United States Office of Water July 1982
Environmental Protection Regulations and Standards (WH-553)
Agency Washington DC 20460
An Exposure
and Risk Assessment for
Benzo[a]pyrene and
Other Polycyclic
Aromatic Hydrocarbons
Volume I. Summary
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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.
-------
SO J72 -101
REPORT DOCUMENTATION '• "wow NO- *•
PAGE EPA-440/4-85-020
4. Title and Subtttta
An Exposure and Risk Assessment for Benzo [a] pyrene and Other
Polycyclic Aromatic Hydrocarbons: Volume I. Summary
7. Authors)
Harris, J.; Perwak, J.; and Coons, S.
. Performing Organization Nam* and Addr*ts
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
12. Sponsoring Organization Name and Address
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Recipient"! Accession No.
5. Report Date
July 1982
8.
8. Performing Organization Rapt. No.
10. Proiect/Task/Work Unit No.
11. Contractor or 6rent(G) No.
(0 68-01-6160
(6)
13. Type of Report & Period Covered
Final
14.
15. Supplementary Notes
Extensive Bibliographies
ft. Abstract (Umlt 200 words)
This report assesses the risk of exposure to polycyclic aromatic hydrocarbons (PAHs).
This is Volume I of a four-volume report, summarizing an analysis of 16 PAHs:
benzofajpyrene, naphthalene, anthracene, acenaphthene, fluoranthene, fluorene,
phenanthrene, pyrene, acenaphthylene, benz[a]anthracene, benzo[b]fluoranthene,
benzo[k]fluoranthene, benzo[g,h,i]perylene, chrysene, dibenz[a,h]anthracene, and
indeno[1,2,3-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 July of
1982.
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.
'. Document Analysis a. Descriptors
Exposure Effluents
Risk Waste Disposal
Water Pollution Food Contamination
Air Pollution Toxic Diseases
b. Identlflers/Open-Ended Terms
Pollutant Pathways
Risk Assessment
e. COSATI Field/Group Q6F Q6T
Polycyclic Aromatic Hydrocarbons
Benz[a]anthracene
Benzo[b]fluoranthene
Benzo[k]fluoranthene
Benzo[g,h,i]perylene
Dibenz[a,h]anthracene
Indeno[1,2,3-c,d]pyrene
Phenanthrene
Acenaphthylene
Pyrene
Benzo[a]pyrene
Naphthalene
Anthracene
Acenaphthene
Fluoranthene
Fluorene
Chrysene
PAHs
.«. Availability Statement
Release to Public
•MANS1-Z39.18)
U.S. Environmental Protection Agency
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, IL 60604-3590
19. Security Class (This Report)
Unclassified
20. Security Class (This Page)
Unclassified
21. No. of Pages
53
22. Price
$10.00
«rse
OPTIONAL FORM 272 (4-77)
(Formerly NTIS-3S)
Department of Commerce
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EPA-440/4-85-020
July 1982
AN EXPOSURE AND RISK ASSESSMENT FOR BENZO[a]PYRENE AND
OTHER POLYCYCLIC AROMATIC HYDROCARBONS:
VOLUME I. SUMMARY
by
Judith Harris, Joanne Perwak,
and Susan Coons
Arthur D. Little, Inc.
U.S. EPA Contract 68-01-6160
John Segna
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 "quires an
understanding of the human and environmental risks associated with the
manufacture, use, and disposal of the ^"1'£M??*O*r[£
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environment^ c«cetl«*;
tions. The risk assessment process integrates health effects data
(e.g., carcinogenicity, teratogenicity) with information on 'xpoaura.
^'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
oatterns 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 IB 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 and 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
111
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TABLE OF CONTENTS
List of Figures
List of Tables
1.0 INTRODUCTION
2.0 TECHNICAL SUMMARY
2.1 Benzo[a]pyrene (BaP) J-l
2.1.1 Risk Conclusions |J~J
2.1.2 Releases of BaP to the Environment 2-3
2.1.3 Fate and Distribution of BaP in the Environment 2-6
2.1.3.1 Transport to the Aquatic Environment 2-6
2.1.3.2 Fate in the Aquatic Environment 2-6
2.1.3.3 Modeling of Environmental Distribution 2-9
2.1.3.4 Concentrations of BaP in the Environment 2-9
2.1.4 Human Effects and Exposure 2-12
2.1.4.1 Human Effects 2-12
2.1.4.2 Human Exposure 2-13
2.1.5 Aquatic Effects and Exposure 2~15
2.1.6 Risk Considerations 2-18
2.1.6.1 Human Risk of Carcinogenicity 2-18
2.1.6.2 Human Risk Associated with Non-Carcinogenic
Effects 2-18
2.1.6.3 Risk to Aquatic Organisms 2-18
2.2 Naphthalene 2-19
2.2.1 Risk Conclusions z~1^
2.2.2 Releases of Naphthalene to the Environment 2-19
2.2.3 Fate and Distribution in the Environment 2-20
2.2.4 Human Effects and Exposure 2-21
2.2.5 Aquatic Effects and Exposure 2-22
2.3 Anthracene, Acenaphthene, Fluoranthene, Fluorene,
Phenanthrene, and Pyrene 2-23
2.3.1 Risk Conclusions 2-23
2.3.2 Releases to the Environment 2-24
2.3.3 Fate and Distribution in the Environment 2-24
2.3.4 Human Effects and Exposure 2~26
2.3.5 Aquatic Effects and Exposure 2-26
2.4 Acenaphthylene, Benz[a]anthracene, Benzo[b]fluoranthene,
Benzo[k]fluoranthene, Benzo[g,h,i]perylene, Chrysene,
Dibenz[a,h]anthracene, and Indeno[1,2,3-c,d]pyrene 2-27
2.4.1 Risk Conclusions 2-27
2.4.2 Releases to the Environment 2-28
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TABLE OF CONTENTS
Continued
2.4.3 Fate and Distribution in the Environment 2-29
2.4.4 Human Effects and Exposure 2-30
2.4.5 Aquatic Effects and Exposure 2-30
REFERENCES 2_32
vi
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LIST OF FIGURES
Figure
.. No- Page
1-1 Structures of the Priority Pollutant Polycyclic
Aromatic Hydrocarbons 1_2
2-1 Sources and Fate of Benzo[a]pyrene in the Aquatic
Environment 2-11
vii
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LIST OF TABLES
Table
No.
1-1 Page
Pollutant PAHs ^^ °T Carcin°Senicity of Priority
2-1 Est 1~5
2-2 ^~^
2-3 Sources of Benzo[a]pyrene to the Environment, 1978 2-5
2"* P^nt"0" °f A«-"-S»^-e Pathway for Benzofa]-
2-5 Basic Physicochemical Properties of Benzo[a]pyrene 2-3
2-6 Fate of Benzo[alpyrene in Generalized Aquatic Systems 2-10
" „
2-8
2-9
Air
2-17
viii
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1.0 INTRODUCTION
The Office of Water Regulations and Standards (OWRS), Monitoring
and Data Support Division, of Che U.S. Environmental Protection Agency
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 summary
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 more 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
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NAPHTHALENE
THE BENZOUJPYRENE GROUP
THE ANTHRACENE GROUP
I
NJ
Phenanthrene
Acenaphthene
Pyrene
BenzofaJpyrene Acenaphthylene Benz [a] anthracene
Chrysene
Benzo[b]fluoranthene
Benzo[g,h.i]perylene
Dibenzfa.hJ anthracene
Benzo[k]fluoranthene
P
Indenof1,2,3-c,d]pyrene
FIGURE M STRUCTURES OF THE PRIORITY POLLUTANT
POLYCYCLIC AROMATIC HYDROCARBONS
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• Benzo[a]pyrene (BaP) and the eight other PAHs in the third
group have no commercial production or use, except as research
laboratory standards. They are released to the environment
inadvertently by combustion sources. With one exception
(acenaphthylene), the chemicals in this group have very low
vapor pressures and water solubilities. Several of the PAHs
in the BaP group had been identified as carcinogens. Much of
the information regarding this group of compounds is for BaP.
The exposure and risk assessment for each of the three groups of
PAHs was treated in a separate chapter of a multivolume report; Chapter
3.0 (Volume II) concerns naphthalene; Chapter 4.0 (Volume III) concerns
the anthracene group PAHs; and Chapter 5.0 (Volume IV) concerns the
benzo[a]pyrene group PAHs. These chapters are bound separately.
Potential waterborne routes of exposure are the primary focus of
these exposure and risk assessments because of the emphasis of OWRS on
aquatic and water-related pathways. Inhalation exposures are also
considered, however, in order to place the water-related exposures into
perspective. Each chapter contains major sections discussing the
following topics:
• 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
balance);
• Description of the fate processes that transform and/or
transport the compounds from the point of release through
environmental media until exposure of humans and other recep-
tors occurs, and a summary of reported concentrations detected
in the environment, with a particular emphasis on aquatic
media;
• Discussion of the available data concerning adverse health
effects of the subject PAHs on humans, including (where known)
the doses eliciting those effects and an assessment of the
likely pathways and levels of human exposure;
• Review of available data concerning adverse effects on aquatic
biota and the levels of environmental exposure; and
• Discussion of risk considerations for various subpopulations
of humans and other biota.
Two comments regarding the materials balance section are appropri-
ate. First, these sections were based in large part on draft material
prepared by Acurex Corporation, under EPA Contract 68-01-6017, and
provided to Arthur D. Little, Inc. by EPA. Second, the phrase "mater-
ials balance" is somewhat inappropriate when applied to chemicals such
as the PAHs that are produced primarily as byproducts of combustion
1-3
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»th.r than
balance production versus use and ~Vr T* approach of trying to
applicable to these chemicals md ^f0™*"*! release is not strictly
tions of these exposure and "isk a^ses^fV J""*^ balance --
releases from major sources such **Sess*ents are focused on estimates of
is associated wii most of tSese StSS^™8 considerable uncertainty
coverall11 l^p^^^ ^ T"" 7* rt* —ts
chemical, benzofajpyrenef was i of «« ?'u, W3S determined that one
than were the oti? 15 compounds studied V^^^ interest tO °^
more extensive data base available for • aL "terest reflects the
ss
^^^
.. -
(Volumes II-IV) . The sumary is focused nyk r V6 ""P"" 3.0-5.0
greatest Interest. The estSated releases to^T'81^""6 a3 the PAH of
mental fate, monitoring data. h™n eff^-V. / enviro™el":. environ-
ed exposure, and risk considerations con«J • '^T"' bI°"C effec"
expanded summary for,. Abbreviated 'Z™"8 *P "* Pres«ted in
naphthalene, anthracene
t , -
without reference to the se^ratelv I f V"7 be read and -nderatood
3
dram, ,»d more ,
sources that were reviewed In thj ° course ^ of thl^ ? vcr^ ^ Ut«"«"
1-4
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TABLE 1-1. SUMMARY OF EVIDENCE FOR CARCINOGENICITY OF
PRIORITY POLLUTANT PAHs
PAH
Benzo[a]pyrene
Dibenz[a,h]anthracene
Benz[a]anthracene
Benzo[g,h,i]perylene
Benzo[b]fluoranthene
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 orally.
1-5
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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
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2.0 TECHNICAL SUMMARY
2.1 BEN20[a]PYRENE (BaP)
2.1.1 Risk Conclusions
BaP is suspected of being a human carcinogen, although there are a
number of limitations regarding the experimental animal data upon which
this conclusion is based. Table 2-1 shows estimates of the relative
potential carcinogenic risks (excess lifetime tumor probability) for the
major BaP exposure routes determined by using a range of risk calculated
using two sets of animal data and three dose-response extrapolation
models. Although these two sets of animal data demonstrate a carcino-
genic 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 assumptions that seriously limit the
degree of confidence associated with the quantitative human risk
extrapolations for BaP. Moreover, there is, as always, no clear
agreement over the most appropriate model for performing such
extrapolations. Additional uncertainty is introduced into the risk
estimates by the conversion techniques used to estimate human equivalent
doses, and by possible differences in susceptibility between humans and
mice. Due to the use of a number of conservative assumptions in the
risk calculations, the results shown in Table 2-1 most likely
over-estimate the actual risk to humans.
The highest potential carcinogenic risks appear to be associated
with cigarette smoking. For non-smokers, the highest potential carcino-
genic risks are associated with dietary exposure to BaP (notably inges-
tion of charcoal-broiled meats and fish). Inhalation exposures at the
upper end of the range in urban areas are higher than dietary exposure,
but the estimates are based upon limited monitoring data. Drinking
water generally represents a less significant source of BaP exposure
than the diet or inhalation.
BaP has also been shown to induce in vivo chromosomal aberrations
in laboratory animals. Because of this indication of mutagenicity, BaP
exposure could be expected to contribute to the genetic burden of a
population; however, since extrapolation procedures for genetic risks
have not been well established, a quantitative risk assessment for these
kinds of adverse health effects is not presently feasible. Little
information is available on other health effects of BaP.
No conclusions could be drawn as to the risk to biota associated
with BaP exposure due to the lack of information regarding effects.
Similarly, no water quality criterion for aquatic life has been set for
this compound.
2-1
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TABLE 2-1, ESTIMATED RANGES OF CARCINOGENIC RISK TO HUMANS DUE
TO BENZO[a]PYRENE EXPOSURE FOR VARIOUS ROUTES
Route
Typical Diet
Average Lifetime
BaP Exposure Size of Exposed Estimated Lifetime Excess Estimated Incidence
Population Probability of Cancer3 (excess cancers/year)
0.05
221 x 10
4 x 10~6 to 6 x 10"4
13 - 1,900
Drinking Water
0.0006
221 x 10
1 x 10"10 to 7 x 10 6
« 1 - 22
to
to
Ambient Air - Urban
- Rural
Smoking
0.02 - 2
0.0002 - 0.2
0.6b
166 x 10
55 x 10
54 x 10
6
-7 -2
6 x 10 to 4 x 10
3 x 10~U to 3 x 10~3
3 x 10~4 to 1 x 10~2
1 - 95,000
« 1 - 2,400
230 - 7,700
A range of probability is given, based on several different dose-response extrapolation models. The
i^k r^ T ?MJ /r°babillty ,°f c*ncer "presents the increase in probability of cancer over the normal
background incidence, assuming that an individual is continuously exposed to BaP at the indicated
dally 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
W6re Utlll2ed' 1C 1S llkel* that these Predictions overestimate the actual risk
a hgher ily exposure
P°pUlation °f smokers <54 mllll°n) «»oked on average 25 cigarettes per
Ci^rettes P« **> andH^quently may receive
Source: Data taken from Volume IV of this report.
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2.1.2 Releases of BaP to the Environment
Combustion is the major source of environmental loading of BaP.
Residential heating is the single largest combustion source, since_ these
emissions are largely uncontrolled. Table 2-2 summarizes the estimates
of BaP releases from these sources and the emission factors that were
used in the calculation.
BaP is also released to the environment as a result of its presence
in petroleum- and coal-derived oils, fuels, and solvents. Coal tar
production and distillation released an estimated total of about 4 kkg
BaP in 1978.2 Creosote oil is used in the wood preserving industry;
however, less than 1 kkg BaP has been estimated to be released from this
source in 1978 (U.S. EPA 1979a).
Publicly-Owned Treatment Works (POTWs) also represent a source of
BaP releases to the environment. The volume of releases is largely
dependent upon variations in industrial disclwrges to POTWs On the
basis of a total POTW flow of approximately 1011 I/day (U.S. EPA 1978a)
and average BaP concentrations of 0.1 yg/1 in the influent (it was not
detected in the effluent), the environmental releases can be estimated.
The total environmental loading of BaP from this source was calculated
to be 3.7 kkg/yr. The amount contained in sludge was calculated to be
less than 1 kkg, assuming 6.0 x 10° kkg dry sludge produced annually
(U.S. EPA 1976- and a concentration of 3.9 yg/kg in the sludge (U.S. EPA
1980a). The difference between the total environmental loading and the
BaP in the sludge was allocated as an atmospheric release. However, an
unknown fraction of this 3.7 kkg may in fact be present in the POTW
effluent at concentrations too low to be detected.
Table 2-3 summarizes the releases of BaP to the environment includ-
ing those from combustion and other sources. Considerable uncertainty
is associated with all of these release estimates. BaP is largely a
combustion product or present at low levels in coal tar and petroleum.
Since this compound is not directly produced, the base of information on
which to apply emission factors does not exist. There are very limited
monitoring data, and the representativeness of the emission factors_is
unknown. Therefore, these estimates should be viewed as an indication
of the relative magnitude of BaP releases to the environment compared
with other compounds, and for identifying roughly the sources that are
important.
ese estimates were developed by Acurex, Inc. for EPA under Contract
No. 68-01-6017. Their data are summarized in Volume IV of this report,
2See footnote 1.
2-3
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TABLE 2-2. ESTIMATED ANNUAL AIR EMISSIONS OF BENZO[a]PYRENE FROM
COMBUSTION SOURCES, 1978
Source
Emission Factor
Residential Coal Combustion 0.0015 g/kg
Fireplaces 0.0008 g/kg
Primary Residential Wood Heating 0.004 g/kg
Auxiliary Residential Wood Heating 0.004 g/kg
Prescribed Burning 0.740 mg/kg (dry fuel)
Wildfire
Agricultural Burning
Gasoline
Tire Wear
0.740 mg/kg (dry fuel)
0.740 mg/kg (dry fuel)
8 yg/mile
Amount Combusted
3.9xl06 kkg
2.9xl06 kkg
6.9xl06 kkg
9.2xl06 kkg
36xl06 kkg (dry wt.)
2x10' kkg (dry wt.)
13x10 kkg (dry wt.)
1.7x10 miles
traveled, 67Z
Emission reduction
Estimated Releases
(kkg)
10
2
30
40
30
20
10
10
Utility Boilers - Coal
Oil
Incinerators
Coal Refuse Pile
Cigarettes
b
b
0.04 ug/kg refuse
0.005 kg/kg POM
0.01 ug/cigarette
4.8x10^ kkg
7.8x10 kkg
municipal - 385 kkg/day
commerical - 8xl06 kkg/yr
6.2xlOcigarettes
< 1
Total 159
SL 12
1.7x10 miles traveled, 0.19 g/vehicle mile airborne particulates,
0.15 g/vehicle-mile is deposited on road surface, rubber - 33Z carbon
black, 17 ug BaP/g carbon black.
Described in Volume IV of this Report.
190x10 m refuse pile volume (21Z burning), dansity 1.5 kkg/m3
POM emission rate of 1.3xlO~8 kg/kkg-hr.
Source: Acurex Materials Balance - Draft Report prepared under Contract So. 68-01-6017. Data summarized
in Volume IV of this report.
2-4
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TABLE 2-3. SOURCES OF BENZO[a]PYRENE TO THE ENVIRONMENT, 1978
Source
Air
Release (kkg)
Water
POTW
Land
Combustion
160
Coal tar production
0.7
0.9
0.6
POTW
not detected
<1
TOTAL
166
0,7
0,9
<2
Source: Acurex. Materials Balance - Draft Report Prepared under
Contract No. 68-01-6017. Data Summarized in Volume IV of
this Report.
2-5
-------
»
of the U.S. is surface water l', t- ^^ely 2% of the total
directly deposited on inUnd sur'fi. ^ P* Ba? annually would be
additional amount would eventuallv „ vT" t™ ^ atmosP*«e. An
runoff, although the total is l«i£t.T^ ^ *" ?"'" V±a SUrface
The effect on water bodies near ^ t l6SS than l kk§ Annually.
cant. The BaP reLininl in the t, ? S°UrC<2S may be more signifL
photolyzed. HoweveT a thorough atl"osPhere i« likely to be rapidly
these compounds
2>1'3'2 late in the Aquatic Environment.
The
volatilization froi surface
this compound. In fact ,
been measured In a simulated
Calculated half -lives '
hours_to 700 hours,
--
«ns"nt s"8gest that
^P0"31": P«h»ay for
-life, of «0- hours has
(Southwo«h- 1979) .
that BaP in the
1979) have suggested that direct
t ,
"Si 1978> NAS 1972-
al. 1978).
factorf up8
signifies
in the presence of humic acid (Smith
et
2-6
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TABLE 2-4. EVALUATION OF AIR-TO-SURFACE PATHWAY
FOR BENZO[a]PYRENE
Near
Combustion
Rural Urban Source
^
yg/in (air)
Percent of atmospheric
emissions deposited
- dry deposition 22 19
- wet deposition 4 4-7
- total 26 23-26
Depends on the proximity to a combustion source.
Source: Data taken from Volume IV of this report.
Fraction of airborne mass
adsorbed on particulate 0.99
Dry deposition velocity
(cm/sec)
Precipitation scavenging
ratio: 6x10 6x10 1.2x10
(water)
2-7
-------
TABLE 2-5. BASIC PHYSICOCHEMICAL PROPERTIES OF BENZO[a]PYRENE
Formula C20H12
Molecular Weight 252.32
Melting Point 179 "C
Vapor Pressure 5,6 x 10"9 torr at 25°C
Water Solubility 0.0038 mg/1 at 25°C
Log octanol/water
Partition Coefficient 6,08 at 25°C
Henry's Law Constant 4.89 x 10~7 atm nfVmole at 25°C
Source: SRI (1980); Versar, Inc. (1979).
2-8
-------
bioaccumulation is not expected to be a significant loss mechanism from
water. In addition, microbial degradation does not appear to be an
important fate process for BaP (Gardner et_ al. 1979, Lu et al. 1977,
Schwall and Herbes 1978).
2.1.3.3 Modeling of Environmental Distribution
The Mackay equilibrium partitioning model (Mackay 1979) was used to
estimate the partitioning of BaP in the environment. This application
is described in Volume IV of this report. The results suggest that
99.9% of the BaP introduced into the air-water sediment system will
reside in the sediment compartment. Less than 0.1% will be present in
the water column, and less than 0.001% will be partitioned to the
atmosphere.
The U.S. EPA EXAMS model (U.S. EPA 1980b) was also used to estimate
BaP fate in aquatic systems using a loading rate of 0.1 kg/hour. Table
2-6 summarizes the fate of BaP in generalized aquatic systems modeled by
EXAMS. The ultimate fate of BaP in these systems is controlled primar-
ily by chemical processes in the static systems, and physical transport
beyond the system boundaries for the river systems. The persistence of
BaP in aquatic systems is reflected in the time for self-purification
predicted by EXAMS. The necessary time for removal of 97% of the BaP
accumulated in the turbid river system was estimated as 89 days, while
the analogous self-purification time predicted for the" static pond
system was as high as 69 years.
Figure 2-1 summarizes the major inputs of BaP to the aquatic
environment, as well as the dominant fate and transport pathways.
2.1.3.4 Concentrations of BaP in the Environment
BaP has been monitored in environmental media. Most of the
observations reported in STORET (the U.S. EPA water quality data base)
are below the detection limits, which are generally 10 yg/1. Data from
other sources indicate that BaP levels in waters are generally less than
1 yg/1 and commonly less than 0.01 ug/1 (White and Vanderslice 1980).
Reported levels of BaP in sediment are much higher than in water.
In the STORET data base, levels up to 1,400 yg/kg have been recorded,
although only 11 of 125 observations were above the detection limit
(often greater than 1,000 ug/kg) (U.S. EPA 1980c). Hites &t_ al. (1977)
reported a high level of 8,000 yg/kg BaP (dry weight) in sediment from
the Charles River in Massachusetts. Concentrations in urban soils
appear to be about two orders of magnitude higher than concentrations in
rural soil (White and Vanderslice 1980).
Concentrations of BaP in drinking water are reported to range from
0.2 ng/1 to 1.6 ng/1, with the highest reported BaP concentration found
in drinking water from New Orleans, LA (Basu and Saxena 1978).
2-9
-------
to
TABLE 2-6. FATE OF BENZO [a] PYRENE IN GENERALIZED AQUATIC SYSTEMS3
Percent Distribution
Percent Lost by Various Processes
Residing in
Water at
System Steadv-State
Pond
Eutrophic Lake
01 igotrophic 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
by Other
Volatilized Processes
0.16 31.03
0.21 4.64
0.02 0.01
0 99.96b
0 lOOb
0.02 97.08b
Time for
System Self-
Purification0
69 years
25 years
393 days
95 days
89 days
376 days
All data simulated by the EXAMS model (U.S. EPA 1980b).
Primarily loss through physical transport beyond system boundaries.
"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.
Source: Data taken from Volume IV of this report.
-------
Direct Discharge
»>
Neg. % env. releases
AIR
100 % env. releases, 180 kkg/yr.
(rapid photolysis. t,/a 5-10 hrs.)
Atmospheric Deposition
23-26 % airborne load.
47 kkg/yr.
to U.S.
inland waters
< 1 kkg/yr.
to U.S. land mass
"v/47 kkg/yr.
Volatilization
(slow)
\\\V ti/ "v 1
•XjJ- Photolysis
(fast)
tya<10hrs.
Oxidation
tyj10.
(limited by concentration of oxidants)
Sorption log KraA, = 6.08 (fast)
— ..,.... Physical
Desorpt,on ^ ,v;:. —_____^ Transport
(slow and
continuous) \ \Sedimentation
FIGURE 2-1
SOURCES AND FATE OF BENZOla] PYRENE IN THE AQUATIC ENVIRONMENT
-------
ported to range from 0.
16 observations were
2-1.4 Human Effects and
2.1.4.1 Human Effects
to l / r, J >»v. been re-
tested for its carcinogenic effects. In
~~ ""••* w=cu suown co be both a ln/».»i -,„-> *. . »-«-vo. j.u
oral, dermal, and intratracheal routes Th SyStemic «rclnogen by
transplacental carcinogen an ±niti£ V ,, "mpound is also a
and carcinogenic in sin'2ltHn« f£ Skin carcinogenesis in mice,
_ "^e-^iij-w iu singxe—dose experiments ('TARP 1070 n
Compounds which have been TV *• A f r s;"1-0 VJ.A«.V- ly/zj Survey of
1970, 1972, 1978). Carcinogenic Activity, 1961, 1968,
allow a quantitative estimate of risk «
raise questions as to the validitv «f t-'h SeV6ral shortcomings, however,
of these studies, the test pooulLio extraP°la'ed results. In both
derably less than the secies Were exP°sed for periods consi-
" -
sensitive as,ay of the carnogiciofp
,
of carcinogenic rislc of
are subject to the foUowing quaUf ltions-
°°deis ha- »—
8S"Mtes
extrapoiation
2-12
-------
• the less-than-lifetime duration of exposure in both the
studies used.
The results of extrapolating these two data sets by use of three
extrapolation models are shown in Table 2-7. Due to different assump-
tions concerning the actual underlying mathematical relationship between
dose and effect, the extrapolated risk estimated at the relatively lower
exposure levels typical of actual environmental exposures varies
appreciably depending upon the model and the data set used. Regardless
of the model, however, higher risk estimates (by about an order of
magnitude) are predicted from the data of Fedorenko and Yanysheva (1966)
than from those of Neal and Rigdon (1967), possibly due to the different
modes of oral administration. [Federenko and Yanysheva (1966) utilized
weekly intubation, while Neal and Rigdon(1967) incorporated BaP into the
diet.]
The U.S. Environmental Protection Agency (1980c) used a linear,
non-threshold model and the data of Neal and Rigdon (1967) to calculate
that a concentration of 2.8 ng/1 in surface water would result in an
estimated lifetime excess probability of cancer of 1x10 due to
consumption of drinking water and fish.
The data concerning health effects other than carcinogenicity are
limited." BaP appears to exert little effect on the developing embryo
(Bulay and Wattenberg 1970, Rigdon and Rennels 1964). However, it is an
active mutagen, inducing in vivo chromosomal aberrations in both hamster
spermatogonia and bone marrow cells (Basler and Rohrborn 1978,
Roszinsky-Kocher et al. 1979), and inducing positive mutagenic responses
in sister chromatid exchange tests in hamsters (Bayer and Bauknecht
1977, Roszinsky-Kocher et al. 1979, Sirianni and Huang 1978). Because
of the compound's mutagenicity, BaP exposure could also be expected to
contribute to the genetic burden of a population. However, since
extrapolation procedures for genetic risks are not well established, a
quantitative risk assessment for these kinds of health hazards is not
presently feasible.
In addition to the effects described above, the possibility exists
of augmentation of effects through synergistic or co-carcinogenic
mechanisms. Current understanding of these processes, however, does not
allow estimation of human risk.
2.1.4.2 Human Exposure
Human exposure to BaP was evaluated considering various routes
(food, drinking water, air, and smoking). These routes were considered
as quantitatively as possible, even though data are often scarce.
Smoking appears to be an important route of exposure. Levels of
0.025 yg BaP per cigarette in mainstream smoke were reported by Schmeltz
et_ al. (1975). At these levels, smokers could be exposed to 0.025-2.5
Ug/day, depending upon the type and number of cigarette smoked, the
2-13
-------
TABLE 2- 7. ESTIMATED LIFETIME EXCESS. PROBABILITY OF CANCER TO HUMANS
DUE TO BENZO[a]PYRENE INGESTION AT VARIOUS EXPOSURE LEVELS
BASED ON THREE EXTRAPOLATION MODELS3
Estimated Lifetime Excess Probability of Cancer at Indicated Exposure Level'
'
Exposure Level (yg/day)
Extrapolation Model
Neal and Rigdon data
Fedorenko
and Yanysheva data
Log-probit Model
Neal and Rigdon data
NJ Fedorenko
M and Yanysheva data
Multi-stage Model
Neal and Rigdon data
Fedorenko
and Yanysheva data
: 0.001
1 x 10~6
1.1 x 10~5
1 x 10~9
3 x 10~7
1.7 x 10~6
7 x 10~6
o
The lifetime excess probability of
0.01
1 x 10~5
1.1 x 10~4
1 x 10~7
2.6 x 10 ~5
1.7 x 10~5
7 x 10~5
cancer represents
°-1 1 10 100
1 x 10~4 1 x 10~3 1 x 10~2 9.2 x 10~2
1.1 x 10"3 1.1 x 10~2 l.l x lO"1 6.7 x 10"1
1.4 x 10~5 7.5 x 10~4 1.5 x 10~2 1.2 x 10"1
1.2 x 10~3 2.1 x 10~2 1.5 x 10'1 4.8 x 10"1
1.7 x 10~4 1.7 x 10~3 3.6 x 10~2 1.5 x 10"1
6.8 x 10~4 6.8 x 10~3 6.5 x 10~2 4.8 x 10"1
the increase in probability of cancer over fhe
» — - — - —-. — — v_u v ^-«.* ^f f. *_ri^fc4.u j. a-J- ujr u±. ^.Oll^C A. \J V Ci. LilC
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 conser-
vative assumptions that were utilized, it is likely that these predictions overestimate the actual
risk to humans.
-------
amount of smoke inhaled, and the number of cigarettes smoked. An
estimated 54.1 million persons in the U.S. smoke cigarettes, and of
these 25-30% smoke more than 25 cigarettes per day (U.S. DHEW 1979).
Thus a large segment of the population (those smoking >25 cigarettes per
day) could be exposed to BaP in the 0.6-2.5 yg/day range resulting from
mainstream smoke alone.
Although levels of BaP in smoke-filled rooms have not been measured
specifically, estimates were made based upon CO levels summarized by
Burns (1975). CO levels of 44-92 mg/m3 were reported for rooms (38-92
m ) where 30-80 cigarettes had been smoked with no ventilation. BaP
levels of about 0.07-0.2 yg/m3 were calculated for a small room with no
ventilation, based upon a CO/BaP ratio of 50,000 in side-stream smoke.
0.085
A non-smoker exposed to such a situation 2 hours/day would be exposed to
about 0.25-0.7 yg BaP/day; however, there are numerous uncertainties in
these calculations.
Levels of BaP in raw foods are generally low. Higher levels,
however, result from cooking processes, especially charcoal broiling and
smoking. Table 2-8 shows daily exposure due to consumption of such
foods and summarizes the assumptions made in developing the estimates.
The estimated "typical exposure" via food ingestion is about 0.05
yg/day. Consumption of large amounts of charcoal-broiled food could
result in exposure amounting to as much as 6 yg/day.
The levels reported by White and Vanderslice (1980) for ambient air
imply that persons in urban areas are exposed to 0.02-2 yg/day, while
persons in rural areas are generally exposed to 0.0002-0.2 yg/day,
assuming respiratory flow of 20 m3/day. Although woodburning has been
shown to increase indoor air levels over outdoor air, these levels (mean
of about 5 ng/m3) still fall within the range for rural and urban areas
(Moschandreas et al. 1980). The U.S. EPA (1978b) has estimated the
population sizes exposed to various concentrations. These results shown
in Table 2-9 suggest that most individuals in the U.S. are exposed to
BaP by inhalation of ambient air in the range of 0.02-0.1 yg/day.
Drinking water does not generally appear to represent a significant
source of exposure to BaP. On the basis of the limited data of Basu and
Saxena (1978), a typical exposure of 0.0006 yg/day, and a maximum of
0.004 yg/day were calculated for drinking water, assuming a consumption
of 2 I/day.
A summary of all exposure pathway estimates appears in Table 2-1.
2.1.5 Aquatic Effects and Exposure
No data from acute toxicity bioassays were available for BaP.
However, tissue damage, abnormal growth, and the production of cancer-
like growths ha^e been reported. Teratogenic and mutagenic effects have
2-15
-------
TABLE 2-8. LEVELS OF BENZO[a] PYRENE GROUP PAHs IN FOOD
AND ESTIMATED INGESTION EXPOSURE
Berizo [ a ] pyrene
(g/day)
Charcoal broiled
beefa
Hamburger
Steak
Smoked pork
Smoked sausage
Smoked fish
Oil
Fruits
Grains
Vegetables
Total
Leafy
Typical
10
3
1
1.5
0.1
18
205
256
248
40
Max.
NA
86
27
30
14
NA
NA
NA
NA
NA
Contamination
Intake
(ug/kg) (ue/dav)
Typical
NA
5
2
NA
1
1
0.02
NA
0.01
NA
Max .
2.6
50
55
4
37
8
6
0.3
0.1
7.5
Typical
NA
0.02
0.002
0.006
0.0001
0.02
0.004 •
NA
0.002
NA
Max.
0.03
4.3
1.5
0.12
0.5
0.14
1.2
0.08
0.2
0.3
Consumption of beef - 86 g/day, 15% charcoal-broiled - 80% hamburger,
20% steak. Worst case maximum 86 g consumption of charcoal-broiled
steak.
Consumption of pork - 27 g/day, 5% smoked. Worst case maximum,
27 g/day smoked.
r+
"Consumption of sausage - 30 g/day, 5% smoked. Worst case maximum
30 g/day smoked.
Consumption of fish - 14 g/day, 1% smoked. Worst case maximum,
14 g/day smoked.
Source: USDA (1978, 1980), U.S. EPA (1980), White and Vanderslice (1980)
2-16
-------
TABLE 2-9 ESTIMATED SIZE OF THE U.S. POPULATION EXPOSED TO RANGES
OF BENZO[a]PYRENE CONCENTRATIONS IN AMBIENT AIR
SaP Concentration (ng/m )
73,294
0.5-1.0
26,731
1.0-5.0
102,132
>5.0
1059
Note- For some locations for which monitoring data were unavailable
(representing about 50% of the population) the upper limits of 95/»
confidence intervals of national average concentrations were used.
These levels were as follows:
o
urban SMSA3 1.3 ng/m
3
urban non-SMSA 1.4 ng/m
3
rural 0.23 ng/m
aStandard Metropolitan Statistical Area
Source: U.S. EPA (1978b).
2-17
-------
also been observed in aquatic invertebrates and lower vertebrates
(Korotkova and Tokin 1968, Neff 1979).
The available data on BaP concentrations in ambient waters suggest
that exposure of aquatic organisms is low. As discussed previously,
levels in surface water of less than 1 ug/1 are most common. The levels
of BaP in sediments may frequently exceed 1000 pg/kg, and represent a
potential source of exposure. However, the bioavailability of sediment-
bound BaP is unknown.
2.1.6 Risk Considerations
2.1.6.1 Human Risk of Carcinogenicity
The results of the extrapolation of the animal studies on
carcinogenicity have been discussed and presented previously in Table
2-7 (p. 2-14). The qualifications and major assumptions have also been
discussed and underline the caution with which these calculations must
be viewed.
The risks based upon these calculations and the exposure estimates
made for specific subpopulations are shown in Table 2-1 (p. 2-2). The
highest estimated excess probability of cancer appears to be for
smokers, especially heavy smokers with an estimated incidence of
230-7700 excess cancers/year. Dietary exposure, primarily due to smoked
and charcoal-broiled foods, may result in an estimated 13-1900 excess
cancers/year. Risk estimates associated with inhalation exposures show
a wide range. Urban residents may experience 1-95,000 excess
cancers/year and residents of rural areas, « 1 to 2400 excess
cancers/year. Drinking water consumption generally appears to present a
lower degree of risk. It should be noted, however, that these estimates
are based upon numerous assumptions and limited monitoring data. These
limitations are discussed in this summary and Volume IV of this report.
2.1.6.2 Human Risk Associated With Non-Carcinogenic Effects
Little information exists regarding other potential adverse effects
of exposure to BaP. Although this compound has been identified as an
active mutagen in numerous systems, a quantitative estimate of genetic
risk is not feasible. In addition, one should not overlook possible
augmentation of risk through synergistic or co-carcinogenic mechanisms;
however, current understanding of the co-carcinogenesis process is not
sufficiently adequate to allow estimation of associated human risks at
this time.
2.1.6.3 Risk to Aquatic Organisms
Data on effects of BaP on biota are extremely limited. As a
result, no statement of potential risk, even qualitative, can be made at
this time. Similarly, the U.S. EPA (1980c) was unable to set water
quality criteria for BaP due to the lack of data. It should be noted,
however, that high sediment levels may pose some risk to aquatic biota,
2-18
-------
although there is at present no way to evaluate the environmental risks
of contaminated sediment.
2.2 NAPHTHALENE
2.2.1 Risk Conclusions
A review of the environmental monitoring and human effects data
indicates that the dose levels at which acute effects of naphthalene
have been observed in humans or mammals are generally more than five
orders of magnitude greater than human exposure levels through inges-
tion, and at least three orders of magnitude higher than inhalation
exposure levels to specific subpopulations associated with mothball
usage and cigarette smoking. Chronic toxicity studies have failed to
demonstrate the carcinogenic activity of naphthalene. The major effects
of naphthalene on humans include cataracts and hemolytic anemia. There
appears to be little acute risk to humans from environmental exposure to
naphthalene; however, severe adverse effects are possible from acciden-
tal ingestion of substantial quantities of naphthalene.3
The U.S. EPA has not established a water quality criterion for the
protection of human health due to the inadequacy of the data on the
chronic toxicity of naphthalene and the lack of epidemiologic studies
(U.S. EPA 1980d).
There is very little information available on the extent of expo-
sure of aquatic biota to naphthalene. However, the available monitoring
data suggest concentrations reported inr:ambient water are about two
orders of magnitude lower than the levels associated with acute or
chronic effects to aquatic organisms.**
2.2.2 Releases of Naphthalene to the Environment
Production of naphthalene in 1978 totaled 2.35 x 105 kkg, 70% from
coal tar and 30% from petroleum (Abshire e_t al. . 1980). Total
environmental releases in 1978 were equivalent to 5% of production:
10,600 kkg were released to air, 300 kkg were released to land, 240 kkg
were released to POTWs, and approximately 340 kkg were discharged
directly to surface waters. Production activities accounted for the
estimated annual release of 83 kkg (Brown 1975); direct uses of
naphthalene released 5,000 kkg, and sources of inadvertently released
naphthalene total more than 6,000 kkg.5
3These conclusions are taken from Volume II of this report.
**See footnote 3.
5These estimates were developed by Acurex, Inc. for EPA under Contract
No. 68-01-6017. Their data are summarized in Volume II of this
report.
2-19
-------
2>2'3 ^te and Distribution in the Environment
»n a Vap°r Press«e "* 0-09 torr at 25°C (SRI
Inc 1979°, ."? octanol:««« partition coefficient of 3?37
-79
«« . .-
ta«Vaif '^ 9e"lmen; V'a adsorP"'»' — sedimentation may be i^rl
tant if there is a significant amount of suspended material in rtL
aquatic system (Neff 1979). Biodegradation mayP also b^ a s?Lif iclnt
6 r° *
-TT ^-^ '^-1SS5
%i^^^^
tt^^^ -^
adsorbed naphthalene
'See footnote 5.
2-20
-------
EXAMS results for six generalized aquatic systems suggest that the
naphthalene in sediment will tend to remain there unless there is
considerable mixing between the sediment and the water column, since
neither photolysis nor anaerobic degradation are important fate path-
ways. In summary, although the sediments and the water columns of
aquatic systems may contain naphthalene, accumulation will occur in the
sediment.
Monitoring data confirm that concentrations in sediment are higher
than those in water. The STORE! data base (U.S. EPA 1980e) reports
actual measurements of naphthalene in ambient waters ranging from 0.005
yg/1 to 17 yg/1; effluent concentrations up to 36,000 yg/1 are reported.
Actual sediment concentrations reported in STORET range from 0.02 yg/kg
to 496 ug/kg. Drinking water concentrations up to 1.4 yg/1 were re-
ported in the literature (U.S. EPA 1980d). Ambient air concentrations
of naphthalene were reported to be 0.35 ng/m3 in an urban area, and 0.05
ng/m3 in a rural area (Krstulovic et, al. 1977). Concentrations to which
industrial workers may be exposed range from 102 ng/m3 to 10° ng/m3 in
the vapor phase, and up to 4 x 103 ng/m3 adsorbed onto particulate
matter (Bjorseth est al. 1978a,b).
2.2.4 Human Effects and Exposure
Naphthalene is absorbed through ingestion, inhalation, and skin
contact; however, the rate 'and extent of absorption and the tissue
distribution have not been studied in detail (U.S. EPA 1980d). There is
little quantitative information on the carcinogenic or long-term effects
of naphthalene. Two experiments by Knake (1956) indicated a slight but
not statistically significant increase in lymphosarcomas in rats and
lymphocytic leukemia in mice; several other skin painting studies were
negative for carcinogenesis. Mutagenicity studies were also negative
(U.S. EPA 1980d). A single study noted retarded heart development and
cranial ossification in rats exposed to high concentrations throughout
gestation (Harris et al. 1979).
The major effects linked to naphthalene exposure include cataracts,
sometimes accompanied by retinopathy and hemolytic anemia. Near blind-
ness was reported in one human upon ingestion of 5 g naphthalene ('WO
mg/kg); bilateral cataracts were also reported among workers exposed to
naphthalene, although details of that study were not available (Ghetti
and Mariani 1956). Cataracts and retinopathy were reported in labora-
tory animals at dose levels of 1,000 mg/kg/day. The oral LDLo (lowest
lethal dose) reported for naphthalene in children was ^100 mg/kg (Sax
1979); the oral LDso (lethal dose to 50% of the subjects) observed in
rodents was ^2,000 mg/kg (U.S. EPA 1980d).
Individuals with relative deficiencies in the enzymes (G6PD) needed
to maintain glutathione levels in red blood cells (approximately 100
million people worldwide) may have increased sensitivity to naphthalene
(Wintrobe et al. 1974); the fetus and the newborn may also have an
2-21
-------
increased sensitivity (Dawson et al losfll IT,
increased risk of develop^ nTmoTv,:^ < t subpopulations are at
damage. «wpin» hemolytic anemia, vhich may lead to renal
W/l. and a fish consumption of 21
Data concerning naphthalene
of 2
about one-third of H.S adults
smoke more than 25 ciga^ttes par day
of the U.S. population
alene doses greate
content in •i
Schmeltz et al. (1976); in a smoke
tration wa7 eTtimated (by
Since
°f the"
lar§e segment
C°Uld be 6Xp°Sed to naPh^~
™*- Naphthalene
46 yg/cigarette by
•'«"
in
inhalation exposures
^
related to domestic use of «flJf n ^
analogy to dichlorobenzene f 1« Sf rL^ed b
Approximately 26 x 10* households in the us ue mot n '
one-third of the mothballs nJrJno ^ ^ U'S'J use mothballs, though only
1980h). mothballs produced contain naphthalene (U.S. EPA
2'2-5 Aquatic Effects and Exposure
2-22
-------
generally about 10 yg/1; sediment levels range from 0.02 pg/kg to less
than 500 yg/kg (U.S. EPA 1980e).
2.3 ANTHRACENE, ACENAPHTHENE, FLUORANTHENE. FLUORENE,
PHENANTHRENE, AND PYRENE ,
2.3.1 Risk Conclusions
The human effects data for this group of PAHs are inadequate to
warrant a quantitative extrapolation of the human risk from environmen-
tal exposure to these compounds. There are virtually no toxicological
data. -)A Nofle_of ,Jth_e_cojippunds in this jgrpup has been reported to be
^carcinogenic by~ the oral jo^te7Ts"cKmahT'l955, Innes'ef-gi". "1969) ;' pyfene
and -fluoranthene, however, have been reported to_ be co-carcinogens
(Salaman and Roe"'T9T67 Scribner 1973). Due to inhalation of "mains tfream
cigarette smoke reported to contain fluoranthene and fluorene (Schmeltz
et^ al. 1975), smokers may be exposed to higher levels of these PAHs than
Is" "the general population. However, the limits on the risk associated
with these environmental exposure scenarios cannot be defined at this
time.
The U.S. EPA reports that sufficient data on acenaphthene were not
available to permit the derivation of a water quality criterion that
would protect humans against the potential toxicity of this compound.
However, the level for controlling undesirable odor and taste quality in
ambient water has been estimated to be 20 ug/1 on the basis of organo-
leptic data which have no demonstrated relationship to adverse human
health effects (U.S. EPA 1980f). For fluoranthene, an ambient water
quality criterion for the protection of human health has been set at 42
yg/1 (U.S. EPA 1980g). This criterion was based on a no-effect level
for mortality in a mouse skin-painting experiment. Ambient surface
water concentrations above these recommended levels have been reported
for both of these compounds. No specific water quality criteria have
been set for the other PAHs in this group (U.S. EPA 1980c).
Risk to aquatic biota exposed to ambient concentrations of these
PAHs is expected to be low. The U.S. EPA has not established ambient
water quality criteria for these compounds for the protection of aquatic
life (U.S. EPA 1980c,f,g). However, all ambient concentrations in the
STORET data base (U.S. EPA 1980e) were below the levels that were
reported to be acutely toxic to freshwater organisms. The STORET
concentration data for surface water do overlap the range of chronic and
acute toxic effects levels for marine organisms, which appear to be more
sensitive to these PAHs (Neff 1979, U.S. EPA 1980g); however, there are
no monitoring data specifically for marine systems. Since the potential
does exist for bioaccumulation of these PAHs in zooplankton (Giddings et
al. 1978), and subsequent biomagnification by fish (Herbes 1976), direct
comparison of ambient concentrations with effects levels may not ade-
quately describe the risk to aquatic organisms.
2-23
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2.3.2 Releases to the Environment
The six PAHs in the anthracene group are all used commercially.
Total use in 1979 amounted to approximately 830 kkg; most (720 kkg) was
imported. The annual (domestic and imported) supply of fluorene and
phenanthrene was reported to be less than 1 kkg of each (U.S. Dept. of
Commerce 1980).
These PAHs are used as intermediates in the synthesis of a variety
of compounds, including Pharmaceuticals, pigments, plastics, pesticides,
and photographic chemicals. Since the PAH compounds are consumed in
these processes, a small, approximately 1%, release to the environment
may be assumed; thus, about 8 kkg of these six PAHs were estimated to be
released in 1979, distributed almost equally among the air, land, and
water compartments.
The chief source of inadvertent releases of anthracene and the
other PAHs in this group is combustion. Burning of wood for residential
heating generates the largest amount of these PAHs, 3,200 kkg or 60% of
the total (5,400 kkg) estimated annual atmospheric emissions of anthra-
cene group PAHs; coal, gas, and oil rired residential heating units
release less than 800 kkg combined. Anthracene and phenanthrene account
for 75% of the total atmospheric emissions from residential wood burning
attributable to the PAHs in this group. Other combustion sources of
these PAHs include agricultural burning, prescribed burning, wildfires,
and combustion of gasoline.8
In 1978, coal tar distillation resulted in the inadvertent produc-
tion of approximately 175,000 kkg of anthracene group PAHs (U.S. DOE
1979, Rhodes 1954). Of this total, the amounts released to the environ-
ment are estimated to be: 30 kkg to air, 14 kkg to land, 17 kkg to
POTWs, 22 kkg to surface water, for a total estimated environmental
release of 83 kkg in 1978. Approximately 15 kkg of the PAHs in this
group were released to water in oil spills and 14 kkg to air in petro-
leum refinery wastestreams, according to 1978 data.9
The total environmental releases of the anthracene group PAHs for
1978 are estimated to be about 5,600 kkg; of this total, 5,400 kkg or
97% is estimated to be released to air, 60 kkg to surface water, 100 kkg
to POTWs, and approximately 1 kkg to land.10
2.3.3 Fate and Distribution in the Environment
The environmental release data indicate that most discharges of
anthracene and the other PAHs in this group are to the atmosphere.
These estimates were developed by Acurex, Inc. for EPA under Contract
68-01-6017. Their data are summarized in Volume III of this report.
8See footnote 7.
9See footnote 7.
10See footnote 7.
2-24
-------
Atmospheric deposition (from both wet and dry processes) may remove
5-26% of the atmospheric load of anthracene in urban areas, accounting
for 75-300 kkg/yr of anthracene fallout. It is estimated that about 2%
will fall directly on inland surface waters, representing 1.5-7-8 kkg/yr
anthracene. The upper limit on this range corresponds to deposition in
areas near combustion sources, where the anthracene will be primarily
adsorbed onto particulates. The percentage of these PAHs that remains
in the atmosphere will be degraded by photolysis to oxygenated com-
pounds, including quinones (Radding &t_ al. 1976).
Since the water solubilities of the anthracene group PAHs are
relatively low and the octanol:water partition coefficients are fairly
high, adsorption onto both organic and inorganic matter is a primary
removal pathway for these compounds in the water column. The particu-
late matter will ultimately be transported to the sediment where these
PAHs will accumulate (Neff 1979, Smith et_ al. 1978); biodegradation and
photo-oxidation in sediments are expected to be quite slow. The
fraction of these PAH that remain in the water column is expected to be
degraded photolytically (Zepp and Schlotzhauer 1979, Radding et al.
1976); however, the extent of this removal pathway will be affected by
the turbidity and light penetration in the actual system (Southworth
1977). Volatilization from water is not expected to be a major fate
process, but the relative importance of this pathway differs among
aquatic systems (Southworth 1979). Bioconcentration factors for
anthracene are on the order of several hundred (Herbes 1976); half-lives
for biodegradation have been determined to be 1-2 weeks in acclimated
cultures (Quave et al. 1980).
EXAMS (U.S. EPA 1980b) calculations for anthracene indicate that in
all model systems, except the oligotrophic lake where sedimentation
rates are low, over 80% of the anthracene resides in the sediment
compartment when the system is at steady state. Rapid photolysis is
predicted by EXAMS for the anthracene remaining in the water column of
clear, quiescent systems; volatilization is important in the pond and
eutrophic lake systems where light penetration is reduced by suspended
matter. Biological degradation is important only in the highly produc-
tive eutrophic lake. In the more dynamic river systems, physical
transport (downstream) accounts for most of the anthracene removal.
Anthracene and the related PAHs have been detected in all environ-
mental media (Kim and Stone 1979; U.S. EPA 1980c,e,f,g; White and
Vanderslice 1980). Monitoring data support the predictions that
significant amounts of anthracene and related PAHs will reside in the
sediments. The majority of the STORET surface water concentrations of
these PAHs are less than 100 Mg/lj STORET effluent data include
concentrations ranging from <1 yg/1 to <1,000 ug/1 for these PAHS (U.S.
EPA 1980e). Various other sources report effluent and sewage
concentrations of fluoranthene from 2 ug/1 to 20 yg/1 (U.S. EPA 1980g).
Levels of pyrene and fluoranthene in soil were high, up to 120,000 wg/kg
(White and Vanderslice 1980). Concentrations of pyrene in several
edible marine species were reported to range from less than 0.6 ug/kg to
2-25
-------
58 yg/kg (wet weight) (Pancirov and Brown 1977)
• * of urban locations -
2'3'4 Human Effects and
t. i
which to determine the dose **ln? ? 5 Z n° toxic°l°Sical data
humans or laboratory immals The ch/onf "V? aCUte tOXiC ef f ects in
have not been studied extensivelv. hn ""ecta °f these compounds
that none has been sho^ to ' bt > c^n^ ^ available d^a indicate
1955). Phenanthrene an? pyrene show wf'f ^ * th* Oral r°Ute (Schmahl
mo "
an pyrene show w
mouse skin carcinogenesis ^xperimen" (Us ^1^0^°" aCtiVity in
studies were negative, and no data ^ were kvSLblf §8)V Muta§enicity
effects of these six compounds. SincTLl «^ p^ °^ the terato8enic
lipid-soluble, absorption and distribution ^ I ^ th±S gr°up are
expected to occur. distribution throughout the body are
tal exposure^ ige^ioof To^?* **"• ^ ^^ -vironmen-
air is estimated to le less than f uWH^'f ^ inhalation of ambient
maximum exposure levels could >, 8/ S uf°r 6ach °f these six PAHs;
anthene. "^ However very SfA J% " Mgh 3S 21 PS/day for f^^~
drinking water ^5^3^ ^ £» "^^^ Particularly for
meats, appears to be the maior rcfui-/ «f particularly charcoal-broiled
in this group (U.I. DOA 1978 1Q8H erfPc°SUre f °r a11 of the six ?AHs
typical exposure to the geneVal population!*""
2.3.5 Aquatic Effects and
in
found
o
however, plants were found to T. °f the Slx PAHs in thls
'
UData taken from Volume III of this
report.
2-26
-------
fluoranthene concentrations as low as 12 yg/1 (U.S. EPA 1978c). Micro-
cosm experiments conducted in the presence of sunlight have shown that
1 yg/1 to 10 ug/1 of anthracene killed all organisms present (Personal
Communication, P. Landrum et al., Savannah River Ecology Laboratory
1980). However, these laboratory data may not be directly representa-
tive of the effects of these PAHs in actual environmental systems.
The monitoring data documenting the exposure of aquatic biota to
these PAHs are quite limited. All of the ambient water concentrations
of anthracene, and most of those for the other PAHs in this group, were
reported to be less than 100 yg/1 (U.S. EPA 19890e); all of the actual
concentrations in ambient waters were reported to be below 1.7 mg/1, the
lowest acute effects level for freshwater organisms (U.S. EPA 1978c).
However, 25-40% of the detectable concentrations for five PAHs in this
group (excluding anthracene) were between 100 yg/1 and 1,000 yg/1;
only 8-17 observations above detection limits were reported (U.S. EPA
1980e). Acute toxic effects and chronic effects for marine organisms
have been attributed to concentrations within this range. Sediment
concentrations of acenaphthene and fluorene were reported to be within
the range of 2 yg/kg to 50 yg/kg; unremarked sediment concentrations for
the other PAHs ranged from not detected to 1,000 yg/kg (U.S. EPA
1980e). The extent of the bioavailability of these compounds bound to
sediments has not been clearly determined at this time.
2.4 ACENAPHTHYLENE, BENZ[a]ANTHRACENE, BENZO[b]FLUORANTHENE.
BENZO[k]FLUORANTHENE. BENZO[g.h.i]PERYLENE, CHRYSENE,
DIBENZ[a,h]ANTHRACENE, AND INDENO[1,2,3-c.d]PYRENE
2.4.1 Risk Conclusions
Data for the PAHs included in this group were inadequate for
purposes of quantitative risk assessments since dose-response data were
unavailable. Bj^z^ajaaehracene and dibenz[a,h]anthracene are both
carcinogenic in mice by the oral route (IARC 1972). The compounds are
also complete carcinogens in mice exposed by the dermal route, as are
benzo [b] fluoranthene and indeno [1,2,3-c td]jvjrene_. Benzo[g,h,i]perylene
is a co-carcinogen with BaP and benz[a]anthracene; benzojb]fluoranthene,.
chrysene, and indeno[1,2,3-c,d]pyrene are all (^±t±ators) of skin
carcinogenesis in mice. No carcinogenicity data were~fouH3~?or acenaph-
thylene (U.S. EPA 1980c, IARC 1972, Habs £t al. 1980).
Only limited data are available describing the acute and chronic
effects of the PAHs in this group for aquatic biota. The results of the
only reported laboratory toxicity test for any of these compounds
indicate that benz[a]anthracene at a concentration of 1 yg/1 caused 87%
mortality in bluegill sunfish in 6 months (Brown et al. 1975). Levels
of these compounds in ambient surface water are generally lower than 1
yg/1, although levels up to about 2000 yg/1 have been reported (U.S. EPA
1980c,e). High sediment levels of PAHs, as may be found near industri-
alized areas, may pose some risk to aquatic biota, although the extent
of bioavailability of sediment-bound PAH is not well documented.
2-27
-------
2.4.2 Releases to the Environment
The PAHs in this group are released primarily to the atmosphere and
result mainly from combustion sources. Residential heating accounts for
the largest releases, since these emissions are largely uncontrolled.
Emission factors indicate that fireplace burning produces a smaller
amount of PAHs per unit of fuel than do the more airtight wood-burning
units used for primary heating. On the basis of emission factors and
quantity of fuel consumed in 1978, the following estimates of annual
atmospheric releases for this group PAHs can be made:
• residential coal combustion — 130 kkg;
• fireplace burning, primary wood heating and auxiliary wood
heating — 40 kkg, 630 kkg, and 800 kkg, respectively;
• two types of forest fires, prescribed burning and wildfire
burning — 450 kkg and 260 kkg, respectively; and
• agricultural burning — 170 kkg.
With the exception of gasoline combustion (accounting for the
release of about 40 kkg of this group of PAHs in 1978), all other
combustion sources are estimated to release total quantities of these
PAHs that are much smaller on a national level than the amounts released
during combustion of coal and wood. Utility boilers, municipal and
commercial incinerators, and industrial internal-combustion engines are
all controlled units, have relatively high combustion efficiencies, and
are believed to release relatively low amounts of these PAHs.12
In addition to combustion sources, these PAHs are released from a
few contained sources, primarily related to coal tar and petroleum.
Coal tar production and distillation activities account for the environ-
mental release of approximately 50 kkg (1978) of these six PAHs; their
distribution is believed to be almost equally divided among releases to
air, land, surface water, and POTWs. Significant environmental releases
associated with petroleum sources (exclusive of gasoline combustion) are
believed to be limited to oil spills and atmospheric releases at refin-
eries. ld
1 9
These estimates were developed by Acurex, Inc. for EPA Under Contract
No. 68-01-6017. These data are summarized in Volume IV of this
report.
13See footnote 12.
2-28
-------
2.4.3 Fate and Distribution in the Environment
The PAHs in this group are released to the environment primarily as
products of combustion. Although photolysis of atmospheric PAHs is
relatively rapid (Versar 1979), wet and dry deposition of the atmo-
spheric PAH emissions probably represent the major input pathways to the
aquatic environment based upon the analysis conducted for BaP described
previously in this summary and in Volume IV of this report.
Calculations using the model of Mackay (1979) indicate that at
equilibrium 99.9% of BaP in the aquatic environment resides in the
sediment compartment; very small amounts will be found in the air (vapor
phase BaP), water, or biota. This distribution of BaP is probably
representative of the fate of other compounds in this group as well.
The U.S. EPA (1980b) 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 10 . 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%). Again, this pattern
of distribution should hold true for other compounds in this group of
PAHs.
The most significant fate processes for these compounds in aquatic
systems include adsorption (with subsequent transport to the sediment)
and chemical degradation (photolysis). Volatilization and biodegrada-
tion are expected to be slow processes for the PAHs in this group (Smith
et_ £LL. 1978, Quave et al_. 1980, Colwell and Sayler 1978, Gardner et al.
1979). These compounds are expected to be relatively persistent in
aquatic systems as was predicted for BaP by use of EXAMS.
There are fewer monitoring data for the other PAHs in this group
than for BaP. Most of the observations in the STORET data base for the
PAHs in this group are reported to be below the detection limits. The
PAH concentrations reported above detection limits for sediment samples
range from 0.002 yg/kg to 2600 yg/kg. Detectable ambient water
concentrations recorded in STORET range from 0.01 ug/1 to 1500 ug/1
(U.S. EPA 1980c).
Data from other sources indicate that the concentrations of these
compounds in ambient waters are generally less than 1 yg/1 (White and
Vanderslice 1980). Concentrations in drinking water were reported to
range from 0.1 ng/1 to 4.0 ng/1 (Basu and Saxena 1978). In this survey,
the highest concentration for the PAHs in the BaP group was 4.0 ng/1,
reported for benzo[g,h,i]perylene in a drinking water sample taken from
Philadelphia, PA.
Ambient air concentrations of these PAHs were also reported to be
significantly higher in urban areas than in rural areas. In a study of
2-29
-------
„<,/ 3 t r •"«"" "« uignesc rAii concentrations in air CUD to 21 1
ng/m for benzore.h.ilDervlen^ «<»^ «««,*«j r-_ „. „ . :;ip " ^i'J
2.4.4 Human Effects and Exposure
m°re active ««t»8«i than any of the compounds
in
with surH1011 " avail/ble on oth« toxic effects associated
"
the b, f t Pr/ay "Presents an important source of exposure
-^
(1978),
water exposures are generally less
ralless
2-4-5 Aquatic Effects and Exposure
There are almost no data describing the acute toxic effects to
aquatic organisms of the PAHs in this group. Benz[a]anthracene at a
ummarized ^ Volume IV of this report.
information is described in Volume IV of this report.
2-30
-------
concentration of 1 ug/1 caused 87% mortality in freshwater bluegill in 6
months (Brown et al. 1975).' No other acute toxicity data for these PAHs
were found.
A limited number of studies of sublethal and chronic effects have
been found as described in Volume IV of this report.' These are gener-
ally inadequate to define the concentration ranges associated with these
effects.
Experiments conducted on a small number of species of aquatic
invertebrates and lower vertebrates have shown that PAHs in the BaP
group may cause tumor production and teratogenic and mutagenic effects
(Neff 1979). Concentration levels associated with these effects were
not given. Increased liver disease in benthic English sole has been
shown to be associated with sediments contaminated with PAHs; however,
no concentration data are available (Malins 1979).
The limited number of positive observations in STORET of the PAHs
in this group indicates a concentration range in surface waters from
0.01 ug/1 to 1500 Ug/1; benzo[k]fluoranthene, with five observations
ranging from 320 ug/1 to 1500 ug/1, was consistently reported at higher
levels than the other PAHs in this group (U.S. EPA 1980c). Other data
sources generally report ambient water concentrations of these PAHs to
be less than 1 ug/1 (White and Vanderslice 1980). Sediment concentra-
tions recorded in STORET are generally less than 1000 ug/kg; however, a
few observations were reported above 1000 ug/kg. In the absence of
quantitative data on toxicologic effects, it is not possible to assess
the significance of exposure of aquatic biota to concentrations in this
range.
The environmental conditions present in an aquatic system actually
determine the extent of exposure to aquatic organisms. Though environ-
mental models predict that most of the BaP (and probably the compounds
in this group as well) in aquatic systems will be transported to the
sediments, the bioavailability of sediment-bound PAHs is not well
understood. Several studies have concluded that any PAHs that are
actually taken up by fish come from the interstitial waters and from the
water column (dissolved and/or adsorbed onto suspended solids); uptake
from the sediment itself does not appear to be significant (Neff 1979).
2-31
-------
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