&EPA
United States
Environmental Protection
Agency
Great Lakes
National Program Office
77 West Jackson Boulevard
Chicago, Illinois 60604
EPA905-R92-007A
December 1992
Assessment and Remediation
Of Contaminated Sediments
(ARCS) Program
BASELINE HUMAN HEALTH
RISK ASSESSMENT:
ASHTABULA RIVER, OHIO,
AREA OF CONCERN
United States Areas of Concern
ARCS Priority Areas of Concern
PKIHTXD OH RECYCLED PAPEB*
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BASELINE HUMAN HEALTH RISK ASSESSMENT:
ASHTABULA RIVER, OHIO, AREA OF CONCERN
by
Judy L. Crane
AScI Corporation
Athens, Georgia 30605
Project Officer
Robert B. Ambrose, Jr.
Environmental Research Laboratory
Athens, Georgia 30613
ENVIRONMENTAL RESEARCH LABORATORY
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
ATHENS, GEORGIA 30613
U.b. L.v/T-.'-.ric.i-o! ,•=,:.!?'..••-.(1 Agency
i';o..-ion u, L!':-:n;,' .''"".. •:'' 5
7'A'V3St Jackson bou.i.A •'!, 12th Floor
Chio-ago, IL 6G604-3590
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DISCLAIMER
The information in this document has been funded wholly or in part by the
United States Environmental Protection Agency under Contract Number 68-C1-
0012 to AScI Corporation. It has been subject to the Agency's peer and
administrative review, and it has been approved for publication as an EPA
document. Mention of trade names or commercial products does not constitute
endorsement or recommendation for use by the U.S. Environmental Protection
Agency.
11
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FOREWORD
Risk assessment has been defined as the characterization of the probability of
adverse effects from human and ecological exposures to environmental hazards. Risk
assessments are quantitative, chemical-oriented characterizations that can use
statistical and biological models to calculate numerical estimates of risk to human
health or the environment. The concept of risk assessment is a cornerstone on which
the U.S. Environmental Protection Agency builds programs to confront pollution
problems in air, water, and soil under the direction of Congressional mandates. One
such mandate is the Clean Water Act, which includes a directive to the Agency to
study the control and removal of toxic pollutants in the Great Lakes, with emphasis
on removal of contaminants from bottom sediments. Charged with performing this
study is EPA's Great Lakes National Program Office (GLNPO) located in Chicago, IL.
GLNPO administers the Assessment and Remediation of Contaminated Sediments
(ARCS) program to examine the problem of contaminated sediments using a
multidisciplinary approach involving engineering, chemistry, toxicology, modeling,
and risk assessment.
In support of the GLNPO, the Environmental Research Laboratory-Athens
began a series of studies under the ARCS program that will culminate in a baseline
risk assessment for each of five Great Lakes Areas of Concern (AOC)-Buffalo River,
NY, Grand Calumet River, IN, Saginaw River, MI, Ashtabula River, OH, and
Sheboygan River, WI. This report describes a baseline human health risk assessment
for the population within the Sheboygan River AOC. The assessment, which is based
on available environmental data, is designed to provide a conservative estimate of
carcinogenic and noncarcinogenic risks to human health under the baseline, no-action
alternative.
Rosemarie C. Russo, Ph.D.
Director
Environmental Research Laboratory
Athens, Georgia
IV
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PREFACE
This risk assessment was prepared as part of the Assessment and
Remediation of Contaminated Sediments (ARCS) program coordinated by the U.S.
EPA Great Lakes National Program Office. The work by AScI Corporation was
completed under contract no. 68-C1-0012 with the U.S. EPA Environmental
Research Laboratory-Athens by Judy Crane, Ph.D. under the supervision of James
L. Martin, Ph.D., P.E., AScI Site Manager. This work was performed through the
U.S. EPA Center for Exposure Assessment Modeling, Mr. Robert Ambrose, Jr.,
P.E., Manager.
111
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ABSTRACT
The Assessment and Remediation of Contaminated Sediments (ARCS)
program, a 5-year study and demonstration project relating to the control and
removal of contaminated sediments from the Great Lakes, is being coordinated
and conducted by the U.S. Environmental Protection Agency's (EPA) Great Lakes
National Program Office (GLNPO). As part of the ARCS program, baseline
human health risk assessments are being performed at five Areas of Concern
(AOCs) in the Great Lakes region. The Ashtabula River, located in northeastern
Ohio, is one of these AOCs.
In this report, exposure and risk assessment guidelines, developed for the
EPA Superfund program, have been applied to determine the baseline human
health risks associated with direct and indirect exposures to sediment-derived
contaminants in the Ashtabula River AOC. These risks were estimated for
noncarcinogenic (e.g., reproductive toxicity, teratogenicity, liver toxicity) and
carcinogenic (i.e., probability of an individual developing cancer over a lifetime)
effects.
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TABLE OF CONTENTS
DISCLAIMER ii
PREFACE iii
FOREWORD iv
ABSTRACT v
LIST OF FIGURES viii
LIST OF TABLES ix
ACKNOWLEDGMENTS xi
1. EXECUTIVE SUMMARY 1-1
1.1 OVERVIEW 1-1
1.2 STUDY AREA 1-1
1.3 EXPOSURE ASSESSMENT 1-2
1.4 RISK ASSESSMENT 1-3
1.4.1 Determination of Risk 1-3
1.4.2 Noncarcinogenic Risks 1-4
1.4.3 Carcinogenic Risks 1-5
1.4.4 Uncertainties 1-6
2. INTRODUCTION 2-1
3. ASHTABULA RIVER AREA OF CONCERN 3-1
3.1 ENVIRONMENTAL SETTING 3-1
3.2 CONTAMINATION PROBLEMS 3-4
3.3 RECREATIONAL USES 3-14
3.4 CONTAMINATION OF FISH 3-15
3.4.1 Routes of Contamination 3-15
3.4.2 Fish and Wildlife Advisories 3-18
3.5 WATER SUPPLY 3-19
3.6 HUMAN HEALTH CONCERNS 3-19
4. RISK ASSESSMENT FRAMEWORK 4-1
4.1 CONCEPT OF RISK 4-1
4.2 RISK FRAMEWORK 4-2
5. EXPOSURE ASSESSMENT 5-1
5.1 EXPOSURE PATHWAYS 5-1
5.2 DATA USED IN THE EXPOSURE ASSESSMENT 5-3
5.2.1 Data Sources 5-3
5.2.2 Data Review 5-4
5.2.3 Data Sets 5-7
VI
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TABLE OF CONTENTS
5.3 EXPOSURE ASSESSMENT 5-7
5.3.1 General Determination of Chemical Intakes 5-7
5.3.2 Intakes: Ingestion of Contaminated Fish 5-11
6. TOXICITY ASSESSMENT 6-1
6.1 TOXICITY VALUES 6-1
6.2 LIMITATIONS 6-1
7. BASELINE RISK CHARACTERIZATION FOR THE ASHTABULA
RIVER AOC 7-1
7.1 PURPOSE OF THE RISK CHARACTERIZATION STEP 7-1
7.2 QUANTIFYING RISKS 7-1
7.2.1 Determination of Noncarcinogenic Risks 7-1
7.2.2 Determination of Carcinogenic Effects 7-2
7.3 HUMAN HEALTH RISKS IN THE ASHTABULA RIVER AOC . . 7-2
7.3.1 Typical and Reasonable Maximum Exposures 7-2
7.3.1.1 Noncarcinogenic Risks 7-2
7.3.1.2 Carcinogenic Risks 7-3
7.3.2 Subsistence Anglers 7-5
8. CHARACTERIZATION OF QUALITATIVE UNCERTAINTIES 8-1
8.1 INTRODUCTION 8-1
8.2 QUALITATIVE LIST OF UNCERTAINTIES 8-1
8.2.1 Data Compilation and Evaluation 8-1
8.2.2 Exposure Assessment 8-2
8.2.3 Toxicity Values 8-2
8.2.4 Risk Characterization 8-3
8.3 SUMMARY 8-4
REFERENCES 9-1
APPEND K A: Importance of other Complete Exposure Pathways in the
Ashtabula River Area of Concern A-l
APPENDK B: Human Toxicity Estimates for Contaminants Present in
the Ashtabula River Area of Concern B-l
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LIST OF FIGURES
Figure
2.1 Map of ARCS priority areas of concern (USEPA, 1991b) 2-3
3.1 Boundaries of the Ashtabula River Area of Concern (Ohio
EPA, 1991) 3-2
3.2 Location of water supply intakes and recreational facilities
in the Ashtabula River AOC (Ohio EPA, 1991) 3-3
3.3 Location of point source dischargers in the Ashtabula River
AOC (Ohio EPA, 1991) 3-5
3.4 Sediment pollution classification of the Ashtabula River AOC
(Ohio EPA, 1991) 3-13
4.1 Components of baseline human health risk assessments 4-3
5.1 Fish sampling locations in the Ashtabula River AOC
(WCC, 1991) 5-5
5.2 Surface water sampling locations in the Ashtabula River
AOC (WCC, 1991) 5-6
vni
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LIST OF TABLES
Table
1.1 Amount of Fish Assumed to be Consumed per Person per Day
from the Ashtabula River AOC 1-3
1.2 Noncarcinogenic Risks Based on the Hazard Index (HI) for
each Exposure Scenario 1-5
1.3 Carcinogenic Risks for the Consumption of Fish in the
Ashtabula River AOC 1-6
3.1 Summary of Ashtabula River AOC Point Source Discharger
Compliance with Final NPDES Permit Limits (Ohio
EPA, 1991) 3-6
3.2 Pollutants Identified in the Ashtabula River Area of Concern
since 1975 (Y = Yes; N = No; X = PoDutant Detected
in Medium) (Adapted from the Stage One RAP (Ohio
EPA, 1991)) 3-8
3.3 A Summary of Ambient Water Quality Standard Violations
Measured in the Ashtabula River AOC (All
Concentrations in ug/L) (Adapted from the Stage One
RAP (Ohio EPA, 1991)) 3-12
5.1 Potential Pathways by which People may be Exposed to
Sediment-Derived Contaminants from the Ashtabula
River AOC 5-2
5.2 Complete Exposure Pathways in the Ashtabula River AOC 5-3
5.3 List of Contaminants Analyzed in the Fish Used in this Risk
Assessment 5-8
5.4 Contaminant Concentrations in Whole Carp and Bluegill
Fillets Collected from the Ashtabula River AOC (WCC,
1991) 5-9
5.5 Contaminant Concentrations in Bluegill and Small/Large
Mouth Bass Fillets Collected from the Ashtabula
River AOC (WCC, 1991) 5-9
5.6 Generic Equation for Calculating Chemical Intakes (USEPA,
1989a) 5-10
5.7 Equation used to Estimate Contaminant Intakes Due to
Ingestion of Fish 5-11
5.8 Parameters used in Estimating Contaminant Intakes Due to
Ingestion of Fish in the Ashtabula River AOC 5-12
6.1 EPA Weight-Of-Evidence Classification System for
Carcinogenicity (USEPA, 1989a) 6-2
6.2 Human Health Risk Toxicity Data for Chemicals of Interest
in the Ashtabula River AOC 6-2
IX
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LIST OF TABLES
Table Page
7.1 Noncarcinogenic Risks Associated with Consuming
Small/Large Mouth Bass Fillets (Taken from the
Ashtabula Harbor) Under Typical, Reasonable Maximum
(RME), and Subsistence Exposure Scenarios 7-6
7.2 Noncarcinogenic Risks Associated with Consuming Small/Large
Mouth Bass Fillets (Taken from the Ashtabula River
Downstream from Fields Brook) Under Typical,
Reasonable Maximum (RME), and Subsistence Exposure
Scenarios 7-7
7.3 Noncarcinogenic Risks Associated with Consuming Bluegill
Fillets (Taken from the Ashtabula Harbor) Under
Typical, Reasonable Maximum (RME), and Subsistence
Exposure Scenarios 7-8
7.4 Noncarcinogenic Risks Associated with Consuming Bluegill
Fillets (Taken from the Ashtabula River Downstream
from Fields Brook) Under Typical, Reasonable Maximum
(RME), and Subsistence Exposure Scenarios 7-9
7.5 Noncarcinogenic Risks Associated with Consuming Whole Carp
(Taken from the Ashtabula Harbor) Under Typical,
Reasonable Maximum (RME), and Subsistence Exposure
Scenarios 7-10
7.6 Noncarcinogenic Risks Associated with Consuming Whole Carp
(Taken from the Ashtabula River Downstream from
Fields Brook) Under Typical, Reasonable Maximum
(RME), and Subsistence Exposure Scenarios 7-11
7.7 Carcinogenic Risks Associated with Consuming Small/Large
Mouth Bass Fillets (Taken from the Ashtabula River
Downstream from Fields Brook) Under Typical,
Reasonable Maximum (RME), and Subsistence Exposure
Scenarios 7-12
7.8 Carcinogenic Risks Associated with Consuming Whole Carp
(Taken from the Ashtabula Harbor) Under Typical,
Reasonable Maximum (RME), and Subsistence Exposure
Scenarios 7-13
7.9 Carcinogenic Risks Associated with Consuming Whole Carp
(Taken from the Ashtabula River Downstream from
Fields Brook) Under Typical, Reasonable Maximum
(RME), and Subsistence Exposure Scenarios 7-14
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ACKNOWLEDGMENTS
Several members of the Ashtabula River RAP Advisory Council provided
useful information about the Ashtabula River Area of Concern including: Julie
Letterhos (RAP Coordinator, Ohio EPA), Carl Anderson (Co-Chair), Leonard
Eames, Karla Auker (Ohio EPA), and Jack Phelps (Co-Chair). In addition, Pete
Redmon (U.S. EPA Region 5) and Rick Fox (Great Lakes National Program Office)
supplied additional information about the Ashtabula River. Jack's Marine
provided a courtesy boat tour of the lower Ashtabula River and Harbor. Members
of the ARCS Risk Assessment and Modeling Work Group have provided useful
feedback for the preparation of this risk assessment. James Martin (AScI Corp.),
Bill Sutton (ERL-Athens), and Bob Swank (ERL-Athens) reviewed this document.
Finally, I would like to thank Tawnya Robinson (AScI Corp.) for typing the tables
in Chapter 3.
XI
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CHAPTER 1
EXECUTIVE SUMMARY
1.1 OVERVIEW
The Assessment and Remediation of Contaminated Sediments (ARCS)
program, a 5-year study and demonstration project relating to the control and
removal of contaminated sediments from the Great Lakes, is being coordinated
and conducted by the U.S. Environmental Protection Agency's (EPA) Great Lakes
National Program Office (GLNPO). As part of the ARCS program, baseline
human health risk assessments are being performed at five Areas of Concern
(AOCs) in the Great Lakes region. The Ashtabula River, located in northeastern
Ohio, is one of these AOCs.
In this report, exposure and risk assessment guidelines, developed for the
EPA Superfund program, have been applied to determine the baseline human
health risks associated with direct and indirect exposures to sediment-derived
contaminants in the Ashtabula River AOC. These risks were estimated for
noncarcinogenic (e.g., reproductive toxicity, teratogenicity, liver toxicity) and
carcinogenic (i.e., probability of an individual developing cancer over a lifetime)
effects under different exposure scenarios.
1.2 STUDY AREA
The lower 3.2 km of the Ashtabula River and the Ashtabula Harbor have
been severely impacted by industrial pollution, especially from contaminant loads
transported into the river from Fields Brook, a Superfund site. Dredging of the
federal navigation channel was stopped in 1964 due to severe contamination
problems in the channel and to a lack of agreement among several agencies on
how to safely dispose of the dredged sediments. Consequently, sediments have
built up in the lower river to the point where it is becoming increasingly difficult
for people with deep draft boats to navigate the river.
The contamination and sedimentation problems in this area have been of
concern to the International Joint Commission (IJC); the IJC designated this
region as an AOC in 1987. In response, the Ohio EPA has nearly completed the
Stage One Remedial Action Plan (RAP) to identify contamination problems in the
Ashtabula River AOC (Ohio EPA, 1991).
Within the AOC, the Ashtabula River is bordered by nine marinas and
yacht clubs in the small city of Ashtabula. The lower river is used by recreational
boaters and charter boat operators as an access point to Lake Erie. Sport fishing
is very popular in the Ashtabula Harbor and in the nearshore Lake Erie area.
The Ohio Department of Health and Ohio EPA issued a fish advisory in 1983
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recommending that no fish caught in the river from the 24th St. Bridge to the
harbor mouth be eaten (Woodward-Clyde Consultants, 1991). Despite these
warnings, some people still fish in the AOC.
1.3 EXPOSURE ASSESSMENT
This assessment focused on only one pathway by which residents of the
lower Ashtabula River were likely to be exposed to sediment-derived
contaminants: the consumption of contaminated fish. Other exposure pathways
were determined to be either incomplete (e.g., ingestion of sediments) or
insignificant in terms of risk (e.g., ingestion of surface water during infrequent
swimming events).
Woodward-Clyde Consultants (WCC) conducted the most recent survey
(1990) of contaminant levels in fish inhabiting the Ashtabula River AOC. In this
study, 12 carp, 16 small/large mouth bass, and 16 bluegill were collected from four
sites in the AOC and were analyzed for a variety of contaminants. Data obtained
from composite samples of fish collected from two of the sites were used in the
exposure assessment: 1) the Ashtabula River just downstream from Fields Brook
(3 carp, 2 large mouth bass, and 11 bluegills), and 2) the Ashtabula Harbor (4
carp, 1 small mouth plus 3 large mouth bass, and 5 bluegills). The carp were
analyzed as whole fish while the other two species were analyzed as skin-on
fillets. The collection and data analysis of the fish appears to have gone through a
rigorous QA/QC program at WCC. Thus, the data were deemed usable for this
baseline risk assessment.
Noncarcinogenic and carcinogenic risks were estimated for three different
exposure scenarios: typical (average), reasonable maximum (i.e., the maximum
exposure that is reasonably expected to occur at a site), and subsistence exposures.
The subsistence pathway was chosen for a small segment of the population that
may be relying on the consumption of fish from the area for their main source of
protein. Different consumption rates were applied to each scenario (Table 1.1),
and it was assumed that only fish collected and consumed from the Ashtabula
River AOC were contaminated. In addition, the exposure duration varied with the
exposure scenario. Typical exposures were assumed to occur over a period of 9
years; reasonable maximum and subsistence exposures were assumed to occur
over a period of 30 years. Noncarcinogenic effects were averaged over the same
time period as the exposure duration, whereas carcinogenic effects were averaged
over a lifetime (i.e., 70 years). For all three exposure scenarios, exposures were
determined for each chemical and added for each pathway. This assumption of
additivity did not account for any synergistic or antagonistic effects that might
occur among chemicals.
Several heavy metals and organic compounds that were detected in some or
all of the fish samples were included in the exposure assessment (i.e., chromium,
copper, mercury, silver, zinc, polychlorinated biphenyls (PCBs), 1,1,2,2-
1-2
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TABLE 1.1.
AMOUNT OF FISH ASSUMED TO BE CONSUMED PER
PERSON PER DAY FROM THE ASHTABULA RIVER AOC
Exposure Scenario
Typical
Reasonable Maximum
Subsistence
* Sources: Typica
Total
Amount
of Fish
Consumed*
(g/day)
19.2
54
132
1 (West et al.,
x FP* =
0.10
0.25
0.7
1989); Reasonable
Amount of
Ashtabula R.
Fish
Consumed
(g/day)
1.9
13.5
92.4
Maximum (USEPA,
1991a); Subsistence [Pao et al. (1982) cited in USEPA (1989a)]
** FI = fraction of fish ingested from the Ashtabula River (study
assumption)
tetrachloroethane, tetrachloroethene, and trichloroethene). In addition,
noncarcinogenic and/or carcinogenic toxicity values were either available or under
review for this set of contaminants. Thus, the exposure and toxicity information
could be integrated into the risk assessment.
1.4 RISK ASSESSMENT
1.4.1 Determination of Risk
This baseline risk assessment did not characterize absolute human health
risks, rather it identified potential sources of unacceptable risks. Risk estimates
were determined for both noncarcinogenic and carcinogenic endpoints.
Noncarcinogenic effects were evaluated by comparing an exposure level over
a specified time period with a reference dose (RfD)1 derived from a similar
1 The RfD provides an estimate of the daily contaminant exposure that is not
likely to cause harmful effects during either a portion of a person's life or
their entire lifetime (USEPA, 1989a).
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exposure period (otherwise known as a hazard quotient (HQ)). Thus, HQ =
exposure level/RfD. An HQ value of less than 1 indicates that exposures are not
likely to be associated with adverse noncarcinogenic effects. HQ values between 1
and 10 may be of concern, particularly when additional significant risk factors are
present (e.g., other contaminants at levels of concern) (USEPA, 1988a). The sum
of more than one HQ value for multiple substances and/or multiple exposure
pathways is represented by the Hazard Index (HI).
Carcinogenic risks were estimated as the incremental probability of an
individual developing cancer over a lifetime as a result of exposures to potential
carcinogens. This risk was computed using average lifetime exposure values that
were multiplied by the oral slope factor2 for a particular chemical. The resulting
carcinogenic risk estimate generally represents an upper-bound estimate, because
slope factors are usually based on upper 95th percentile confidence limits.
Carcinogenic effects were summed for all chemicals in an exposure pathway. This
summation of carcinogenic risks assumed that intakes of individual substances
were small, that there were no synergistic or antagonistic chemical interactions,
and that all carcinogens produced the same effect (i.e., cancer). The EPA believes
it is prudent public health policy to consider actions to mitigate or minimize
exposures to contaminants when estimated excess lifetime cancer risks exceed the
10"5 to 10~6 range, and when noncarcinogenic health risks are estimated to be
significant (USEPA, 1988a).
1.4.2 Noncarcinogenic Risks
Noncarcinogenic risks, as represented by the Hazard Index (HI), were below
levels of concern (i.e., less than 1) for most of the typical and reasonable maximum
exposure scenarios (Table 1.2). For fish collected from the Ashtabula Harbor, only
the consumption of whole carp under the subsistence exposure scenario resulted in
a significant risk. The subsistence consumption of large mouth bass fillets,
bluegill fillets, and whole carp collected from below Fields Brook could pose a
potential noncarcinogenic risk to anglers and their families; the reasonable
maximum consumption of carp at this site was also of concern. The estimated
risks were mostly attributable to methyl mercury and copper contamination.
Methyl mercury has been shown to cause central nervous system effects in
humans at the lowest adverse effect level of 0.003 mg/kg/day (IRIS data
baseretrieval for methyl mercury, 1992). Information about the types of
noncarcinogenic effects one might experience from chronic exposure to copper is
not available at this time from the IRIS data base.
Slope factors are estimated through the use of mathematical extrapolation
models, most commonly the linearized multistage model, for estimating the
largest possible linear slope (within 95% confidence limits) at low
extrapolated doses that is consistent with the data (USEPA, 1989a).
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TABLE 1.2. NONCARCINOGENIC RISKS BASED ON THE HAZARD
INDEX (HI) FOR EACH EXPOSURE SCENARIO
Exposure Scenario
Site and Fish Type Typical RME* Subsistence
Ashtabula Harbor
S/L Mouth Bass FiUet 0.02 0.1 0.9
Bluegill Fillet 0.02 0.1 0.8
Whole Carp 0.05 0.3 2
Ashtabula R. (Downstream
from Fields Brook)
L. Mouth Bass Fillet 0.02 0.1 1
Bluegill Fillet 0.04 0.2 2
Whole Carp OA 3 20_
* RME = Reasonable Maximum Exposure
1.4.3 Carcinogenic Risks
A carcinogenic risk estimate could not be calculated for the consumption of
small/large mouth bass collected from the Ashtabula Harbor and for bluegills
collected from both the river and harbor; this was because no carcinogens were
detected in these fish fillets (Table 1.3). The upper-bound carcinogenic risk
estimates associated with the consumption of large mouth bass fillets collected
below Fields Brook were below concern levels (i.e., less than 10"6) under all three
exposure scenarios. Methylene chloride was the only carcinogen detected in the
bass for which a toxicity value was available. The consumption of whole carp was
of concern at both the harbor and river under all three exposure scenarios. The
carcinogenic risk from consuming carp was attributable to PCB contamination.
There is a possibility that people who ingest, inhale, or have dermal contact with
certain PCB mixtures may have a greater chance of incurring liver cancer;
however, this statement is based on suggestive evidence rather than on verified
data (IRIS data base retrieval for PCBs, 1992).
The human health risks attributable to carp consumption were probably
overestimated because the risk estimates were based on data derived from whole
carp instead of fillets. In addition, the data were also based on raw fish; different
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TABLE 1.3. CARCINOGENIC RISKS FOR THE CONSUMPTION OF FISH
IN THE ASHTABULA RIVER AOC
Exposure Scenario
Site and Fish Type Typical RME* Subsistence
Ashtabula Harbor
S/L Mouth Bass FiUet
Bluegill Fillet
Whole Carp 4E-06 9E-05 6E-04
Ashtabula R. (Downstream
from Fields Brook)
L. Mouth Bass Fillet 5E-09 1E-07 7E-07
Bluegill Fillet
Whole Carp 2E-05 5E-04 3E-03
* RME = Reasonable Maximum Exposure
preparation and cooking techniques may reduce concentrations of hydrophobic
organic contaminants (e.g., PCBs) in fish if the fat is trimmed away prior to
cooking.
1.4.4 Uncertainties
Several assumptions and estimated values were used in this baseline risk
assessment that contributed to the overall level of uncertainty associated with the
noncarcinogenic and carcinogenic risk estimates. As with most environmental risk
assessments, the uncertainty of the risk estimates probably varied by around an
order of magnitude or greater. The uncertainties were addressed in a qualitative
way for the parameters and assumptions that appeared to contribute the greatest
degree of uncertainty. One of the greatest sources of uncertainty was the
assumption that exposure intakes and toxicity values would not change during the
exposure duration. This assumed that human activities and contaminant levels
would remain the same over the exposure duration, and that toxicity values would
not be updated.
1-6
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CHAPTER 2
INTRODUCTION
Sediments in the Great Lakes have become a repository for a variety of
nutrients and contaminants, mostly as a result of industrial and municipal
pollution. More stringent pollution control measures have generally reduced point
sources of contamination during the past twenty years. However, problems
remain with nonpoint sources of pollution (ranging from agricultural runoff to
groundwater contamination) and with permit violations of effluent dischargers. In
some areas of the Great Lakes, contaminated sediments now represent the
primary source of anthropogenic chemicals to the aquatic environment.
Consequently, concern has been raised about what remediation measures, if any,
are needed to deal with the problem of contaminated sediments. In addition,
these contaminants may pose a potential health risk to aquatic life, wildlife, and
to human populations residing in the area of concern.
The 1987 amendments to the Clean Water Act, in Section 118(c)(3),
authorize the U.S. Environmental Protection Agency's (EPA) Great Lakes National
Program Office (GLNPO) to coordinate and conduct a 5-year study and
demonstration project relating to the control and removal of contaminated
sediments from recommended areas in the Great Lakes region. To achieve this
task, GLNPO has initiated the Assessment and Remediation of Contaminated
Sediments (ARCS) program. The overall objectives of the ARCS program (USEPA,
199Ib), for selected Areas of Concern (AOCs), are to:
1. Assess the nature and extent of contaminated sediments,
2. Evaluate and demonstrate remedial options (e.g., removal,
immobilization, and advanced treatment technologies) as well
as the "no action" alternative,
3. Provide risk assessments for humans, aquatic life, and wildlife
exposed to sediment-related contaminants, and
4. Provide guidance on the assessment of contaminated sediment
problems and on the selection and implementation of necessary
remedial actions in the Areas of Concern and other locations in
the Great Lakes.
As one part of the ARCS program, baseline human health risk assessments
for exposure to sediment-derived contaminants are being prepared for five AOCs:
Ashtabula River, OH; Buffalo River, NY; Grand Calumet River/Indiana Harbor
Canal, IN; Saginaw River, MI; and Sheboygan River, WI (Figure 2.1). The
objectives of these risk assessments are to: 1) estimate the magnitude and
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frequency of human exposures to sediment-derived contaminants in the AOC, and
2) estimate the risk of adverse effects resulting from both typical and reasonable
maximum exposures (i.e., the highest exposure that is reasonably expected to
occur at a site) to contaminants. Risk estimates are determined for both
noncarcinogenic (i.e., chronic or subchronic effects) and carcinogenic (i.e.,
probability of an individual developing cancer over a lifetime) effects resulting
from direct and indirect exposures to sediment-related contaminants. These risk
estimates are made using conservative assumptions about exposure scenarios
when complete data are not available. Thus, the risk estimates are designed to be
overprotective of human health.
This document presents a baseline human health risk assessment for the
Ashtabula River AOC. The next chapter describes the AOC and its contamination
problems. Successive chapters describe the risk assessment framework and
provide details on how the exposure and risk estimates were generated. The final
chapter gives a qualitative assessment of the uncertainties associated with the
risk estimates.
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ARCS1 PRIORITY
AREAS OF CONCERN
GREAT LAKES AREAS OF CONCERN
1. SHEBOYGAN HARBOR
2. GRAND CALUMET/INDIANA HARBOR
3. SAGINAW RIVER/BAY
4. ASHTABULA RIVER
5. BUFFALO RIVER
1 Assessment and Remediation of Contaminated Sediments
N
o JO too m am
I.I 111
iMCNvmoNMonM.pi
Figure 2.1.
Map of ARCS priority Areas of Concern (USEPA, 1991b).
2-3
-------
CHAPTERS
ASHTABULA RIVER AREA OF CONCERN
3.1 ENVIRONMENTAL SETTING
The lower 3.2 km of the Ashtabula River and the Ashtabula Harbor in
northeastern Ohio (Figure 3.1) have been identified as one of 43 Great Lakes
AOCs by the International Joint Commission. This ranking is given to areas
where environmental quality is degraded and designated uses of the water are
impaired. The Ashtabula River AOC has been severely impacted by industrial
pollution, especially from contaminant loads transported into the river from Fields
Brook, a Superfund site. A Stage One Remedial Action Plan (RAP) for the
Ashtabula River AOC has been prepared by the Ohio EPA, in cooperation with the
Ashtabula River RAP Advisory Council, to identify impaired uses in the AOC
(Ohio EPA, 1991). The RAP will also serve as a guidance document for future
remedial clean-up measures. The RAP was the major source of information for
this chapter, and the reader should refer to it for a thorough description of the
physical site as well as for detailed information on the sources and extent of
multimedia contamination in the AOC.
Within the AOC, the Ashtabula River is bordered by nine marinas and
yacht clubs in the small city of Ashtabula (Figure 3.2). The lower river is used by
recreational boaters and charter boat operators as an access point to Lake Erie.
However, it is becoming increasingly difficult for people with deep draft boats to
navigate the lower river due to the accumulation of sediments in the channel; in
some areas, the water column is only 0.6 m deep (Ohio EPA, 1991). The river has
not been dredged for about 30 years because of a decline in commercial shipping in
the area (Ohio EPA, 1991). In addition, a suitable solution has not been reached
between the U.S. Army Corps of Engineers, U.S. EPA, City of Ashtabula, and
other parties for deciding how to dredge and dispose of contaminated sediments in
the AOC.
The hydrologic and topographic features of the Ashtabula River have
enhanced the settling and deposition of suspended particulate matter (SPM) (and
associated contaminants) to the sediments. Low flow conditions prevail
approximately 90% of the time in the river with an average flow of 4.5 cubic
meters per second (Ohio EPA, 1991). In addition, the AOC lies within the former
lake bottom of Lake Erie where the vertical gradient in this 4.8 to 8 km wide band
is only 76 cm per km (Ohio EPA, 1991). Thus, a net accumulation of sediments
arises from these conditions of low flow, narrow vertical gradient, and high SPM
load. The resuspension of these sediments by boat propellers or wind induced
waves may be important mechanisms for reintroducing contaminants back into
the water column.
3-1
-------
Figure 3.1. Boundaries of the Ashtabula Eiver Area of Concern (Ohio EPA, 1991).
3-2
-------
1. Ashtabula Public Water Supply Intake
2. CEI Intake
3. ASHCO Intake
4. Walnut Beach
5. Lakeshorc Park
6. Point Park
7. Sutherland Marine
8. Marshall Marine
9. Ashlabula Yacht Club
10. Kister Marine
11. Jack's Marine North
12. Riverside Yacht Club
13. Harbor Yacht Club
14. Jack's Marine
15. Recreation Unlimited
16. Community Boating Center
* Water Supply Intake
• Recreational Facility
Figure 3.2.
Location of water supply intakes and recreational facilities in the Ashtabula River AOC (Ohio
EPA, 1991).
3-3
-------
Most of the Ashtabula River discharge flows north through the Ashtabula
Harbor mouth to an area adjacent to the Lake Erie Central Basin sediment
depositional area [Thomas and Mudrock (1979) cited in the RAP (Ohio EPA, 1991].
The river discharge typically remains within 2.4 km of the shoreline and moves
eastward due to prevailing southwest winds [U.S. Department of Health,
Education, and Welfare (1965) cited in Ohio EPA (1991)]. Thus, suspended
sediment loads (and associated contaminant loads) transported from the
Ashtabula River may be deposited in the nearshore area of Lake Erie. Although
the nearshore area is included in the AOC of the RAP, it will not be included in
this risk assessment because of insufficient information on contaminant levels in
the water column and sediments.
The Ashtabula River drainage basin (approximately 355 km2) is the
smallest watershed of all the major tributaries entering Lake Erie (Ohio EPA,
1991). The basin includes mostly rural and agricultural land in northeastern
Ohio. The city of Ashtabula, with a 1990 census population of 21,633, is the only
urban area in the watershed that has contributed extensively to contamination in
the AOC (Ohio EPA, 1991). The industrial zone of Ashtabula is concentrated
around Fields Brook and is dominated by several chemical industries and waste
disposal sites (Figure 3.3). Another industrial area exists by the river mouth
where large quantities of coal are stored at the Conrail coal dock; coal is the major
commodity shipped from Ashtabula. The next section will describe some of the
contamination problems in the Ashtabula River AOC arising from this industrial
development.
3.2 CONTAMINATION PROBLEMS
The Ashtabula River AOC has a history of contamination problems due to
previously unregulated industrial and municipal discharges of metals and organic
chemicals into Fields Brook and the Ashtabula River beginning in the late 1940s
(Ohio EPA, 1991). The greatest source of contamination to the AOC today is
through the release of in-place pollutants contained in the sediments (Ohio EPA,
1991). Other secondary sources include point sources (e.g., effluent discharges,
combined sewer overflows) and nonpoint sources (e.g., industrial and agricultural
runoff). The location of point source dischargers in the Ashtabula River AOC is
shown in Figure 3.3, and their recent record of compliance with final NPDES
permit limits is given in Table 3.1. Fines have been levied against some of the
industries who have violated their NPDES permits.
Twenty-four unregulated hazardous waste sites have been identified in the
Ashtabula River AOC (Ohio EPA, 1991), and runoff from these waste sites could
contribute to the contaminant load in Fields Brook and the Ashtabula River.
Strong Brook, a small tributary entering the Ashtabula River west of Jack's
Marine, has been an important source of oil and grease, lead, and zinc in the past
[Aqua Tech (1979) cited in Ohio EPA (1991)]. The highest concentrations of zinc
and lead in the sediments of the AOC are still found in Strong Brook (WCC, 1991).
3-4
-------
TABLE 3.1. CONTINUED
Discharger __^_ Compliance Action
18. Vygen No Currently operating under interim
limits. Compliance schedule in
permit.
19. SCM #1 No Findings and Orders - 4/91
20. SCM #2 No Findings and Orders - 4/91
Thus, this small brook may continue to provide a source of zinc and lead to the
rest of the AOC.
Other possible sources of contamination to the Ashtabula River AOC do not
appear to be important. Groundwater contamination has not been observed to
intrude on the Ashtabula River; this is because there is little groundwater
recharge to the river due to the low permeability of surface deposits (Ohio EPA,
1991). Agricultural runoff and other upstream watershed inputs do not appear to
contribute substantially to contaminant loads in the river although much of the
sediments in the AOC have originated from these upstream sources. Regular air
quality standards (i.e., ozone, total suspended particulates, sulfur dioxide, nitrogen
dioxide, carbon monoxide, and lead) have not been violated in Ashtabula County
(Ohio EPA, 1991). It is unlikely that atmospheric contamination contributes
significantly to the contaminant burden in the AOC because of the small size of
the watershed. In addition, no studies have been conducted to evaluate whether
the AOC itself may serve as a source of contaminants to the atmosphere via the
volatilization of hydrophobic organic compounds (HOCs) (e.g., PCBs).
A number of contaminants have been detected in the sediments, water
column, and fish tissue collected from the Ashtabula River (Table 3.2) (Ohio EPA,
1991). The sediments have become a repository for metals, pesticides, nutrients,
PCBs, polyaromatic hydrocarbons (PAHs), and a number of other chlorinated
organic compounds. The contaminants of greatest concern in the AOC, because of
their prevalence and potential toxicity, include PCBs, mercury, zinc,
hexachlorobenzene, hexachlorobutadiene, chromium, and volatile organic
compounds (Ohio EPA, 1991).
While a portion of these contaminants will become permanently buried in
the sediments, contaminants in the surface sediment layer may be released to the
water column through processes such as bioturbation, molecular diffusion, and
resuspension. Furthermore, ionic species of chemicals (e.g., metals) in the
sediments may undergo changes in solubility due to changes in reaction kinetics,
pH, redox conditions, and other variables. In addition, benthic (i.e., bottom
3-7
-------
TABLE 3.2.
POLLUTANTS IDENTIFIED IN THE ASHTABULA RIVER AREA OF CONCERN SINCE
1975 (Y = YES; N = NO; X = POLLUTANT DETECTED IN MEDIUM) (ADAPTED FROM
THE STAGE ONE RAP (OHIO EPA, 1991))
PARAMETER
WATER
SEDIMENT
PRIORITY OUTER ASHTABULA FIELDS OUTER ASHTABULA FIELDS
POLLUTANT HARBOR RIVER BROOK HARBOR RIVER BROOK
FISH
Inorganics
Aluminum
Arsenic
Barium
Beryllium
Cadmium
Chromium
Copper
Cyanide
Iron
Lead
Manganese
Mercury
Nickel
Nitrogen (Ammonia)
Nitrate + Nitrite
Phosphorus
Oil and Grease
Silver
Zinc
Total Dissolved Solids
Phenols
Organics
Aldrin + Dieldrin
PCBs
N
Y
N
Y
Y
Y
Y
Y
N
Y
N
Y
Y
N
N
N
N
Y
Y
N
Y
Y
Y
X
.
X
-
X
X
X
-
X
X
X
X
X
X
X
X
-
.
X
X
-
X
-
X
-
X
-
X
X
X
X
X
X
X
X
-
X
X
X
-
-
X
X
-
X
-
X
-
X
-
X
X
X
-
X
X
X
X
-
X
X
X
.
-
X
X
-
_
-
X
X
X
-
X
X
X
X
X
X
X
X
X
X
X
X
X
-
X
.
X
_
X
X
X
X
X
X
X
X
X
X
X
X
X
X
-
.
-
X
X
X
.
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
-
-
-
-
X
X
-
-
_
X
.
X
-
X
-
-
X
-
-
X
-
X
-
-
-
-
-
X
X
-
-
-
X
3-8
-------
TABLE 3.2.
CONTINUED
PARAMETER
WATER
SEDIMENT
PRIORITY OUTER
POLLUTANT HARBOR
ASHTABULA FIELDS
RIVER BROOK
OUTER ASHTABULA FIELDS
HARBOR RIVER BROOK
FISH
PAHs
Acenaphthene
Anthracene
Benzo(a)anthracene
Benzo(a)pyrene
Benzo(b)fluoroanthene
Chrysene
Fluoranthene
Fluorene
Naphthalene
Phenanthrene
Pyrene
2-chloronaphthalene
Benzo(k)fluoranthene
Other Organics
Acetone
Benzene
Bis(2-ethylhexyl
phthalate
2-butanone
Butylbenzyl phthalate
Chlorobenzene
Chloroform
1,1-dichloroethene
Diethyl phthalate
Dimethyl phthalate
Di-n-butyl phthalate
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
Y
.
Y
N
Y
Y
N
Y
Y
Y
Y
Y
Y
Y
X
X
X
X
X
X
X
X
X X
X
X
-
-
_
-
X
-
-
-
X
-
X
-
-
_
X
X
X
X
X
X
X
X
X
X
X
X
X
-
X
X
X
X
-
-
-
X
X
-
-
-
X
-
-
X
-
-
X
-
-
-
X
X
X
X
X
-
X
X
X
X
X
-
-
-
-
-
-
X
-
-
-
-
-
-
_
-
-
-
-
-
-
-
-
-
-
3-9
-------
TABLE 3.2.
CONTINUED
PARAMETER
WATER
SEDIMENT
PRIORITY OUTER ASHTABULA FIELDS OUTER ASHTABULA FIELDS
POLLUTANT HARBOR RIVER BROOK HARBOR RIVER BROOK
FISH
Other Organics (Continued)
Ethylbenzene
Fluorotrichloromethane
Hexachlorobenzene
Hexachlorobutadiene
Hexachloroethane
Methylene chloride
1,2-Dichlorobenzene
1,3-Dichlorobenzene
1,4-Dichlorobenzene
n-nitrosodiphenylamine
Carbon tetrachloride
Octachlorostyrene
Xylene
Pentachlorobenzene
1,1,1,2-tetrachloroethane
1,1,2,2-tetrachloroethane
Tetrachloroethene
1,2-transdichloroethene
1,1,2-trichloroethane
1,1,1-trichloroethane
Trichloroethene
Toluene
Vinyl chloride
1,2,4-trichlorobenzene
1,2-dichloroethane
1,3,5-trichlorobenzene
1,2,3,4-tetrachlorobenzene
Y
N
Y
Y
Y
Y
Y
Y
Y
Y
Y
N
N
N
N
Y
Y
N
Y
Y
Y
Y
Y
N
Y
N
N
.
X
X
-
X XX
X
X
X
X
X
.
-
-
-
XX X -
XX X -
X
X
.
XX X -
-
.
.
x
-
-
X
-
X
X
X
X
-
X
X
-
-
X
X
-
X
-
X
-
-
-
X
X
-
X
-
-
-
X
X
X
X
X
X
-
-
-
-
-
-
X
-
-
X
X
X
X
X
X
X
X
-
-
-
-
-
X
X
-
-
-
-
-
-
-
X
-
X
-
-
X
-
-
-
X
-
-
-
-
-
-
3-10
-------
dwelling) organisms may ingest sediments while feeding which may result in
biological transformations of some contaminants. Thus, the cycling of these
contaminants in the environment will affect their availability for biotic uptake and
human exposure.
The physical-chemical properties of the contaminants detected in the
Ashtabula River AOC affect their fate in the environment. Hydrophobic organic
compounds, like PCBs, are especially persistent and ubiquitous in the
environment due to their low aqueous solubilities, high octanol-water partition
coefficients, high molecular weights, etc. HOCs preferentially partition to organic-
rich particles in the water column and sediment, but will also partition to a lesser
extent to dissolved and colloidal phases in the porewater and water column. Thus,
HOCs are often difficult to detect in the water column because they are usually
present at very low concentrations. Since HOCs preferentially partition into the
lipids of organisms and will biomagnify through the higher orders of the food
chain, fish can provide a good indication of contamination problems in the area.
Unlike HOCs, ionic (e.g., metal species) and polar compounds are more
susceptible to the solvating properties of water. However, metal complexes can
precipitate out of the water column under certain conditions, and both ionic and
polar compounds may become associated with suspended particulate matter which
may also settle out of the water column. Besides settling, contaminants may
undergo a variety of other processes (e.g., volatilization, photolysis, advective
transport, uptake into biota, hydrolysis, oxidation, microbial biotransformation)
depending on the physical-chemical properties of the chemical. It is beyond the
scope of this risk assessment to describe the importance of these mechanisms in
the Ashtabula River and Harbor.
Contamination of the water column by metals has been a problem for some
areas of the Ashtabula River AOC. Ambient Water Quality Standards (WQS)
have recently been violated in the Ashtabula River for copper, cadmium, iron,
lead, and zinc (Table 3.3) (Ohio EPA, 1991). However, the Ashtabula River is not
used as a drinking water source, and these violations do not appear to pose an
immediate threat to human health.
The upper turning basin, including the area near the mouth of Fields Brook,
is the most contaminated area of the Ashtabula River (Figure 3.4). Most of the
toxic sediments in the AOC are found in this area and are covered by 1.2 to 3.6 m
of moderately to heavily polluted sediments. Current U.S. EPA classification lists
the upper turning basin and area immediately downstream from Fields Brook as
toxic, most of the river channel as heavily polluted, and the outer harbor as non-
to-moderately polluted (Ohio EPA, 1991). Sediments in the outer harbor may be
dredged and disposed of in Lake Erie approximately 3.2 km from the east
breakwater light, when necessary. However, PCBs appear to be migrating from
the river to the harbor and this could curtail future dredging operations if PCB
levels continue to increase in the harbor sediments (Ohio EPA, 1991).
3-11
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TABLE 3.3.
A SUMMARY OF AMBIENT WATER QUALITY STANDARD VIOLATIONS MEASURED IN THE
ASHTABULA RIVER AOC (ALL CONCENTRATIONS IN UG/L) (ADAPTED FROM THE STAGE ONE
RAP (OHIO EPA, 1991))
Site
Parameter
Ashtabula River*
Copper
Cadmium
Iron
Lead
Zinc
Endosulfan
Lake Erie, (Water Intake)*
Copper
Iron
Zinc
Total Diss. Solids (mg/1)
Mercury
Bis (2-ethylhexyl)phthalate
Concentrations
Max.
129
3.5
4850
7.8
62.3
0.13
35.5
4810
41.0
22V
0.5
13.0
Min.
ND
ND
353
ND
6.8
ND
4.8
892
6.0
169
ND
ND
Mean
13.5
0.15
900
1.29
16.0
0.01
17.5
2502
19.7
194.2
0.05
1.08
Standard
Deviation
30.6
0.7
860
2.26
14.6
0.03
0.75
1610
9.81
17.1
0.15
3.59
Number of
Samples
23
23
23
23
23
23
12
12
12
12
12
12
Detection
Limits
2.4
3.2
13.7
1.5
1.4
0.05
2.4
13.7
1.4
10
0.4
10
Ohio WQS
Aquatic Human
Life Health1
16(2)
1.8(1)
1000(2)
11
140
.003(2) 2.0
16(7) 1000
1000(8)
140 5000
1500
0.2(1) 0.012(1)
8.4(1) 59
U.S. EPA Criteria
Aquatic Human
Life Health
16(2)
1.5(1)
1000(2)
4.9(4)
141
.056(2) 159
16(7)
1000(8) 300(12)
141
0.012(1) 0.146(1)
50000
GLWQA
Objectives
5(9)
0.2(1)
300(23)
25
30(2)
5(11)
300(12)
30(2)
200(4)
0.2(1)
0.6(1)
Human health standards for the Ashtabula River are based on surface water concentrations that could
bioaccumulate in fish tissue making fish consumption potentially deleterious to human health. Human
health standards for Lake Erie include consumption of water as well since Lake Erie is designated as a
public water supply.
Woodward Clyde Consultants (1991)
3-12
-------
,/^ /-VSES==*^
^A /' *'**fiOTA V
' :' //^7^^^"~^=^^ ^
ASHTABULA HARBOR, OHIO
DRIOCC ANDCONFlNt DiSPOSll PROJtCl
SEDIMENT POLLUTION
CLASSIFICATION
US «Bur CNCINllN UlilfliCI fcufF«LO
CHCtMBCR I96J
Figure 3.4. Sediment pollution classification of the Ashtabula River AOC (Ohio EPA, 1991).
3-13
-------
The latest sediment sampling of the Ashtabula River AOC was conducted
during 1989 and 1990 by Woodward-Clyde Consultants (WCC). The WCC
investigation involved an intensive sampling effort of 115 stations located in Lake
Erie, the harbor, the main navigation channel, outside the channel, in slips off the
river itself, and upstream from the navigation channel. The draft Stage One RAP
has provided a synopsis of WCC's results (Ohio EPA, 1991). A few major points to
make about this study are: 1) metal (especially iron and arsenic) and PCB
contamination is extensive at nearly all sites in and around the main channel; 2)
pollutant concentrations generally increase with depth to some maximum level
(PCB concentrations as high as 660 mg/kg were observed in a buried layer of
sediment in the navigation channel); 3) all contaminants show a decreasing
concentration gradient with distance downstream from Fields Brook, especially for
organics; 4) heavily polluted (i.e., >10 mg/kg) concentrations of PCBs were never
detected in the surficial sediments; and 5) very high concentrations of chromium,
copper, lead, and zinc were observed downstream from the 5th St. Bridge (WCC,
1991).
3.3 RECREATIONAL USES
The greatest recreational opportunities on the Ashtabula River and Harbor
involve fishing and boating. Recreational land along the Ashtabula River AOC
consists mostly of marina facilities and launching ramps that provide an access
point to Lake Erie. There are currently nine marinas and yacht clubs in the area
with an estimated 1200 slips (Figure 3.2). Fishing for perch and walleye has
improved greatly in Lake Erie, and there are now more than 50 registered fishing
charters operating out of Ashtabula (Ohio EPA, 1991). The marinas and improved
fisheries in Lake Erie have contributed to local efforts to increase tourism and to
promote economic development hi the region.
The economic base of Ashtabula has been weakened by industrial layoffs
and closures. Ashtabula, like other small cities in the Great Lakes region that are
undergoing economic problems, is searching to increase tourism by capitalizing on
their access to one of the Great Lakes, on the history of the town, and on the
natural resources of the area. The area is being promoted for sport fishing in
Lake Erie, deer hunting, snowmobiling, visiting historical covered bridges in the
county, and enjoying the scenic beauty of the area (Ashtabula Area Chamber of
Commerce, 1991). In addition, Ashtabula is trying to promote its small size, rural
lifestyle, and easy access to the major metropolitan centers of Cleveland, Erie and
Youngstown/Warren to people and businesses who might want to settle there.
Although sport fishing in Lake Erie is very popular, fishing also occurs in
the Ashtabula Harbor. The species composition of fish in the harbor is typical of
the warmwater fish community in Lake Erie river mouths (Ohio EPA, 1991). The
protected areas of the harbor usually contain relatively large numbers of yellow
perch, white bass, pumpkinseed, white crappie, goldfish and emerald shiner. The
more open water areas contain lower densities of gizzard shad, yellow perch, carp,
3-14
-------
goldfish, brown bullhead, and emerald shiner. Fish migrate to and from the lower
Ashtabula River when water conditions are favorable. Spawning migration runs
for walleye and smallmouth bass occur in the spring [U.S. Fish and Wildlife
Service (1984) cited in Ohio EPA (1991)]. The construction of vertical bulkheads
at the commercial shipping facilities from River Mile 0.7 to the mouth of the river
severely affected the ability of this portion of the river to support a diverse fish
community.
Swimming is another recreational activity that takes place near the
Ashtabula River AOC. Two official swimming beaches are located along the
nearshore of Lake Erie. Walnut Beach, located west of the harbor mouth, has a
large sand beach. Lakeshore Park, located east of the harbor mouth, has a
smaller beach with recurring erosion problems. Both beaches consistently meet
bacteriological water quality standards for bathing waters (Ohio EPA, 1991).
Boaters may occasionally anchor and swim in the outer harbor by a sheltered sand
bar near the west breakwater; this sand bar is also accessible by car, but it would
probably be used only occasionally for swimming because Walnut Beach is nearby.
No swimming areas or beaches exist along the lower 3.2 km of the
Ashtabula River. Although the river is classified by the State of Ohio for primary
contact, the poor water quality of the river does not make it aesthetically pleasing
for swimming. In addition, parts of the banks of the river are walled off; thus it is
not likely that anyone would be exposed to contaminants through contact with
river bank sediments. Some sporadic swimming may occur in the river from
people jumping off their boats and swimming in the water. In addition, a railroad
bridge, located just downstream from where Fields Brook enters the Ashtabula
River, is used infrequently by kids who jump off the bridge into the river (J.
Letterhos, Ohio EPA, personal communication, 1991). Water skiing is not likely to
take place on the lower Ashtabula River because of the shallow depth of the river
and busy boat traffic. Other activities that may result in immersion in the water,
such as wind surfing, are unlikely to occur in the river because of heavy boat
traffic and flow reversals in the surface water.
3.4 CONTAMINATION OF FISH
3.4.1 Routes of Contamination
One of the primary ways in which people in the Great Lakes region have
been exposed to sediment-derived contaminants is through the consumption of
contaminated fish. The specific mechanisms by which contaminants may be
transferred from sediments to fish are still being elucidated. Part of the problem
with determining these mechanisms is that different fish species occupy different
habitats in the water column (e.g., benthic (bottom) versus pelagic (open water)
habitats) and their diet and metabolism may change with age. This section will
examine some of the ways in which fish occupying a river/harbor area of the Great
3-15
-------
Lakes may accumulate contaminants, assuming that the major source of
pollutants comes from in-place contaminated sediments.
The group of contaminants that have been of major concern in the Great
Lakes are hydrophobic organic compounds (HOCs) such as PCBs and DDT. These
compounds are persistent in the environment, due to their physical-chemical
properties, and will preferentially accumulate in the lipids of organisms relative to
other compartments (e.g., muscle, bone). Many of the commercially exploited
Great Lakes fish have relatively high amounts of body fat (e.g., lake trout, lake
whitefish, and channel catfish), and thus would be expected to contain higher
levels of lipid-soluble HOCs than species characterized by low body fat (e.g., yellow
perch and suckers) (Kononen, 1989).
The accumulation of contaminants in fish lipids can occur by two routes: 1)
diffusion across the gills into the body and 2) transfer from the gut into the body
after the consumption of contaminated food (Swackhamer and Kites, 1988). For
the first route, the uptake of contaminants from water is functionally dependent
on fish respiration and is related to the transfer of dissolved oxygen across the gill
surfaces (Weininger, 1978). For the second route, the flux of contaminant transfer
through feeding is dependent on the following factors: a) contaminant
concentration in food, b) rate of consumption of food, and c) degree to which the
ingested contaminant in the food is actually assimilated into the tissues of the
organism. The assimilation of pollutants is affected by the desorption and
excretion of contaminants from body tissues, and by the growth of the organism
(Thomann and Connolly, 1984).
There is some uncertainty as to whether compounds sorbed to sediment
particles will be available to fish for uptake. A chemical equilibrium model would
assume that contaminant concentrations in the fish and sediments would be in
equilibrium through their individual equilibrium coefficients with the water
column (Connor, 1984). Studies with marine bottom fish in urban bays seem to
indicate that the concentration of organic contaminants in the fish is correlated
with the sediment concentration of those compounds (Connor, 1984; Mallins et al.,
1984). This correlation may depend on the area's physical flushing capacity
(residence time of water in a basin) and the metabolism of the organism (Connor,
1984). Similarly, a good correlation between the types of contaminants found in
sediments collected from areas of industrial and urban development with the types
of contaminants detected in freshwater carp from the same area has been made
(Jaffe et al., 1985). Carp tend to remain in a local territory and, for the most part,
are benthic feeders; thus, they would be expected to serve as a reasonable
barometer of the types of contaminants (especially organic compounds) found in
their aquatic environment. In another study, Brown et al. (1985) hypothesized
that PCB concentrations in pelagic (i.e., open water) consumers of benthic-feeding
organisms in the Hudson River were largely controlled by PCB levels in the
surficial sediments. While the aforementioned studies seem to indicate some
causal linkage between contaminant concentrations in sediment and fish, there is
3-16
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a degree of uncertainty associated with this linkage. One of the difficulties with
assessing the impacts of sediment contaminants on fish is that the factors
controlling their bioavailability are not well understood, nor is there a basic
understanding of trophic transfer from benthic to pelagic food chains (Biennan,
1990).
Due to the difficulty involved with assessing sediment-fish linkages in the
field, controlled laboratory experiments have been conducted. Seelye et al. (1982)
exposed young-of-the-year perch to a slurry of contaminated sediments for 10-days
to simulate the conditions these fish would encounter during dredging. Although
the perch accumulated organic compounds and heavy metals from the resuspended
sediments, it is not known whether the contaminants in the fish reached steady
state. In another experiment, by Kuehl et al. (1987), carp exposed to Wisconsin
River sediment for 55 days accumulated 7.5 pg/g 2,3,7,8-TCDD; maintaining
exposed fish in clean water for an additional 205 days resulted in the depuration
of 32-34% 2,3,7,8-TCDD. The most likely uptake route for 2,3,7,8-TCDD in the
carp was through the ingestion of contaminated sediments while feeding (Kuehl et
al., 1987). In another experiment, lake trout that were exposed to Lake Ontario
sediment and smelt in long term lab experiments appeared to bioaccumulate
2,3,7,8-TCDD primarily through the food chain and secondarily through contact
with contaminated sediment (Batterman et al., 1989). These lake trout did not
bioaccumulate a significant concentration of 2,3,7,8-TCDD from the water column,
even under simulated equilibrium conditions and with low suspended solids
concentrations (Batterman et al., 1989).
Recent evidence indicates that concentrations of HOCs in fish are primarily
the result of food chain biomagnification and not equilibrium partitioning from the
sediments or water column (Oliver and Niimi, 1988; Batterman et al., 1989). In
Lake Ontario, samples from all trophic levels in the planktonic (water to plankton
to mysid to alewive/smelt to salmonid) and the benthic (water to
sediment/suspended sediment to amphipod/oligochaete to sculpin to salmonid) food
chains showed classic biomagnification of PCBs with successive trophic levels
(Oliver and Niimi, 1988). Thus, the rate at which contaminant concentrations
increase with body size will be a function of how efficiently the contaminant is
excreted after assimilation (Borgmann and Whittle, 1991). In turn, the
assimilation of contaminants in fish will be affected by declines in feeding and
clearance rates as growth occurs (Pizza and O'Connor, 1983). Temperature has
also been found to affect the accumulation of PCBs in certain adult species of fish
because temperature controlled food consumption, growth, and lipid content
(SpigareUi et al., 1983).
Other contaminants, such as mercury, are also of concern in the Great
Lakes. Unlike HOCs, mercury appears to accumulate in fish tissues through
direct uptake from the water column (Gill and Bruland, 1990). The major form of
mercury in the water column is the highly toxic methylated mercury species.
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Because of the problem of mercury contamination in fish in the Great Lakes
region, fish advisories have been issued for certain size classes of sport fish.
3.4.2 Fish and Wildlife Advisories
The Great Lakes jurisdictions have issued consumption advisories for sport
fish since the late 1960s and early 1970s. These consumption advisories are based
on the relationship between tissue concentrations of contaminants in individual
size classes and species of fish and on specific trigger levels. When tissue
concentrations exceed some trigger level (usually Food and Drug Administration
action levels), consumption advice is issued by tile states. The Governors of the
Great Lakes States called for the uniform development of fish consumption
advisories by the states in the 1986 Great Lakes Toxic Substances Control
Agreement (Foran and VanderPloeg, 1989). However, this mandate has not been
followed by all states, and this inconsistent consumption advice may serve to
confuse the fishing public and those consuming Great Lakes sport fish.
Ultimately, confusion about fish consumption advice may result in it being ignored
entirely.
The Ohio Department of Health and Ohio EPA issued a fish advisory for the
Ashtabula Harbor and lower 3.2 km of the Ashtabula Kiver in 1983. This advisory
recommends that no fish caught hi the river from the 24th St. Bridge to the
harbor mouth be eaten (Ohio EPA, 1991). In addition, signs are posted at several
access points to the AOC warning against the consumption of any fish from the
lower Ashtabula River. A general advisory against the consumption of carp and
channel catfish in Lake Erie is in effect.
Despite these warnings, many anglers do not heed these advisories (J.
Letterhos, Ohio EPA, personal communication, 1991). People still fish from the
river banks. Fishing is also popular from the west breakwall and along rip rap in
the outer harbor. The Ohio Department of Health does not have any specific
information on fish consumption patterns and rates of consumption in the
Ashtabula River area (T. Shelley, Ohio Department of Health, personal
communication, 1991). As will be discussed in Chapter 5, standard fish
consumption rates approved by the EPA were used in this risk assessment.
During 1989, an Ohio EPA survey discovered brown bullheads with
numerous lip and skin tumors inside the west breakwall in the Ashtabula River
(Ohio EPA, 1991). The source of the tumors has not been determined; the U.S.
Fish and Wildlife Service is investigating this matter. The Conrail coal storage
piles and the coal conveyor spanning the river are sources of coal dust problems at
the river mouth. There may be some link between PAHs in the coal dust and
tumors in the fish.
Although the Ashtabula River lies on a major migration corridor for ducks
and geese, there is currently no information on deformities or tissue
3-18
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concentrations of contaminants in any birds. Because the Ashtabula River AOC
lies within an urban area, hunting for waterfowl would not be occurring there.
3.5 WATER SUPPLY
The drinking water supply for Ashtabula comes from Lake Erie. Very little
groundwater is used in Ashtabula County (Ohio EPA, 1991). The Ohio American
Water Company provides drinking water to approximately 38,000 people in the
city of Ashtabula and surrounding townships. The company has two, 457 m
intake pipes in Lake Erie west of the river mouth (Figure 3.2). Concern has been
raised that the quality of the water supply may be threatened by river discharges
under certain weather conditions or during river dredging.
Sampling at the intake under varying weather conditions was conducted in
1990 to determine if the Ashtabula River plume impacted water quality at the
intake (WCC, 1991). Violations of Ohio WQS were noted for copper, iron, and
mercury (Table 3.3); however, these metals are frequently violated along the Lake
Erie southshore nearshore zone (Ohio EPA, 1991). The WQS for bis(2-ethyl-hexyl)
phthalate was also violated. Although raw water sometimes exceeds WQS for
metals, finished water meets all drinking water standards (Ohio EPA, 1991). The
U.S. Army Corps of Engineers (1988) has calculated that a 40 kilometer per hour
northeast wind coupled with a river flow greater than 12.7 cubic meters per
second would be needed for the river discharge to affect the water supply intake.
These conditions rarely occur.
3.6 HUMAN HEALTH CONCERNS
Several human health studies have been conducted for the Fields Brook
area that are relevant to the Ashtabula River AOC population. The Ohio
Department of Health conducted a cancer surveillance study of the human
population in close proximity to Fields Brook. The study concluded that the total
cancer incidence and mortality in the population close to Fields Brook did not
differ significantly from the rest of Ohio or the United States [Indian and Hundley
(1987) cited in Ohio EPA (1991)]. However, the incidence of mortality of brain and
other central nervous system cancers was significantly higher, but it was not
known whether exposure to chemicals in the area had contributed to this
situation. A follow-up study, the Adverse Reproductive Outcomes Survey,
examined congenital anomalies, low birthweight and fetal deaths hi the Fields
Brook area; these factors did not differ significantly from the rest of Ashtabula
County or Ohio [Indian and Rao (1988) cited in Ohio EPA (1991)].
A risk assessment was completed for Fields Brook as part of the CERCLA-
Superfund requirements. This assessment determined that public health and
welfare may be affected adversely, under existing and future exposure scenarios,
by contaminants in Fields Brook and its tributaries (CH2M Hill, 1986).
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Public concern has been raised about uranium contamination in the
Ashtabula River AOC. Although uranium was found above background levels in
river sediments (2.4-22.3 pCi/g), the concentrations were below Nuclear Regulatory
Commission guidelines (i.e., 30 pCi/g) and ruled not to be of concern [U.S. EPA
(1990) cited in Ohio EPA (1991)].
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CHAPTER 4
RISK ASSESSMENT FRAMEWORK
4.1 CONCEPT OF RISK
People are subject to a number of risks throughout their day which may
cause them immediate or delayed harm. Some risks arise from personal choices
(e.g., driving a car, participating in sports) while other risks may result from
things people have little control over (e.g., breathing urban air, being a victim of a
random crime). In terms of human health risks resulting from exposure to some
chemical, biochemical, or physical agent, risks are classified into two categories:
carcinogenic and noncarcinogenic risks.
Cancer is the leading cause of death for women in the United States, and
most cancers, for both men and women, are caused by factors resulting from life
style choices (e.g., smoking, drinking alcohol, consuming a diet high in animal fat,
being overweight, or staying out in the sun too long (ultraviolet light exposure))
(Henderson et al., 1991). In particular, tobacco (alone or in combination with
alcohol) accounts for one of every three cancer cases occurring in the U.S. today
(Henderson et al., 1991). Occupational exposures to specific carcinogens
(especially asbestos) account for only about 4% of the cancers in the United States
(Henderson et al., 1991). Although nonoccupational exposures to environmental
contaminants probably cause an even smaller fraction of the cancers reported in
the United States, it is important to safeguard the public's health from
unnecessary risks. In addition, environmental contaminants may also pose a
noncarcinogenic risk to human health.
Noncarcinogenic risks include chronic and subchronic effects to people.
Included in this risk category are birth defects, respiratory diseases (e.g., asthma),
liver diseases, learning disabilities, etc. One way to examine incidences of these
risks in human populations is through epidemiological studies. Three sets of
studies of the impacts of human exposure to PCB contaminated fish from the
Great Lakes basin~the Michigan Sports Fisherman Cohort, the Michigan
Maternal/Infant Cohort, and the Wisconsin Maternal/Infant Cohort were evaluated
using epidemiologic criteria (Swain, 1991). The results from comparing the
studies against each other, and against comparable data from other geographic
locales, strongly suggest a causal relationship between PCB exposure and
alterations in both neonatal health status and in early infancy (Swain, 1991).
However, there is no evidence that these short-term effects lead to any chronic
health effects (Bro, 1989). Possible developmental effects in infants and children
will not be addressed in this risk assessment because complex pharmacokinetic
models, which are not well developed in the risk assessment field, would have to
be used. Thus, it is beyond the scope of the ARCS Program to address this issue
in any great depth (USEPA, 1991b).
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4.2 RISK FRAMEWORK
Risks associated with environmental exposures to contaminants are difficult
to assess because 1) the exposure itself is often difficult to document and 2) the
exposure does not always produce immediately observable effects. Due to these
difficulties, human health risks associated with exposures to contaminants must
often be estimated via scenarios using standard EPA exposure parameters.
The approach used for this baseline human health risk assessment followed
exposure and risk assessment guidelines established by the EPA for use at
Superfund sites (USEPA, 1988b; 1989a,b; 1991a). Although the Ashtabula River
is not a Superfund site, the risk assessment procedures developed for the
Superfund Program can be applied to this site to estimate current risks to people
residing in the AOC. Unlike the Superfund risk assessments, this risk
assessment did not consider risks resulting from future scenarios (e.g., future
risks associated with turning a contaminated site into a playground). Instead,
this risk assessment was based on the most up-to-date information available to
estimate current noncarcinogenic and carcinogenic risks to human populations in
the lower 3.2 km of the Ashtabula River and in the Ashtabula Harbor.
The procedures used in this risk assessment are outlined briefly in Figure
4.1. The first step in the process was to obtain information about the Ashtabula
River from the draft Stage One RAP (Ohio EPA, 1991) and from other documents.
In addition, a search for the latest data on contaminant levels in the
environmental media of interest was conducted to characterize the extent of
contamination at the site. The next step was to determine the exposure pathways
by which people could come in contact with sediment-related contaminants from
the river. The most complete and current data sets were then evaluated to judge
whether adequate quality assurance/quality control (QA/QC) protocols were
followed. Next, based on the exposure pathways and sites of exposures, the most
current, environmental data were used to determine contaminant intake levels.
Intake levels are essentially equivalent to administered doses and are expressed in
units of nog chemical/kg body weight-day. These chemical intake levels were then
integrated with noncarcinogenic and carcinogenic toxicity data, obtained from
verified and interim EPA sources, to estimate the respective human health risks
to people in the Ashtabula River AOC. Finally, because of the number of
assumptions that went into each step of the risk assessment procedure, a
qualitative listing of the uncertainties involved in these assumptions was made.
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Site Character Izat Ion
1
Review & Evaluation
or Ex Ist1ng
Chemical Data
1
Tox1cIty Prof I Ies
Eva Iuat r on of
Base I Ine Risks
1
DetermlnatI on of
ProbabIe Expos ure
Pat. hways
i
Determination of
Exposure Point
ConcentratIons
I
DetermInatIon or
ContamInant
Intakes/Exposure
Risk/Hazard
Character IzatI on
Character IzatIon
of UncertaInty
Figure 4.1.
Components of baseline human health risk assessments.
4-3
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CHAPTER 5
EXPOSURE ASSESSMENT
5.1 EXPOSURE PATHWAYS
In this exposure assessment, the magnitude, frequency, duration, and route
of direct and indirect exposures of people to sediment-derived contaminants from
the Ashtabula River AOC will be determined. Exposures to these pollutants can
potentially occur via three pathways: dermal contact, inhalation, and ingestion.
Dermal contact involves direct contact of the skin with either contaminated
sediments, riverplain soils, or overlying water. Inhalation of airborne vapors or
dust may introduce chemicals of potential concern into the respiratory system.
Ingestion of contaminants through the consumption of contaminated soils,
sediment, or food (e.g., fish, waterfowl) is potentially significant because of the
direct transfer of contaminants across the gut.
The Ashtabula River AOC was toured during 28-29 August 1991 so that
researchers could become familiar with the AOC and determine relevant exposure
pathways. A meeting of the Ashtabula River RAP Advisory Council, held the
evening of August 28, provided a means of informing the Council about this
human health risk assessment. For the most part, the Ashtabula River AOC is
not accessible for detailed viewing by car. Consequently, Julie Letterhos (RAP
Coordinator) arranged a boat tour of the lower Ashtabula River and Harbor area
courtesy of Jack's Marine; the tour included Ms. Letterhos and members of the
Ashtabula River RAP Advisory Council. In addition, Ms. Letterhos provided a
short driving tour of the Ashtabula River AOC and Fields Brook area. The input
and cooperation of the Ashtabula River RAP Advisory Council was extremely
valuable for evaluating exposure pathways in the AOC.
The potential pathways by which people may be exposed to contaminants
from the Ashtabula River AOC are given in Table 5.1. These pathways were then
examined to determine whether they were complete or incomplete. A pathway is
complete if there is: 1) a source or chemical release from a source, 2) an exposure
point where contact can occur, and 3) an exposure route by which contact can
occur (USEPA, 1989a). The exposure pathway is incomplete if one of these
conditions is not met. Five pathways appear to be incomplete:
1) Ingestion of contaminated drinking water: the Ashtabula
River is not used as a source of drinking water in the AOC.
2) Ingestion of sediments: the ingestion of bottom sediments
does not appear to be occurring. Only the bottom sediments
near shore would be accessible if, for example, a child reached
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TABLE 5.1. POTENTIAL PATHWAYS BY WHICH PEOPLE MAY BE
EXPOSED TO SEDIMENT-DERIVED CONTAMINANTS
FROM THE ASHTABULA RIVER AOC
INGESTION OF CONTAMINATED:
• Surface Water
• Fish and Wildlife
• Drinking Water
• Sediments
• River Bank/Flood Plain Soils
DERMAL CONTACT WITH CONTAMINATED:
• Surface Water
• Sediments
• River Bank/Flood Plain Soils
INHALATION OF AIRBORNE CONTAMINANTS
into the water and grabbed some sediments; however, no
evidence of this behavior was available.
3) Ingestion of contaminated soils: the ingestion of
contaminated soils from the river banks does not appear to be
occurring. The banks are either walled off or are not easily
accessible, thus limiting the opportunities for human contact.
4) Dermal contact with contaminated soils: the river bank
soils are mostly inaccessible to people; thus, this pathway may
not be occurring.
5) Ingestion of wildlife: hunting is not allowed within the city
limits of Ashtabula, including the AOC.
Although five exposure pathways were considered complete in the
Ashtabula River (Table 5.2), not all of these exposure pathways may result in
significant human health risks. In particular, it was assumed that if insignificant
risks were associated with the ingestion of surface water while swimming then
the risk associated with dermal exposure to surface water or sediments in the
Ashtabula River AOC would also be insignificant (see Appendix A for the rationale
behind this assumption). Under a reasonable maximum exposure scenario in
which a 70-kg person swam 3 days/yr for 0.5 hr/event over a 30-year period, the
noncarcinogenic and carcinogenic risks resulting from ingesting surface water at a
rate of 50 mL/hr could be estimated (Appendix A). The surface water, collected
below Fields Brook, contained detectable concentrations of barium, copper,
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TABLE 5.2. COMPLETE EXPOSURE PATHWAYS IN THE ASHTABULA
RIVER AOC
• Consumption of Contaminated Fish
• Ingestion of Surface Water while Swimming or Playing in the
Water
• Dermal Contact with Water while Boating, Fishing, Swimming,
etc.
• Dermal Contact with Sediments while Entering or Leaving the
Water
• Inhalation of Airborne Contaminants
manganese, zinc, acetone, methylene chloride, and vinyl acetate. The resulting
noncarcinogenic risk (Hazard Index (HI) = 0.0003) and upper-bound, lifetime
carcinogenic risk (4 x 10"10) were far below levels of concern (i.e., HI > 1, cancer
risk exceeding 10"4 to 10"6). Thus, infrequent dermal exposure to water and
sediments were also assumed to be insignificant. No swimming areas are
designated along the AOC and swimming may only occur infrequently (e.g., if
someone jumps off his or her boat into the water).
Although the air pathway is complete, it cannot be quantitatively assessed
with the currently available data. In addition, it would be difficult to separate out
the contribution of airborne contaminants from the river and that from industrial,
municipal, and background sources.
The only complete exposure pathway that will be considered for this risk
assessment is the consumption of contaminated fish. Noncarcinogenic and
carcinogenic risks will be determined for typical (i.e., average) and reasonable
maximum exposures (i.e., the maximum exposure that is reasonably expected to
occur at a site), as well as for exposures resulting from subsistence fishing. The
subsistence exposure scenario was chosen because of economic problems in the
area which might contribute to an underemployed/unemployed person to rely on
locally caught fish for their main source of protein.
5.2 DATA USED IN THE EXPOSURE ASSESSMENT
5.2.1 Data Sources
Data on contaminant levels in fish and water were obtained from a recent
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study by Woodward-Clyde Consultants (WCC, 1991). WCC also sampled and
analyzed sediment cores from the Ashtabula River AOC, but these data were not
used in this risk assessment. No assumptions about the temporal and spatial
variability of contaminants data in the Ashtabula River and Harbor will be made
here because of a general lack of historical data.
Fish samples were collected by WCC at three locations in the lower
Ashtabula River and at one site in the harbor (Figure 5.1) from 4-17 October 1990.
Thirteen of the planned 16 fish samples were collected during sampling. Ten
brown bullheads, collected by the U.S. Fish and Wildlife Service (USFWS) in the
harbor, were provided to WCC for analysis. A total of 66 fish were caught: 20
carp, 26 small and large mouth bass, 4 rock bass, and 16 bluegill. Seven of the
fish caught had tumors; of this number, one whole fish and two fillets were
analyzed for contaminants. The species of fish with tumors were not identified by
WCC. Of the total fish caught at the four sites, 12 carp, 16 small/large mouth
bass and 16 bluegill were selected at the request of the Ohio EPA for laboratory
analysis. The criteria by which fish were selected for analysis was not given. The
carp were analyzed as whole fish; the other species were analyzed as fillets. Eight
carp had detectable concentrations of PCBs of less than 2 mg/kg, the U.S. Food
and Drug Administration recommended limit for PCBs in fish. No fillets had
detectable levels of PCBs.
WCC collected water samples at several locations in the Ashtabula River
AOC (Figure 5.2). All water samples were grab samples collected mid-stream at
mid-depth and at the deepest depth where river water was more than 1 m deep.
The samples were analyzed for basic water chemistry parameters, for target
compound list compounds (i.e., base/neutral and acid extractable organic
compounds, pesticides, PCBs), and for a select group of metals. The only water
samples used in this risk assessment were collected just below Fields Brook; the
concentrations of contaminants were greatest at this site (see Appendix A).
5.2.2 Data Review
All of the data used in this risk assessment underwent a QA/QC review by
Lockheed Engineering and Sciences Company (Lockheed-ESC) under a contract
with the EPA Environmental Monitoring Systems Laboratory in Las Vegas, NV.
A complete evaluation of the data could not be made because of difficulty with
obtaining WCC's QA/QC data. However, it appears that the data were generated
following contract laboratory program (CLP) protocols. The CLP protocols are
more extensive in their incorporation of QA/QC samples than those specified in
the ARCS QA/QC program. In addition, rigorous data verification and validation
procedures were used by WCC to ensure that the data were acceptable in terms of
the QA/QC requirements as well as correct in terms of data entry and the final
released values (i.e., few to no transcription errors). Therefore, it was the opinion
of Brian Schumacher, the ARCS QA/QC reviewer (formerly of Lockheed-ESC), that
the WCC data should be acceptable for use in this risk assessment; however, the
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Figure 5.1. Fish sampling locations in the Ashtabula River AOC (WCC,
5-5
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SURFACE WATER
SAMPLE LOCATION (TCL. T*L)
D 1000 2000
SCALE 1(4 FEET
Figure 5.2.
Surface water sampling locations in the Ashtabula River AOC
(WCC, 1991).
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supporting data to confirm its acceptability were not available (B. Schumacher
(EPA Environmental Monitoring Systems Laboratory-Las Vegas), personal
communication, 1991).
5.2.3 Data Sets
Not all of the fish species sampled by WCC for contaminants were used in
this risk assessment because some of the fish were collected upstream from the
limits of the Ashtabula River AOC (i.e., 24th Street Bridge). In addition, other
fish were collected from the mouth of Strong Brook, upstream from Fields Brook.
Data obtained from composite samples of fish collected from two locations
were used in this exposure assessment: 1) the Ashtabula River just downstream
from Fields Brook (3 carp, 2 large mouth bass, and 11 bluegills), and 2) the
Ashtabula Harbor (4 carp, 1 small mouth plus 3 large mouth bass, and 5
bluegills). Thus, data were obtained from both bottom feeders (i.e., carp) and open
water feeders (i.e., bluegills, small/large mouth bass). Although carp are not a
favored sport fish, they were included since they generally accumulate high levels
of contaminants in water bodies due to their feeding habits and high fat content.
Thus, carp were representative of an "upper-bound" level of contaminants in fish.
The data for both bluegills and small/large mouth bass were used because both
may be consumed by anglers. By determining separate exposures for the
consumption of carp, bluegill, and small/large mouth bass, a range of risk
estimates could be determined for typical, reasonable maximum, and subsistence
exposure scenarios.
The fish were analyzed for a number of contaminants (Table 5.3). The
mean contaminant levels of the fish data sets used in the exposure assessment are
given in Tables 5.4 and 5.5. The highest contaminant concentrations were
generally observed in fish collected below Fields Brook. The only exceptions were
for concentrations of 1,1,2,2-tetrachloroethane, tetrachoroethene, and
trichloroethene in whole small/large mouth bass collected from the mouth of
Strong Brook. However, these data were not used in the exposure assessment
since data for bass fillets were available from the Fields Brook site.
5.3 EXPOSURE ASSESSMENT
5.3.1 General Determination of Chemical Intakes
Once the complete exposure pathways were identified and contaminant
concentrations for fish were obtained, an exposure assessment could be conducted.
Exposures were normalized for time and body weight to determine chemical
"intakes," expressed in units of mg chemical/kg body weight-day. For the
ingestion of contaminated fish, intakes represent the amount of chemical available
for absorption in the gut. The general equation for calculating chemical intakes is
given in Table 5.6. Several variables are used to determine intakes, including
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TABLE 5.3. LIST OF CONTAMINANTS ANALYZED IN THE FISH USED
IN THIS RISK ASSESSMENT
DETECTED
CHEMICAL Yes No
ORGANICS
Chlorobenzene X
1,1,2,2-Tetrachloroethane X
Tetrachloroethene X
Hexachlorobenzene X
Hexachlorobutadiene X
Trichloroethene X
Pentachlorobenzene X
Octachlorostyrene X
Fluoranthene X
Phenanthrene X
PCBs
Aroclor 1242 X
Aroclor 1248 X
Aroclor 1254 X
Aroclor 1260 X
INORGANICS
Arsenic X
Beryllium X
Cadmium X
Copper X
Chromium X
Lead X
Mercury X
Silver X
Zinc X
specific information about the exposed population and the period over which the
exposure was averaged. Noncarcinogenic effects were averaged over the same
time period as the exposure duration [i.e., 9 years for typical exposures and 30
years for reasonable maximum exposures (RME)]. Carcinogenic effects were
averaged over a lifetime (i.e., 70 years). Intake variable values were selected so
that the combination of all values resulted in an estimate of either the typical,
reasonable maximum, or subsistence exposure intakes.
The exposure parameters used in the typical scenario were assumed to be
applicable to the general angling population of Ashtabula while the reasonable
maximum exposure scenario applied to recreational anglers and their families.
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TABLE 5.4.
CONTAMINANT CONCENTRATIONS IN WHOLE CARP
AND BLUEGILL FILLETS COLLECTED FROM THE
ASHTABULA RIVER AOC (WCC, 1991)
Chemical
METALS
Chromium
Copper
Mercury
Silver
Zinc
ORGANICS
PCBs (Aroclor 1260)
1, 1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
Whole
Carp
Ashtabula
River
(nag/kg)
2.0E+00
1.7E+01
4.6E-02
3.2E-01
9.6E+01
8.1E-01
2.8E-02
2.7E-01
4.0E-02
Whole
Carp
Ashtabula
Harbor
(mg/kg)
1.5E+00
1.5E+00
ND
ND
8.3E+01
1.5E-01
5.5E-03
3.0E-02
7.3E-03
Bluegill
Fillets
Ashtabula
River
(mg/kg)
1.4E+00
5.5E-01
1.7E-01
ND
2.2E+01
ND
ND
ND
ND
TABLE 5.5.
CONTAMINANT CONCENTRATIONS IN BLUEGILL AND
SMALL/LARGE MOUTH BASS FILLETS COLLECTED FROM
THE ASHTABULA RIVER AOC (WCC, 1991)
Chemical
METALS
Chromium
Copper
Mercury
Silver
Zinc
ORGANICS
PCBs (Aroclor 1260)
1, 1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
Bluegill
Fillets
Ashtabula
Harbor
(mg/kg)
1.6E+00
ND
7.3E-02
ND
1.6E+01
ND
ND
ND
ND
L. Mouth
Bass
Fillets
Ashtabula
River
(mg/kg)
1.2E+00
ND
1.5E-01
ND
1.1E+01
ND
6.8E-03
1.2E-01
1.3E-02
S/L Mouth
Bass
Fillets
Ashtabula
Harbor
(mg/kg)
1.4E+00
ND
1.2E-01
ND
1.2E+01
ND
ND
ND
ND
5-9
-------
TABLE 5.6.
GENERIC EQUATION FOR CALCULATING CHEMICAL
INTAKES (USEPA, 1989a)
_ C X CR X EFD
BW X AT
where:
I
CR
EFD
BW
AT
Intake = the amount of chemical at the exchange boundary (mg/kg body weight-
day)
Chemical-Related Variables
Chemical Concentration = the average concentration contacted over the exposure
period (e.g., mg/L)
Variables that Describe the Exposed Population
Contact Rate = the amount of contaminated medium contacted per unit time or
event (e.g., L/day)
Exposure Frequency and Duration = how long and how often exposure occurs.
Often calculated using two terms, EF and ED, where:
EF = exposure frequency (days/year)
ED = exposure duration (years)
Body Weight = the average body weight over the exposure period (kg)
Assessment-Determined Variables
Averaging Time = period over which exposure is averaged (days)
The subsistence exposure scenario was chosen for a sensitive subpopulation of
people who would be consuming about four 8-ounce servings of locally caught fish
per week. At the present time, specific information on fish consumption rates and
trends in the Ashtabula River AOC is lacking. Results from the Michigan Sport
Anglers Fish Consumption Survey, conducted by West and co-workers at the
University of Michigan, may give a better indication of typical ingestion rates of
fish by Ashtabula anglers than the default EPA parameter value. West et al.
(1989) found that, for their survey conducted during the January-June, 1988 time
frame, the average fish consumption was 18.3 g/person/day with a standard total
deviation of 26.8 g/person/day; approximately 26% of the sample household
5-10
-------
TABLE 5.7.
EQUATION USED TO ESTIMATE CONTAMINANT
INTAKES DUE TO INGESTION OF FISH
Intake ,
where:
Intake
C
IR
FI
EF
ED
BW
AT
Intake Rate (mg/kg-day)
Contaminant Concentration (mg/kg)
Ingestion Rate (kg/day)
Fraction Ingested from Contaminated Source (unitless)
Exposure Frequency (days/yr)
Exposure Duration (yr)
Body Weight (kg)
Averaging Time (days)
persons who ate fish consumed between 20-40 g/person/day while another 10%
consumed between 40-75 g/person/day. West et al. (1989) estimated a year-round
fish consumption rate of 19.2 g/person/day. This exposure assessment used a
reasonable maximum ingestion rate of 54 g/person/day; this number seems
appropriate because it falls within the upper 10% ingestion rate of the Michigan
anglers. This exposure assessment also assumed that the only contaminated fish
ingested by local residents came from the Ashtabula River AOC.
5.3.2 Intakes: Ingestion of Contaminated Fish
The equation used to estimate intakes of contaminants due to the ingestion
of contaminated fish is provided in Table 5.7. The parameter values used in that
equation are given in Table 5.8. Parameter values were obtained from
recommended EPA sources except for the fraction of fish assumed to be ingested
from the Ashtabula River AOC. This latter parameter had to be estimated, in a
conservative way, because of a lack of information about what proportion of the
fish consumption was attributable to locally caught fish. Since chemical intake
values will be incorporated into the estimation of risk presented in Chapter 7,
separate tables of intake values will not be presented here.
5-11
-------
TABLE 5.8.
PARAMETERS USED IN ESTIMATING CONTAMINANT
INTAKES DUE TO INGESTION OF FISH IN THE
ASHTABULA RIVER AOC
Var.
IR
FI
EF
ED
BW
AT:
Units
kg/day
-
day/yr
yrs
kg
days
Value
Used
0.0192
0.054
0.13
0.1
0.25
0.7
350
9
30
70
3285
10950
25550
Comment
Typical: West et al. (1989)
RME: USEPA (1991a)
Subsistence fishing: used the 95th percentile daily
intakes averaged over 3 days for consumers of fin
fish (Pao et al. (1982) cited in USEPA (1989a))
Typical: study assumption
RME: study assumption
Subsistence fishing: study assumption
USEPA (1991a)
Typical: USEPA (1989a)
RME and Subsistence: USEPA (1989a)
50th percentile average for adult men and women
(USEPA, 1989b)
9 yrs x 365 days/yr (typical noncarcinogenic risk)
30 yrs x 365 days/yr (RME and subsistence
noncarcinogenic risk)
70 yrs x 365 days/yr (carcinogenic risk)
5-12
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CHAPTER 6
TOXICITY ASSESSMENT
6.1 TOXICITY VALUES
Two types of toxicity values were used in combination with exposure
estimates (i.e., chemical intake values) to estimate human health risk. One
toxicity value, the reference dose (RfD), provides an estimate of the daily
contaminant exposure that is not likely to cause harmful effects during either a
portion of a person's life or his/her entire lifetime. The RfD is the toxicity value
used most often in evaluating noncarcinogenic effects. The other toxicity value,
the slope factor, is used in risk assessments to estimate an upper-bound lifetime
probability of an individual developing cancer as a result of exposure to a
particular level of a potential carcinogen. In addition, the EPA weight-of-evidence
classification scheme indicates the strength of evidence that the contaminant is a
human carcinogen (Table 6.1). Slope factors are typically calculated for potential
carcinogens in classes A, Bl, and B2 as well as for class C on a case-by-case basis.
A more detailed description of these toxicity values, summarized from "Risk
Assessment Guidance for Superfund. Volume 1. Human Health Evaluation
Manual (Part A)" (USEPA, 1989a), is given in Appendix B.
Chronic oral RfD values and oral slope factors were used for the fish
ingestion pathway examined in this risk assessment. Toxicity values, which had
undergone an EPA review process, were obtained from the EPA's Integrated Risk
Information System (IRIS) data base. For chemicals lacking a "verified value,"
interim toxicity values were obtained from the Health Effects Assessment
Summary Tables (HEAST), if available. Table 6.2 lists the toxicity data used for
the chemicals of interest. This table also includes the form in which the chemical
was administered to the test animal or patient (e.g., drinking water, diet, or
gavage) for determination of the oral RfD. In addition, the source of the toxicity
value is given. The endpoints of concern for evaluating noncarcinogenic risks are
listed in Table B-l of Appendix B.
6.2 LIMITATIONS
This risk assessment was limited by the current availability of toxicity
information. In some cases, toxicity values were not available for some of the
chemicals (e.g., RfD value for PCBs). In other cases, toxicity values were available
for a particular metal species rather than for the total metal (e.g., mercury). In
particular, methyl mercury was assumed to be the major form of mercury present
in this system, and chromium VI was assumed to be the major valence state of
chromium in the system. For other chemicals (i.e., tetrachloroethene and
trichlorethene), the oral slope factors have been withdrawn from IRIS pending
further review.
6-1
-------
TABLE 6.1.
EPA WEIGHT-OF-EVIDENCE CLASSIFICATION SYSTEM
FOR CARCINOGENICITY (USEPA, 1989a)
Group
Description
Bl or
B2
C
D
E
Human carcinogen
Probable human carcinogen
Bl indicates that limited human data are available
B2 indicates sufficient evidence in animals and
inadequate or no evidence in humans
Possible human carcinogen
Not classifiable as to human carcinogenicity
Evidence of noncarcinogenicity for humans
TABLE 6.2.
HUMAN HEALTH RISK TOXICITY DATA FOR CHEMICALS
OF INTEREST IN THE ASHTABULA RIVER AOC
Cham leal
"METAIS"
Chromium VI
Copper
Mercury, methyl
Silver
Zinc
"ORGANICS"
PCBB
1, 1, 2, 2— Tetrachlorethane
Tetrachloroethene
Trichlorethene
Sources :
a:
b:
Oral RED
-------
CHAPTER?
BASELINE RISK CHARACTERIZATION FOR THE ASHTABULA RIVER AOC
7.1 PURPOSE OF THE RISK CHARACTERIZATION STEP
The purpose of the risk characterization step is to combine the exposure and
toxicity estimates into an integrated expression of human health risk. This
section presents the calculated potential human health risks associated with the
consumption of contaminated fish from the Ashtabula River AOC under the no
action alternative. It is important to recognize that these calculated risk
estimates are not intended to be used as actual values. Risk assessment is a
regulatory process that provides risk managers with quantitative estimates that
are to be used for comparative purposes only. These risk estimates must be
interpreted in the context of all the uncertainties associated with each step in the
process. Some of the major uncertainties in this risk assessment are addressed in
the next chapter.
Two means of expressing the carcinogenic and noncarcinogenic risks of
adverse health effects are presented in this chapter. First, chemical specific risks
were estimated. Secondly, chemical specific risks were added to estimate the
cumulative risk resulting from the consumption of a particular species of fish
under one of three exposure scenarios.
7.2 QUANTIFYING RISKS
7.2.1 Determination of Noncarcinogenic Risks
Noncarcinogenic effects do not generally occur below a minimum or
threshold level of exposure. These effects are evaluated by comparing a site-
specific exposure level over a specified time period with a RfD derived from a
similar exposure period (otherwise known as a hazard quotient (HQ)). Thus, HQ
= exposure level (or intake)/RfD. Hazard quotients are usually expressed as one
significant figure in a nonprobabilistic way. In this risk assessment, HQ values
were expressed to two significant figures for each chemical; this was done to
reduce round-up error when HQ values were summed for each pathway. An HQ
value of less than 1 indicates that exposures are not likely to be associated with
adverse noncarcinogenic effects (e.g., reproductive toxicity, teratogenicity, or liver
toxicity). As the HQ approaches or exceeds 10, the likelihood of adverse effects is
increased to the point where action to reduce human exposure should be
considered. Owing to the uncertainties involved with these estimates, HQ values
between 1 and 10 may be of concern, particularly when additional significant risk
factors are present (e.g., other contaminants at levels of concern). However, the
level of concern does not increase linearly as the RfD is approached or exceeded
7-1
-------
because RfDs do not have equal accuracy or precision; nor are RfDs based on the
same severity of toxic effects (USEPA, 1989a).
In assessing health risks, all HQ values are representative of long term
chronic exposures (i.e., exposures assumed to occur over a period of 9 or 30 years).
The sum of more than one HQ value for multiple substances and/or multiple
exposure pathways is the Hazard Index (HI). This assumption of additivity does
not account for any synergistic or antagonistic effects that may occur among
chemicals. In addition, no attempt was made to distinguish between risk
endpoints (e.g., target organs and related effects) when calculating the HI. Thus,
this expression of total risk may be extremely conservative; it would be better to
refine the HI to specific endpoints for HQ values greater than one. Additional
limitations of HQ values and the segregation of hazard indexes have been
described elsewhere (USEPA, 1989a).
7.2.2 Determination of Carcinogenic Effects
Unlike noncarcinogenic effects, carcinogenic effects are thought to pose some
degree of risk at all exposure levels. These effects are estimated as the
incremental probability of an individual developing cancer over a lifetime as a
result of exposure to a potential carcinogen. The carcinogenic risk is computed
using average lifetime exposure values that are multiplied by the oral slope factor
for each carcinogen of interest. Slope factors are used to convert estimated daily
intakes averaged over a lifetime of exposure directly to the incremental risk of an
individual developing cancer. The resulting carcinogenic risk estimate is generally
an upper-bound estimate, because slope factors are usually based on upper 95th
percentile confidence limits. The EPA believes it is prudent public health policy to
consider actions to mitigate or minimize exposures to contaminants when
estimated excess lifetime cancer risks exceed the 10"5 to 10~6 range, and when
noncarcinogenic health risks are estimated to be significant (USEPA, 1988a).
Carcinogenic effects were summed for all chemicals in an exposure pathway
(i.e., consumption offish). This summation of carcinogenic risks assumes that
intakes of individual substances are small, that there are no synergistic or
antagonistic chemical interactions, and that all chemicals produce the same effect
(i.e., cancer). The limitations to this approach are discussed in detail elsewhere
(USEPA, 1989a).
7.3 HUMAN HEALTH RISKS IN THE ASHTABULA RIVER AOC
7.3.1 Typical and Reasonable Maximum Exposures
7.3.1.1 Noncarcinogenic Risks
Based on typical and reasonable maximum exposure (RME) levels over a 9-
and a 30-year period, respectively, estimated noncarcinogenic risks were below
7-2
-------
levels of concern (i.e., Hazard Index <1) for all three fish species except for carp
taken from the Ashtabula River (below Fields Brook) under RME conditions
(Tables 7.1-7.6). For these carp, the estimated Hazard Index of 3 was mostly
attributable to copper contamination. Thus, high consumption rates of carp from
the Ashtabula River near Fields Brook may result in adverse noncarcinogenic
effects. Information about the types of noncarcinogenic effects one might
experience from chronic exposure to copper is not available at this time from the
IRIS data base.
Since some of the chemicals (e.g., PCBs) detected in fish from the Ashtabula
River AOC are lacking RfD values, it would be premature to state that no
noncarcinogenic risk exists from consuming fish (e.g., bluegills, bass) from the
Ashtabula River and Harbor. The noncarcinogenic risk reported here is an
estimated risk based on currently available exposure/intake data and toxicity
information, and should not be construed as an absolute risk.
7.3.1.2 Carcinogenic Risks
A carcinogenic risk estimate could not be calculated for the consumption of
small/large mouth bass collected from the Ashtabula Harbor and for bluegills
collected from both the river and harbor because no carcinogens were detected in
these fish fillets. However, the carcinogenic risk could be determined, under
typical and reasonable maximum exposure scenarios, for the consumption of both
large mouth bass and carp collected from the Ashtabula River (below Fields
Brook) and for carp from the Ashtabula Harbor.
The upper bound carcinogenic risk estimates associated with the
consumption of large mouth bass fillets from the river were below concern levels
(i.e., less than 10"6) under typical and RME scenarios (Table 7.7). However, carp
collected from both the harbor (Table 7.8) and river (Table 7.9) appear to pose a
potential risk to human health; the upper bound cancer risk ranged from 4 x 10~6
to 5 x 10~4. The potential carcinogenic risk resulting from the consumption of carp
was up to an order of magnitude greater for fish collected near Fields Brook than
for carp from the harbor. This upper bound risk was attributable to a PCB
mixture resembling Aroclor 1260 in the whole carp.
There is a possibility that people who ingest, inhale, or have dermal contact
with certain PCB mixtures may have a greater chance of incurring liver cancer;
however, this statement is based on suggestive evidence rather than on verified
data. Studies with three strains of rats and two strains of mice have verified the
carcinogenic toxicity of PCBs through the occurrence of hepatocellular carcinomas
(IRIS data base retrieval for PCBs, 1992). This evidence was used to classify
PCBs as a probable human carcinogen.
As discussed in Chapter 3, fish will preferentially accumulate PCBs and
other hydrophobic organic contaminants in their lipids. Since carp are mostly
7-3
-------
benthic feeders that generally reside in a local area, they can be used as an
indicator of local contamination problems. In addition, carp have a high lipid
content which may readily accumulate contaminants through the ingestion and
assimilation of contaminated food and possibly through the consumption of
sediment while feeding. It is not possible to estimate how much of the
carcinogenic risk is directly attributable to contaminants in the sediments.
However, the Stage One RAP (Ohio EPA, 1991) indicates that the sediments in
the Ashtabula River AOC are presently the major source of contamination to this
area; thus, one could make the conservative assumption that nearly all of the
human health risk is attributable to the direct and indirect (e.g., food chain
transfer) exposure of fish to contaminants in the sediments.
The carcinogenic risk calculated for the consumption of carp is probably
overly conservative because it is based on the assumed consumption of whole carp
rather than on fillets. These risk estimates should be updated as new data
becomes available, especially for data on contaminant levels in carp fillets.
Although carp are generally regarded as an undesirable "trash" fish by many
anglers, some people do consume them. In addition, food scientists are examining
ways in which carp flesh can be deboned and restructured to form fabricated
seafood products (Stachiw et al., 1988); this is of particular interest to Michigan
firms as a way of exploiting an underutilized fish.
These noncarcinogenic and carcinogenic risk levels are based on raw fish.
Depending on how one prepares and cooks the fish, the risk could be lessened.
For the past 20 years, Mary Zabik and coworkers from Michigan State University
have been investigating whether cooking methods can reduce pesticide and PCB
residues in meat and fish (Smith et al., 1973; Zabik et al., 1979; Zabik et al., 1982;
Stachiw et al., 1988). The results have not been consistent between and within
species of fish. In one instance, different cooking methods did not result in
significant changes in the level of PCBs, DDE, or DDD in cooked carp fillets
(Zabik et al., 1982). In another case, cooking resulted in reductions of TCDD in
restructured, deboned carp fillets (Stachiw et al., 1988). In order to further assess
how cooking techniques may reduce the level of contaminants in fish, the
Michigan Department of Public Health and Michigan State University have just
begun a 2-year investigation (H. Humphrey, Michigan Department of Public
Health, personal communication, 1991). This study will include a variety of sport
fish in the Great Lakes (e.g., chinook and coho salmon) for skin-on and skin-off
fillets. The results of the Michigan study will be useful for future human health
risk assessments for determining better estimates of contaminant levels in cooked
fish. At the present time, the following cooking techniques are recommended for
reducing the risk of hydrophobic organic contaminants in fish: 1) trim fatty areas,
2) puncture or remove skin before cooking so that fats drain away, or 3) deep-fry
trimmed fillets in vegetable oil and discard the oil (Michigan Department of
Natural Resources, 1991).
7-4
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7.3.2 Subsistence Anglers
Subsistence anglers increased their risks to contaminants by nearly an
order of magnitude over recreational anglers in the reasonable maximum exposure
scenario. The noncarcinogenic risks associated with the separate subsistence
consumption of small/large mouth bass and bluegill fillets from the Ashtabula
Harbor were below concern levels (i.e., HI<1) (Tables 7.1 and 7.3). The
noncarcinogenic risk increased for the same fish species when they were obtained
downstream from Fields Brook (HI = 1-2) (Tables 7.2 and 7.4). Whole carp had
the highest Hazard Index from the harbor (HI = 2) (Table 7.5) and from the river
(HI = 20) (Table 7.6). These risk estimates for carp are probably overestimated
since they are based on whole fish instead of fillets. Still, these risk levels are
high enough to warrant continued fish advisories in the Ashtabula River AOC.
For all three fish species, the estimated noncarcinogenic risk was due mostly to
methyl mercury contamination. Methyl mercury has been shown to cause central
nervous system effects at the lowest adverse effect level of 0.003 mg/kg/day (IRIS
data base retrieval for methyl mercury, 1992).
The carcinogenic risk could only be estimated for large mouth bass fillets
(Ashtabula River) and for whole carp (both locations). The estimated cancer risk
resulting from the consumption of bass did not appear to be of concern (i.e., less
than 1 x 10"6) (Table 7.7). The estimated cancer risk was much higher for carp
collected from the Ashtabula Harbor (6 x 10'4) (Table 7.8) and by Fields Brook (3 x
10"3) (Table 7.9). In all cases, the risk was attributable primarily to PCB
contamination. These carcinogenic risk levels represent an upper bound risk and
are probably overestimated for carp since the risk estimates are based on raw,
whole carp. These risk estimates confirm that the greatest human health risk
associated with the consumption of fish resulted from fish inhabiting the most
contaminated area of the Ashtabula River AOC (i.e., by Fields Brook).
7-5
-------
TABLE 7.1.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING SMALL/LARGE MOUTH
BASS FILLETS (TAKEN FROM THE ASHTABULA HARBOR) UNDER TYPICAL,
REASONABLE MAXIMUM (RME), AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
ORGANICS
PCBs (Aroclor 1260)
1,1, 2,2-Tetrachloroethane
retrachloroethene
Trichloroethene
CUMULATIVE NONCARCINOGENIC RISK
Fish Cone.
(mg/kg)
1.5E+00
ND
1.2E-01
ND
1.2E+01
ND
ND
ND
ND
Noncarcinoqenic Intake Hazard Index
(mg/kg-day) (Intake/RfD)
Typical RME Subsistence Typical RME Subsistence
3.8E-05 2.7E-04 1.8E-03 0.0076 0.054 0.37
3.2E-06 2.2E-05 1.5E-04 0.010 0.074 0.51
3.0E-04 2.1E-03 1.5E-02 0.0015 0.011 0.073
0.02 0.1 0.9
7-6
-------
TABLE 7.2.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING LARGE MOUTH BASS
FILLETS (TAKEN FROM THE ASHTABULA RIVER DOWNSTREAM FROM FIELDS
BROOK) UNDER TYPICAL, REASONABLE MAXIMUM (RME), AND SUBSISTENCE
EXPOSURE SCENARIOS
Noncarcinogenic Intake
Chemical
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
ORGANICS
PCBs (Aroclor 1260)
1,1, 2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
CUMULATIVE NONCARCINOGENIC RISK
Fish Cone.
(mg/kg)
1.
1.
1.
6.
1.
1.
2E+00
ND
5E-01
ND
1E+01
ND
8E-03
2E-01
3E-02
Typical
3
A
2
1
3
3
.2E-05
.OE-06
.9E-04
.8E-07
.OE-06
.4E-07
(mg/kg-day)
RME
2
2
2
1
2
2
.2E-04
.8E-05
.OE-03
.3E-06
.IE-OS
.4E-06
Subsistence
1.5E-03
1.9E-04
1.4E-02
8.6E-06
1.5E-04
1.6E-05
Hazard Index
(Intake/RfD)
Typical RME Subsistence
0.0063 0.044 0.30
0.013 0.092 0.63
0.0014 0.010 0.069
0.0003 0.0021 0.015
0.02 0.1 1
7-7
-------
TABLE 7.3.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING BLUEGILL FILLETS
(TAKEN FROM THE ASHTABULA HARBOR) UNDER TYPICAL, REASONABLE MAXIMUM
(RME), AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
ORGANICS
PCBs (Aroclor 1260)
1,1,2, 2-Tetrachloroethane
Tetrachloroetbene
Trichloroetbene
CUMULATIVE NONCARCINOGENIC RISK
Noncarcinoqenic Intake
Fish Cone. (mg/kg-day)
(mg/kg) Typical RME Subsistence
1.6E+00 4.2E-05 3.0E-04 2.0E-03
ND
7.3E-02 1.9E-06 1.4E-05 9.2E-05
ND
1.7E+01 4.3E-04 3.1E-03 2.1E-02
ND
ND
ND
ND
Hazard Index
(Intake/RfD)
Typical RME Subsistence
0.0084 0.059 0.40
0.0064 0.045 0.31
0.0022 0.015 0.10
0.02 0.1 0.8
7-8
-------
TABLE 7.4.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING BLUEGILL FILLETS
(TAKEN FROM THE ASHTABULA RIVER DOWNSTREAM FROM FIELDS BROOK) UNDER
TYPICAL, REASONABLE MAXIMUM (RME), AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Noncarcinoqenic Intake
(mg/kg-day)
Typical RME Subsistence
Hazard Index
(Intake/RfD)
Typical RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
1.4E+00
5.5E-01
1.7E-01
ND
2.3E+01
3.7E-05
1.4E-05
4.5E-06
5.9E-04
6E-04
OE-04
3.1E-05
4.2E-03
1.8E-03
7.OE-04
2.2E-04
2.8E-02
0.0074
0.011
0.015
0.0030
0.052
0.078
0.10
0.021
0.35
0.54
0.72
0.14
ORGANICS
PCBs (Aroclor 1260)
1,1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
ND
ND
ND
ND
CUMULATIVE NONCARCINOGENIC RISK
0.04
0.2
7-9
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TABLE 7.5.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP (TAKEN
FROM THE ASHTABULA HARBOR) UNDER TYPICAL, REASONABLE MAXIMUM (RME),
AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Typical
Noncarcinogenic Intake
(mg/kg-day)
RME
Subsistence
Typical
Hazard Index
(Intake/RfD)
RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
1.5E+00
1.5E+00
ND
ND
8.3E+01
4.0E-05
4.0E-05
2.2E-03
2.8E-04
2.8E-04
1.5E-02
1.9E-03
1.9E-03
l.OE-01
0.0079
0.030
0.011
0.055
0.21
0.077
0.38
1.5
0.53
ORGANICS
PCBs (Aroclor 1260)
1,1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
1.5E-01
5.5E-03
3.0E-02
7.3E-03
4.0E-06
1.4E-07
7.9E-07
1.9E-07
2.8E-05
l.OE-06
5.5E-06
1.4E-06
1.9E-04
7.0E-06
3.8E-05
9.2E-06
0.00008
0.0006
0.0038
CUMULATIVE NONCARCINOGENIC RISK
0.05
0.3
7-10
-------
TABLE 7.6.
NONCARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP (TAKEN
FROM THE ASHTABULA RF7ER DOWNSTREAM FROM FIELDS BROOK) UNDER
TYPICAL, REASONABLE MAXIMUM (RME), AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Typical
Noncarcinoqenic Intake
(mg/kg-day)
RME
Subsistence
Typical
Hazard Index
(Intake/RfD)
RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
2.0E+00
1.7E+01
4.6E-02
3.2E-01
9.6E+01
5.3E-05
4.5E-04
1.2E-06
8.4E-06
2.5E-03
3.7E-04
3.2E-03
8.5E-06
5.9E-05
1.8E-02
2.5E-03
2.2E-02
5.8E-05
4.0E-04
1.2E-01
0.010
0.35
0.0040
0.0017
0.013
0.074
2.4
0.028
0.012
0.089
0.51
17
0.19
0.081
0.61
ORGANICS
PCBs (Aroclor 1260)
1,1,2, 2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
8.1E-01
2.8E-02
2.7E-01
4.0E-02
2.1E-05
7.4E-07
7.1E-06
l.OE-06
1.5E-04
5.2E-06
5.0E-05
7.4E-06
l.OE-03
3.5E-05
3.4E-04
5.1E-05
0.0007 0.0050 0.034
CUMULATIVE NONCARCINOGENIC RISK
0.4
20
7-11
-------
TABLE 7.7.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING LARGE MOUTH BASS
FILLETS (TAKEN FROM THE ASHTABULA RIVER DOWNSTREAM FROM FIELDS
BROOK) UNDER TYPICAL, REASONABLE MAXIMUM (RME), AND SUBSISTENCE
EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Typical
Carcinogenic Intake
(mg/kg-day)
RME
Subsistence
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
1.2E+00
ND
1.5E-01
ND
1.1E+01
4.1E-06
5.1E-07
3.7E-05
9.5E-05
1.2E-05
8.6E-04
6.5E-04
8.1E-05
5.9E-03
ORGANICS
PCBs (Aroclor 1260)
1,1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
ND
6.8E-03
1.2E-01
1.3E-02
2.3E-08
3.9E-07
4.4E-08
5.4E-07
9.2E-06
l.OE-06
3.7E-06
6.3E-05
7.0E-06
4.6E-09
1.1E-07
7.4E-07
CUMULATIVE CARCINOGENIC RISK
5E-09
1E-07
7E-07
7-12
-------
TABLE 7.8.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP (TAKEN FROM
THE ASHTABULA HARBOR) UNDER TYPICAL, REASONABLE MAXIMUM (RME), AND
SUBSISTENCE EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Typical
Carcinogenic Intake
(mg/kg-day)
RME Subsistence
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
1.5E+00
1.5E+00
ND
ND
8.3E+01
5.1E-06
5.1E-06
2.8E-04
1.2E-04
1.2E-04
6.6E-03
8.1E-04
8.1E-04
4.5E-02
ORGANICS
PCBs (Aroclor 1260)
1,1,2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
1.5E-01
5.5E-03
3.0E-02
7.3E-03
5.1E-07
1.9E-08
l.OE-07
2.5E-08
1.2E-05
4.4E-07
2.4E-06
5.8E-07
8.1E-05
3.0E-06
1.6E-05
4.0E-06
3.9E-06
3.7E-09
9.2E-05
8.7E-08
6.3E-04
6.0E-07
CUMULATIVE CARCINOGENIC RISK
4E-06
9E-05
6E-04
7-13
-------
TABLE 7.9.
CARCINOGENIC RISKS ASSOCIATED WITH CONSUMING WHOLE CARP (TAKEN FROM
THE ASHTABULA RIVER DOWNSTREAM FROM FIELDS BROOK) UNDER TYPICAL,
REASONABLE MAXIMUM (RME), AND SUBSISTENCE EXPOSURE SCENARIOS
Chemical
Fish Cone.
(mg/kg)
Carcinoqenic Intake
(mg/kg-day)
Typical RME Subsistence
Lifetime Cancer Risk
(Intake*Slope Factor)
Typical RME Subsistence
METALS
Chromium VI
Copper
Mercury (methyl)
Silver
Zinc
Z.OE-l-00
1.7E+01
4.6E-02
1.1E-06
9.6E+01
6.8E-06
5.8E-05
1.6E-07
1.1E-06
3.3E-04
1.6E-04
1.4E-03
3.6E-06
2.5E-05
7.6E-03
1.1E-03
9.3E-03
2.5E-05
1.7E-04
5.2E-02
ORGANICS
PCBs (Aroclor 1260)
1,1, 2,2-Tetrachloroethane
Tetrachloroethene
Trichloroethene
8.1E-01
2.8E-02
2.7E-01
4.0E-02
2.7E-06
9.5E-08
9.1E-07
1.4E-07
6.4E-05
2.2E-06
2.1E-05
3.2E-06
4.4E-04
1.5E-05
1.5E-04
2.2E-05
2.1E-05
1.9E-08
4.9E-04
4.4E-07
3.4E-03
3.0E-06
CUMULATIVE CARCINOGENIC RISK
2E-05
5E-04
3E-03
7-14
-------
CHAPTERS
CHARACTERIZATION OF QUALITATIVE UNCERTAINTIES
8.1 INTRODUCTION
A number of assumptions and estimated values are used in baseline human
health risk assessments that contribute to the overall level of uncertainty about
the risk estimates. For most environmental risk assessments, the uncertainty of
the risk estimates varies by at least an order of magnitude or greater (USEPA,
1989a). In this chapter, the key site-related variables and assumptions that
contribute the greatest degree of uncertainty will be examined in a qualitative
way.
8.2 QUALITATIVE LIST OF UNCERTAINTIES
8.2.1 Data Compilation and Evaluation
The data compilation and evaluation step is one part of the risk assessment
process where uncertainties arise. These uncertainties are listed below for the
following assumptions and statements.
• The available data for contaminant levels in fish and water
samples collected from the Ashtabula River and Harbor were
representative of the true distribution of contaminants in the
Ashtabula River AOC. A moderate level of uncertainty is probably
associated with this assumption. Additional sampling over a longer
period of time would be needed to look for any temporal or spatial
variability in contaminant levels, and to obtain a more representative
profile of contaminant concentrations in the media of interest.
• Contaminant burdens in fish may decrease depending on how
the fish is prepared and cooked. Contaminant levels may be
reduced 10-70% depending on how the fish is prepared and cooked (H.
Humphrey, Michigan Department of Public Health, personal
communication, 1991). Because of this wide range, the uncertainty
associated with the resulting overestimation of risk is not well
established.
• The selection of a subset of fish by the Ohio EPA for
laboratory analysis was appropriate. The criteria by which fish
were chosen for analysis was not described in the Ashtabula River
Report (WCC, 1991). A low to moderate level of uncertainty is
probably associated with this assumption.
8-1
-------
8.2.2 Exposure Assessment
A number of assumptions were made in the exposure assessment step of
this baseline human health risk assessment.
• An adequate assessment of complete and incomplete exposure
pathways was made. There is a low uncertainty that some
exposure pathways were either not identified or else were incorrectly
classified as a complete or incomplete exposure pathway.
• The exclusion of some complete exposure pathways (i.e.,
dermal exposure to water and sediments) from the exposure
assessment was justifiable because of the low probability that
these pathways would result in significant human health
risks. The uncertainty associated with this assumption is probably
low. The estimated risk from ingesting contaminated water from the
Ashtabula River (near Fields Brook) while swimming (3 events per
year) was very low, and this pathway usually results in a greater risk
than the dermal exposure pathways (for similar exposure
frequencies).
• The complete exposure pathways chosen for the exposure
assessment represent the primary pathways by which people
in the Ashtabula River AOC were exposed to contaminants.
The pathways chosen were based primarily on observed activities and
on available data. A low level of uncertainty is probably associated
with not being able to include these incomplete exposure pathways.
• The assumptions made about exposure frequency and
duration variables, body weight, life expectancy, and
population characteristics were appropriate. Many of these
assumptions (e.g., body weight, life expectancy, exposure frequency)
were based on EPA guidance (USEPA, 1989a,b; 1991a) and probably
have a low to moderate level of uncertainty associated with them. A
similar level of uncertainty may be attributed to professional
judgments about the fraction of fish ingested from contaminated
sources.
8.2.3 Toxicitv Values
The toxicity values (i.e., oral RfDs and oral slope factors) used in this risk
assessment were either verified values obtained from IRIS or interim values
obtained from other sources. RfDs and slope factors are subject to change as the
result of new information and updates of the IRIS data base. In addition,
chemicals will be added to IRIS in the future to expand the data base. Thus, this
risk assessment is "dated" to the toxicity values available at the time it was
8-2
-------
prepared. Listed below are the uncertainties associated with using these toxicity
values.
• R£D values and slope factors have a certain amount of
uncertainty associated with them. Uncertainty and modifying
factors are incorporated into the calculation of RfDs (see Appendix B)
and take into consideration factors such as extrapolating data from
long-term animal studies to humans, etc. In general, RfD values
have an uncertainty range of about one order of magnitude. Since
slope factors represent an estimate of an upper-bound lifetime
probability of an individual developing cancer, these values are
already conservative. Thus, the amount of uncertainty associated
with slope factor values may be minimized.
• A conservative assumption for metal speciation in the
Ashtabula River AOC was made for chromium and mercury
because toxicity values for the total metal form were not
available. Thus, toxicity values for chromium VI and methyl
mercury were used to represent the major forms of these heavy
metals. The use of this more toxic chemical species resulted in a
conservative estimate of risk. A moderate level of uncertainty is
probably associated with this uncertainty.
• Two organic chemicals were excluded from the risk
assessment because their toxicity values have been retracted
from IRIS for further review. The oral slope factors for
tetrachloroethene and trichlorethene have been withdrawn from IRIS.
The exclusion of these chemicals from the carcinogenic risk
assessment was probably minor because the use of the old oral slope
factors resulted in a small proportion of the total risk estimate.
8.2.4 Risk Characterization
The uncertainties associated with the risk characterization step are listed
below.
Exposure intakes and toxicity values will remain the same
over the exposure duration. This assumes that human activities
and contaminant levels will remain the same over the exposure
duration, and that toxicity values will not be updated. A moderate to
high level of uncertainty is probably associated with this assumption
since it does not take into consideration the implementation of
remedial actions or the deposition of cleaner sediments over
contaminated sediments. Furthermore, toxicity values are frequently
updated in the IRIS data base as new information becomes available.
8-3
-------
The level of uncertainty will probably increase with longer exposure
durations.
• Health risks are additive for both noncarcinogenic and
carcinogenic effects. The uncertainty associated with this
assumption is unknown. The toxicity exhibited by a mixture of
chemicals may involve synergistic and antagonistic effects. However,
no guidelines are available to judge the complex interactions a
mixture of contaminants may possess in terms of its potential toxicity
to humans. At the present time, standard risk assessment guidance
assumes that health risks are additive.
8.3 SUMMARY
Based on the information available, a complete description of the level of
uncertainty associated with all of the assumptions and data used in this risk
assessment cannot be made. This baseline human health risk assessment was
based on data and assumptions that, in reality, represent a snapshot in time. One
of the greatest sources of uncertainty in this risk assessment arises from assuming
that estimated risks will remain constant over the exposure duration (i.e., 9 years
for typical exposures and 30 years for reasonable maximum and subsistence
exposures). The overall uncertainty of the risk estimates probably varies by over
an order of magnitude. As additional data are collected from the Ashtabula River
and as additional (or revised) toxicity values are generated, a better estimate of
human health risk can be determined for people living in this area. Thus, updates
of this risk assessment will probably reduce the level of uncertainty associated
with it.
8-4
-------
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Batterman, A.R., P.M. Cook, K.B. Lodge, D.B. Lothenbach, and B.C. Butterworth.
1989. Methodology Used for a Laboratory Determination of Relative
Contributions of Water, Sediment and Food Chain Routes of Uptake for
2,3,7,8-TCDD Bioaccumulation by Lake Trout in Lake Ontario.
Chemosphere. 19:451-458.
Bierman, V.J., Jr. 1990. Equilibrium Partitioning and Biomagnification of
Organic Chemicals in Benthic Animals. Environ. Sci. Technol. 24:1407-
1412.
Borgmann, U. and D.M. Whittle. 1991. Contaminant Concentration Trends in
Lake Ontario Lake Trout (Salvelinus namavcush): 1977 to 1988. J. Great
Lakes Res. 17:368-381.
Bro, K.M. 1989. Setting Priorities for Investigating Chemical Contaminants in
the Great Lakes. Ph.D. thesis. University of Wisconsin-Madison.
Brown, M.P., M.B. Werner, R.J. Sloan, and K.W. Simpson. 1985. Polychlorinated
Biphenyls in the Hudson River. Environ. Sci. Technol. 19:656-661.
CH2M Hill. 1986. Public Comment - Feasibility Study Fields Brook Site.
Sediment Operable Unit, Ashtabula, Ohio. EPA 19.5L46.0, July 3, 1986.
Prepared for U.S. Environmental Protection Agency Hazardous Site Control
Division under EPA Contract No. 68-01-6692.
Connor, M.S. 1984. Fish/Sediment Concentration Ratios for Organic Compounds.
Environ. Sci. Technol. 18:31-35.
Foran, JA. and D. VanderPloeg. 1989. Consumption Advisories for Sport Fish in
the Great Lakes Basin: Jurisdictional Inconsistencies. J. Great Lakes Res.
15:476-485.
Gill, G.A. and K.W. Bruland. 1990. Mercury Speciation in Surface Freshwater
Systems in California and other Areas. Environ. Sci. Technol. 24:1392-
1400.
Henderson, B.E., R.K. Ross, and M.C. Pike. 1991. Toward the Primary
Prevention of Cancer. Science. 254:1131-1138.
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Jaffe, R., E.A. Stemmler, B.D. Eitzer, and R.A. Kites. 1985. Anthropogenic,
Polyhalogenated, Organic Compounds in Sedentary Fish from Lake Huron
and Lake Superior Tributaries and Embayments. J. Great Lakes Res.
11:156-162.
Kononen, D.W. 1989. PCBs and DDT in Saginaw Bay White Suckers.
Chemosphere. 18:2065-2068.
Kuehl, D.W., P.M. Cook, A.R. Batterman, D. Lothenbach, and B.C. Butterworth.
1987. Bioavailability of Polychlorinated Dibenzo-p-dioxins and
Dibenzofurans from Contaminated Wisconsin River Sediment to Carp.
Chemosphere. 16:667-679.
Malins, D.C., B.B. McCain, D.W. Brown, S-L. Chan, M.S. Myers, J.T. Landahl,
P.G. Prohaska, A.J. Friedman, L.D. Rhodes, D.G. Burrows, W.D. Gronlund,
and H.O. Hodgins. 1984. Chemical Pollutants in Sediments and Diseases
of Bottom-dwelling Fish in Puget Sound, Washington. Environ. Sci.
Technol. 18:705-713.
Michigan Department of Natural Resources (MDNR). 1991. Michigan Fishing
Guide. Michigan Department of Natural Resources, Fisheries Division,
Lansing, MI.
Ohio EPA. 1991 (August). Ashtabula River RAP. Stage 1 Draft. Ohio EPA,
Division of Water Quality Planning and Assessment.
Oliver, B.G. and A.J. Niimi. 1988. Trophodynamic Analysis of Polychlorinated
Biphenyl Congeners and other Chlorinated Hydrocarbons in the Lake
Ontario Ecosystem. Environ. Sci. Technol. 22:388-397.
Pizza, J.C. and J.M. O'Connor. 1983. PCB Dynamics in Hudson River Striped
Bass. n. Accumulation from Dietary Sources. Aquatic Toxicol. 3:313-327.
Seelye, J.G., R.J. Hesselberg, and M.J. Mac. 1982. Accumulation by Fish of
Contaminants Released from Dredged Sediments. Environ. Sci. Technol.
16:459-464.
Smith, W.E., K. Funk, and M.E. Zabik. 1973. Effects of Cooking on
Concentrations of PCB and DDT Compounds in Chinook (Qncorhynchus
tshawvtscha) and Coho (O. kisutch) Salmon from Lake Michigan. J. Fish.
Res. Board Can. 30:702-706.
Spigarelli, S.A., M.M. Thommes, and W. Prepejchal. 1983. Thermal and
Metabolic Factors Affecting PCB Uptake by Adult Brown Trout. Environ.
Sci. Technol. 17:88-94.
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Stachiw, N., M.E. Zabik, A.M. Booren, and M.J. Zabik. 1988. Tetrachlorodibenzo-
p-dioxin Residue Reduction through Cooking/Processing of Restructured
Carp Fillets. J. Agric. Food Chem. 36:848-852.
Swackhamer, D.L. and R.A. Kites. 1988. Occurrence and Bioaccumulation of
Organochlorine Compounds in Fishes from Siskiwit Lake, Isle Royale, Lake
Superior. Environ. Sci. Technol. 22: 543-548.
Swain, W.R. 1991. Effects of Organochlorine Chemicals on the Reproductive
Outcome of Humans who Consumed Contaminated Great Lakes Fish: an
Epidemiologic Consideration. J. Toxicol. Environ. Health. 33:587-639.
Thomann, R.V. and J.P. Connolly. 1984. Model of PCB in the Lake Michigan
Lake Trout Food Chain. Environ. Sci. Technol. 18:65-71.
U.S. Army Corps of Engineers. 1988. Ashtabula River and Harbor Suspended
Sediment Movement During Dredging. Prepared in response to Ohio EPA
comments on Final Environmental Impact Statement for dredging
Ashtabula Harbor (1987).
U.S. EPA. 1988a. Risk Management Recommendations for Dioxin Contamination
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U.S. EPA. 1988b. Superfund Exposure Assessment Manual. Office of Remedial
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Weininger, D. 1978. Accumulation of PCBs by Lake Trout in Lake Michigan.
Ph.D. thesis. University of Wisconsin-Madison, Madison, WI.
West, P.C., J.M. Fly, R. Marans, and F. Larkin. 1989. Michigan Sport Anglers
Fish Consumption Survey. University of Michigan School of Natural
Resources, Natural Resource Sociology Research Lab Technical Report #1.
Woodward-Clyde Consultants (WCC). 1991 (March 29). Ashtabula River
Investigation. Draft Report: Ashtabula, Ohio. Prepared for: The Ashtabula
River Group. 86C3609F-510.
Zabik, M.E., P. Hoojjat, and C.M. Weaver. 1979. Polychlorinated Biphenyls,
Dieldrin and DDT in Lake Trout Cooked by Broiling, Roasting or
Microwave. Bull. Environm. Contain. Toxicol. 21:136-143.
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9-4
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APPENDIX A
IMPORTANCE OP OTHER COMPLETE EXPOSURE PATHWAYS IN THE
ASHTABULA RIVER AREA OF CONCERN
The dermal exposure of people to water and sediments in the Ashtabula
River was assumed to be insignificant based on the frequency with which these
exposures would take place and also in comparison to the estimated
noncarcinogenic and carcinogenic risk from ingesting surface water while
swimming in the Ashtabula River. In this appendix, these assumptions and
estimated risk estimates will be described.
Dermal contact with Ashtabula River sediments may occur infrequently
because there are no designated swimming areas along shore where someone could
wade into the water. Another place where dermal contact with sediments may
occur is at the boat ramps when people are putting in or taking out their boats;
however, most people would probably be wearing some kind of foot protection to
shield their feet from rocks, broken glass, etc. People may have dermal contact
with water as their boats travel from the marina areas out to the harbor or Lake
Erie.
Although limited dermal exposures to water and sediment may take place
in the Ashtabula River, it is more difficult to determine the risks from these
pathways than from an ingestion or inhalation pathway. This is because toxicity
values are not developed specifically for dermal sorption, nor are absorption rates
developed well for contaminants. Thus, the estimation of exposure for the dermal
pathway, calculated as an absorbed dose, has a greater amount of uncertainty
associated with it than exposures that are based on an actual intake of
contaminant into the body. Based on dermal exposures calculated for other more
contaminated ARCS sites, dermal exposures to water and sediments in the
Ashtabula River are not likely to result in significant noncarcinogenic and
carcinogenic risks. In addition, a greater risk is likely to be encountered due to
the ingestion of surface water from the Ashtabula River than dermal exposures to
it. This is because of the direct intake of contaminants into the gut versus the
absorption of contaminants (with varying levels of permeability) across the skin
interface.
The human health risk resulting from the ingestion of surface water from
the Ashtabula River (collected at the mouth of Fields Brook) was estimated based
on exposure and risk assessment guidance developed for the EPA Superfund
program (USEPA, 1989a). The noncarcinogenic and carcinogenic intake values
were calculated using the following equation:
A-l
-------
Intake (mg/kg-day) = CW x CR x ET x EF x ED
BWxAT
where:
CW = Chemical concentration in water (mg/L)
CR = Contact rate: used 0.05 L/hr
ET = Exposure time: used 0.5 hr/day (study assumption)
EF = Exposure frequency: used 3 days/year (study assumption)
ED = Exposure duration: used 30 years for a reasonable maximum
exposure scenario
BW = Body Weight: used 70 kg
AT = Averaging Time: ED x 365 days/year for noncarcinogenic risk
(i.e., 1.09 x 104 days) and 70 years x 365 days/year (i.e.,
2.56 x 104 days) for carcinogenic risk
The assumptions incorporated into the above equation were either study
assumptions, where noted, or else were recommended values given in EPA
Superfund Guidance (USEPA, 1989a).
The chemical intake values were incorporated with toxicity estimates to
produce the risk estimates. The estimated noncarcinogenic risk is given in Table
A.I. The Hazard Index was very low (i.e., HI = 0.0003); thus the consumption of
Ashtabula River water during infrequent swimming events appears to pose little
noncarcinogenic risk. The upper-bound carcinogenic risk estimate was also quite
low (i.e., 4 x 1Q-10) (Table A.2). The EPA believes it is prudent public health policy
to consider actions to mitigate or minimize exposures to contaminants when
estimated excess lifetime cancer risks exceed the 10"5 to 10"6 range (USEPA,
1988a). Based on this low carcinogenic risk estimate for the ingestion of surface
water, dermal exposures to water and sediments were assumed to be insignificant.
A-2
-------
TABLE A.I.
NONCARCINOGENIC RISK ASSOCIATED WITH THE INGESTION OF WATER FROM THE
ASHTABULA RIVER DURING INFREQUENT SWIMMING EVENTS
Chemical
METALS
Barium
Copper
Manganese
Zinc
Water
Cone.
(mg/L)
8.77E-02
1.29E-01
3.19E-01
2.03E-02
Noncarc.
Intake
(mg/kg-day)
2.68E-07
3.95E-07
9.77E-07
6.21E-08
Oral RfD
(mg/kg-day)
7.00E-02
1.30E-03
l.OOE-01
2.00E-01
HI
Intake/RfD
3.8E-06
3.0E-04
9.8E-06
3.1E-07
ORGANICS
Acetone
Methylene Chloride
Vinyl Acetate
8.70E-02
3.90E-02
4.60E-01
2.66E-07
1.19E-07
1.41E-06
l.OOE-01
6.00E-02
l.OOE+00
2.7E-06
2.0E-06
1.4E-06
0.0003
A-3
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TABLE A.2.
CARCINOGENIC RISK ASSOCIATED WITH THE INGESTION OF WATER FROM THE
ASHTABULA RIVER DURING INFREQUENT SWIMMING EVENTS
Chemical
METALS
Barium
Copper
Manganese
Zinc
Water
Cone.
(mg/L)
8.77E-02
1.29E-01
3.19E-01
2.03E-02
Carcinogenic
Intake
(mg/kg-day)
1.10E-07
1.62E-07
4.01E-07
2.55E-08
Slope
Factor
l/(mg/kg/day)
Cancer
Risk
ORGANICS
Acetone
Methylene Chloride
Vinyl Acetate
8.70E-02
3.90E-02
4.60E-01
1.09E-07
4.91E-08
5.79E-07
7.50E-03
3.7E-10
4E-10
A-4
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APPENDIX B
HUMAN TOXICITY ESTIMATES FOR CONTAMINANTS PRESENT IN THE
ASHTABULA RIVER AREA OF CONCERN
B.I TOXICITY ASSESSMENT
The toxicity assessment step is an integral part of the human health
baseline risk assessment. This step includes four tasks: 1) gather qualitative and
quantitative toxicity information for substances being evaluated, 2) identify
exposure periods for which toxicity values are necessary, 3) determine toxicity
values (i.e., reference doses (RfDs)) for noncarcinogenic effects, and 4) determine
toxicity values (i.e., slope factors) for carcinogenic effects (USEPA, 1989a). The
EPA has performed the toxicity assessment step for a limited number of chemicals
and these assessments have undergone extensive peer review. Therefore, the
toxicity assessment step of this study involves primarily a compilation of available
toxicity data.
Once a "verified" toxicity value is agreed upon by the EPA's toxicologists, it
is entered into the EPA's Integrated Risk Information System (IRIS) data base;
these values are updated as necessary. IRIS is the primary source of toxicity
information used in baseline risk assessments. The Health Effects Assessment
Summary Tables (HEAST) are the second most current source of toxicity
information and include both verified and interim RfD and slope factor values.
Interim values are used for chemicals that have not yet been approved by the
EPA. Specific EPA workgroups, such as the Carcinogen Risk Assessment
Verification Endeavor (CRAVE) and RfD Workgroups, are another source of
interim toxicity values. If toxicity values are not available in the aforementioned
sources, then interim values from other reports may be used.
This appendix summarizes pertinent toxicity information obtained from
IRIS and other sources for chemicals in the lower 3.2 km of the Ashtabula River
and Harbor. Also included in this appendix are brief descriptions of the most
important toxicity values used to evaluate noncarcinogenic and carcinogenic
effects; these subsections were summarized from the EPA guidance document:
"Risk Assessment Guidance for Superfund. Volume 1. Human Health Evaluation
Manual (Part A)" (USEPA, 1989a).
B.I.I Noncarcinogenic Chronic Toxicitv
The RfD is the toxicity value used most often in evaluating noncarcinogenic
effects. RfDs are based on tile assumption that thresholds exist for certain toxic
effects (e.g., cellular necrosis) but may not exist for other toxic effects (e.g.,
carcinogenicity). The RfD is defined as an estimate of the daily exposure to the
B-l
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human population that is likely to be without an appreciable risk of deleterious
effects during either a portion of the lifetime (i.e., subchronic RfD or "RfD8") or
during the lifetime (i.e., chronic RfD or "RfD"). This toxicity value has an8
uncertainty range of about an order of magnitude and includes exposures to
sensitive subgroups in the population. For each chemical, the RfD is calculated
from the following equation:
RfD - NOAEL or LQAEL
UF X MF
where:
NOAEL = No-Observed-Adverse-Effect-Level
LOAEL = Lowest-Observed-Adverse-Effect-Level
MF = Modifying Factor
UF = Uncertainty Factor
The NOAEL and LOAEL are derived from dose-response experiments. The
NOAEL represents the highest exposure level tested at which no adverse effects
occurred (including the critical toxic effect), whereas the LOAEL represents the
lowest exposure level at which significant adverse effects occurred. Uncertainty
factors usually consist of multiples of ten, with each factor representing a specific
area of uncertainty included in the extrapolation from available data. An
uncertainty factor of ten is usually used to account for variation in the general
population so that sensitive subpopulations are protected. An additional ten-fold
factor is usually applied for each of the following extrapolations: from long-term
animal studies to humans, from a LOAEL to a NOAEL, and when subchronic
studies are used to derive a chronic RfD. A modifying factor (MF), ranging from
>0 to 10, is included as a qualitative assessment of additional uncertainties; the
default value for the MF is one.
Table B-l includes the uncertainty and modifying factors, confidence
classifications, and critical effects of the contaminants examined for this risk
assessment. Uncertainty factors ranged from 3 to 1000, and either a low or
medium level of confidence was given for these RfD values. Better estimates of
oral RfD values are needed to reduce these levels of uncertainty.
B.1.2 Carcmogenicity
Human carcinogenic risks are usually evaluated for a chemical by using its
slope factor (formerly designated as a cancer potency factor) and corresponding
weight-of-evidence classification. These variables were listed in Table 6.2 for the
Ashtabula River chemicals. Slope factors are estimated through the use of
mathematical extrapolation models, most commonly the linearized multistage
model, for estimating the largest possible linear slope (within 95% confidence
limits), at low extrapolated doses, that is consistent with the data. The slope
B-2
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TABLE B-l.
ORAL RfD SUMMARY FOR CHEMICALS LISTED IN IRIS AS
OF 24 DECEMBER 1991
Chemical
UF1
MF2
Confidence
in Oral
RfD
Critical Effects
METALS
Chromium VI
Copper
Mercury, methyl
Silver
Zinc
ORGANICS
Tetrachloroethene
500 1 Low
Under Review
10 1 Medium
3 1 Low
Under Review
1000 1 Medium
No effects reported
Central nervous system effects in humans
Argyria (bluish-gray discoloration of the
skin) in humans
Hepatotoxicity in mice, weight gain in
rats
UF = Uncertainty Factor
MF * Modifying Factor
factor is characterized as an upper-bound estimate so that the true risk to
humans, while not identifiable, is not likely to exceed the upper-bound estimate.
The weight of evidence classification for a particular chemical is determined
by the EPA's Human Health Assessment Group (HHAG). Chemicals are placed
into one of five groups according to the weight of evidence from epidemiological
studies and animal studies. These groups are designated by the letters A, B, C, D,
and E which represent the level of carcinogenicity to humans (see Table 6.1).
Quantitative carcinogenic risk assessments are performed for chemicals in Groups
A and B, and on a case-by-case basis for chemicals in Group C.
B.2 UNCERTAINTIES
A number of uncertainties are involved with using toxicity values for
estimating noncarcinogenic and carcinogenic risks. Some of these qualitative
uncertainties are listed below:
• Using dose-response information from healthy animal or human
populations to predict effects that may occur in the general
population, including susceptible subpopulations (e.g., elderly,
children),
• Using dose-response information from animal studies to predict
effects that may occur in human populations,
• Using NOAELs derived from short-term animal studies to predict
effects that may occur in humans during long-term exposures,
• Using dose-response information from effects observed at high doses
to predict the adverse health effects that may occur following
exposure of humans to low levels of the chemical in the environment,
and
B-3
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Using a toxicity value derived from exposure to a particular chemical
mixture (e.g., Aroclor 1260) to represent the level of toxicity for other
similar chemical mixtures (e.g., Aroclor 1242, 1248, and 1254).
B-4
*U-S. GOVERNMENT PRINTING OFFICE 1993-747-249
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