Point
Little Toms Cove
Darien, Conn. Scotts Cove
Fish Market, Linden, NJ
Chesapeake Bay
Raritan Bay
Atlantic Ocean
Long Branch, NJ
S. of Long Island
Falmouth, MA
Little Sippextfisset
Wild Harbor
Palacios, Texas
Atlantic Ocean
25 mi. off Toms River, NJ
Marine
Tissue
Oyster
Concentration (yg/kg wet weight)
Benzfaj-
anthracene
8
BaP
Other
PAHsa
<2-15
Oyster
Clam
Clam
Clam
Crab
Crab
Menhaden
Flounder
Flounder
Mussel
Mussel
Shrimp
Codfish
0.1
0.3
1
<1
<1.5
2
<0.3
<]L
1
<0.2-0.3
<0.5-1.2
<0.5-<5
:
Source: Pancirov and Brown 1977.
Includes chrysene, benzo[b]fluoranthene, benzo[eJpyrene, perylene, and
benzo[g,h,i]perylene.
Source: Pancirov and Brown (1977).
5-30
-------
TABLE 5-41. REPORTED LEVELS OF BENZO[a]PYRENE GROUP
PAHs IN AIR OF U.S. CITIES
Compound
Benz[a]anthracene
Benzo[b]fluoranthene
Concentration
Range (ng/m3)a
0.18-4.6
0.1-1.6
Reference
Fox and Staley (1976),
Gordon (1976)
Gordon and Bryan (1973)
Benzo[k]fluoranthene
0.18-5.2
Fox and Staley (1976)
Benzo[a]pyrene
Indeno[1,2,3-c,d]pyrene
Chrysene
Benzo[g,h,i]perylene
0.13-3.2
0.03-1.34
0.2-6.4
0.2-9.2
Colucci and Begeman (1971)
Gordon (1976), Gordon and
Bryan (1973
Gordon and Bryan (1973)
Gordon and Bryan (1973)
a
The concentration data for air can be converted to ppt (parts per
trillion) by multiplying the value in ng/m3 by the following factors
(F-24.47/M.W.): benz[a]anthracene and chrysene, F=0.107; benzo[a]pyrene
and benzofluoranthenes, F=0.097; indeno[1,2,3-c,d]pyrene and benzo[g,h,i]-
perylene, F=0.089.
5-81
-------
TABLE 5-42. CONCENTRATIONS OF BENZO[a]PYRENE GROUP PAHs IN THE AIR OF
SELECTED U.S. CITIES, AVERAGE OF SUMMER AND WINTER VALUES
City
Concentration
Atlanta, GA
Birmingham, AL
Detroit, MI
Los Angeles, CA
Nashville, TN
New Orleans, LA
San Francisco, CA
Range
Mean
Benzo[a]pyrene Benzo [k] fluoranthene Benzo[g,h,i]perylene
4«5 3,7 7.0
15.7 8.8 13.2
18.5 12.5 21.3
2-9 3.1 10.2
13.2 8.0 10.2
3-1 2.9 6.0
1-3 1.0 5.1
1.3-18.5
8.5
1.0-12.5
5.7
5.1-21.3
10.4
a
Concentration data for air samples can be converted to ppt (parts per
trillion) by multiplying the value in ng/m3 by the following factors
(F-24.47/M.W.): benzo[a]pyrene and benzo[k]fluoranthene. F=0.097;
benzo[g,h,i]perylene, F=0.089.
Source: Sawicki et _al. (1962).
5-32
-------
TABLE 5-43. FREQUENCY OF AMBIENT CONCENTRATIONS OF BENZO[a)PYRENE CROUP I'AUs IN URBAN AIR
Ol
I
00
U)
PAH
Benzo[a]pyrene
Benzlajanthracene
Bcnzo[b]fluoranthene
Benzofk]fluoranthene
Benzo[g,h,Ijperylene
Chrysene
Indenof1,2,3-c,d]pyrene
Total
No. of
Observations
116
24
29
12
No.
0.01-0.1
1
4
3
1
1
Observations in
.o±Ari
6
5
4
7
6
2
1
Indicated Concentration (ng/m )
1-10 10-100 100-1000
45 54 9
852
4
13 6
21 24 2
6 2 1
1
> 1000
Source: White and Vanderslice (I960).
-------
Air samples collected in areas surrounding combustion sources show
the highest levels of BaP in air. Table 5-44 presents some data showing
that oil refineries, for example, can be associated with air levels of
BaP 30 times those near airports. Katz and Chan (1980) note that an
earlier U.S. EPA study found BaP levels in urban air to be 1.42 to 3.34
times higher in cities with coke oven facilities than in cities without
coke ovens. Table 5-42 shows relatively high ambient levels of BaP
in cities such as Detroit and Birmingham, compared with San Francisco,
for example. These differences are due probably in considerable part
to the^different degrees of industrialization, although meteorologic
and climatologic factors are also important.
Rural areas have been shown to have detectable levels of PAHs in
ambient air, though the levels are well below any levels measured in
heavily populated or industrial areas (U.S. EPA 1980a). Table 5^5
presents a frequency distribution for reported concentrations in rural
air compiled by White and Vanderslice (1980).
_ Moschandreas et al. (1980) examined BaP levels in a few locations,
indoors and outdoors, on woodburning and non-woodburning days. In
the Boston metropolitan area, they found mean levels for various residences
of 0.4-1.1 ng/m-3 indoors, and 0.4-0.9 ng/m3 outdoors. On woodburnin*
days in one residence, the mean level indoors was 4.7 ng/in3, and the°
mean level outdoors was 1.3 ng/m3. These levels suggest that there is
little difference between indoor and outdoor concentrations of BaP
except on days on which wood is being burned.
In order to place the ambient air data in perspective, Table 5-46
presents some data on PAHs in mainstream cigarette smoke (Severson _e_t al.
1976). Note that these data are in ug/m3 vs_. ng/in3 for ambient air
concentrations and thus generally at least~an order of magnitude higher.
5.2.5 Summary - Ultimate Fate and Distribution
Benzo[a]pyrene and the other PAHs in this group are released to the
environment primarily as products of combustion. Virtually all of the
BaP in the atmosphere is adsorbed onto airborne particulates. Even
though photolysis of BaP in the atmosphere is expected to be rapid, wet
and dry deposition of these PAHs are estimated to be the major input
pathways to the aquatic environment. On the basis of transport model
calculations, it was estimated that ^44 kkg/yr BaP may be deposited on
the surface of the U.S.; only a fraction of that will be introduced
directly or indirectly to aquatic systems.
The relative composition of the PAH mixtures released from high-
temperature combustion sources indicates that production of the unsub-
stituted, parent compound is favored. The fact that, within a PAH series,
unsubstituted PAHs are the most abundant homologs in sediments from
industrial areas (despite their higher solubility) further supports
the conclusion that combustion is the major source of PAHs in
the environment.
5-34
-------
TABLE 5-44. RELATIONSHIP BETWEEN CONCENTRATION OF BENZO[a]PYRENE IN AIR
AND DISTANCE FROM EMISSION SOURCE
Concentration of BaP (yg 3aP/kg of particulate material)
—
Location
Airport - USSR
Oil refinery - USSR
Highway (in town)
(rural)
At
Source
400
12,000
176
120
I
50
64
100
)istance from Source (n
i
51-250 | 251-500
!
46 | 17
1,200
6 21
15
i
0
501-1500
1.3
120
i
5
Maximum.values
blotal POM yg/kg
Source: White and Vanderslice (1980).
5-35
-------
TABLE 5-45. FREQUENCY OF AMBIENT CONCENTRATIONS OF BEN20[a]PYRENE
GROUP PAHs IN KURAL AIR
Observations ___Njjmbej:, "f Observations in Indicated Concentration (ng/m Range
0.001-0.01 Ml-PjJ: OJ.-J: I-IQ 30-100
DI l>enz[ a, h] anthracene
Ln
I
GJ
CT.
Benzo[a]pyrene
16
Bunzolg,h,i]perylene 10
Source: White and Vanderslice (1980).
-------
TABLE 5-46. CALCULATED CONCENTRATIONS OF BENZO[a]PYRENE AND
RELATED PAHs IN MAINSTREAM CIGARETTE SMOKE
PAH
Benzo[ajpyrene plus
Benzo[e]pyrene
Concentration (yg/m )
Non-Filter
Cigarette
85-86
Filter
Cigarette
28-32
"Low Tar"
Cigarette
(10 mg)
16
Benzo[a]anthracene plus
Chrysene plus
Triphenylene
310-680
96-210
73
Analysis method used did not give complete resolution of the
PAHs; data are for partially resolved mixtures of PAHs.
Source: Calculated from data of Severson _et al. (1976).
5-87
-------
The Mackay equilibrium partitioning model was run for BaP, and
the^calculations indicate that 99.9% of the environmental BaP will
reside in the sediment compartment; very small amounts will be found
in the air (vapor phase BaP), water, or biota. The U.S. EPA EXAMS
model was used to predict the fate and distribution of BaP in six
generalized aquatic systems. The results indicate that in all of the
systems modelled, maximum BaP concentrations in sediment can be expected
to be higher than total water concentrations by factors up to 104. Aqueous
BaP concentrations were estimated to range from 0.1 yg/1 to 1.9 ug/1;
sediment concentrations predicted by EXAMS range from 90 ug/kg to
1.9 x 104 ug/kg. The EXAMS data also indicate that more than 90% of
the BaP will reside in the sediment for all aquatic systems examined,
with the exception of the oligotrophic lake (81%).
The most significant fate processes for BaP in aquatic systems
include adsorption (with subsequent transport to the sediment), and
chemical degradation (photolysis). Volatilization and biodegradation,
with half lives on the order of a number of days to months, are expected
to be slow processes for BaP and the other PAHs in this group. The EXAMS
calculations indicate that the relative importance of the various fate
processes is determined by the actual conditions characteristic of the
environmental systems. In the static pond and lake systems, chemical
degradation will be the dominant fate process. However, in the more
dynamic river systems, physical transport of BaP downstream is largely
responsible for determining the ultimate fate. The persistence of BaP
in aquatic systems is reflected in the self-purification times predicted
by EXAMS. The times estimated for removal of 97% of the BaP accumulated
in the turbid river system is 89 days, whereas the self purification
time predicted for the static pond system is as high as 69 years.
Figure 5-9 gives a representation of the major inputs of BaP to the
aquatic environment, as well as the dominant fate and transport pathways.
BaP has been extensively monitored in environmental media; there are
fewer data for the other PAHs in this group. Most of the monitoring data
in the STORET data base for the PAHs in the BaP group are remarked, i.e.,
reported to be below the detection limits. The PAH concentrations actually
reported for sediment samples range from 0.002 ug/kg to 2600 ug/kg. Ambient
water concentrations recorded in STORET range from 0.01 ug/1 to 1500 ug/1.
However, since sediment and aqueous samples were not taken from the same
locations, very few conclusions can be based entirely on the limited
data in STORET.
Data from other sources indicate that BaP concentrations in ambient
waters are generally less than 1 ug/1; concentrations of BaP in industrial
effluents were reported to be as high as 300 ug/1. Concentrations of BaP
in drinking water were reported to range from 0.2 ng/1 to 1.6 ng/1; the
highest BaP concentration was in New Orleans, LA. In this survey, the
highest concentration for the PAHs in the BaP group was 4.0 ng/1, reported
5-33
-------
Direct Discharge
•v
Neg. % cn\i. releases
Ul
I
oo
AIR
100 % env. releases, 17O kkg/yr.
(rapid photolysis. t,/2 5-10 hrs.)
Atmospheric Deposition
23-26 % airborne load.
44 kkg/yr.
to U.S.
inland waters
< 1 kkg/yr.
to U.S. land mass
44 kkg/yr.
Biotranslocation
Photolysis
(fast)
t,/2<10hrs.
ty2102-105hrs.
(limited by concentration of oxidants)
Sorption log K = 6.08 (fast)
Physical
Transport
Desorption
(slow and
continuous)
Biotransformation
t,, months
SEDIMENT
FIGURE 5- 9 SOURCES AND FATE OF BENZOfa] PYRENE IN THE AQUATIC ENVIRONMENTS
-------
for benzo[g,h,i]perylene in a drinking water sample taken from Philadelphia,
PA. Benzo[a]pyrene has been reported at concentrations up to 300,000 yg/kg
(dry weight) in lake sediment samples. In contrast, a Charles River, MA
sediment sample showed a BaP level of 8000 ug/kg dry weight. Concentra-
tions of these PAHs in urban soil were reported to be about two orders
of magnitude higher than concentrations in rural soils.
Ambient air concentrations of these PAHs were also reported to be
significantly higher in urban areas than in rural areas. In a study
of seven urban areas, the highest PAH concentrations in air were reported
for Detroit, MI, up to 21.3 ng/m3 benzo[g,h,i]perylene, probably due to
the high degree of industrialization in that city. Data presented in a
separate review of ambient levels of PAHs indicate that most rural air
concentrations are less than 10 ng/m3; urban air concentrations up to
100 ng/m3 were reported for many of these PAHs.
5-90
-------
5.3 HUMAN EFFECTS AND EXPOSURE
5.3.1 Human Toxicity
5.3.1.1 Introduction
Data on the effects of ingestion of individual polycyclic aromatic
hydrocarbons included in the benzo[a]pyrene group (i.e., acenaphthylene,
benz[a]anthracene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[k]fluor-
anthene, benzo[g,h,i]perylene, chrysene, dibenz[a,h]anthracene, indeno-
[l,2,3-c,d]pyrene) on man or laboratory animals are few. We have con-
centrated our efforts on benzo[a]pyrene (BaP), the prototype PAH carci-
nogen since regulatory action to reduce levels of BaP will also re-
sult in the simultaneous reduction of other PAHs as well as non-
carcinogenic compounds, and BaP is a major source of exposure.
5.3.1.2 Pharmacokinetics
There are no pharmacokinetic data for this group of PAHs in humans.
Considerable animal data are available, however, for BaP from which
generalizations can be drawn for other PAHs in this group.
Absorption and Distribution
Animal studies indicate that BaP is readily transported across
the intestines, primarily by passive diffusion (Rees et. al.. 1971). It
is also easily absorbed through the lungs (Kotin et. _ad. 1969, Vainio
et. al. 1976). Rodent studies indicate wide tissue distribution follow-
ing absorption of BaP (USEPA 1980). In rats, BaP disappears from blood
and liver very rapidly following intravenous administration; the half-
time for BaP disappearance from liver is about 10 minutes. This rapid
elimination phase is followed by a slower disappearance phase lasting
6 hours or more in which the concentration of BaP increases in body fat
and fatty tissues (e.g., breast) (Schlede et al.. 1970). Since BaP has
been shown to induce microsomal enzyme activity, prior exposure can ac-
celerate both the rate of disappearance from tissues and excretion of
metabolites into bile.
Metabolism
Most tumorigenic PAHs in themselves are not direct carcinogens but
require metabolic activation before biological activity such as PAH-
induced carcinogenesis can be expressed. Current understanding of the
mechanisms involved in this process (Yang et. al_. 1978; Sims 1976, Lehr
et al. 1978, Selkirk et al.. 1975a,b Jerina et. al. 1977a,b, Selkirk 1977)
is as follows: PAHs are metabolized by the cytochrome P-450 dependent:
microsomal mixed function oxidase (MFO) system (often designated as the
aryl hydrocarbon hydroxylase system). This enzyme system is readily
inducible by exposure to a variety of chemicals and is found in most
5-91
-------
™"
with PA»ltal considfratio* ^ the extrapolation of risks associated
-
_.
^ Carcino§enesi^ This issue remains unresolved
at this time.
Excretion
The primary routes of BaP excretion in mice and rats are the
bioaccumulation as such-iJ-believed to occur 19?°a'b)
to occur Ho
5.3.1.3 Human and Animal Studies^
Carcino^enicity
rn group are well established
"— r*88?^8' c?-c«?it»8ena and/or tumor initiators; others
no tumorxgenic responses, ^^capacity-orfiaKffial PAHs to
inouce positxve responses in humans is^n^-so Veil established^ Th
5-92
-------
6-PIIENOXY RADICAL
HP-},f>-QI)INONE
PHENOL
CONJUGATES
[DIOI, EPOXIDESI
BP-6.12-QU1NONK
CONJUGATES
TETKOI.S
IlP(-)TRANS-7 ,8-DIOL
11 0 SOLUBLE CONJUGATES
UP-7,8-I)IOL-9,10-EPOXri)E
HOUND TO
MACKOMOI.r.CULES
UNA
UNA
1'kOTEINS
Source: L.I et al. TJ76; Selkirk 1977; U.S.EPA 1980.
FICUUP, 5-]0. I'OSSTIiT.K PATHWAYS OF BENZOla] PYUKNK MlJTAliOLISM
-------
is primarily due to the fact that human exposures have not been to in-
dividual chemicals but rather to combinations as they occur in coke
oven emissions, coal-tar, soot or from environmental exposures to to-
bacco smoke or exhaust fumes. Numerous studies have shown increased
incidences of lung, skin and other types of cancer among workers ex-
posed to coke oven emissions, coal gas, coal tar and pitch (IARC 1972).
These studies, however, do not allow identification of the individual
chemical(s) responsible, do not account for possible synergistic or
co-carcinogenic effects resulting from other components, often are un-
able to clearly define exposure levels and generally are not amendable
to quantifying human risk.
For the most part, available data for specific PAH compounds are
from skin painting and subcutaneous or intramuscular injection experi-
ments in_mic.e. Few oral or inhalation experiments have been conduc_te_d^
and those that are available are generally inadequate for risk assess-
ment purposes.
Ben2o[a]pyrene
Among the compounds in the benzo[a]pyrene group, BaP itself has
been the most extensively studied. The published literature on BaP
is vast. A few representative studies of the positive carcinogenic
effects of BaP in a variety of animal models are presented in Table 5-
47. BaP has been shown to be both a local and systemic carcinogen by
oral, dermal and intratracheal routes. It is also a transplacental
carcinogen, an initiator of skin carcinogenesis in mice and is carcino-
genic in single dose experiments. Additional documentation of the car-
cinogenicity of BaP may be found in IARC (1972) or the Survey of Com-
pounds . . . Tested for Carcinogenic Activity (1961, 1968, 1970, 1972,
1978).
Few studies have adequately examined the carcinogenic effects of
orally administered BaP. Available studies are generally of very
short duration with small test populations and frequently without ap-
propriate control animals. Incidence data for the two best available
oral studies for BaP (Neal and Rigdon 1967, Fedorenko and Yanysheva
1966) are presented in Table 5-48. Forestomach tumors were found in
CFW mice fed BaP in their diet for an average of 110 days (Neal and
Rigdon 1967) as well as in CC57 mice administered BaP by gavage once
a week for 10 weeks and then maintained up to 19 months (Federenko and
Yanysheva 1966). Although both these studies are by the oral route,
several shortcomings raise questions as to their relevance to possible
induction of cancer in humans from ingestion of BaP. Test populations
in both studies were exposed for periods considerably less than life-
time and tumors were limited to the forestomach. The site of
tumor development and the probabla underlying mechanism are possibly
unique to laboratory rodents. Unlike the fundus portion of the human
stomach (which is homologous to the forestomach of rodents), the rodent
forestomach is nonglandular and similar in histology to skin epithelium.
5-94
-------
TABLE 5-47. CARCINOGENIC ACTIVITY OF BENZO[a]PYRENE BY VARIOUS EXPOSURES
Exposure
n[>t-i:j.us \ao.i Major Krtects
A/lle.f female Fores tomach
mice (12) turaors
lla/ECK female Forestomacli
mice tumors
Mice Tumors
Spraguu Dawley Mammary turaors
female rats (9)
Rose (ff administrations) Route
1 rng/g dlot Ave. 3 x/wk for 2 wka Diet
4.8 iiig 11 a I'/ mo 11 .so
exposure
Controls
1 ing/mouse In corn 2 x/wk for 4 wks Gavage
oil
0.3 rag/mouse In corn 3 x/wk for 8 wks Gavage
oil
Control (no treat-
ment)
°-2 H'g Single administration Cavage
0.05 ing " "
0.012 mg " "
In PEG
1Q0 »'8 Single administration Oral
Incidence
12/12
0/12
36/39
33/33
0/19
5/11
0/9
2/10
8/9
Comments
Duration 29 uks
Duration 21 wks
Duration 31 wks
Oiirdtioii 31 wks
Cr)7UI./6j female Skin tumors
mice (30)
0.02 itmolea
O.I iimoles
Once every two wks
for 60 wks
(Same as above)
Skin painting
12/30
26/27
Mostly squamous
cell carcinomas
-------
TABLE 5-47. CARCINOGENIC ACTIVITY OF BENZO[a]PYRENE BY VARIOUS EXPOSURES (continued)
I
cr>
Species (No.) Major Effects |>
ni'/re (30) ^ pap"lomas 200 mnolea
Spr«i(»ue Dawl ey Sarrr»n»M« « •» ,
***"**'* U • *, iifnoj £*s
i"ti t s \ J 3)
""*—"•"••—••••"-•-———-•-— _ .... „ , _ _ _ ___-__-_— .____._ __
Hlc-e.male (14) Sarcomas 2.4 ,1BOlea
Mice, female (16) " » „
Ral a i
l-»ng tumors 2.5 rag
0.25
0.05
0.01
0.002
0.0005
Mixed with a
blood substitute
RK-8 and India
Ink
Syrian Golden Respiratory ] ra.,
hamsters tract tumors
0.5
0.25
0.125
0.0625
In saline
Exposure
vtf adin t n 1 R hm i ^ mm\
— ™iUUi«>i»ii2.tioiJs2_ Route
Single application skin palntlno
followed by twice
weekly applications
of 10 pg TPA for 23
weeks
Alternate days for Subcutaneous In-
30 dosea jection
At monthly Intervals Injection
for 3 treatments
(Same as above) »
Once monthly for Intratracheal
10 m0' instillation
Once weekly for 52 Intratracheal
weeks . instillation
ln_cldence Comments
94%; 4.8 Initiator
paplllomas/ of skin carclno-
Diouse genesis
J3/13 Average latency
101 d,lys
13/14 Average latency:
129 d.lys
8/J6 160 days
80* Observed for 2
yr beyond treat-
ment
43%
28%
14%
0%
07.
26/28
25/29
9/30
4/30
3/30
-------
TABLE 5-47. CARCINOGENIC ACTIVITY OF BENZO[a]PYRENli BY VARIOUS EXPOSURES (continued)
Dose
Exposure
_(_> administrations)
ST/A mice Mammary tumors 10 mg Single Injection
Route
Intrapnrltoneal
Incidence
2/10
At one year
Pregnant ]CR/Ila Uing adenomas;
mice Initiation of
skin earcino-
genesis
2-4 mg
Dama treated on
daya 11, 13 and
15 of gestation
IntrapcrJ toiifial
or subcutaneous
Injections
TranuplaceiHal
carcinogen
Ui
I
Source of data: USEPA 1980, IAKC 1972.
-------
TABLE 5-48. INCIDENCE OF ORALLY ADMINISTERED, BENZO[a]PYRENE-INDUCED FORESTOMACH TUMORS IN MICE
Strain
CC57 mice
2-3 mo.
Ui
i
vo
oo
Treatment
1 mg BaP in 0.2 ml trie thylcue
glycol, Ix/wk for 10 wk by in-
tubation (fasted)
As above except 0.1 nig
As above except 0.01 mg
As above except 1 ug
As above except 0.1 ng
Control
Incidence of
Forestomach
Tumors
23/27 (85%)
23/30 (77%)
5/24 (21%)
2/26 (8%)
0/16 (0%)
not given
Comments
All mice were held for 19
months prior to sacri-
fice.
Reference
Fedorenko and
Yanysheva
(1966).
CFW mice
32.5 mg BaP mg/kg/day in the
diet
As above except 13 mg
As above except 6.5 mg
As above except 5.85 mg
As above except 5.2 mg
As above except 3.9 mg
As above except 2.6 mg
As above except 1.3 mg
As above except 0.13 mg
_ Control
66/73 (90%)
19/23 (83%)
24/34 (71%)
4/40 (10%)
1/40 (3%)
0/37 (0%)
1/23 (4%)
0/24 (0%)
0/25 (0%)
0/289 (0%
The various treatment
groups were put on test
at different times.
The mice at different
exposure levels varied in
age from 17 to 116 days
at the start of the experi-
ment and were exposed for
an average of 110 days
(range: 70-197 days) over
a 183 day average study
duration (range: 85-219
days).
Neal and Rig-
don (1967).
-------
This suggests that the rodent forestomach may be unusually sensitive to
repeated localized exposure to Ba? akin to skin painting bioassays.
This presumably local effect of ingested BaP on rodent forestomach epi-
thelium, in the absence of tumors at other sites, appears to be of
questionable relevance to humans with a wholly different stomach ana-
tomy.
Other PAHs in the Benzo[a]pyrene Group
The carcinogenic activity of other PAHs included in the benzo[a]-
pyrene group is summarized in Table 5-49. No carcinogenicity data were
found for acenaphthylene; the^majority of other compounds in this group
have been tested only in the mouse with exposures generally limited to
skin painting experiments. Only benz[a]anthracene and dibenz[a,h]an-
thracene have been tested by the oral route. Both were found to be
carcinogenic by the oral route (IARC 1972). Dibenz[a,h]anthracene in-
duced forestomach tumors in mice following oral administration of this
compound (IARC 1972, USEPA 1980). Repeated gavage administration of
benz[a]anthracene (15 doses of 1.5 mg over 5 week period) produced a
95% incidence of lung adenomas, 64% incidence of hepatomas and a 3% in-
cidence of forestomach papillomas in the test population of 59 B6AF1/J
mice. Another group of 20 mice given only two treatments 3 days apart
developed 16 hepatomas and 17 lung adenomas. Controls for these test
groups had 2 hepatomas, 10 lung adenomas and no forestomach tumors
among 59 control animals (IARC 1972).
Difaenz[a,h]anthracene, benz[a]anthracene, benzo[b]fluoranthene,
chrysene and indeno[l,2,3-c,d]pyrene are'complete carcinogans for mouse
skin and all are also initiators of skin carcinogenesis in this species
(USEPA 1980, IARC 1972, Habs et al.. 1980). No carcinogenic response
was noted in a skin painting study with benzo[k]fluoranthene in NMRI
mice treated twice a week with up to 9.2 pg/mouse/application for their
lifetime (Habs et al. 1980).
A pronounced co-carcinogenic effect was observed in a single experi-
ment conducted with benzo[g,h,i]perylene (2000 pg) plus 5 yg BaP applied
to skin of ICR/Ha Swiss mice 3 times per week for 52 weeks (USEPA 1980).
Local sarcomas have also been produced at the site of subcutaneous
or intramuscular injections of benzo[b]fluoranthene, chrysene, dibenz-
[a,h]anthracene and indeno[l,2,3-c,d]pyrene (USEPA 1980, IARC 1972).
Ultimate Carcinogenic Metabolites
Investigators have long sought a common molecular feature among
carcinogenic PAHs such as BaP. Recent attention has focused on the
increased reactivity of diol epoxide metabolites of PAHs in which the
oxirane oxygen forms part of a "bay region." Carcinogenicity studies
conducted with various potential oxidative metabolites of BaP, for
example, suggest that the 7,8-diol-9,10-epoxide is the most active neta-
bolite (Wislocki et al. 1977).
5-99
-------
TABLE 5-49, SUMMARY OF THE CARCINOGENIC ACTIVITY FOR OTHER POI.YCYCLIC AROMATIC HYDROPARRnMc:
IN THE BENZO[a]PYRENE GROUP1 "lUKUUVKUONS
Exposure
t_n
I
C
o
Chemical
Ht'iizf a] An tli racene
l)enz[ a] Anthracene
Kunz[ a] Anthracene
llt;nz[ a J Anthracene
Controls
BenzCalAnthracene
Be nz[ a] Anthracene
Be nz[ a] Anthracene
Species lNo.J[
Mice (13)
Mice (27)
Mice (16)
B6A?1/J
mice (59)
Mice (20)
Mice (59)
Mice (20)
(nil/lie
Mice
Mice (75)
Mai or effects
No tumors in 16
months
1'apilloma of fore-
stomach
Ho tumors
Lung adenomas ;
hepatomas; papil-
loraa.s (stomach)
Hepatomas; lung
adenomas
Hepatomas; lung
adenomas
Papllloma
Tumors (type not
specified - mostly
malignant)
Tuino rs
Paplllomas
Dose
0.5 mg In mineral oil
0.5 mg in mineral oil
Mineral oil
1.5 nig/mouse metho-
celaerosol OF
1.5 ing/mouse
Untreated
0.4% In mineral oil
.002% in toluene
.02% "
.2% " "
1.0% "
.0002% in dodecane
.0027. " "
.02%
0.2% " "
1% " "
.05% in acetone
+5% croton oil
(8 administrations)
Single dose
8 or 16 X at 3-7
day Intervals
Vehicle controls
15 treatments in
5 weeks
2 treatments, 3
days apart
2 X/wk, 68 wks
3 X/wk/50 wks
II II II 81 II
II II II tl II
II II II II II
II II II II II
M II II II II
II II II II II
II II II tl II
II II II II II
Alternate once
weekly applications
Route
Gavage
Gavage
Cavage
Gavage
Gavage
Skin
Painting
Skin
Painting
it ii
M it
ii ii
ii ii
it ii
ii n
ii n
Skin
Painting
Incidence Comments
2/27
0/16
56/59; 2 hepatomas in
38/59; 20 animals with
2/59 median age of
death 547-600
days
16/20; Median death
17/20 age 547-600 days
2/59;
10/59
1/20 No control data
0/32
1/18
3/32
8/29
4/31 Dodecane Is a
8/21 cocarcinogen
4/20
11/21
17/22
17/17 at 9 months
18/9 at 12 months
Tumors
controls - 5% croton
oil
1/13
-------
TA1JLE 5-49. SUMMARY OF THE CARCINOGENIC ACTIVITY FOR OTHER POLYCYCLIC AROMATIC HYDROCARBONS
LN THE HENZO[a]PYRENE CROUP1 (continued)
Ul
I
CjicuiJ ca 1 Species (No.) Major effects
Benzla] Anthracene Mice (20) Skin tumors
Doae
Exposure
(t atlmlnlstratlons) Route
Incidence
Comments
6 ing/mouse total
followed by cro-
lon oil
10 X over 5 wka Skin 21 tumors In DA alone gave
weekly applications Painting 7/18 mice no tumors
llunzla lAnthraoeiie Hamsters (10) No tumors
(Syrian gold.)
0.5% in mineral oil
Bi-weekly for 10 wka Skin
Painting
6/10 alive at
50 wks. all
dead at 85 wka
llenzLa (Anthracene C57B1. mice Tumors
0.05 nig in tricaprylJn Single
0.2 mg "
1.0 nig "
5.0 mK "
10.0 ing "
Injection 5/43 mice Surviving at
" 11/A3 9 months
15/31
49/145
5/16
lleiiz|.
14 mob.
-------
TABLE 5-49. SUMMARY OF THE CARCINOGENIC ACTIVITY FOR OTHER POLYCYCLIC AROMATIC HYDROCARBONS
IN THE BENZO[a]PYRENIi CROUP1 (continued) «IUKUI,AKIIUNJ>
Chemical
SjiocleB (No.) Major effects
Dose
Exposure
Route
Incidence
lienzo[h JPJ uoran-
thene
l!«mzo[l>] Fluoran-
thenc
Benzo[ b] Fluoran-
thenc
Benzo[k]Fluoran-
thene
Oi
1
Q CliryHt'no
to
Chrysene
Chrysene
Chrysene
Cbrysene
Mice
Mice
(20)
16 rf. 14 *
XVlInc/z
mice
NMRI
NMRI
Mice
(40)
(AO)
(20)
CFl mice
Mice
Mice
Mice
Mine
(50)
(30)
No tumors
Pap J] lomas
Carcinomas
Sarcoma at injec-
tion site
Pap 11 lomas, sarcomas.
and carcinomas
No tumors
I'apll Ionian
Carcinoma
Epi the] loma
No tumors
Papll lomas
Carcinomas
No tumors
Negative
1.0 mg in acetone
1.0 mg in acetone
and croton resin
0.6 mg/lnj action
3.4 pg In acetone
5.6 PB "
9.2 pg »
3.4 pg In acetone
5.6 PB "
9.2 pg "
1 .02 In acetone
0.2Z In acetone
1 mg In acetone
] ing in acetone
and croton resin
2 mg (purified)
10 mg/ Implantation
Single application
Single application
Repeated applica-
tion
3 injections in 2
months
2 X/wk for lifetime
II II II II II
II II II II II
2 X/wk for lifetime
M ii ti ii it
II M II II II
3 X/wk for ?
Hi weekly for 31wka
Single application
Single application
Repeated applica-
tion
Single injection
2 Implantations
Skin painting
Skin painting
n n
Subcutaneous
Skin painting
M n
n n
Skin painting
n n
ii ii
Skin painting
Skin painting
Skin painting
Skin painting
n n
Subcutaneous
Subcutaneous
63 weeks observ.
18/20 Initiator of
5/20 skin carcinog.
18/24 Avg. latent
period of 4.5
months
5.3% No tumors in
14.7% controls
54. 1Z
- - - No tumors In
controls
9 After Obvious shortened
8 8 mos. life-span
1/16
— - 63 wks observ.
16/20 Initiator of
2/20 skin carcinog.
— - 45 wks observ.
Cliry.se ne
Mice (40-50) Sarcomas
(C57BL)
5 mg in trycaprylene Single injection Subcutaneous 5/22?
Avg. Induction
time = 271 days
22 alive at 150
days
-------
TABLE 5-49. SUMMARY OF THE CARCINOGENIC ACTIVITY FOR OTHER POLYCYCLIC AROMATIC HYDROCARBONS
IN THE BENZO[a]PYRENE CROUP1(continued)
Chemical Swedes (No.jl_
Chrysenu Mice
(57BI.)
Chryscne Ral.s
Chrysene Rats (10)
Chrysene Mice (50)
Dlhenz[a,h]An- Mice
ihrarenc
Dllmnzf d,h]An- Mice (20)
1 Ihracene
1 — i
O
LJ Mice
DIbenzr.-i,li]Aii- Mice (42)
fhracene DBA/2
Mice (35)
(>lbunz[n,li]Aii- Mice (BALB/c)
thracene
Major effects Dose (jf administrations)
Tumors (?) 1 mg in arachis oil 10 injections
Sarcomas 2-3 mg/lnjection Repeated (?)
No tumors 0.05Z (aq.) Bi-weekly
No tumors 2 mg in lard Single
Tumors (1 carcinoma 9-l!> mg total dose Over 5-7 months
of forestomach)
Sqnamous-cell carci-
noma, Papllloma of 0.4 mg/day in oil »/in 406 days
forestomach emulsion
Lung, heart and 0.4 mg/day in NaOll ?
Intestinal tumor
Pulmonary adenoma- 0.76-0.85 mg/day 200 days
losis In olive oil
Aveologenlc carci- " " " "
noma
llemangio-endollie- " " " »
1 1 oma
Mammary carcinoma " " " "
Mammary carcinoma — roMTnni <:
Pulmonary adenoma- — "
toses
Mammary carcinoma 0.5% In almond oil Twice weekly for
Route
Injection
Injection
Injection
Injection
Dietary
Drinking
water
Drinking
water
Drinking
water
ii ii
ii ii
it ii
Stomach lube
Incidence
2/20
4/10
0/4 at 18 mos
7/22 after
1 year
'2/20
11/20
?
27/27
24/27
16/27
12/13?
0
0
1/20
Comments
No tumors in
vehicle control
2/10 sarcomas
In vehicle
controls
•
50 wk observ.
Pseudopreg. Mairmary carcinoma
Mice (UALB/c)
" " " "
" " " " "
ii ii
13/24
-------
TABLE 5-49.
«,«» POLYCYaK AUOMATIC HV,,KOCA,tl!,,NS
o
-IN
Chemical Species (No.) Major effects
l)Ihenz[a,h]An- C3II mice Mammary tumors
thracene " "
Swiss mice (20) Skin tumors
l>ibenz[a,h]An- ICK/Ila Swiss Tumors (some
lliracene mice carcinomas)
l)ll.ony.[a,h]An- C3ll mice Local sarcomas
thracene
nibenz[a.h]An- Mlce (2Q) Sarcomas
thracene
i i)eiv/i_'*t n J An- Mice (new— Local sarcomas
thracene boril) Lung Al)enomas
l)lbenz[a,li]An- Rats Tumors
l)ll>enx[a,h]An- Rats Sarcomas
lhr.ic.ene
DJbeiii'l a,h]An- Guinea pigs Sarcomas
lliracene
l>lbenz[a,ls]Au- Fowl Sarcomas
thracene
Dose
0.25% 1 n benzene
Controls
30 tig/dose in ace-
tone-benzene
0.001%
0.01%
0.1%
0.00019 ing/dose
0.0078 ing/dose
0.016 mg/dose
0.03 ing/dose
0.06 mg/dose
0.12 mg/dose
0.25 mg/dose
0.0125 mg In lard
> 0.08 |ig
> 0.2 ug
8 rag/1 njectlon
, "n In olive oil
8-48 ing (total dose)
in oil
0.4% in lard
bxpomire
(II administrations)
Twice weekly
Untreated
Bi-weekly
3 X weekly
n n n
Single dose
5 injections
5 Injections
9 injections at
monthly Intervals
Single dose
II M
Multiple
Single dose
Route Incidence Comments
Skin painting 10/11
50%
Skin painting 16/20
Skin painting 1/30
" " 43/50 (3
-------
TABLE 5-49. SUMMARY OF TIIK CARCINOGENIC ACTIVITY FOR OTHER POLYCYCLIC AROMATIC HYOROCAKIJONS
TN THE BENZOLaJPYKENE GROUP1 (continued)
C! it'in i ra 1
DlhenzCn.il] An- Mice
thracene
l)lbenz[a,h]An- Frogs
thracene
Dllicn7.[a,h]An- Mice
thracene
DII)cnz[a,h]An- Mice
thrdcene
Olhcnzf a,h]An- Mice
Y' thracene Mice
Ui
lndeno[J , 2, 3-c,d] Tyrone
liuleno[l , 2, 3-c,d3l'yrene
lnclono[l ,2,3-c, tumors
(40)
Dose
> 0.1 mp, colloidal
dispersion (uq.)
0.3-0.5 mg In olive
oil
36 pmoles/kg
?
179 mg (total)
236 niR (total)
(in olive oil)
0.05 or 0.1% In
dloxanc
0.01% in acetone
0.05% " "
0.1% "
0.1% "
0.5% "
0.5% "
250 pg total
0 .6 mg 1 n ol ive
oil
3.4 pg in acetone
c r II II
'•> '2 PR "
Kxposure
(t administrations)
Single dose
Single dose
Single dose
7
237-279 days
II II II
3X/wk for 12 months
3 X/uk for 12 months
n n n n ii n
n n n n n n
ii ii n n n n
n n n n n n
n n M M M ii
10 paintings at 2
day interval
3 Injections at 1
month Intervals
2 X/uk for J ifetlme
it n n n n
ti ii ii n n
Kouto. Incidence
i.v.
1 n tra renal 26%
i.v. 10/10
Skin painting 8/65
33/65
Drinking water 77%
100*
Skin painting - - -
Skin painting 0
n n ()
" " 6/20
" " 3/20
" " 7/20
" 5/20
II II
Injection 10/14
1/14
Skin painting - - -
Comments
Dose- response
relationship
3% Incidence
controls
63% tumor Inci-
dence/239 day
avg. latent
period " 26
II. all Index
Dose- response
Relationship
n ii n
n ii ii
n n n
n ii ii
W/Jn 265 days
W/ln 145 days
No tumors In
controls.
Source of data: HSlil'A 1980, IARC 1972, llabs e^
-------
Wislocki and coworkers (1977) found that BP7,8-oxide was the most
active carcinogen among 4 BaP arene oxides tested (and only slightly
less effective than BaP) following skin application of 0.3-0.4 umol
to C57BL/6J mice once every two weeks for 60 weeks. Since 4-,5-,6-,7-,
8-,9- and 10-hydroxyBP were all inactive as complete carcinogens at
0.4 ymol/dose (Kapitulnik _e_t al. 1976), carcinogenic activity could not
be attributed to phenolic isoraerization products of BP7,8-oxide.
Further tests with metabolic products of BP7,8-oxide implicated BP7,8-di-
hydrodiol as a more potent proximate carcinogen; the dihydrodiol was
presumably formed when BP7,8-oxide was hydrated by epoxide hydrase
(Jerina _et al. 1977a,b). BP7,8-dihydrodiol induced 100% incidence of
skin tumors (as did BaP itself) compared to <20% incidence induced by
BP7,8-oxide at doses of 0.15 ymol by the above schedule; at lower doses
the dihydrodiol was more active than BaP (Levin et al. 1977a,b). The
lack of carcinogenic activity of 7,8,9,10-tetrahydro-BP7,8-epoxide and
7,8,9,10-tetrahydro-BP7,8-diol at 0.3 pmol/dose indicated that the 9,10-
double bond was important in metabolic transformation to ultimate carci-
nogenic products (Levin _et al. 1976a,b, Jerina _et al. 1978). The most"
probable candidates for this ultimate metabolite, would again be the
BP7,8-diol-9,10-epoxides formed by oxidation of the 7,8-dihydrodiol at
the 9,10-position by the monooxygenase system (Conney ejt al. 1980,
Jerina _e£ al. 1977a,b). In tests with newborn Swiss-Webster mice,
intraperitoneal injection of a 28 nmol dose of either BaP, BP7,8-dihy-
drodiol or BP7,8-diol-9,10-epoxide-2 resulted in a definite sequential
increase in tumorigenic activity of BaP, BP7,8-dihydrodiol and BP7,8-
diol-9,10-epoxide-2, respectively, clearly implicating the dihydrodiol
as the proximate carcinogenic metabolite and the epoxide as the ul-
timate carcinogenic metabolite. The BP7,8-diol-9,10-epoxide-l iso-
mer was too toxic for an adequate assessment of tumorigenic activity
(Kapitulnik et al. 1977).
These and other studies have generated the "bay-region" (i.e., hin-
dered area between the 10- and 11-positions) theory to correlate struc-
ture of polycyclic hydrocarbons with carcinogenic activity. Presumably
benzylic carbonium ions derived from epoxides of a saturated angular
benzo ring have a greater ease of formation when the carbonium ion is
located in the bay region, thus enhancing the chemical reactivity and
perhaps the mutagenicity and carcinogenicity of the epoxide (Jerina
.e_t al. 1977a, 1977b, 1978, Conney jet al.. 1930).
A number of recent experiments with bay region diol epoxides of
benz[a]anthracene, dibenz[a,h]anthracene and chrysene indicate that
they, also, are more active than the parent compounds or other oxidative
metabolites.
Skin painting studies with various metabolites in CD-I mice suggest
that BA3,4-dihydrodiol is at least 10 times more tumorigenic than benz-
[ajanthracene itself or other metabolites (Wood jet al.. 1977b,c, Levin
_ejt _al_. 1978, Slaga .et. al. 1978). In newborn mice treated with various
5-106
-------
metabolites of benz[a]anthracene, BA3,4-dihydrodiol induced at least
30-fold more pulmonary adenomas than the parent compound or 4 other
dihydrodiols tested (Wislocki _ejt al. 1978) ,
Similarly, Buening and coworkers (1979b) found DBA 3,4-dihydrodiol
to be equal to dibenz[a,h]anthracene and considerably greater than DBA
1,2-dihydrodiol, DBA 5,6-dihydrodiol and DBA H^-S^-diol in tumor-in-
ducing activity on mouse skin following single applications. In the
same study, the incidence of pulmonary adenomas induced in newborn
Swiss-Webster mice following intraperitoneal injection was similar for
dibenz[a,h]anthracene and DBA 3,4-dihydrodiol, while tumor incidences
caused by DBA 1,2-dihydrodiol and 5,6-dihydrodiol were significantly
lower. Again, the much lower tumorigenic activity on mouse skin of
DBA 3,4-diol compared to DBA 3,4-dihydrodiol is consistent with the pre-
diction of the bay-region theory that metabolism at the 1,2 double bond
would yield the ultimate carcinogenic diol epoxide, DBA 3,-4-diol-l,2-
epoxide (Buening _et_ al. 1979b).
Initiation-promotion studies in CD-I mice with chrysene and various
chrysene metabolites applied once at doses of 0.4, 1.25 or 4.0 jamoles
and followed by twice weekly applications with TPA, a phorbol ester,
for 25 weeks resulted in significantly greater tumorigenic activity for
chrysene 1,2-dihydrodiol above chrysene itself (Levin _e_t al. 1978).
Similar findings were reported by Buening e_t al. (1979a) who found en-
hanced lung tumor activity for chrysene 1,2-dihydrodiol in newborn mice
given intraperitoneal injections on days 1,8 and 15 of life.
In summation, benzo[a]pyrene has been most extensively studied of
all PAHs in the benzo[a]pyrene group. BaP has been shown to be both
a local and systemic carcinogen by oral, dermal and intratracheal routes.
It is also a transplacental carcinogen and an initiator of skin carcino-
genesis in mice. Few studies have adequately examined the carcinogenic
effects of orally administered BaP but it has been shown to induce fore-
stomach tumors in mice exposed to BaP by the oral route. The absence of
tumors at sites other than in the forestomach and the unique anatomy of
rodent forestomach in contrast to humans raises questions as to the sig-
nificance of the induction of forestomach tumors in mice to human risks
associated with the ingestion of BaP.
With respect to other PAHs included in this group, benz[a]anthra-
cene and dibenz[a,h]anthracene are both carcinogenic in mice by the
oral route as well as complete carcinogens for mouse skin as are benzo-
[bjfluoranthene and indeno[l,2,3-c,d]pyrene. Benzo[g,h,i]perylene is a
co-carcinogen with BaP and benz[a]anthracene, benzo[b]fluoranthene,
chrysene and indeno[l,2,3-c,d]pyrene are all initiators of skin carcino-
genesis in mice.
Recent studies on the mechanisms of carcinogenic activity of some
PAHs suggest increased reactivity of the diol epoxides of PAHs in
which the oxirane oxygen is located in the "bay-region." Experiments
5-107
-------
with possible metabolites of BaP indicate that one or more of the BP7,8-
diol-9,10-epoxides are the ultimate carcinogenic form. The bay-region .
theory of polycyclic hydrocarbon carcinogenesis is further supported by
findings of increased carcinogenic activity of the bay-region diol
epoxides of benz[a]anthracene, dibenz[a,h]anthracene and chrysene above
that of the parent compounds.
Adverse Reproductive Effects
BaP appears to exert little effect on the developing embryo (Bulay
and Wattenberg 1970). Rigdon and Rennels (1964) found only one mal-
formed fetus among 7 litters of rats from dams exposed to 1 mg BaP/g
diet during gestation. Increased resorptions and dead fetuses were
noted, however.
Juchau and coworkers (1978) reported that several human fetal tis-
sues (i.e., liver, lung, kidney, adrenals and placenta) possess the
requisite monooxygenase enzyme systems needed to bioactivate and bio-
transform BaP into metabolites that induce positive mutagenic effects
in the Ames Salmonella assay.
No other data were available for compounds in this group.
Mutagenicity
€
A summary of the mutagenic activity exhibited by compounds compris-
ing the benzo[a]pyrene group is presented in Table 5-50. No data were
found for faenzo[k]fluoranthene or indeno[l,2,3-c,d]pyrene. BaP is the
most active mutagen of the group, exhibiting positive mutagenic
responses in all of the test systems including induction of _tn vivo
sister chromatid exchange in hamster cells (Bayer and Bauknecht 1977,
Roszinsky-KScher _e_t al. 1979, Sirianni and Huang 1973) and chromosomal
aberrations in both spermatogonia and bone marrow cells of hamsters in
vivo (Basler and Rohrfaorn 1978; Roszinsky-Kocher et al. 1979). Studies
conducted with various potential metabolites of BaP suggest that the
BP7,8-diol-9,10-epoxide is the most potent mutagen in the presence of
a metabolic activation system and may in fact be the ultimate carcino-
gen (Conney _et al. 1977, Wislocki _et ail. 1976a,b, Wood _et al. 1976,
Huberman _et_ al_. 1976, Newbold and Brookes 1976).
Mixed responses have been found for several of the other compounds
in this designated group. In vivo studies with benz[a]anthracene have
been generally positive. Increased chromosomal aberrations were ob-
served in mouse oocytes and hamster spermatogonia and bone marrow cells
(Peter _et al. 1979, Basler and Rohrborn 1978). Roszinsky-Kocher and
coworkers (1979) noted a weak induction of sister chromatid exchange
in hamster cells exposed in vivo to benz[a]anthracene. Both positive '
and negative results have been reported in host-mediated assays with
Salmonella typhimurium TA1538 (Simmon 1979, Simmon £t _al. 1979, Rosen-
kranz and Poirier 1979). 3enz[a]anthracene induced positive mutagenic
5-108
-------
TABLE 5-50. SUMMARY OF MUTAGEN1C ACTIVITY FOR COMPOUNDS COMPRISING THE BBNZO[a]PYRENI£ CROUP
Chromosomal
Aberrations
In Tn
Vivo Vitro
Sister
Chromatic!
Exchange
In Vivo
Host
Mediated
Assay
Mammal Ian
Cells
In Vitro
Salmonella typlilmurlum
TA98 TA100 TA1535 TA1538
Unscheduled
DNA
Synthesis
Acena phi hyl cue
References
Kaden et al. 1979.
Belli1 [ajanthra-
cene
01
I
Basler and Rohrhurn 1978;
lluberman 1977; lluhernuin and
Sachs 1976; Kaden c^l al_. 1979;
Martin £t a]_. 1978; Peter et^ al.
1979; Rosenkranz and PoJrler
1979; Roszinsky-Kocher ct_ al.
1979; Simmon 1979; Simmon et al.
1979.
Benzo[b] fluor-
anthenu
Roszlnsky-Kochcr e^ a]. 1979.
Ucnzo[g,h, 1 ]
perylene
Gibson e
-------
TABLE 5-50.
SUMMARY OF MUTAGENIC ACTIVITY FOR COMPOUNDS COMPRISING THE BENZO[a]PYRENE GROUP
(conLuiuecl)
Chromosomal
^Aberrations
Ct>IB|>t»UUl
Chrysene
In
Vivo
In
Vitro
Sister
Cliroin;iti(]
Exchange
In Vivo
Host
Mediated
Assay
Maiiuuul Jan
CeJls
In Vitro
Salmonella typhtiwirliini
TA98 TAIOO TA153S TA1538 TM677
Unscheduled
ONA
Synthesis
References
Basler .££ .aJL, 1977; Baslur and
Rohrborn 1978; lluberman et al.
1972; Kaden et_ £l. 1979; Kamel
1980; Poirler ami de Surres 1979;
Ricliter-Relclihelin et al. 1979;
Kosenkranz and Polrier 1979;
Roszlnsky-Kocher e£ ;U. 1979;
Salanonc et. al. 1979; Simmon ^
al. 1979; Simmon 1979.
DJbtmz [a,b ]
anthracene
Ui
I
Gibson et^ al. 1978; lluberman
1977; Wood et^ aj^. 1978;
Hubernian and Sachs 1976; Kaden
SL Si- !979; take et _a_l. 1978;
Martin et^ al^. 1978; Roszinsky-
KOcher et al. 1979;
-------
responses in in vitro bacterial tests with several strains of Salmonella
typhimurium in the presence of liver microsomal activation (Kaden et al.
1979, Simmon 1979) and induced unscheduled DNA synthesis in Hela cells
(Martin _et_ al. 1978). No significant increase in the number of mutants
was seen, however, in hamster cells exposed in culture (Huberman and
Sachs 1976). Tests with possible metabolites of benz[a]anthracene in-
dicate that the bay-region BA 3,4-diol-l,2-epoxides are the most potent
mutagens and probable ultimate carcinogens for this compound (Wood et
al. 1977a).
Weak induction of sister chromatid exchange but no induction of
chromosomal aberrations of marrow cells was observed in hamsters ex-
posed to dibenz[a,h]anthracene in vivo. Positive induction of unsched-
uled DNA synthesis was noted in both human epithelial and Hela cell
cultures (Lake _et_- al. 1978, Martin £t_ al. 1978) and a significant num-
ber of mutations observed in V79 hamster cells exposed in culture in
the presence of metabolic activation (Huberman and Sachs 1976).. Mixed
results have been reported in tests with various strains of Salmonella
typhimurium (Kaden _e_t al. 1979; Wood _e_t al_. 1978, Gibson et_ al. 1978).
In contrast to the generally positive findings for BaP, benz[a]-
anthracene and dibenz[a,h]anthracene, results with chrysene have been
either negative or, at most, only weakly positive. In vivo tests
indicate no induction of chromosomal aberrations in hamster bone mar-
row cells (Easier .et al. 1977, Easier and Rohrborn 1978), a weak sister
chromatid exchange response in this species (Roszinsky-Kocher _et_ al.
1979) and a slight increase in aberrations in mouse oocytes (Basler _et_
al. 1977, Basler and Rohrborn 1978, Roszinsky-Kocher et al. 1979).
Generally negative findings were noted in tests with Salmonella typhi-
murium (Basler _e_t al_. 1977, Simmon _et aJL. 1979, Rosenkranz and Poirier
1979) and negative results reported for a host-mediated assay (Poirier
and de Serres 1979).
Limited data are available for acenaphthylene, benzo[b]fluoran-
thene and benzo[g, h, i]perylene. A single experiment with acenaphthylene
produced positive findings in one strain of Salmonella typhimurium TM677
in the presence of rat liver activation but only at concentrations that
were toxic to the bacteria (Kaden _ejt al. 1979). An in vivo study with
benzo[b]fluoranthene resulted in a weak induction of sister chromatid
exchange but no significant induction of chromosomal aberrations in
hamster marrow cells (Roszinsky-KScher _e_t aJL. 1979). Benzo[g,h,i]peryl-
ene has been tested in Salmonella typhimurium, producing negative results
in strain TA1535 (base-pair mutant) and positive results in strains
TA1538 and TA98 (frameshift mutants) with 60Co gamma irradiation activa-
tion (Gibson et al. 1978). Positive results were also noted in S_. .
tvphimurium TM677 in the presence of liver microsomal activation
(Kaden et al. 1979).
5-111
-------
Other Toxic Effects
The major focus of studies conducted with PAHs in the Ba? group
has been their potential for inducing carcinogenic effects. Overt
signs of toxicity are generally not evident except for the carcinogenic
PAHs and then only at doses sufficient to produce a high tumor incidence
(NAS 1977).
Normally proliferating tissues are the selected targets for car-
cinogenic PAHs such as BaP, This may be attributable to specific
attack on the DNA of cells in the S-phase of the mitotic cycle (Philips
£t al. 1973). Other contributing factors are alterations of enzyme
activity and immunologic competence. A single carcinogenic dose of
BaP xvas reported to produce a prolonged depression of the immune
response to sheep red blood cells (Stjernsward 1966, 1969). Damage to
the hematopoietic and lymphoid systems has been frequently reported in
experimental animals (USEPA 1980).
Bond and coworkers (1981) have noted the development of athero-
sclerotic plaques in groups of eleven 4-week-old Sc strain chickens
injected weekly for 20 weeks with 0.1, 1 or 10 mg/kg BaP dissolved
in dimethyl sulfoxide. The specific route of exposure was unspecified.
Solvent and untreated control groups were also included in the study.
At 20 weeks, detectable lesions were found in 44, 45 and 75% of animals
in the 0.1, 1 and 10 mg/kg BaP groups, respectively, compared to 50%
of solvent controls and 22% of untreated control animals.
5.3.1.4 Human Risk Considerations — Benzo[a]pvrene Group
Carcinogenicity of Ben2o[a]pvrene
The quantitative estimate of potential carcinogenic risk to humans
resulting from ingestion of benzo[a]pyrene (BaP) is calculated below.
Ideally, human data relating carcinogenic response at known dailv dose
levels in the dose range of interest would be utilized in an appropriate
mathematical model to predict risk. Usually, such ideal data are not
available and extrapolations of risk must be made from either:
1) epidemiological data involving relatively high level
exposures such as may occur in occupational settings, or
2) controlled experiments on laboratory animals involving
very high total dosages.
In the first case, the overriding uncertainty is often in the data
themselves; the exposure levels, lengths of exposure, and even response
rates are usually "best estimates," and, furthermore, unknown factors
(e.g., co-existent carcinogenic exposure) may bias the data. In the
second case, the data are usually more accurate, but the quantitative
5-112
-------
extrapolation from animal models to humans is uncertain. At present,
there is no universally accepted solution to this species to species
extrapolation problem. In short, in the former case one has relevant
data of questionable accuracy, whereas in the latter case, one has ac-
curate data of questionable relevance. Further complicating the issue
is the present lack of an indisputable basis for judging the relative
merits of the various mathematical models relating dose and effect.
The available data concerning human and other mammalian effects
have been presented above. Many experiments involving exposure of
laboratory animals to BaP have been done, but surprisingly few experi-
ments have been done in which significant populations of animals were
given a wide range of doses of BaP. Two ingestion studies are considered
whose data appear to lend themselves to dose/response extrapolation, one
by Federenko and Yanysheva (1966) on CC57 mice, the other by Neal and
Rigdon (1967) on CFW mice. Three commonly used mathematical models have
been applied to each set of data to extrapolate the potential carcinogenic
risk of BaP to humans. These assessments of potential human risk are
subject to important qualifications:
• The experimental data chosen for extrapolation are for fore-
stomach tumors induced either by weekly intubation (Federenko and Yany-
sheva 1966) or incorporation of BaP into the diet (Neal and Rigdon
1967). While apparently relevant with respect to route of administra-
tion, the site of tumor production and probable underlying mechanism
are possibly unique to laboratory rodents because of the anatomy of the
rodent stomach. The forestomach in both rat and mouse is non-glandular
and has a stratified squamous epithelium with a cornified covering
(Chiasson 1979). The fundus portion of the human stomach (homologous
to the forestomach in rodents) is glandular and has a columnar epithe-
lium. The similarities between the epithelium of rodents and that of
skin suggest that the induction of forestomach tumors in mice may be
analogous to the induction of skin tumors in skin-painting bioassays.
This possibility calls into question the relevance of forestomach tu-
mors in mice to the potential for human cancer from BaP ingestion. Al-
though it is recognized that a carcinogen can cause different types of
cancer in varying target organs in different species, even when the
same route of exposure is used, it is considered possible that the fore-
stomach tumors in mice induced by BaP may represent an unusually sensi-
tive assay of the carcinogenicity of BaP by the oral route.
• The EPA guidelines call for the adjustment of dose between
species to be based on body surface area not on body weight (USEPA
1979). In the case of forestomach tumor induction in rodents, neither
adjustment would appear to reflect the presumably local effect of BaP on
the rodent forestomach epithelium. If it were hypothesized that stom-
ach tumors from BaP ingestion are unlikely in humans because of the dif-
ferences in anatomy between rodent and human stomach, but other tumor
sites were considered possible, one could reasonably adjust upwards
5-113
-------
the human equivalent daily dose to account for the wider distribution
in the body and consequent dilution of BaP. Conceivably, however,
stomach tumors (or other intestinal tract tumors) are possible in humans due
to ingested BaP. The analysis that is carried out below adjusts dose
on a body surface basis, but it is regarded as the probable worst
case - tending to overstate the risk due to BaP ingestion in humans.
• Both animal studies were of less than lifetime duration, espe-
cially in the study by Neal and Rigdon (1967). Doses were administered
for about half the duration of the experiment in both studies. In order
to adjust animal dose schedule to an equivalent daily lifetime human
dose, two assumptions were utilized as recommended by the USEPA (1979).
First it was assumed that the response would be the same if the total
dose was distributed evenly over the entire experimental lifetime of
the animal. Second, it was assumed that a short-duration study attri-
butable to either early mortality or early termination leads to an
over-estimation of the dose required to produce the observed effect.
The EPA guidelines (1979) suggest reducing the average daily dose by
(Le/L)3 where Le is the actual experimental lifetime and L is the theo-
retical lifetime of the experimental animal. In treating the Neal and
Rigdon data, this adjustment leads to a marked reduction (^1/40) in the
effective daily dose level. These dose adjustments tend to ignore that
detoxification processes and repair mechanisms generally reduce the ef-
fectiveness of low dose/long duration exposures.
The first set of data (Neal and Rigdon 1967) selected for extra-
polation of possible risk is shown in Table 5-51 and indicates the in-
cidence of forestomach tumors in CFW mice treated with BaP in their diet
for an average of 110 days. The mice ranged in age from 17 to 116 days
at the outset of the study.
To obtain a quantitative human risk, the human equivalent daily
lifetime dose was computed as follows:
human dose _ animal dose /IIP days i f 183 davs \
(mg/day) = (mg/kg/day) x \183 days/ X 190 wks x 7 d/wk X
/human weight , . . . . , _,
- : - :: - • ; • • x (animal kg weignt)
animal weight
That is,
1 mg/day human dose is approximately equivalent to 13.7 mg/kg/day animal
dose.
The second set of data (Federenko and Yanysheva 1966) selected for
extrapolation is shown in Table 5-52, and indicates the incidence of
forestomach tumors in CC57 mice treated with BaP in triethylene glycol
5-114
-------
TABLE 5-51. CARCINOGENIC RESPONSE IN CFW MICE
TREATED WITH BENZO[a]PYRENE
Mouse Dose a
(mg/kg/day)
0.0
0.13
1.3
2.6
3.9
5.2
5.85
6.5
13.0
32.5
Equivalent
Human Dose
(mg/day)
0.0095
0.095
0.190
0.285
0.380
0.428
0.476
0.95
2.38
Incidence of
Forestomach
Tumors
0/289
0/25
0/24
1/23
0/37
1/40
4/40
24/34
19/23
66/73
Percent
0
0
0
4
0
3
10
71
83
90
Doses administered in diet for 110 days of a 183-day average study duration.
Source: Neal and Rigdon (1967).
5-115
-------
TABLE 5-52. CARCINOGENIC RESPONSE IN CC57 MICE
TREATED WITH BENZOfaJPYRENE
Mouse Dosea
(mg/kg/day)
1.0
0.1
0.01
0.001
0.0001
Equivalent
Human Dose
(mg/day)
2.68
0.268
0.0268
0.00268
0.000268
Incidence of
Forestomach
Tumors
23/27
23/30
5/24
2/26
0/16
Percent
85
77
21
8
0
BaP in 0.2 ml triethylene glycol was administered by intubation one time
per week for ten weeks of 83-week (19 months) study duration, beginning
when mice were 2-3 months old.
Source; Fedorenko and Yanysheva (1966).
5-116
-------
solution by intubation once a week for 10 weeks. It is assumed that
the control group response would be zero as in the previous study,
since this was the response of the group treated with 0.1 ug, and the
response of the group treated with 1 yg (8%) was also quite low. Thus,
it is presumed that all forestomach tumors reported here are attribu-
table to 3a? ingestion.
To obtain the human equivalent lifetime daily dose, the following
calculation was used:
human dose (mg/day) = animal dose (mg/mouse/wk) x - ,•• x ^: x
7 days 83 WKS
2/3
human weight
.animal weight
\ /
That is, 1 mg/day (human dose) is approximately equivalent to .373 (mg/
mouse/wk).
Estimation- of Human Risk
The three dose/response models used to extrapolate human risk
were the linear "one-hit" model, the multistage model and the log-
probit model. The multistage model is actually a generalization of the
one-hit model, in which the hazard rate function is taken to be a
quadratic rather than a linear function of dose. The one-hit and multi-
stage models assume that the excess probability (P) of a carcinogenic
response to daily dose (D) is described by:
~ e
- P(0)
where h(D) is the "hazard rate" function, and P(D) and P(0) are the
response rates at doses D and zero, respectively. For the one-hit
model, the hazard rate function is simply BD, while in the multistage
model, it is a quadratic function, B]D + B^2. The coefficients, B
or B-^ and 62, of the hazard rate functions are solved by least squares
regression of the data using linearized forms of the model equations.
For the "one-hit" model: BD = loge (1-P) ;
for the multistage model, B-j^D + B.^2 = log£ (1-P).
The log-probit model assumes that human susceptibility varies with
dose according to a log-normal distribution as follows:
P = £ (z) where z = A -f log10D and <£ is the cumulative normal
distribution function. Values of z are obtained from cumulative nor-
mal probability tables relating response rate P such that o (z) = P. Once
5-117
-------
th for the "probit"
the linear equation:
2 - A + log,. D.
j. 'J
All of the data applicable to the models were utilized to calcu-
late the parameters B, B-, + * or A. Although the EPA (USEPA 1979) ha
the°oTnhed f A" ^ gr°"P WMch S±VeS the l-rgest value of B in
the one-hit model should be used, this procedure was not followed here
because of the relatively small number of animals per group. Table
the DaT6f S the reSUll:S °f thS mathe-tical calculations! Values of
the parameters are given in the footnotes.
levelshindi^^e^an" P"dicted/esP°^es at the equivalent human dose
levels indicate the 'goodness of fit". Within each data set, comparable
fits are obtained by the three models. The extrapolated risk estimates
based on the^data of Neal and Rigdon (1967) and Fedorenko and Ya^e"
(1966) are given in Tables 5-54 and 5-55, respectively. Due to different
' the aCtUal -denying mathematical relationship
at thp r*ia,.< 11 "' "" extraP°lated risks are somewhat different
at the relatively lower exposure levels typical of human environmental
~*---*!gardl!ss--°f the mode1' higher risk esti— (by abrtal
v fTQ£.£\ j " * —~*" wii*. data of Fedorenko and Yany—
study. 6 t0 ChS hl§her equation "efficients calculated for this
1, -t, P°JS, °aUSe f°r the differen" ^ results for the two studies
tL Jrf ,V,tem f,r°m the dlfferent mod«s of oral administration. In
the study of Fedorenko and Yanysheva (1966), relatively higher doses
were administered by intubation once a week, which probably resulted in
higher exposure concentrations at the susceptible sites in the mouse
Alt"natively> food ™? have diminished the bio-availa-
in the experiments of Neal and Rigdon (1967) .
USEPA Risk Estimate
The U.S. EPA (1980) has established a zero ambient water concentra-
S?° f°r f Qaximum P^tection of human health from potential carcinogenic
effects of exposure to PAHs through ingestion of water and contaminated
ITal eachrSniSmS; -^ W** qU3lity Criterion is based on the assumption
^nL ^ff, rP?U\ 1S SS P°tent a carcino§en as BaP and that the carcino-
genic effect of the compounds is proportional to the sum of their concen-
ona^°nf' * g E Un?ar> non-threshold model, the EPA estimated, based
on the findings of Neal and Rigdon (1967), that a concentration of 2.8 ng
of 10-6 ^ 3Ce WatSr W°Uld reSUlt ^ 3n additional lifetime cancer risk
5-113
-------
TABLE 5-53. COMPARISON OF DOSE/EFFECT ANALYSES
USING THREE MATHEMATICAL MODELS
Response (%)
Equivalent Human
Dose (rag/day)
Based on
Neal and Rigdon
(1967):
.0095
.095
.19
.285
.38
.428
.476
.95
2.38
Based on
Federenko and
Yanysheva
(1966):
2.68
0.268
0.0268
0.00268
0.000268
* P = l-e-97D; B =
b p . ^-(1-670 -
c P = $(-.182 + log
d P = l-e"11'50; B
e p = !_e-C6.78D-2.
Observed
0
0
4
0
3
10
71
83
90
85
77
21
8
0
0.97
.272D2). B =1
10 D); A = -•
= 11.5
25I)2) . * - fi
; B- - b
One-hit
0.9*
8.8
17
24
31
34
37
60
90
d -
100
95
26
3
0.3
.67; B2= -0.272
182
.78; B,, = -2.25
Predicted
Multi-stage
1.6b
14
26
36
44
48
52
74
91
86£
81
16
1.8
0.2
log-0/probit
1.4°
11
18
23
27
29
31
41
58
92f
65
27
5.4
0.5
0(0.96 + log1QD> ; A = 0.96
5-119
-------
TABLE 5-54. PROBABLE UPPER BOUNDS ON EXPECTED EXCESS CANCERS PER
MILLION POPULATION DUE TO BENZO[a]PYRENE INGESTION
(Based on Neal and Rigdon (1967) Study)
Exposure Level (yig/day)
Linear
Model
Log-Probit
Model
Multi-Stage
Model
0.001 .01 0.1 1
1 10 100 1,000
10~3 10'1 14 750
1.7 17 170 ' 1,700
10 100
10,000 92,000
14,600 120,000
I6.ooo 151. onn
5-120
-------
TABLE 5-55. PROBABLE UPPER BOUNDS ON EXPECTED EXCESS CANCERS PER
MILLION POPULATION DUE TO BENZO[a]PYRENE INGESTION
(Based on Fedorenko and Yanysheva (1966) Study)
Linear
Model
Exposure Level (pg/day)
0.001 0.01 0.1
10
100
11 110 1,100 11,000 106,000 670,000
Log-Probit
Model
0.3 26 1,200 21,000 150,000 480,000
Multi-Stage
Model 7
70
680 6,800 65,000 480,000
5-121
-------
Possible Shortcoming in BaP Risk Calculations Utilizing Less
Than Lifetime Exposures _ ^ _
The range of possible excess cancers in humans ingesting BaP de-
termined in the preceding section is based on an assumption that the
total effective dose is equal to dose rate times dose duration. Ad-
ditional information presented by Neal and Rigdon (1967) allowed an
examination of the validity of this assumption in extrapolating short
duration animal exposures to BaP to the human situation. As the fol-
lowing discussion indicates, it appears that in the case of the two
available BaP studies, this assumption may not be valid.
Neal and Rigdon (1967) varied both the daily dose of BaP incor-
porated into the diet and the duration of feeding of the BaP-containing
diet. Animals were returned to a basal, untreated diet after a vari-
able period on the BaP-containing diet with most animals killed between
140 and 200 days from the start of the BaP exposure.
Their data, presented in Table 5-56, were analyzed by multiple
regression analysis using linear transformations of the log/probit and
one-hit models. In the log/probit model:
P(z) = 0(8., + B log Dat),
where: z - the value of B]_ + B2 logg Dat at the response rate P(z), and
D = daily dose of BaP
t = number of days on BaP diet
3^ and B2 = the probit intercept and slope, respectively.
The total effective dose is shown to be directly proportional to t
but a power function (Da) of daily dose. The exponent "a" should be close
to 1 if total effective dose can be approximated by D times t.
The linear transformation of this equation is z = 3± + (B2 a log D)
+ B2 loget. The coefficients B^, B2a, and B2 are obtained by least
squares regression. From this analysis, "a" was determined to be 1.6 which
is significantly greater than 1 (p <.01) suggesting that the total ef-
fective dose is not a simple product of D and t but is probably more
accurately estimated by the power function, D^'^) t. This result means
that dose rate has a stronger influence on response than dose duration.
This relationship between dose rate and dose duration can also be
demonstrated in the one-hit model:
P - 1 - e
5-122
-------
TABLE 5-56. COMPARISON OF DOSE/EFFECT ANALYSES WHERE
EFFECTIVE DOSE IS A POWER FUNCTION
Dailv Dose (D)
0.10
0.16
0.18
0.20
0.4
1.0
1.0
1.1
1.0
0.9
0.40
12.0
Duration (t)
110 (days)
110
110
%110
VL10
"-11 0
2
4
5
7
30
1
Observed
0.017
0.025
0.10
0.71
0.83
0.90
0.11
0.10
0.44
0.30
0.67
0.50
Response
Predicted (1)
0.10
0.23
0.27
0.31
0.61
0.90
0.07
0.19
0.20
0.23
0.27
0.79
(2)
0.07
0.15
0.19
0.22
0.55
0.98
0.07
0.15
0.16
0.19
0.20
0.91
Multiple Regression Results:
(1) log/probit model: P = (E^ + B a log D + B log t), 3 = -1.957;
B2a = 1.113; B2 = 0.692, a = 1.113/0.692 = 1.61
(2) one-hit model: P = l-e~(B D t), B = .035 a = 1.71
Source of data for columns 1-3: Neal and Rigdon (1967).
3-123
-------
where D, t and "a" are defined as above and "a" should again be close to
one if D times t is a good approximation of total effective dose. The
linear transformation is:
loge [-logg (1-P) ] -log t = log£B + a log D.
Solving for the coefficients by multiple regression "a" equals 1.71 and
B equals 0.035. Thus, the effective dose is more appropriately given
by: D^1-7' t. Again, the exponent of D is significantly greater than
one (p ^ .01).
Thus, both analyses indicate that in the case of BaP, dose rate is
more important than dose duration in determining the incidence of BaP-
induced forestomach tumors in mice. These results appear to contradict
the validity of the assumptions inherent in the established guidelines
(USEPA 1979) for computing risk to humans from ingestion of BaP, and
suggest that in addition to the possible increased sensitivity of the
rodent forestomach to tumor induction by BaP, extrapolation of high
exposure/short duration animal studies to determine excess lifetime
human risk may overestimate true risk.
Other Risk Considerations and Overview
Although the two animal studies discussed in the previous section
demonstrate a carcinogenic response to BaP in mice by the ingestion
route, the quantitative estimates of human risk must be treated with
considerable caution since they are dependent on a number of stated
assumptions that have high levels of uncertainty. Several considera-
tions which seriously undermine the validity of quantitative human risk
extrapolations for BaP have been discussed. For example, the mouse
forestomach has a different anatomy than the human stomach and may be
particularly sensitive to BaP. This difference in anatomy is indicative
of the fundamental problem of species to species extrapolation. Slight
differences in dose-effect relationship were obtained between the Neal
and Rigdon (1967) and the Fedorenko and Yanysheva (1966) studies which
were primarily attributed to the difference in mode of administration
but which may also have been caused by differences in dosing schedules.
Analysis of additional data from the Neal and Rigdon (1967) study indi-
cates that the total effective dose is probably not a simple product of
daily dose times duration but, in fact, may be a more complex power
function in which the dose rate has a greater influence on response
than treatment duration.
Another vital consideration in the extrapolation of carcinogenic
risks associated with PAH exposure is the metabolic differences, both
qualitatively and quantitatively, in the inducibility of the P-450 de-
pendent microsomal mixed function oxidase system which is involved in
the activation of tumorigenic PAHs to their ultimate carcinogenic
forms. Considerable variations are known to exist among various species
and significant individual variations have been documented for humans.
5-124
-------
Among the other PAH compounds in this group, benz[a]anthracene,
dibenz[a,h] anthracene, benzo[b]fluoranthene, and indeno[l,2,3-c,d]
pyrene are complete carcinogens for mouse skin; benzo[§,h,i]perylene is
a co-carcinogen with BaP; and benzfa]anthracene, benzo[b] fluoranthene,
chrysene and indeno[l,2,3-c,d]pyrene are all initiators of skin car-
cinogenesis in mice. Thus, for the most part, published reports on the
other PAHs in this group deal with localized tumor production and are
generally not considered relevant to the assessment of systemic car-
cinogenicity. We have, therefore, focused our attention on the risks
associated with BaP because (1) it is the dominant substance in this
group with respect to human exposure (see Section 5.3.2); and (2) re-
duction of BaP levels will presumably lead to reduction in exposure to
the other PAHs in this group. In addition to ingestion studies, BaP
has been shown to be animal carcinogen by dermal and intratracheal
routes. It is also a transplacental carcinogen, an initiator of skin
carcinogenesis in mice, and is carcinogenic in single dose experiments.
3enzo[a]pyrene is also the most active mutagen of the group, in-
ducing in vivo chromosomal aberrations in both hamster spermatogonia
and bone marrow cells and inducing positive mutagenic responses in
sister chromatid exchange tests. Mixed mutagenic responses have been
reported for the other PAHs in this group. Because of its mutagen-
icity, BaP exposure could also be expected to contribute to the genetic
burden of a population, but since extrapolation procedures for genetic
risks have not been well established, a quantitative risk assessment
for these kinds of health hazards is not presently feasible.
BaP appears to exert little effect on the developing embryo; data
were unavailable for the other compounds in this group regarding adverse
reproductive effects.
The major focus of studies conducted with PAHs in this group
has been their potential for inducing carcinogenic effects. Thus
little information is available on other possible toxic effects asso-
ciated with exposure to these compounds. However, in assessing the
risks to humans associated with exposure to these PAHs, one should not
overlook possible augmentation of effects through synergistic or co-
carcinogenic mechanisms. Current understanding of the co-carcinogen-
SUf
*» 11- estiation
5-125
-------
5.3.2 Human Exposure
5.3.2.1 Introduction
As is apparent from the preceding sections, monitoring data are
limited for the PAHs comprising the BaP group. This section examines
human exposure to benzo[a]pyrene and the other chemicals in this group
via ingestion (food and drinking water), inhalation, and dermal contact.
5.3.2.2 Ingestion
Drinking Water
Basu and Saxena (1978) sampled ten finished water supplies for
several PAHs, including BaP, benzo[g,h,i]perylene, indeno[l,2,3-c,d]-
pyrene, and benzo[k]fluoranthene. All of these chemicals were detected
in at least seven of the 10 samples (see Table 5-38). Most values
range from 0.2 ng/1-1 ng/1, and these as well as maximum reported values
are shown in Table 5-57. Removal efficiencies ranged from 77-100% for
plants using activated carbon; thus in plants of this type, concentra-
tions of BaP and related compounds would be expected to be low.
No data on drinking water levels were found for the other chemicals
in this group (chrysene, benz[a]anthracene, acenaphthylene, benzo[b]-
fluoranthene, and dibenz[a,h]anthracene). In addition, these chemicals
are rarely detected in ambient water (see Section 5.2.2). Table 5-57
shows estimated exposures for these other compounds based upon the
limited data available.
Food
Levels of the PAHs in raw foods appear to be generally low. However,
vegetables or fruits grown in the vicinity of air releases may contain
higher levels (U.S. EPA 1980). The highest levels of the BaP group PAHs
in food, however, appear to result from the cooking process, especially
charcoal broiling and smoking. Table 5-58 estimates daily exposure by
consumption of such foods, and lists the various assumptions made in
deriving the estimates. The data on contamination levels were taken
from the U.S. EPA Criteria Document (U.S. EPA 1980) and White and
Vanderslice (1980). It is apparent that data are limited for many of
these chemicals. As a result, the columns in Table 5-58 were not totaled,
since the exposure estimates shown represent only an unknown portion of
the actual total exposure. In addition, the maximum intakes represent a
level of maximum contamination and consumption of the food item. Hence
the total is meant to represent a worst case and is not representative
of widespread exposure. Charcoal broiling represents the major source
of exposure to the BaP group PAHs via food. Consumption of large amounts
of food cooked in this manner could result in a high exposure, perhaps up
to about 6 yg/day (intake from charcoal-broiled beef and smoked pork).
5-126
-------
TABLE 5-57. ESTIMATED HUMAN EXPOSURE TO THE BENZO[a]PYRENE
GROUP PAHs VIA DRINKING WATER
Benzo[a]pyrene
Acenaphthylene
Benz[a]anthracene
Benzo[b]fluoranthene
Benzo[k]fluoranthene
Benzo[g,h,i]perylene
Qirysene
Dibenz[a,h]anthracene
Indeno[l,2,3-c,d]pyrene
Concentration (ng/1)'
Typical Maximum
0.3
NAC
NA
NA
0.3
2.0
NA
NA
1
1.6
NA
NA
NA
0.7
4.0
NA
NA
1.7
Estimated Daily
Exposure (ng/day)
Typical Maximum
0.6 3.2
0.6
4.0
1.4
8.0
3.4
For locations see Table 5-38. Typical concentrations are average values,
the data on Ba? from New Orleans was excluded from the average.
Intake assumed to be 2 liters of water per day (ICRP 1975).
'NA = Not Available.
Source: Basa and Saxena, 1978.
5-127
-------
•I-AHI.I: •,-•,». I.KVU.S OK uKNa.|.i|rvki-.Ni-: <;K,.
IS IN
AND I-STIMAI'CII l-.Xr<>:.ll|{|-. VIA INCISTIIlN (IK KIM ID
•-- - »r>L'">I-'ll'*"•'<•• _ . Ben/lajanlliiaeene lleiiioli;,!., i J.-oryJoiif »-|lr>
(.onsnnipi luii (.oiit.-imlii.il Ion Intake Com ami nal ion Intake Com ami nal ion Intake Himl ami nai ion Intake
Typical yM.,»7 Tyi-J-al ^Max. Ty,ura, '"fa. ', vn , ^."'Ix. Typ^M.!,. Typiea^axV TVP ,'.' a, ''" M.L Ty,, S [" "L. , V1,'"a^Nax
rh.irciM 1 hro i K'tl
1., Ci'1
tLiuibur^h NA
V.-ijelaMe-. loial 2/.8 NA
l.ealy 40 NA
NA 2.1, NA
S •)!) 0.02
2 V. 0.002
NA 4 O.OOli
1 1? O.dOOl
1 H 0.1)2
O.O/ 1, O.OO'i
NA 0. 1 NA
<>.UI 0. 1 0.002
NA 7.i NA
O.O!
>. . 1
I.S
0. 12
(I. '>
(I. U
1.2
(1.08
0. 2
0. 1
NA
J
)
0.2
1
1
NA
NA
NA
NA
J) 0.00)
2 O.OOOJ
IB'» .11001
)o 0.02
NA NA
NA NA
NA NA
50 NA
.0 1
2.7
0.9
(1.06
2.«,
0. ')
NA
NA
NA
NA
i r>
6 12
2 2')
NA 1.0
1 .'.4
1 4.0
NA NA
H,\ NA
N^ NA
NA 8
0.01
0.02
0.002
0.005
O.O001
0.02
NA
NA
NA
NA
0. li
1.0
0. J
O.O 9
O.OJ
0.07
NA
NA
NA
0. 1
NA I
1 ')
NA 2 . .'
NA NA
1 171
NA I.'
NA NA
NA NA
NA NA
NA Ml
NA
.11(11
NA
NA
O.IIOOI
NA
NA
NA
fn
NA
0.01
(I. 8
0.06
NA
2.4
0. 2
NA
NA
NA
1.2
(:oiu-,i.i«|.li.,n ol lici-f - 86 g/il.iy, t'.Z ch.ircoul- l.roi h-d - KO,: li.i»ilnirK>-r, 20J: btuak.
Win si rase maximiim 86 g cimaunipt ion of rlurco.il-l.r.ii I, tion of fi.sh - l/i is/day. 1% tinoked. Worst case ni.ixiinniii. I', K/^-IV .-.nMikeil.
NOUJ: TypJtdl roiisiuoptiuii refers to av^rat;e ionsuiii|>t ma Ic.r in.il.-s
2 )•)'.; ivpu-al i-unoenir.it Ions are not actual .ir! linnet i<-
.•ive.rjt-t.-s due to I lie widely varied nature of III. simile-., lull
are meant l_o approximate such an average.
boime: IISliA (1978, IWU). U.S. El'A (1980), White and Vandersl I.-e (1980).
-------
5.3.2.3 Inhalation
The U.S. EPA (1980) has summarized the available data for PAH levels
in air, mostly for urban areas. These data, although limited, were
utilized in developing exposure estimates for an assumed respiratory
flow of 20 m-Vday (ICRP 1975). These results are shown in Table 5-59
As was found for food and drinking water, BaP generally appears to
represent the largest exposure of chemicals in this group.
As discussed in Section 5.2.4, Moschandreas et al. (1980) examined BaP
concentrations indoors. These authors found concentrations indoors to be
similar to those outdoors on non-woodburning days, but higher indoor con-
centrations on wood-burning days. The mean level indoors on woodburning
days, however, was 4.7 ng/m3, which is within the range for urban and
rural shown in Table 5-59.
In addition to ambient air, smoking can contribute to inhalation of
PAHs Schmeltz et al. (1975) reported that mainstream smoke contained
0.025 ug BaP and 0.044 ug benz[a]anthracene per cigarette. A side-
stream rmainstream ratio of 3.4 for BaP was also reported, resulting in
a sidestream smoke content of 0.085 ug BaP per cigarette. Thus, exposure
of smokers to BaP in mainstream smoke could range from .025-2.5 ug/day
depending upon the type of cigarette smoked, the amount inhaled, and the
number of cigarettes smoked, assuming a range of consumption of 1-100
cigarettes per day (U.S. DHEW 1979). An estimated 33.2% of adults over
17 years old smoke cigarettes or 54.1 million persons in the United
States. Of smokers, 25-30% smoke more than 25 cigarettes per day
(U.S. DHEW 1979); thus, a large segment of the population could be
exposed to BaP at levels greater than 0.6 ug/day.'
In addition, nonsmokers nay be exposed to BaP through inhalation
of sidestream smoke. Although only a few measurements of BaP have been
taken in smoke-filled rooms, concentrations may be estimated from measure-
ments of CO levels, which have been summarized by Burns (1975). The
results are not consistent, and apparently depend upon a number of
variables. They show levels of 44-92 mg/m3 C0 in rooms (38-92 in3) where
30-80 cigarettes had been smoked with no ventilation. The Surgeon
General's Report (U.S. DHEW 1979) reported levels up to 50 mg CO produced
in sidestream smoke per cigarette, as compared with the 0 085 ua BaP pro-
duced per cigarette. Thus, by analogy, a room concentration of 0 08-0 •>
Ug/m-3 can be calculated. Alternatively, using Q.Q85 ug BaP/cigarette
and assuming a room size of 48 mj with no ventilation in which 40
cigarettes were smoked, a concentration of about 0.07 ug/m3 can be
calculated. A nonsmoker exposed to such a situation 2 hours/day would
receive about 0.25-0.7 ug/day, assuming a respiratory flow of 1.8 m3/hr.
These values would tend to overestimate exposure since no ventilation was
assumed, and a high respiratory flow was used in the calculation.
Smokers in the same situation would receive the combined intake from
sidestream and mainstream smoke.
5-129
-------
TABLE 5-59. ESTIMATED EXPOSURE TO BENZOfa]PYRENE GROUP PAHs VIA
INHALATION OF AMBIENT AIR
Ambient Concentration (nR/m )
3, a
Co
O
Benzofajpyrene
Benzfa]anthracene
Benzofb]fluoranthene
Benzofk]fluoranthene
Benzo[g,h,i]perylene
Chrysene
Indeno|l,2,3-c,d]pyrene
Urban
1-100
0.1-20
o.i -10
0.1-10
0.2 -50
0.2 -10
0.3 -1.3
Rural
0.01-10
7-50C
Intake (ng/day)
Urban Rural
20-2000 0.2-200
2-400
2-200
2-200
4-lpOO 140-1000
4-200
6-30
U.S. EPA (1980), White and Vanderslice, 1980.
Based on respiratory flow of 20 m3/day (ICRP 1975).
CThere are not enough monitoring data to explain this apparent
lack of difference between urban and rural areas.
-------
There are problems with using CO levels to estimate BaP levels in
a smoke-filled room since they would be due to sidestream smoke and
exhaled mainstream smoke. In addition, the concentration of CO and
BaP would be influenced by type and amount of tobacco smoked, extent of
inhalation, size of room, ventilation, and duration of exposure. The
estimates provided above are probably on the high side since worst-case
assumptions were frequently made.
The U.S. EPA (1978) estimated the sizes of populations exposed to
various levels of BaP in the United States using SRI data for areas
with coke ovens and ambient data or national average concentrations for
other areas. Their results are shown in Table 5-60.
5.3.2.4 Dermal Contact
No direct information is available regarding the dermal exposure
of humans to this group of PAHs. However, due to the low levels found
in drinking water, dermal exposures are expected to be low.
5.3.2.5 Overview
Estimated typical daily exposures to the BaP group PAHs are shown
in Table 5-61. Data are unavailable for estimating exposures to some
of the compounds in the group. Smoking appears to be the most
significant exposure route for benzo[a]pyrene and benz[a]anthracene.
A smoker consuming 25 cigarettes per day could be inhaling 600 ng and '
1100 ng of these compounds, respectively.
Food, primarily charcoal-broiled and smoked meats and fish, is
also a significant exposure medium for BaP, benzo[g,h,i]perylene, and
benz[a]anthracene, although inhalation exposures at the upper limit of
the concentration ranges reported for urban areas are greater in every
case. By contrast, although monitoring data are very limited, drinking
water appears to contribute relatively small amounts to typical daily
exposures.
Data concerning levels of these compounds in foods are variable,
as are atmospheric concentrations reported for urban areas. Therefore,
some subpopulations (i.e., those consuming large amounts of charcoal-
broiled and smoked meat) may be exposed to considerably higher levels
(possibly as high as 6 ug/day from food consumption alone).
5-131
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TABLE 5-60. ESTIMATED SIZE OF THE U.S. POPULATION EXPOSED TO RANGES
OF BENZO[a]PYRENE CONCENTRATIONS IN AMBIENT AIR
Population (1000's) exposed to BaP Concentration (ng/m3)
>5.0 1.0-5.0 0.5-1.0
-------
TABLE 5-61. ESTIMATED HUMAN liXI'OSIIKK TO THE Bf.N/.O| .1 | I>YKENE CKOUI' I'Allh
1
U)
Exposure Ben.:|a|- Duniolb)- Hi-n/o|k|-
Koiiti- flaP Aceiiapjitliyjcnu ant liraci-ne 1 1 not .inthein' 1 1 not ant hem'
ln(!'-.st ion
l)i ink in;; Water O.fe 0.6 NA NA NA
Food 50 NA H>c NA NA
hiha} at ion
Urban 10-60 [IA t,-'tl> 2-10 4 100
Kural 2
Sinr.klliR 600 HOD
Bi-nxol (; ,h , 1 1 - Dil>en^|^
|>crylene Chi^s^ni- .inihi.tr
».'. NA1' NA
'ill1 'Jc NA
4 -1811 4 -1JO NA
J"Tyi>ic.il" as used IKTC i^ a qualitative eat imaic ba&ed on avuraj;L> coiisnuipt ion and a ranyi-' ol n'|">ii>-il fiincent rat inns,
NA - not avallable.
,h|- Ind.-nol I ,2,3-c,
lVcry lii.iilrd data ,iro dvailablu conccrniiiR tlu- diulary intake- of tlu-sc compounds. Tims, this ..nly n-pn;si-nl b a |iartial pa t iin.il.-.
Soun e : For assuiiipt ions and rcforcnccs, see text.
NA
-------
5-4 EFFECTS AND EXPOSURE—SON-HUMAN BIOTA
5.4.1 Effects on Non-Human Biota
5.4.1.1 Introduction
No data from acute toxicity bioassays were available for benzo[a]-
pyrene or any o.ther PAHs in this group, but several studies have been dene
that indicate the general concentration ranges that cause toxic effects
in marine and freshwater organisms.
5.4.1.2 Plants and Microorganisms
In studies on the effects of PAHs on Escherichia coli, BaP was
found to be highly toxic when in colloidal suspension in the presence of
light and oxygen. The authors suggest that the toxicity of BaP was
probably due to its photo-oxidation products. The concentrations of BaP
at which toxicity occurred, however, were not reported (Harrison and
Raabe 1967).
Haas and Applegate (1975) studied the effect of PAHs at concentrations
of 10-->, 10~°, and 10" M on _E. coli; (approximate calculated concentra-
tion range, 25-2500 ug/1 BaP). Benz[a]anthracene, dibenz[a,h]anthracene,
and benzo[a]pyrene all promoted growth in bacteria at these concentrations.
Similar growth-stimulating effects of PAHs have been shown with
freshwater algae. Graff and Nowak (1966) reported that concentrations of
10-20 ug/1 of BaP, benz[a]anthracene, benzofbjfluoranthene, indeno[1,2,3-
c.djpyrene, and benzo[g,h,i]perylene promoted growth in the algae
Chlorella yulgaris, Scenedismus obliquus, and Ankistrodesmus oraundii.
5.4.1.3 Animals
No standard toxicity tests were found for the compounds in this
group. In the only study examining mortality, benz[ajanthracene was
found to cause 87% mortality to the freshwater fish, bluegill (Lepomis
macrochirus) at 1.0 ug/1 in 6 months (Brown et^ al. 1975).
Various other effects have been reported in the literature. For
example, Haranghy (1956) reported that concentrations of 0.2-1.0 ug/1
BaP injected into the visceral sac of freshwater mussels resulted in a
significant decrease in filtration rate. The author suggested that Ba?
inhibited ciliary activity or possibly the entire metabolism of the
mussels. Exposure of marine calcarious sponges, Leucosolenia complicata
and _L. variabilis. to 5 g/1 BaP caused tissue damage and abnormal growth
(Korotkova and Tokin 1968).
Several studies on aquatic invertebrates and lower vertebrates,
including sponges, newts, and toads, have shown that PAHs in this
group can produce cancer-like growths and cause teratcgenetic and
5-134
-------
mutagenic effects. The number of species examined is small; however
though no exact concentration levels for these effects were given it
is believed that they were caused by concentrations higher than those
generally found in the environment (Neff 1979).
Flat fish (English sole, Parophrys vetulus) exposed to hydrocarbon-
contaminated sediments near the industrialized City of Seattle'were
found to have a significant number (32% of the adult population) of liver
tumors (Malins 1979). It appeared that these fish had absorbed PAHs and
PCBs from the sediment. Fish of the same species taken from relatively
clean areas of the Washington coast were almost free of this disease.
PAHs specifically were not detected in liver samples of these fish, but
the authors theorized that these compounds had been absorbed to some
degree and metabolized. It is known that metabolites (e.g., diol-epoxides)
of certain higher-molecular-weight aromatic hydrocarbons are carcinogenic,
(Slins^gT * W6re n0t identified in liver samples in this study
In related work, Malins (1979) showed that liver enzymes of English
;*f nsf elv.metab°lize benzo^pyrene to intermediates that interact
fnrnJ-n' ^ AJnterac5lons aTe thought to be a starting point for tumor
formation. Studies with freshwater trout (Salmo trutta lacustris) have
shown that trout liver microsomes actively biotra^ifo^ed benzo[a]pyrene
into a variety of electrophilic metabolites and catalyzed binding of
activated BaP to DNA. Similar studies showed that liver enzymes'from
. echo salmon (Onchorhynchus kisutch) and starry flounder (Platichthvs
Mfrf^vA^6113^617 metabolized Bap ^to reactive intermediates that
found i ?h (Varnast^' 1979>« Although no data on BaP concentrations
f2fTfHV "a^al Washington sediments were available, it is strongly
felt (Malins 1979) that the liver disease seen in the benthic English sole
was associated with contaminated sediments. "ignsn sole
5.4.1.4 Conclusions
Since the toxicity data for the BaP group PAHs are very limited it
is not possible to make any conclusions as to the toxicily of BaP or"
another PAHs. The toxicity data that are available are sularlzed
Concentration
(ug/1) Compound Effect
1'° (benz[a]anthracene) Caused 87% mortality
in Bluegill in 6 months
10~20 (BaP, benz[a]anthracene, benzofb]- Promoted growth in
fluoranthene, indeno[l,2,3-c,d]- freshwater algae.
pyrene, benzo[g,h,i]perylene)
25-2500 (benz[a]anthracene, dibenz[a,h]- Promoted growth
anthracene, and BaP) in bacteria.
5-135
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5.4.2 Exposure of Non-human Biota
5.4.2.1 Introduction
PAHs are found in various aquatic and terrestrial environments.
From monitoring data, it appears that higher concentrations are generally
found near industrialized areas, major ports, and areas of petroleum or
other fossil-fuel related activities. In some remote locations, such as
the coast of Greenland and areas of peat deposits, concentrations of
PAHs, particularly BaP, may be higher than general background levels in
pristine" areas. The source of these high concentrations is believed
to be biosynthesis of PAHs from naturally-occurring quinones in anaerobic
sediments, and leaching of BaP from peat deposits, which are known to
contain high concentrations of PAHs (Neff 1979).
This section will examine the exposure of biota to PAHs, considering
both the levels and the types of locations where it may occur.
5.4.2.2 Monitoring Data
The STORET monitoring data provide a basis for examining aquatic '
exposure. Summary descriptions and concentration distributions for each
PAH in the BaP group are given in Section 5.2.2. Observations of values
greater than the detection limit (unremarked data) are infrequent, with
only 17 such observations of a total of 3,261 observations in water for
this group. A greater percentage (14%) of the sediment values were
unremarked; 83 of 600 total observations. Unremarked observations for
both sediment and surface water are presented in Table 5-62.
Overall there were three observations of the PAHs in the BaP group
greater than 1000 yg/kg in sediment.
Many of the higher sediment values occurred consistently in several
locations, including Puget Sound, coast of Washington State and Oregon,
San Francisco Bay and north coastal California, a hazardous waste site
in North Carolina, and the Houston ship channel.
5.4.2.3 Aquatic Fate
Environmental conditions have a significant influence on the
disposition of BaP and related PAHs in aquatic systems and, hence, on
the exposure conditions. These compounds are quite insoluble in water
and chemical transformation processes; e.g., photolysis, are not as signif-
icant as with the lower-molecular-weight PAHs. EXAMS data for BaP
indicate that in five of the six environments examined, nearly all
(^98%) of the compound is accumulated in the sediments. These observa-
tions are confirmed by monitoring data that indicate a propensity of
these PAHs to accumulate in the sediments. In the oligotrophic lake,
a greater percentage (18.75%) of BaP remained in the water column, but
5-136
-------
TABLE 5-62. SUMMARY OF UNREMARKED OBSERVATIONS OF CONCENTRATIONS
OF 3ENZO[a]PYRENE GROUP PAHs IN SURFACE WATER AND
SEDIMENT—STORET, 1980
Compound
Number of
Observations
Range of
Observations
Acenaphthylene
Benz[a]anthracene
Benzo[k]fluoranthene
Chrysene
Benzo[a]pyrene
Acenaphthylene
Benz[a]anthracene
Benzo[k]fluoranthene
Benzo[g,h,1]perylene
Chrysene
Dibenz[a,h]anthracene
Surface Water (ug/1)
6
5
5
1
Sediment (us/kg dry weight)
11
12
12
12
5
11
0.01-0.12
1-400
320-1500
0.02
0.02-1400
0.002-93
6.2-340
0.9-1300
4.3-40.9
0.06-120
15.7-2600
Source: See Table 5-34.
5-13:
-------
the remainder still went to the sediments. BaP in sediment is less
likely to be physically transported than BaP in the water column. It
is likely to persist chemically unchanged because the conditions con-
ducive to chemical degradation (light, oxygenation) are not present.
In addition, microbial biodegradation is not a significant fate process
for any of the BaP group compounds. These characteristics suggest that
although monitoring data for sediment are limited, this medium may present
an important exposure route. Therefore, uptake from sediment was
examined.
5-4.2.4 Factors Affecting Bioavailability of Sediment Concentrations
It is known that aquatic biota are exposed to PAHs directly from
water, but the extent to which they may be exposed to sediment con-
centrations of these compounds is less well understood.
Accumulation of hydrocarbons, including PAHs from oil-contaminated
sediments by the English sole Parophrys vetulus has been investigated
(McCain _et_ al. 1978). Results from several separate studies (Roesjadi
et al. 1978, Fucik et al. 1977, Anderson et al. 1974) indicate that
overall uptake of PAHs is not significant, but is greater by suspension
feeding benthic invertebrates than deposit feeders, and that accumula-
tion by fish is greater from water than from sediment. The conclusion
has been made that any PAH that is taken up comes, to a greater extent,
from dissolved PAH in interstitial waters and from PAH in the water
column (dissolved and/or adsorbed onto suspended solids) rather than
desorbed from the sediment itself (Neff 1979).
These studies also indicated that sediment adsorbed PAHs are not
readily metabolized by benthic invertebrates. However, based on the
few species studied, it is impossible to quantify the degree to which
accumulation of PAHs in sediment represents a major source of exposure
to aquatic biota.
5.4.2o5 Conclusions
Scattered observations for the PAHs in this group reveal that
they are detected infrequently in water and when found are in the low
yg/1 range. Unremarked observations indicate that these PAHs may be
found to a greater extent and in higher concentrations in sediment.
The possible contribution of naturally-occurring PAHs to these levels
is unknown. Sediment concentrations do appear to be consistently
higher near industrialized areas, however, and levels as high as
2600 ug/kg have been detected.
Environmental fate and monitoring data indicate that BaP group
PAHs may accumulate to potentially high levels in the sediments. The
extent to which these compounds are available to biota from the sediments
is not well understood or quantifiable at this time, but experimental
evidence indicates that although some PAHs are taken up by benthic
organisms directly from sediment, the PAHs present in interstitial
waters and adsorbed to suspended particulates are more available for
uptake by biota.
5-133
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5.5 RISK CONSIDERATIONS
5.5.1 Introduction
An objective of the risk assessment process is the quantification
of risks to various subpopulaticn groups of humans and other
classes of biota. Quantifying such risks requires:
• Careful identification of the subpopulations at risk and
the populations exposed;
• Evaluation of the ranges of exposure for each subpopula-
tion;
• Determination of the effects levels or dose-response data
in the species of concern and/or proxies for these species
(for example, laboratory animals as a proxy for humans);
and
• Extrapolation of dose/response data to the subpopulations
at risk.
The largest data base available for estimating the risks associ-
ated with human exposure to PAH compounds in the benzo[a]pyrene group
is that available on BaP. Dose-response data for BaP-induced fore-
stomach tumors in mice and information on the range and types o'f human
exposure to BaP are sufficient to allow estimation of the potential
risks associated with continuous lifetime exposure to some level of
BaP. Information on exposure and effects for the other PAHs in this
group is lacking and no quantitative estimates of risks associated with
exposure to these compounds is possible at this time.
Extensive uncertainties are inherent in the extrapolation of car-
cinogenic findings in laboratory animals to humans. Additionally,
because of an inadequate understanding of the mechanisms of carcino-
genesis, a scientific basis has not been developed for selecting among
several alternative dose-response models, which yield widely differing
results. Therefore, we have applied three dose-response models to the
data, and the results provide a range of potential human risk associated
with exposure to BaP.
In the case of risks to other forms of biota, insufficient data
are available on most toxic effects and on exposure levels to assess
risk quantitatively.
5-139
-------
5.5.2 Human Exposure
A series of possible exposure routes for humans with an indication
of the size of the population at risk and typical exposure levels are
presented in Table 5-61 and also in Table 5-63 with the estimated population
sizes. Exposure levels of BaP appear to be the largest of the chemicals
in the group via drinking water, food, and air (see Section 5.3.2), but
this may be because monitoring data are limited for the other compounds.
Smoking appears to be the most significant exposure route for benzo[a]-
pyrene and benz[a]anthracene. A smoker consuming 25 cigarettes per day
could inhale 600 ng and 1100 ng of these compounds, respectively.
Food, primarily charcoal-broiled and smoked meats and fish, is also
t1K ' >,ne, « benzfa]-
anthracene, although inhalation exposures at the upper limit of the
concentration ranges reported in urban settings are greater in everv
case. By contrast, although monitoring data are very limited dr-nkin^
water appears to contribute relatively small amounts to typical daily °
exposures. •*
Data concerning levels of these compounds in foods are variable
as are atmospheric concentrations reported for urban areas. Therefor
some subpopulations (i.e., those consuming large amounts of charcoal-
broiled and smoked meat) may be exposed to considerably higher levels
(possibly as high as 6 ug/day from food consumption alone)
5=5.3 Human Risk
5.5.3.1 Carcinogenicity
_ Several PAHs in the benzo[a]pyrene group are well established an-
imal carcinogens, co-carcinogens and/or tumor initiators; others have not
been demonstrated to induce tumorigenic responses (see Section 5313)
The capacity of individual PAHs to induce positive responses in humans is
not so well established. This is primarily due to the fact that human ex-
posures have not been to individual chemicals but rather to combinations*
as they occur in coke oven emissions, coal-tar, soot or from environmental
exposures to tobacco smoke or exhaust fumes. Numerous studies have shown
increased incidences of lung, skin and other types of cancer among
??lJjr?o5??08ed t0 C°ke °V6n emlssions, coal gas, coal tar and pitch
(IARC 1972). These studies, however, do not allow identification of the
individual chemical(s) responsible, do not account for possible syner-
gistic or co-carcinogenic effects resulting from other components, often
are unable to clearly define exposure levels and generally are not
amenable to quantifying human risk.
For the most part, available data for specific PAH compounds ar»
from skin painting and subcutaneous or intramuscular injection exper--
ments in mice. Few oral or inhalation experiments have been conducted
and those that are available are generally inadequate for risk assess-'
ment purposes.
5-140
-------
TAIIIJ- V-ftJ. KSTIMAII.I) HUMAN KXTObUKL TO HII' IlKNZOf.i ll'YKENK CltOlM' I'AMs
llHlenO
I'opolallon-1 llenzolal Honz|.i|~ lien/o|b|- Henzo|k|- tk-n/ol K,b, 11- IHben/.|a,li | - | I , 2, l-i- ,il |-
Lx!^'*J."L!:_J^i".t>l IL^..... -__rXJ"SJlu ^enapbi by lene .inijirai-ene f luouiiithi-ne I luorjntlitMie perylene Clirysene aiithrai-eni- pvrene
lni;ebt ion
III inMilB Water 220.6 x 10 0.0006 0.0006 NA' NA NA 0.0004 NA NA U.IKIL'
I'ood 220.6 x 106 0.05 NA O.Ol'1 NA NA 0.06'1 0.001d NA NA
(j, luli.il.il Ion
I 6
^J. Urban 165.6 x 10 0.02 - 2 NA 0.1102 - 0.4 0.002 - 0.2 0.002 - 0.2 0.004 - 1 0.004 - 0.2 NA O.OOii - 0.0)
liural V).l x U/' 0.0002 - 0.2 0.14 - 1
Smoking V, .1 x 106 0.6 I.I
'U.S. Di'partiiiunl of Coiwncrie (1980).
"ryi.lc.il" a-., na<-J lu-ie is a c|ualltatlvc csLlraan- based on aviTj^L- i-oiibnmpl ion .in.I ,i range of n-porti-J < onrtntr.it ions.
NA - not aval lalile.
'Vciy limited data .ire dv.il 1,-ible conLernlni; the tlleinry Intake ol I lies.e fonptiun.lb. Ibiis, till:, only i.presents a (.arti.il ebtiuiale.
IJWW'L: KOI iis.suiii|iL iona anJ lelereiues, but S.'diun 5..1.2.
-------
Benzo[a]pyrene has been most extensively studied of all PAHs in
the benzo[a]pyrene group. BaP has been shown to be both a local and
systemic carcinogen by oral, dermal and intratracheal routes in animals.
It is also a transplacental carcinogen and an initiator of skin carcin-
ogenesis in mice. Few studies have adequately examined the carcinogenic
effects of orally administered BaP but two ingestion studies whose
data appear to lend themselves to dose/response extrapolation, one by
Neal and Rigdon (1967) on CFW mice, the other by Fedorenko and
Yanysheva (1966) on CC57 mice, resulted in the production of forestomach
tumors in this species. Dose-response values based on these two studies
were estimated using three extrapolation models (see Section 5.3.1.4), A
summary of the risk estimates obtained for these two data sets from the
various models is presented in Table 5-64. Risk estimates are shown for
continuous lifetime daily exposures ranging from one nanogram to 100
micrograms. The gap between the estimates is large in the low-dose
region. However, present scientific methods do not permit a more ac-
curate or definitive assessment of human risk.
The interpretation of these calculated risk estimates is subject
to a number of important qualifications and assumptions which were
discussed in Sections 5.3.1.3 and 5.3.1.4:
• The site of tumor production and probable underlying mech-
anisms are possibly unique to laboratory rodents. The rodent
forestomach has a different anatomy than the human stomach
and may represent an unusually sensitive assay of the car-
cinogenicity of BaP by the oral route. The absence of tumors
at sites other than in the forestomach raises questions as
to the significance of these findings to the risks to hu-
mans from ingestion of BaP.
• Assuming that the positive findings indeed provide a basis
for extrapolation to humans, although dosing route may be
significant, we have assumed that absorbed dose by inhala-
tion or ingestion has the same effect.
• A vital consideration in the extrapolation of risks asso-
ciated with PAHs in general, and BaP specifically, is the
existence of metabolic differences, both qualitatively
and quantitatively, between humans and other species.
The degree of individual genetic variation of some activating
enzymes is suspected to be a key factor in an organism's susceptibility
to PAH-induced carcinogenesis. The highly heterogeneous nature of human
populations exposed to BaP introduces a confounding factor in reliably
predicting excess cancer incidences due to Ba? exposure.
• Both animal studies, and especially the study by Neal and
Rigdon (1967), were of less than lifetime duration. Doses
were administered for about half the duration of the experi-
ment in both studies. In order to adjust animal dose
5-142
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TABLE 5-64. ESTIMATED LIFETIME EXCESS PROBABILITY OF CANCER TO HUMANS
DUE TO BENZO[alPYRENE INCESTION AT VARIOUS EXPOSURE LEVELS
BASED ON THREE EXTRAPOLATION MODELS''1
r T i t /, Estimated Lifetime Excess Probability of Cancer at Indicated Exposure Level
Exposure Level dig/Jay) Q.QQ1 Q.Q1 QJL 1 1Q ' ~ToO~
Extrapolation Model
Linear Model
Neal and Rigdon data 1 x 1Q~6 1 x 1Q~3 1 x 1Q~4 1 x 10~3 1 x 10~2
Fedorenko
and Yanysheva data 1.1 x 10~5 1.1 x 10~4 1.1 x 10~3 1.1 x 10~2 1.1 x 10~3
Logj-probit Model
Neai and Rigdon data 1 x 10~ 1 x 10~7 1.4 x 10~5 7.5 x 10~4 1.5 x 10~2
Ln
,L Fedorenko
£ and Yanysheva data 3 x 10~7 2.6 x 10~5 1.2 x 10~3 2.1 x 10~2 1.5 x 10'1
Multi-stage Model
Neal and Rigdon data 1.7 x 10~6 1.7 x 10~5 1.7 x 10~4 1.7 x 10~3 1.6 x 10~2
Fedorenko
and Yanysheva data 7 x 10~6 7 x 10~5 6.8 x 10"4 6.8 x 10~3 6.5 x 10~2
9.2 x 10 2
6.7 x HT1
1.2 x 10"1
4.8 x 10"1
1.5 x 10-1
4.8 X 10"1
a
The lifetime excess probability of cancer represents the increase in probability of cancer over the
normal background incidence, assuming that an individual is continuously exposed to BaP at the indi-
cated daily intake over a 70-year lifetime. There is considerable variation in the estimated risk
due to uncertainty Introduced by the use of laboratory rodent data, by the conversion to equivalent
human dosage, and by the application of hypothetical dose-response curves. In view of several
conservative assumptions that were utilized, it is likely that these predictions overestimate the
actual risk to humans.
-------
schedule to an equivalent daily lifetime human dose, two
assumptions were utilized as recommended by the USEPA
(1979). First it was assumed that the response would be
the same if the total dose was distributed evenly over the
entire experimental lifetime of the animal. Second, it was
assumed that a short-duration study attributable to either
early mortality or early termination leads to an'over-
estimation of the dose required to produce the observed
effect. The average daily dose for the Neal and Rigdon
data was adjusted to reflect the actual experimental life-
time versus the theoretical lifetime of the experimental
animal. In treating the Neal and Rigdon data, this adjust-
ment lead to a marked reduction (vL/40) in the effective
daily dose level.
• Slight differences in dose-effect relationship
between the Neal and Rigdon (1967) and the Fedorenko
and Yanysheva (1966) studies which were primarily
attributed to the difference in mode of administration
(diet vs. gavage, respectively). These may also have
been caused by differences in dosing schedules.
• It appears that the total effective dose for the Neal and
Rigdon study is probably not a simple product of daily dose
times duration but, in fact, may be a more complex power
function in which the dose rate has a greater influence on
response than treatment duration.
• Development of PAH-induced tumors can be altered by compo-
nents in the diet, exposure to inducers or inhibitors of
microsomal enzymes, as well as cocarcinogenic effects such
as from substances present in cigarette smoke.
Keeping these qualifiers in mind, the risks shown in Table 5-64
were combined with the known BaP exposure levels (Table 5-63) to
estimate per capita lifetime risks and incidence (excess cancers/year)
for BaP exposure routes as shown in Table 5-65.
The highest estimated carcinogenic risks appear to be associated
with the subpopulation that smokes. In the general population, the
highest estimated risks are associated with exposure to Ba? in the
diet (e.g., charcoal-broiled meats and fish). Inhalation exposure at the
upper limit of the reported concentration ranges in urban areas are
higher but are based on limited monitoring data. In contrast, continu-
ous lifetime consumption of BaP-contaminated drinking water at typical
concentration levels presents the lowest potential carcinogenic risks.
5-144
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TABLE 5-65. ESTIMATED RANGES OF CARCINOGENIC RISK TO HUMANS DUE
TO BENZ()[a]l'YRENE EXPOSURE FOR VARIOUS ROUTES
UoiiL_e_
Typical Diet
Average Lifetime
Bal' Exposure Size of Exposed Estimated Lifetime Excess Estimated Incidence
(jliiAliiyJ Population Probability of Caticej:' (e_xces_s cancers/year)
0.05
x LO
x 10 to 6 x 10 '*
3 - L.900
!)r i nk Lug Water
0.0006
221 Y. 10
6
I. x 10 t.o 7 x 10
Ui
I
h-1
-f>
Oi
Ambient Air - Urban
- Rural
Smoking
0.02 - 2
0.0002 0.2.
l).6b
166 x LO
r>5 x 10
'34 x 10
-1 ->
6 x 10 to l\ x JO ~
\ x
t:o 3 x 10
-/I -9
x LO to I x 10 "
I - ()5,000
7,;oo
A ran^e of probability is given, based on several Different dose-response extrapolation models. The
lifetime excess probability oL cam-er represents the increase in probability ot cancer pver the normal
background incidence, assuming that an individual is continuously exposed to BaP at the indicated
daiLy intake over a /0-year lifetime. There is considerable variation in the estimated risk clue to
uncertainty introduced by the use of laboratory rodent data, by the conversion to equivalent human
dosage, and by the application of hypothetical dose-response curves. Tn view of several conservative
assumptions (.hat were utilized, it is likely that these predictions overestimate the actual risk
to humans.
25 cigarettes per
It was assumed that the total population of smokers (54 million) smoked oji -^
day. From 25% ID il)% OL smokers consume snore than 25 cigarettes per day and consequently may receive
.1 higher daily exposure.
-------
With respect to other PAHs included in this group, data were in-
adequate for quantitative risk assessment purposes. Benz[a]anthracene
and dibenzfa,h]anthracene are both carcinogenic in mice by the oral
route. They are also complete carcinogens for mouse skin as are benzofb]-
tluoranthene and indeno[l,2,3-c,d]pyrene. Benzo[g,h,i]perylene is a
co-carcinogen with BaP and benz[a]anthracene, benzo[b]fluoranthene
chrysene and indeno[l,2,3-c,d]pyrene are all initiators of skin car-
cinogenesis in mice. No carcinogenicity data were found for acenaph-
thylene.
5.5.3*2 Non-Carcinogenic Risks
The major focus of studies with compounds in the benzo[a]pyrene
group has been their potential for inducing carcinogenic effects.
Little information is available on other potential risks to humans from
exposure to these compounds (see Section 5.3.1). BaP has been shown
to be the most active mutagen of the group, inducing in vivo chromo-
somal aberrations and sister chromatid exchange in hamstirTT Mixed
mutagenic responses have been noted with other compounds in this group
Because of its mutagenicity, BaP exposure could also be expected to
contribute to the genetic burden of a population, but since extrapola-
tion procedures for genetic risks have not been well established, a
quantitative risk assessment for these kinds of health hazards is not
presently feasible.
BaP appears to exert little effect on the developing embryo; data
were unavailable for the other compounds in this group.
Little information is available on other possible toxic effects
associated with exposure to these compounds. However, in assessing the
risks to humans associated with exposure to these PAHs, one should not
overlook possible augmentation of effects through synergistic or co-
carcinogenic mechanisms. Current understanding of the co-carcinogenesis
process is not sufficiently adequate to allow estimation of human risk
at this time.
5.5.4 Risk to Biota
Data on acute and chronic effects of PAHs are limited and water
quality criteria have not been set (USEPA 1980). The only laboratory
toxicity test for any of these compounds indicates that 1.0 yg/1 of
benz.[a]anthracene caused 87% mortality in bluegill sunfish in six
months. Concentrations in this general range (0.2 - 20 ug/1) have also
been found to stimulate growth in some organisms including baceria and
freshwater algae. Several field studies have attributed certain tumors
found in benthic marine fish to BaP from hydrocarbon-contaminated sedi-
ments, but the concentrations of BaP causing these effects were not
known.
5-146
-------
Monitoring data at detectable levels were very scarce, but those
which were available indicate that benz[a]anthracene and benzo[k]fluoran-
thene have been found in surface water at concentrations from 1 - 1500
yg/1. Sediment concentration data were somewhat more extensive and
indicated that all of the eight PAHs in this group have been detected
in concentrations exceeding 1.0 yg/kg. Maximum sediment concentrations
for this group ranged from 35.8 yg/kg (indeno[l,2,3-c,d]pyrene) to
2600 yg/kg (dibenz[a,h]anthracene)i. Uptake of PAHs from sediments
by benthic organisms is believed to occur, but the extent of bio-
availability of sediment-bound PAHs is not known at this time. Although
no data were found attributing specific sediment PAH concentrations to
toxic effects, it is believed that PAHs from hydrocarbon-contaminated
sediments have caused liver tumors in fish. Many of the higher sediment
monitoring observations were found in Puget Sound, the area in which
liver tumors in fish have been observed. PAH sediment levels, therefore,
which are often found near industrialized areas, may pose some risk to
aquatic biota.
5-147
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Cancer Institute; 1961-1967, 1968-1969, 1970-1971, 1972-1973, 1978.
U.S. Department of Agriculture (U.S. DA). Food consumption, prices, and
expenditures. Supplement for 1976 agricultural economic report no. 138.
Washington DC: U.S. Department of Agriculture; 1978.
U.S. Department of Agriculture (U.S. DA). Food and nutrient intakes of
individuals in 1 day in the United States, Spring 1977. Preliminary
Report No. 2. Washington, DC: Science and Education Administration,
U.S. Department of Agriculture; 1980.
U.S. Department of Health, Education, and Welfare (U.S. DHEW). Smoking
and health: A report of the Surgeon General. PHS 79-50066. Washing-
ton DC: U.S. Public Health Service, U.S. Department of Health, Educa-
tion and Welfare; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Preliminary assess-
ment of the sources, control and population exposure to airborne poly-
cyclic organic matter (POM) as indicated by benzo[a]pyrene (BaP). Re-
search Triangle Park, NC: Office of Air Quality Planning and Standards,
U.S. Environmental Protection Agency; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Water quality cri-
teria. Requests for comments. Federal Register 44(52):15977-15981;
1979.
U.S. Environmental Protection Agency (U.S. EPA) Ambient water quality
criteria for polynuclear aromatic hydrocarbons. Washington, DC: Cri-
teria and Standards Division, Office of Water Regulations and Standards;
1980: 180pp. Available from: OTIS, Springfield, VA; EPA 440/5-80-069.
5-168
-------
Vainio, H. _et_ al. The fate of intratracheally installed benzo[a]pyrene
in the isolated perfused rat lung of both control and 20-methylcholan-
threne pretreated rats. Res. Comm. Chem. Pathol. Pharmacol. 13:259;
1976. (As cited by U.S. EPA 1980).
Wang, I.Y. _et_ _al_. Enzyme induction and the difference in the metabolite
patterns of benzo[a]pyrene produced by various strains of mice. Freuden-
thal, R.I.; Jones, P.W.; eds. Carcinogenesis - a comprehensive survey.
Vol. 1. Polynuclear aromatic hydrocarbons: Chemistry, metabolism, and
carcinogenesis. New York: Raven Press; 1976: p.77. (As cited by
U.S. EPA 1980).
White, J.B.; Vanderslice, R.R. POM source and ambient concentration
data: review and analysis. Research Triangle Park NC: U.S. Environ-
mental Protection Agency; 1980.
Wislocki, P.G.; Wood, A.W.; Chang R.L.; Levin, W.; Yagi, H.; Hernandez,
0.; Dansette, P.M.; Jerina, D.M.; Conney, A.M. Mutagenicity and cyto-
toxicity of benzo[a]pyrene arene oxides, phenols, quinones and dihydro-
diols in bacterial and mammalian cells. Cancer Res. 36:3350-3357;
1976a. (As cited by Conney et al. 1980, Jerina _et al. 1977a,b).
Wislocki, P.G.; Wood, A.W.; Chang, R.L.; Levin, W.; Yagi, H.; Hernandez,
0.; Jerina, D.M.; Conney, A.H. High mutagenicity and toxicity of a
diol epoxide derived from benzo[a]pyrene. Biochem. Biophys. Res. Comm.
68:1006-1012; 1976b. (As cited by Conney _e_t a_l. 1980, Jerina et al.
1977b).
Wislocki, P.G.; Chang, R.L.; Wood, A.W.; Levin, W.; Yagi, G.; Hernandez,
0.; Mah, H.D.; Dansette, P.M.; Jerina, D.M.; Conney, A.H. High carci-
nogenicity of 2-hydroxy-benzo[a]pyrene on mouse skin. Cancer Res. 37:
2608-2611; 1977. (As cited by Conney _et_ al. 1980; Jerina _et_ al. 1977a;
U.S. EPA 1980).
Wislocki, P.G.; Kapitulnik, J.; Levin, W.; Lehr, R.; Schaefer-Ridder,
M.; Karle, J.M. Jerina, D.M.; Conney, A.H. Exceptional carcinogenic
activity of benzo[a]anthracene3,4-dihydrodiol in the newborn mouse and
the bay region theory. Cancer Res. 38:693-696; 1978. (As cited by
Conney _et al. 1980).
Wood, A.W.; Chang, R.L.; Levin, W.; Lehr, R.E.; Schaefer-Kidder, M.;
Karle J.M.; Jerina, D.M.; Conney, A.H. Mutagenicity and cytotoxicity
of benzo[a]anthracene diol epoxides and tetrahydroepoxides. Exceptional
activity of the bay region 1,2-epoxides. Proc. Natl. Acad. Sci. U.S.A.
74:2746-2750; 1977a. (As cited by Conney _et_ aJL. 1980).
Wood, A.W.; Levin, W.; Chang, R.L.; Lehr, R.E.; Schaefer-Ridder, M.;
Karle, J.M.; Jerina, D.M.; Conney, A.H. Tumorigenicity of five dihydro-
diols of benzo[a]pyrene on mouse skin. Exceptional activity of benzo
[a]anthracene, 3,4-dihydrodiol. Proc. Natl. Acad. Sci. USA 74: 3176-
3179; 1977c.
5-169
-------
Wood, A.W.; Levin, W.; Lu, A.Y.N.; Yagi, N.; Hernandez, 0.; Jerina, D.M.;
Conney, A.H. Metabolism of benzo[a]pyrene and benzo[a]pyrene deriva-
tives to mutagenic products by highly purified hepatic microsomal en-
zymes. J. Biol. Chem. 251:4882-4890; 1976. (As cited by Jerina et
al. 1977a,b, Conney et al. 1980), —
Wood, A.W.; Levin, W.; Thomas, P.E.; Ryan, D.; Karle, J.M.; Yagi, H.;
Jerina, M.; Conney, A.H. Metabolic activation of dibenzo[a]anthracene
and its dihydrodiols to bacterial mutagens. Cancer Res. 38:1967-1973-
1978.
Yang, S.K.; Roller, P.P.; Gelboin, H.V. Benzo[a]pyrene metabolism:
Mechanism in the formation of epoxides, phenols, dihydrodiols, and the
7,8-diol-9,10-epoxides. Jones, P.W.; Freudenthal, R.I., eds. Carcino-
genesis-a comprehensive survey. Vol. 3. Polynuclear aromatic hydro-
carbons. New York: Raven Press; 1978: pp. 285-301.
5-170
-------
REFERENCES FOR 5.4
Anderson, J.W.; Kiesser, S.L.; Blaylock, J. W. Comparative uptake of
naphthalenes from water and oiled sediment by benthic aniphipods. Am.
Petrol. Instit. Pub. 4308:579-584; 1979.
Anderson, J.W.; Neff, J.M.; Cox, B.A.; Tatem, H.E.; Hightower, G.M.
Characteristics of dispersions and water-soluble extracts of crude
and refined oils and their toxicity to estuarine crustaceams and fish.
Marine Biology 27:75-88; 1974.
Brown, E.R. e£ al. Tumors in fish caught in polluted waters: Possible
explanations. Comparative Leukemia Res. 1975, Leukemogenesis. Univ.
Tokyo Press/Karger, Basel; 47 p. (As cited by U.S. EPA 1980)
Dunn, B.P.; Stich, H.F. The use of mussels in estimating benzo[a]pyrene
contamination of the marine environment. Proc. Soc. Exp. Biol Med
150:49-51; 1975. (As cited by Neff 1979)
Dunn, B.P.; Stich, H.F. Monitoring procedures for chemical carcinogens
in coastal waters. J. Fish Res. Bd. Canada 33:2040-2046; 1976. (As
cited by Neff 1979)
Dunn, B.P.; Young, D.R. Baseline levels of benzo[a]pyrene in southern
California mussels. Mar. Pollut. Bull. 7:231-234; 1976. (As cited
by Neff 1979)
Fucik, K.W.; Armstrong, H.W.; Neff, J.M. The uptake of naphthalenes
by the clam, Rangia cuneata, in the vicinity of an oil-separator
platform in Trinity Bay, Texas. Proc. 1977 oil spill conference
(prevention, behavior, control, cleanup). Washington, DC: American
Petroleum Institute; 1977.
Graf, W.; Nowak, W. Promotion of growth in lower and higher plants
by carcinogenic polycyclic aromatics. Arch. Hyg. (Berlin) 150:513-528-
1966. (As cited by Neff 1979)
Haranghy, L. Effects of 3,4-benzpyrene on freshwater mussels. Acta
Biol. Acad. Sci. Hungary. 7:101-108; 1956. (As cited by Neff 1979)
Harris, R.D.; Raabe, V.E. Factors influencing the photodynamic action
of benzopyrene in E. Coli. J. Bact. 93:618-626; 1967. (As cited by
Neff 1979)
Haas, B.S.; Applegate, H.G. Effects of unsubstituted polycyclic aromatic
hydrocarbons on the growth of escherichia coli. Chem. Biol. Interact.
10(4):265-268; 1975.
5-171
-------
Korotkova, G.P.; Tokin, B.P. Stimulation of the process of somatic
embryogenesis in some porifera and coelenterata. I. Effect of carcino-
genic agents on some porifera. Acta Biol. Hungary 19:465-474- 1968
(As cited by Neff 1979) ' '
°f the marine
Environ. Sci. Technol,
McCain, B.B.; Hodgins, H.O.; Gronlund, W.D.; Hawkes, J.W.; Brown, D.W.-
Myers, M.S.; Vandermeulen, J. H. Bioavailability of crude oil from
experimentally oiled sediments to English sole (Parophrys vetulus) . and
pathological consequences. J. Fish. Res. Board Canada 35(5) : 657-664:
1978. (As cited by Anderson 1979)
Neff, J.M. Polycylic aromatic hydrocarbons in the aquatic environment.
London: Applied Science Publishers; 1979.
Roesijadi, G.; Anderson, J.W.; Blaylock, J.W. Uptake of hydrocarbons
trom marine sediments contaminated with Prudhoe Bay crude oil: Influence
of feeding type of test species and availability of polycyclic aromatic
hydrocarbons. J. Fish. Res. Board. Can. 35:608-614; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for polynuclear aromatic hydrocarbons. EPA 440/5-80-069
Washington, DC: Office of Water Regulations and Standards, U.S. EPA; 1980
Varanasi y. ; Gmur, D.J. ; Krahn, M.M. Metabolism and subsequent binding
of benzo[a]pyrene to DNA in pleuronectic and salonid fish. Bj«5rseth A •
Dennis, A.J. eds. Polynuclear aromatic hydrocarbons: Chemistry and' '"
biological effects (4th International Symposium on Polynuclear Aromatic
Hydrocarbons, Battelle Columbus Laboratories 1979). Columbus OH-
Battelle Press; 1980. ' '
5-17;
-------
REFERENCES FOR 5.5
Fedorenko, Z.P.; Yanysheva, N.Y. Hyg. and Sanit. 31(8):168-173; 1966.
(As cited by Survey of Compounds Which Have Been Tested For Carcino-
genic Activity 1970-1971.)
International Agency for Research on Cancer (IARC). Monographs on the
evaluation of carcinogenic risk of the chemical to man, Vol. 3. Cer-
tain polycyclic aromatic hydrocarbons and heterocyclic compounds.
Lyon, France:World Health Organization; 1972.
Neal, J.; Rigdon, R.H. Gastric tumors in mice fed benzo[a]pyrene: a
quantitative study. Texas Rep. Biol. Med. 25(4):553-557; 1967.
Survey of Compounds Which Have Been Tested For Carcinogenic Activity.
Bethesda, Maryland: Department of Health and Human Services, National
Cancer Institute; 1970-1971.
U.S. Department of Commerce, 1980. Statistical Abstract of the United
States. Washington DC: Bureau of Census.
U.S. Environmental Protection Agency (U.S. EPA). Water quality criteria.
Requests for comments. Federal Resister 44(52):15977-1598l; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for polynuclear aromatic hydrocarbons. EPA 440/5-80-069.
Washington, DC: Office of Water Regulations and Standards, U.S. EPA;
1980.
5-173
-------
APPENDIX A
NOTE 1:
Fireplaces
Emissions were calculated from emission factors (see Table A-l)
that represented the average of three tests (EPA 1980b). The total
mass of wood burned in fireplaces in 1976, 2.7 x 10° kkg (EPA,
1980a) was extrapolated to 1977, based upon the number of housing
units in each region of the country, the percentage of those housing
units with fireplaces an average consumption of 98.3 kg/housing unit
(EPA 1980a). These assumptions led to the estimate that 2.9 x 106
kkg of wood were burned in 1977.
NOTE 2:
Carbon Black
An estimated 1.0 x 105 kkg of carbon black were produced in
19/7 (SRI, 1979). The emission factors in Table A-l (Serth and Hughes,
1980) were used to estimate PAH emissions, although the resulting
estimates are limited by the fact that testing was performed upstream
of an emissions control device (burner).
An estimate of PAH production associated with carbon black
manufacture is presented in Table A-3.
Tire Wear
A crude estimate of PAH emission from tire wear associated with
carbon black (see Table A-4) was developed from the following data:
- 365 da/yr.
- 7.4 x 10^ bbl/da gasoline consumption (Oil and Gas Journal
1979).
- 14.7 miles/gal average (EPA 1975).
- 42 gal/bbl.
- 0.19 g/vehicle-mile is airborne particulates and 0.15
g/vehicle-mile is deposited on road surface (EPA 1979c).
- Rubber composed of 33% carbon black (SRI 1979).
- Average PAH composition of carbon black in Table A-°. (Locati
et al_. 1979).
5-175
-------
NOTE 3:
Motor Vehicles
Motor vehicle PAH emissions were calculated by using the emission
factors in Table A-l (Hangebrauck, 1967), and estimated 2.7 x 10*5
meters/yr travelled (see note on tire wear fcr estimation of vehicle miles
travelled), and an assumed emission reduction of two thirds, this
emission reduction was based upon the following information:
Fraction of Automobile
Population Control Present Reduction
0«32 catalytic Conventer 99
°«58 Engine Modification 65
0.10 None 0
The.automobile population is from EPA (1978b), and the percent
reductions are based on ranges mentioned in that document.
The concentrations of PAHs in used crank case oil are shown in
Table A-5. Releases to sewers and landfills were assumed to account
totally for 2 x 10y t of oil disposed of by the public (Tanacredi
1977); however, this figure does not take into account used oil that
is recycled.
MOTE 4:
a. Oil:
Water figure based on 3.6 x 107 * of various oils -
crude (36%), diesel (18%), fuel (42%), waste (2%), lube
(0.3%) other (1.7%) - spilled in navigable waters in 1978
(U.S. Coast Guard, 1980).
Land figure based on 5.1 x 105 i of crude oil spilled
in 1978 by common carrier (23%), private carrier (22%),
rail (6%), and "other" (49%) (U.S. Dept. of Transportation
1980). Average oil Density = 0.85.
b. Gasoline:
Water - 1.1. x 107 i spilled: aviation/automobile
gasoline (98%) and natural (Casinghead) Gasoline (2%) (U.S.
Coast Guard 1980).
Land - 3.7 x 106 i spilled: common carrier (53%),
private carrier (47%), rail (0.8%), "other" (<0.01%) U.S.
Dept. of Transportation 1980). Gasoline density: 0.73.
5-176
-------
Table A-l. Linission Factors
Ul
i
Acenaphthene
Acenaphthylene
Anthracene3
Benzo[a]anthracene
Benzo[b]fl uoranthene0
Benzo[k]f 1 uoranthene
Benzo[ghi]perylene
BenzoCalnyrene1*
Chrysene"
Uibenzo[a,h]anthracenee
Fluroanthene
Fluorene
Indeno[l ,2,3-cd]pyrene
Naphthalene
Phenanthrene
Pyrene
Residential
Coal
Combustion
(gAg)
0.039
0.008
0.002
0.002
0.002
0.0015
0.002
0.003
0.005
0.026
0.002
0.15
0.008
0.005
Primary and
Auxil iary
Fireplaces
(9Ag)
0.0012
0.010
0.010
0.0008
0.0008
0.0008
0.0009
0.0008
0.0008
0.0001
0.0028
0.0047
NO
0.0403
0.010
0.0028
Wood
Heating
—iii/kyj
0.0076
0.057
0.076
0.0071
0.0058
0.0058
0.0053
0.0040
0.0071
0.0007
0.019
0.016
NO
0.25
0.076
0.016
Cigarettes
(ug/cig)
0.17
0.02
0.01
0.02
0.01
0.006
3
0.36
0.16
Coal
Refuse
Piles
(kg/kg)
POM
0.1
0.01
0.01
0.005
<0.001
0.05
<0.001
0.1
0.05
Forest
Mres
(dry fuel )
2,500
3,100
1,300
1,300
2,500
740
3,100
5,500
1,700
2,500
4,600
Carbon
Black
ug/kg
800
35
4.5
15
15
12
4.5
60
-------
Table A-2. Fireplace Populati
on
Region
Northeast
North Central
South
West
Total
Number of
Housing
Units (1977)
17,707,000
21,181,000
26,422,000
15,406,000
Percentage
w/Fi replace
47
33
29
46
Fireplaces
8,300,000
7,000,000
7,700,000
7,100,000
30,100,000
Sources: Census 1979 and EPA 1980a
5-173
-------
Table A-5. Concentrations of PAHs in Used Crankcase Oils (mq/1}
Anthracene 0.3
Benzo[a]anthracene 0.9
Benzo[k]fluoranthene 1.4
Benzo[ghi]perylene 1.7
Benzo[a]pyrene 0.4
Chrysene 1.2
Fluoranthene 4.4
Fluorene 1.5
Phenanthrene 7.8
Pyrene 6.7
Source: Peake and Parker 1980.
5-181
-------
Table A-6. Municipal Incinerators Release Factors (ug/kg refuse)
Benzo[a]anthracenec
Benzo[b]fi uoranthened
Benzo[k]f 1 uoranthened
Benzo[ghi]perylene
Benzo[a]pyrenee
Chrysenec
Fl uoranthene
Indeno[l,2,3-cd]pyrene
Aira
1.5
0.5
0.5
1.8
0.04
1.5
2.5
0.77
Land
18
21
21
10
16
18
12
<2.1
Waterb
0.08
0.01
0.01
0.007
0.016
0.08
0.14
<0.002
a) after scrubber
b) taken as one half reported benzo[a]anthracene + chrysene emissions
cj taken as one third of benzo[b+k+j]fluoranthene emissions
d) taken as one half of benzo[a+e]pyrene emissions
e) scrubber water
Source: Davies 1976.
5-182
-------
Table A-3. PAH Associated with Carbon Black (yg/g)a
Oi
I
VO
Carbon
PAH Black
Type
Anthracene*3
Benzofluoranthenesc
Benzo[ghi ]peryl ene
Benzopyrenes
Fl uoranthene
Indenopyrene
Phenanthrene
Pyrene
Vulcan J
0.5
10
166
20
68
24
0.5
314
Regal 300
i ND
ND
16
1
9
1
ND
58
*
330 HAF
0.05
<0.9
25
3
10
0.3
0.05
47
660 GPF
ND
4
41
8
13
7
ND
52
339
1
7
164
32
52
35
1
207
Avg
0.3
4
82
17
30
13
0.3
140
Contained
Carbon Black
0.5
6
100
30
50
20
0.5
200
in
(Meg)
a) Based 1.6 x 106 kkg carbon black production (SRI 1979).
b) Reported as antnracene/phenanthrene, assumed equal division among them.
c) Excluding benzo[ghi]fluoranthene, reported separately.
Source: Locati et al. 1979
-------
Table A-4. PAH Releases from Tire Wear (kkg)a
Airborne
Initial Reentrained
Anthracene
Benzofl uoranthenes
Benzo[ghi]perylene
Benzopyrenes
Fluoranthene
Indenopyrene
Phenanthrene
Pyrene
1
0.3
0.5
0.2
2
7
1
3
1
10
Sedimentary or
directly trans-
ferred to Roadway Total
7
1
2
1
10
20
2
6
2
20
See Appendix text for calculations and sources
a) Blanks indicate <1 kkg/yr. For all entries, totals may not add due
to rounding.
5-180
-------
Table A-9. Concentrations of Various PAHs in Coal and Coal Tar Derivatives (mg/kg)a
Ul
I
CO
t_n
Coal
Acenaphthene
Anthracene
Phenanthene
Benzo[a]anthracene
Benzo[a]pyrene 0.7
Chrysene
Fluoranthene
Fluorene
Naphthalene
Pyrene
Coal
Tar
10,000^
9,000b
30,000d
<0.007d
30d
4,000d
6,000b
10,000°
90,000f
3,0009
Coal Tar
Pitch
<10d
10d
<10d
Creosote
Oil
40,000C
20,000C
100,000C
<3d A
negd.e
-------
Table A-10. PAII WasLi>w,ilor Oischanjo: Hy-1'rodiict Cokc-mak iwja
Aiiinonia L
0.000/3
to 0.000006
0.000032
0.000045
0.000196
0.000145
0.00395
0.000393
P_!>tji_aryc_ jjtc_tors (ky/kki
i([uor Cooler Blowdown
0. 00009 /
0.000032
0.000024
O.OOOOIH
0.000323
0. 00004 H
0.0115
0.000026
j coke)
lion/ol I'lant
0.000129
0.000125
0.000155
O.OOOlfW
0.000049
0.00341
0.000109
Ui
I
00
Ac<'iiaphthyl
-------
Table A-7. Emissions of PAHs from Coal-fired Plants and Intermediate/smal1 Oil-fired Units, iig/109 j Fuel
Benzo[a]- Benzo[ghi]- Phenan-
Type of Unit pyrene Pyrene perylene threne
Pulverized coal (vertically-fired,
dry-bottom furnace) 18 - 123 70 - 218 79
Pulverized coal (front-wall-fired,
dry-bottom furnace) 16 - 20 152 - 190 13 190
Pulverized coal (tangential ly-
fired, dry-bottom furnace) 123 133 142 30
Pulverized coal (opposed-, down-
ward inclined burners; wet
£ bottom furnace) 20 - 133 37 - 114 142 - 1,042
00
Crushed coal (cyclone-fired,
wet-bottom furnace) 72 - 351 237 - 1,706 34 - 341
Spreader stoker (traveling
grate) <14 - 23 20 - 56
Oil-fired:
Steam atomized <19 - 45 46 - 284 1,700
Low pressure air atomized 853 5,780 285 3,320
Pressure atomized <38 - <57 14 - 1,700 8,440
Vaporized <95 1,140
Fluoran-
thene
80 - 389
12 - 152
370
52 - 199
42 - 104
20 - 56
53 - 256
1,800
72 - 4,470
14,200
NOTE: Blanks indicate data not available.
Source: llangebrauck et a^. 1967.
-------
Table A-8.
Coke-Oven Tar Produced in the United States, Used by Producers, and Sold in 1978
by State (Thousand Liters)
Cn
I
CO
-P-
Produced
State
Cal if. Colo Utah
Illinois
Ken., Mo., Tenn. , Tex.
Mi nn6sotd Ui scons i n----
Ohio
Virginia, West Virginia—-
Undistributed
Total (1978)b 2,
At Merchant Plants
At Furnace Plants 2,
Total (1977)b 2,
Used by Producers
L/kkg of For Refinery As
Total Coal Coked or Topping Fuel
130,000
130,000
59,000
350,000
34,000
170,000
a
20,000
330,000
580,000
a
240,000
100,000
89.000
000,000
200,000
27
35
25
33
25
32
a
23
31
35
a
30
44
34
44
32
a
a
a
a
500,000
500,000
c
500,000
570,000
a
a
a
a
170,000
a
190,000
360,000
360,000
550,000
Other
a
a
a
32,000
32,000
32 ,000
38,000
Sold for Refining Into Tar Products
Quantity
130.000
130,000
60,000
120,000
31,000
120.000
a
19,000
180.000
280.000
a
150,000
1,200.000
89.000
1,100,000
1,100,000
Value
Thousand Average
Dollars Per Liter
$11,970
11,905
5,593
12,840
3.021
12.911
a
1,938
17.529
29.425
a
12.904
120,036
8.986
111,050
106,728
30.09
0.09
0.09
0.11
0.10
0.11
a
0.10
0.10
0.11
a
0.09
0.10
0.10
0.10
0.10
On -hand
Dec. 31
9.700
13,000
5,700
21,000
2.700
25,000
a
a
27.000
55.000
5,700
14 000
180.000
4.900
170.000
160.000
a) Included with "Undistributed" to avoid disclosing individual company data.
b) Data may not add to totals shown due to independent rounding.
c) Included with "Furnace Plants" to avoid disclosing individual company data.
Source: DOE 1979.
-------
Table A-ll. Concentration of Select PAHs in Petroleum Products, rng/kg
Ut
M
CO
Crude Oil
Acenaphthene
Acenaphthylene
Anthracene
Berizo( a) anthracene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Benzo(ghi)perylene
Benzo(a)pyrene
Chrysene
Dibenzo( a, b) anthracene
Fluoranthene
Fluorene
Indeno[l ,2,3-cd]pyrene
Naphthalene
Phenanthrene
Pyrene
a) ND means not detected.
Source: Guerin 1978; Guerin et
NDa
400
trace
trace
<5
<5
.02
1
<100
100
200
1,000
100
100
al. 1978;
Gasol ine
3
3
2
2
2
7
5
EPA 1979f
Petroleum Diesel
Kerosene Asphalt Fuel
0.4 3
<0.1 0.04 0.1
<0.1 0.03
0.01 0.01 0.07
ND 0.02 0.5
0.09 0.5
ND ND
0.2 0.4
Number 2
Heating Oil
4
0.04
0.03
0.03
0.6
2
ND
1
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Table A-12. Emissions of PAHs from Petroleum Refining
Emissions, ug/100 m3a
Benzo(a)- Benzo(ghi)-
Process pyrene perylene
Straight run distillation
Pyrolysis
Asphalt production
Petroleum coke production
0.015
0.30
0.74
25.5
0.11
0.170
1.58
0.4
Petroleum products
purification 0.024 -b
a) Mean values of multiple samples.
b) Not available.
Source: Samedov and Kurbanov 1971, as cited in EPA 1979h.
5-188
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Table A-13. Emissions of PAHs from Catalyst Regeneration in Petroleum Cracking,
Oil Charges
Ul
I
OO
Type of Unit
FCC:a
Regenerator outlet
Carbon monoxide boiler
outlet
HCC:b
Regenerator outlet
TCC:C
Air lift, regenerator
outlet
TCC:
Brucket lift, regen-
erator outlet
NOTE: Blanks indicate data
Benzo(a) Benzo(ghi)-
pyrene Pyrene perylene
0.7 - 73 6.4 - 24-67
4,450
1.7 - 3.4 3.9 - 26 8.8
32,600 - 20,700 - 47,700 -
36,700 20,800 60,400
8,900 - 21,000 - 7,000 -
19,100 41,300 11,450
*
5 46-57
not available.
Anthra- Phenan- Fluoran-
cene threrie thene
63,560 7.0 - 3,180
330 3.2-13
146 - 3,340 - 1,320 -
318 4,600 1,810
1,640 - 52,500 - 1,685 -
1,685 56,000 4,610
9.17
a) Fluid catalytic cracking.
b) lloudriflow catalytic cracking.
c) Thermofor catalytic cracking.
Source: llangebrauck, Q aj_. 1967,
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Wet deposition is controlled by the precipitation scavenging
ratio, r, which expresses the ratio of pollutant concentration in
precipitation (ng/1) to pollutant concentration in air (ug/nrb . The
scavenging ratio is calculated by contributions from the vapor and
sorbed fractions, i.e.:
rs + rv
where r, rs and rv are scavenging ratios for the total airborne mass,
the sorfaed contaminant, and the vapor phase, respectively. Once the
scavenging ratio is known, the wet deposition flux is given by wet
flux = rRCair, where R is the rainfall rate. These parameter values
have been estimated, as shown below:
PAH
Precipitation Scavenging Ratios
r *
s
6xl04
6xl04
6xl04
rv
53
14
5.4xl04
r
Combustion
Rural
53
130
6xlOA
Urban
71
3.6xl03
6xl04
Sources
2.5x103
1.2xl05
1.2xl05
Naphthalene
Anthracene
Benzo[a]pyrene
For the purpose of further analysis a generic urban environment
has been modeled on the basis of characteristics of Philadelphia and
Cleveland. The average wind speed is 10.25 kts (5.3 m/s) and the
annual rainfall is 1.0 m/yr. The urban area is 100 mi2 (2.6 x 108 m2).
The generic rural area is defined as a volume of air within which
an associated urban source would contribute to rural concentrations.
The size of the area is constrained by the half-life in air, such that
the concentration is typical of an area significantly affected by the
urban source. At a half-life of 5 hours, and typical wind speed of 5.3
m/sec., naphthalene contamination from an urban area could be significant
over an area of 1010 m2 (roughly 40,000 square miles).
Median observed ambient concentrations for three PAHs in urban and
rural areas are presented below (White and Vanderslice 1980):
-Tabulated rs values apply for rural and urban conditions. Near a com-
bustion source the adsorbed phase is expected to be associated with
larger particles resulting in a scavenging ratio, rs = 1.2x10^.
5-193
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Median Observed
Concentration
PAH Rural
Naphthalene 7x10"^
Anthracene 1x10"^
Benzo[a]pyrene IxlO"3
Using the pathway evaluation method we have estimated the emission
that would result in a specific ambient concentration, given the degra-
dation rate, deposition velocity, rainfall rate, and precipitation
scavenging ratio. Applying the equation for wet flux and dry flux we
also estimated the amount deposited in the generic rural and' urban study
areas. Then, by comparison of the deposition rates with emission rates,
we estimated the fraction of total atmospheric emissions of each of the'
three PAHs which would be deposited within the urban and rural study
areas. These results are shown below:
Deposition Rate
% of Emissions % of Emissions
Dry Deposited Wet Deposited % Deposited
£AH Rural Urban* Rural Urban Rural' Urban
Naphthalene 2 2-3 <1
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APPENDIX B. APPLICATION OF THE AIR-TO-SURFACE PATHWAY EVALUATION
METHOD FOR POLYNUCLEAR AROMATIC HYDROCARBONS
A method has been developed for estimating airborne toxicant
deposition rates (air-to-surface pathway evaluation method, Arthur D.
Little, Inc., 1981). The method accounts for both wet and dry
deposition to land and water surfaces. When deposition to a water-
shed or other land area is estimated, this can be interpreted as an
upper bound on the chemical loading to an associated surface water
body resulting from air deposition, since only a fraction of the
mass deposited on land surfaces will be delivered to the water body.
The air-to-surface pathway evaluation method accounts for the parti-
tioning of an airborne contaminant between adsorbed and vapor phases,
with differing deposition rates inferred for the separate phases. It
relies on fundamental physicochemical properties and is designed to
use available data, while filling in data gaps with estimated values of
various parameters. The evaluation method has been applied to naphtha-
lene, anthracene, and benzo[a]pyrene. Each of the three PAHs modeled has
an atmospheric chemical degradation of roughly 0.1 hr.-l leading to half-
lives of 5-10 hours (Radding _e_t al. 1976) . Under typical meteorologic con-
ditions this corresponds roughly to the travel time across major urban areas,
Since urban areas also would be expected to have much greater emission
densities than rural areas, significant urban/rural differences in air
concentrations of PAHs are expected, and indeed observed. These factors
suggest that deposition rates under urban and rural conditions should
be considered separately.
One of the most important chemical properties influencing air-to-
surface transfer is the vapor pressure. The vapor pressure affects the
partitioning of airborne contaminants between vapor and adsorbed phases.
The deposition rate is typically much greater for the adsorbed fraction
of the airborne contaminant. The effect of vapor pressure is expressed
by equation (5) of the Arthur D. Little report (1981) :
.1659
-------
than in rural areas. In the plume from a combustion source, the aerosol
surface area is even higher than typically found in urban air. Appli-
cation of the above equation results in aerosol partitioning for the
three PAHs as shown below:
Adsorbed Fraction of Total Airborne Mass
PAH
Naphthalene
Anthracene
Benzo[a]pyrene
Rural
7xlO'6
0.002
.99
Urban
3xlO~4
0.06
1.00
Near Combustion Sources
0.02
0.97
1.00
Benzo[a]pyrene is strongly partitioned with the aerosol phase, regard-
less of ambient conditions, while at the other extreme naphthalene
exists primarily as a vapor in the atmosphere. Anthracene exhibits
intermediate properties, and the adsorbed fraction is sensitive to
ambient conditions.
The dry deposition flux is proportional to the dry deposition
velocity, Vd> i.e.,
Dry Flux = V, C .
d azr
where
•_
d-L. L
is the ground-level air concentration.
The dry deposition velocity with respect to the total airborne con-
taminant is calculated as the (mass) weighted average of the deposition
velocity for the vapor and sorbed fractions, i.e.,:
V - V 4> + V,
d d,s d,v
(Eq. 6 of Arthur D. Little 1981)
According to the air-to-surface pathway method (Arthur D. Little
1981), the respective dry deposition velocities are given below:
Dry Deposition Velocity
'd,v vd,s
Combustion
PAH
Naphthalene
Anthracene
Benz o [ a ] pyrene
(cm/sec)
0.04
0.02
0.02
(on/sec)
1
1
1
Rural
0.04
0.02
1.00
Urban
0.04
0.08
1.00
Source
0.06
1.00
1.00
5-192
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APPENDIX
REFERENCES
Arthur D. Little, Inc. Air-to-surface pathway evaluation methodology.
Draft final report. Contract N. 68-01-5949. Washington, DC: Monitoring
and Data Support Division, Office of Water Regulations and Standards,
U.S. Environmental Protection Agency; 1981.
Radding, S.B.; Mill, T.; Gould, C.W.; Liu, D.H.; Johnson, K.L.; Bomberger,
D.C.; Fojo, C.V. The environmental fate of selected polynuclear aromatic
hydrocarbons. Washington, D.C.: Office of Toxic Substances, U.S. Environ-
mental Protection Agency; 1976.
White, J.B.; Vanderslice, R.R. POM source and ambient concentration
data review and analysis. Research Triangle Park, NC: U.S. Environ-
mental Protection Agency; 1980.
5-195
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